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Tuesday, July 31, 2007

Evidence of anti-obesity effects of the pomegranate leaf extract in high-fat diet induced obese mice

OBJECTIVE: To investigate the anti-obesity effects of the pomegranate leaf extract (PLE) in a mouse model of high-fat diet induced obesity and hyperlipidemia. DESIGN: For the anti-obesity experiment, male and female ICR mice were fed with a high-fat diet to induce obesity. When the weight of the high-fat diet group was 20% higher than the normal diet group, the animals were treated with 400 or 800 mg/kg/day of PLE for 5 weeks. Body weight and daily food intake were measured regularly during the experimental period. The various adipose pads were weighed and serum total cholesterol (TC), triglyceride (TG), glucose and high-density lipoprotein cholesterol (HDL-C) were measured after 5 weeks, treatment with PLE. In the fat absorption experiment, both the normal and obese mice were given 0.5 ml lipid emulsion and PLE at a dose of 800 mg/kg at the same time. Serial serum TG levels were measured at times 1, 2, 3, 4 and 6 h after the treatment. TGs in fecal excretions were measured after the mice were orally given a lipid emulsion. Effects of PLE and its isolated compounds (ellagic acid and tannic acid) on pancreatic lipase activity were examined in vitro. RESULTS: The PLE-treated groups showed a significant decrease in body weight, energy intake and various adipose pad weight percents and serum, TC, TG, glucose levels and TC/HDL-C ratio after 5 weeks treatment. Furthermore, PLE significantly attenuated the raising of the serum TG level and inhibited the intestinal fat absorption in mice given a fat emulsion orally. PLE showed a significant difference in decreasing the appetite of obese mice fed a high-fat diet, but showed no effect in mice fed a normal diet. CONCLUSION: PLE can inhibit the development of obesity and hyperlipidemia in high-fat diet induced obese mice. The effects appear to be partly mediated by inhibiting the pancreatic lipase activity and suppressing energy intake. PLE may be a novel appetite suppressant that only affects obesity owing to a high-fat diet.


PMID: 17299386 [PubMed - in process]


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Int J Obes (Lond). 2007 Jun;31(6):1023-9

Authors: Lei F, Zhang XN, Wang W, Xing DM, Xie WD, Su H, Du LJ

Punica granatum (pomegranate) extract is active against dental plaque

In the present work, we studied the effect of the hydroalcoholic extract (HAE) from Punica granatum (pomegranate) fruits on dental plaque microorganisms.

The study was conducted on 60 healthy patients (33 females and 27 males, with age ranging from 9 to 25 years) using fixed orthodontic appliances, and randomly distributed into 3 groups of 20 patients each.

The first group (control) used distilled water, while the second and third groups used chlorhexidine (standard) and HAE as mouth-rinses, respectively. The dental plaque material was collected from each patient, before and after a 1-min mouth-rinse with 15 ml of either distilled water, chlorhexidine or HAE. In both dental plaque collections, the material was removed from patients without oral hygiene, for 24 h (no tooth brushing). Dental plaque samples were diluted in phosphate buffered saline (PBS) plated on Mueller-Hinton agar, and incubated for 48 h, at 37 degrees C.

Results, expressed as the number of colony forming units per milliliter (CFU/mL), show that the HAE was very effective against dental plaque microorganisms, decreasing the CFU/ml by 84% (CFU x 10(5)), before mouth-rinse: 154.0 +/- 41.18; after mouthrinse: 25.4 +/- 7.76). While similar values were observed with chlorhexidine, used as standard and positive control (79% inhibition), only an 11% inhibition of CFU/ml was demonstrated in the distilled water group, negative control (CFU x 10(5)), before mouth-rinse: chlorhexidine, 208.7 +/- 58.81 and distilled water, 81.1 +/- 10.12; after mouth-rinse: chlorhexidine, 44.0 +/- 15.85 and distilled water, 71.9 +/- 8.68). The HAE presented also an antibacterial activity against selected microorganisms, and may be a possible alternative for the treatment of dental plaque bacteria.


PMID: 17182487 [PubMed - indexed for MEDLINE]



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J Herb Pharmacother. 2006;6(2):79-92

Authors: Menezes SM, Cordeiro LN, Viana GS


Evaluation of antioxidant activity and preventing DNA damage effect of pomegranate extracts by chemiluminescence method

The antioxidant activities of three parts (peel, juice, and seed) and extracts of three pomegranate varieties in China were investigated by using a chemiluminescence (CL) method in vitro.


The scavenging ability of pomegranate extracts (PEs) on superoxide anion, hydroxide radical, and hydrogen peroxide was determined by the pyrogallol-luminol system, the CuSO4-Phen-Vc-H2O2 system, and the luminol-H2O2 system, respectively. DNA damage preventing the effect of PE was determined by the CuSO4-Phen-Vc-H2O2-DNA CL system.

The results showed that the peel extract of red pomegranate had the best effect on the scavenging ability of superoxide anion because its IC50 value (4.01 +/- 0.09 microg/mL) was the lowest in all PEs.

The seed extract of white pomegranate could scavenge hydroxide radical most effectively of the nine extracts (the IC50 value was 1.69 +/- 0.03 microg/mL).

The peel extract of white pomegranate had the best scavenging ability on hydrogen peroxide, which had the lowest IC50 value (0.032 +/- 0.003 microg/mL) in the nine extracts.

The seed extract of white pomegranate (the IC50 value was 3.67 +/- 0.03 microg/mL) was the most powerful on the DNA damage-preventing effect in all of the PEs.

Also, the statistical analysis indicated that there were significant differences (at P < 0.05) among the extracts of the different varieties and parts in each system.


PMID: 17381116 [PubMed - indexed for MEDLINE]



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J Agric Food Chem. 2007 Apr 18;55(8):3134-40

Authors: Guo S, Deng Q, Xiao J, Xie B, Sun Z


Effect of pomegranate (Punica granatum) juice intake on hepatic oxidative stress

Pomegranate juice (PJ) possesses a high antioxidant activity, which has been related to beneficial health properties. However, in vivo confirmation and characterization of these effects on biological systems are lacking and needed. This study was performed in order to investigate the effect of prolonged PJ ingestion on general oxidation status.

For this purpose, mice ingested PJ (or water in control group) during four weeks, after which damage to lipids, proteins and DNA were evaluated as oxidative cell biomarkers. Levels of hepatic glutathione and the activities and expression of enzymes involved in its metabolism were determined. Catalase and SOD activities were quantified as these enzymes have a crucial role in antioxidant defence.

Protection against protein and DNA oxidation was found in PJ group. There was also a significant decrease in GSH and GSSG, without change in the GSH/GSSG ratio. All studied enzymatic activities (GPx, GST, GR, SOD and catalase) were found to be decreased by PJ treatment. Additionally, RT-PCR results showed that GST and GS transcription were also decreased in this group.


These results are compatible with a protective effect of PJ against systemic oxidative stress in mice.


PMID: 17514376 [PubMed - in process]



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Eur J Nutr. 2007 Aug;46(5):271-8

Authors: Faria A, Monteiro R, Mateus N, Azevedo I, Calhau C


Inhibition of UVB-mediated Oxidative Stress and Markers of Photoaging in Immortalized HaCaT Keratinocytes by Pomegranate Polyphenol Extract POMx.

In recent years there has been an increase in use of botanicals with antioxidant properties as skin photoprotective agents. Pomegranate (Punica granatum L.) fruit possesses strong antioxidant and antiinflammatory properties. Recently, we have shown that pomegranate-derived products rich in anthocyanidins and ellagitannins inhibit UVB-mediated activation of nuclear factor kappa B and modulate UVA-mediated cell proliferation pathways in normal human epidermal keratinocytes. In this study, we evaluated the effect of polyphenol-rich pomegranate fruit extract (POMx) on UVB-induced oxidative stress and photoaging in human immortalized HaCaT keratinocytes.


Our data show that pretreatment of HaCaT cells with POMx (10-40 mug mL(-1)) inhibited UVB (15-30 mJ cm(-2))-mediated (1) decrease in cell viability, (2) decrease in intracellular glutathione content and (3) increase in lipid peroxidation. Employing immunoblot analysis we found that pretreatment of HaCaT cells with POMx inhibited UVB-induced (1) upregulation of MMP-1, -2, -7 and -9, (2) decrease in TIMP-1, (3) phosphorylation of MAPKs and (iv) phosphorylation of c-jun, whereas no effect was observed on UVB-induced c-fos protein levels.


These results suggest that POMx protects HaCaT cells against UVB-induced oxidative stress and markers of photoaging and could be a useful supplement in skin care products.


PMID: 17645659 [PubMed - in process]



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Photochem Photobiol. 2007 Jul-Aug;83(4):882-8

Authors: Zaid MA, Afaq F, Syed DN, Dreher M, Mukhtar H


Pomegranate Wine Has Greater Protection Capacity Than Red Wine on Low-Density Lipoprotein Oxidation.

Although there is a large body of evidence on the main role of red wine in protection of low-density lipoprotein (LDL) against oxidation, there are few data on the role of pomegranate juice, which has high phenolic content. We conducted this study considering the possible importance of pomegranate wine as an antioxidant and in order to make a comparison between red and pomegranate wines.

The phenol levels of pomegranate and red wines (4,850 mg/L gallic acid equivalents and 815 mg/L gallic acid equivalents, respectively) were in accordance with their total antioxidant activity (39.5% and 33.7%, respectively).

Both wines decreased LDL-diene levels following a 30-minute incubation period compared with controls (145 +/- 3.2 mumol/mg of LDL protein). However, pure pomegranate wine demonstrated a greater antioxidant effect (P < .01) on diene level (110 +/- 4.6 mumol/mg of LDL protein) than pure red wine (124 +/- 3.2 mumol/mg of LDL protein).


In conclusion, we suggest that pomegranate wine has potential protective effects toward LDL oxidation, and it may be a dietary choice for people who prefer fruit wines.


PMID: 17651077 [PubMed - as supplied by publisher]



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J Med Food. 2007 Jun;10(2):371-374

Authors: Sezer ED, Akçay YD, Ilanbey B, Yıldırım HK, Sözmen EY


Antioxidant, antimalarial and antimicrobial activities of tannin-rich fractions, ellagitannins and phenolic acids from Punica granatum L.

The Punica granatum L. (pomegranate) by-product POMx was partitioned between water, EtOAc and n-BuOH, and the EtOAc and n-BuOH extracts were purified by XAD-16 and Sephadex LH-20 column chromatography to afford ellagic acid (1), gallagic acid (2), punicalins (3), and punicalagins (4). Compounds 1 - 4 and the mixture of tannin fractions (XAD-16 eluates) were evaluated for antioxidant, antiplasmodial, and antimicrobial activities in cell-based assays.

The mixture of tannins (TPT), XAD-EtOAc, XAD-H2O, XAD-PJ and XAD-BuOH, exhibited IC50 values against reactive oxygen species (ROS) generation at 0.8 - 19 microg/mL.

Compounds 1 - 4 showed IC50 values of 1.1, 3.2, 2.3 and 1.4 microM, respectively, against ROS generation and no toxicity up to 31.25 microg/mL against HL-60 cells.

Gallagic acid (2) and punicalagins (4) exhibited antiplasmodial activity against Plasmodium falciparum D6 and W2 clones with IC50 values of 10.9, 10.6, 7.5 and 8.8 microM, respectively.

Fractions XAD-EtOAc, XAD-BuOH, XAD-H2O and XAD-PJ compounds 1 - 4 revealed antimicrobial activity when assayed against Escherichia coli, Pseudomonas aeruginosa, Candida albicans, Cryptococcus neoformans, methicillin-resistant Staphylococcus aureus (MRSA), Aspergillus fumigatus and Mycobacterium intracellulare.

Compounds 2 and 4 showed activity against P. aeruginosa, C. neoformans, and MRSA.

This is the first report on the antioxidant, antiplasmodial and antimicrobial activities of POMx isolates, including structure-activity relationships (SAR) of the free radical inhibition activity of compounds 1 - 4.


Our results suggest a beneficial effect from the daily intake of POMx and pomegranate juice (PJ) as dietary supplements to augment the human immune system's antioxidant, antimalarial and antimicrobial capacities.


PMID: 17566148 [PubMed - in process]



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Planta Med. 2007 May;73(5):461-7

Authors: Reddy MK, Gupta SK, Jacob MR, Khan SI, Ferreira D


The Ultimate No-Weight Workout

Use your own body weight to burn fat for this 8-minute workout


Sometimes, you can't get to the gym or even access the workout gear you have stashed in your basement. Maybe you're stuck in some godforsaken Motel 6. Maybe you're trapped at your in-laws' house. Maybe the Feds discovered you gave stock advice to Martha Stewart.

Well, that's still no excuse. This full-body routine requires no equipment and only 8 minutes of your time. Perform each exercise below for 30 seconds. Do one move after another without rest and repeat the sequence without rest for a total of four times, if you can.

The intensity of this workout conditions your muscular and cardiovascular systems, helps improve flexibility, and melts fat. You'll burn hundreds of calories.

Jumping Jack. Just like grade school. Start with your hands on your hips and your feet together. Raise your hands out to your sides and up overhead as you move your feet out to the sides. Then bring your feet back together and lower your hands to your sides.

Split Hop. Stand with your hands on your hips and your feet together. Move your left foot 6 inches forward and your right foot 6 inches back. Now jump up and switch leg positions so that your right foot is forward.

Squat Thrust with Pushup. Stand with your arms at your sides. Bend your knees and lower your hands to the floor. Kick your legs behind you so that you're in a Pushup position. Now do a Pushup. Thrust your knees to your chest so that your feet are back underneath you and stand back up.

Squeeze in a Workout

A new circuit workout you can do in less than 20 Minutes

Try to squeeze in this 15-minute full-body workout from Mark Philippi, C.S.C.S., the strength coach at the University of Nevada at Las Vegas. The benefit: It hits multiple body parts with just one weight plate. At home, try a rock or one of the concrete blocks that's holding up your neighbor's car. Do two or three sets of 10 repetitions of each move.

* Stiff-legged deadlift curl and press

Works lower back, hamstrings, shoulders, biceps, and triceps

Hold the weight at waist level, with your legs slightly bent. Lower the weight by bending at your waist; keep your back straight. Return to the starting position. Curl the weight to your chest, then press it above your head. Finish in the starting position.




* Bench-press pullover

Works shoulders and chest

Lie faceup on a bench and grasp the sides of the weight plate. Press the weight to arm's length. Keep your arms extended and lower the weight behind your head until it's in line with your body. Raise the plate to position A again, then lower it back to your chest.

* Front-raise plate rotation

Works shoulders and abdominals Start in the same position as for the stiff-legged deadlift curl and press. Raise the weight to eye level by extending your arms. Slowly turn your head and torso 90 degrees to the left. Now reverse the movement and twist 180 degrees to the right. Turn back so that you're facing straight ahead again.


Stretch for More Strength

Start your workout with this 3-minute flex and you'll build muscle quicker


Can you touch your toes? If you fail this simple test (done the proper way, with legs straight), you've discovered a major flaw in your physique. That's because poor flexibility in this movement inhibits your ability to build muscle and makes you more susceptible to injuries, especially those involving your lower back. But don't worry: You can loosen up in just 3 minutes. So start the clock. Your physical therapy begins now.


Flexibility 101

If you fall short of touching your toes, as most guys do, you may think that tight hamstrings are the culprit. After all, that's probably where you feel the stretch most. But the problem could be elsewhere on the back side of your body.

You see, most men tend to think of their muscles in specific groups, such as "biceps" and "hamstrings." But the reality is that a thin film of connective tissue called fascia surrounds every bone, organ, and muscle in your body like a big sheet of plastic wrap. The fascia unites seemingly separate muscle groups, causing them to function together.

One of the best examples of this is the "superficial back line," a chain of fascia-linked muscles that run from the top of your head, down your back, and all the way to your toes. The fascia ties these muscles together in such a way that if one muscle is stiff, it can limit movement at any joint up or down the chain. So if you can't touch your toes, don't necessarily blame your hamstrings. The limiting factor could be the muscles of your lower back, in your calves, or even on the bottom of your feet.

Here's why this matters: Stiffness in your superficial back line prevents you from working your lower-body muscles through their entire range of motion--for instance, during a squat or a lunge. It also leads to poor lower-back posture when you're performing these movements. All of this results in a less-effective workout and a higher risk of injury. Eliminate these problems with the four-step plan that follows.



Touch Your Toes in 4 Easy Steps

Try this 3-minute flexibility plan. It's designed to diagnose and loosen your tight spots with simple exercises that you can perform at the gym, at home, or even in the office.


1. Loosen Your Back

The Erector spinae are back muscles that run from the top of your spine down to your tailbone. Stiffness of this muscle group limits the degree to which you can bend your spine and torso.

The Exercise: The Camel-Cat

How to do it: Get down on all fours. Your hands should be directly below your shoulders, and your knees directly below your hips. To create the hump-of-a-camel position, round your back by pushing it upward. Pause for one count, then push your lower back toward the floor to create the arched position of a cat. That's one repetition. After 10 repetitions, try touching your toes. No luck? Move on to Step 2.




2. Loosen Your Hips

This exercise stretches your hip muscles--the glutes and hamstrings--while removing tension from your calves, the next link in the chain.

The Exercise: Hip Hinge with heels elevated

How to do it: Place your heels on a 25-pound weight plate or a 2x4. Maintaining the natural curve in your lower back, bend forward at your hips and reach for your toes. Pause for one count, and then raise your torso back to the start. Do 10 reps, step off the weight plate, and retest yourself. Still reaching in vain? Go to Step 3.




3. Loosen Your Calves

By tweaking the exercise in Step 2, you'll move the tension from your hips to your Achilles tendons and gastrocnemii, or calf muscles. This stretch often produces the most dramatic results.

The Exercise: Hip Hinge with toes elevated

How to do it: Place the balls of your feet on a 25-pound weight plate or a 2x4, and perform the same movement as in Step 2, again completing 10 repetitions. Then try touching your toes again. If you're still not there, head to Step 4.




4. Loosen Your Soles

Most people don't realize that they have muscles on the bottom of their feet. They're called Toe Flexors, and they influence the flexibility of your entire lower body. Prepare to be amazed.

The Exercise: Tennis-ball foot roll

How to do it: While standing, roll the bottom of your bare foot over a tennis ball. Work your entire sole over the ball for 60 seconds, and repeat with your other foot.

Now try to touch your toes one last time. If you haven't found success, go through the routine once more. Note that the steps in which you achieve the most improvement indicate your tightest muscles. These are the muscles you need to focus on.




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By: Bill Hartman, P.T., C.S.C.S., Photo Illustrations by: Christian Hogue

Saturday, July 28, 2007

Inhibitory effect of fermented milk on delayed-onset muscle damage after exercise

Milk fermented with a starter containing Lactobacillus helveticus and Saccharomyces cerevisiae is drunk on a daily basis by many people in Japan and has several beneficial effects. We studied the influence of this fermented milk product on muscle damage after prolonged exercise in rats.

Wistar rats were divided into four groups: rested controls, rested rats given fermented milk diet, exercised rats and exercised rats given fermented milk diet. After 3 weeks of acclimatization, both exercise groups were made to run on a treadmill at 26 m/min for 60 min.
Exercise increased the serum creatine kinase level, as well as myeloperoxidase activity and the level of thiobarbituric-acid-reactive substances in the gastrocnemius muscle after 24 h. These changes were ameliorated by intake of fermented milk. An increase of CINC-1 was also ameliorated by fermented milk. Furthermore, milk diet increased the mRNA and protein levels of protective proteins such as antioxidants and chaperone proteins.

These results indicate that fermented milk can ameliorate delayed-onset muscle damage after prolonged exercise, which is associated with an increased antioxidant capacity of muscles.


PMID: 16781862 [PubMed - indexed for MEDLINE]



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J Nutr Biochem. 2007 Feb;18(2):140-5

Authors: Aoi W, Naito Y, Nakamura T, Akagiri S, Masuyama A, Takano T, Mizushima K, Yoshikawa T


Anti-inflammatory metabolite production in the gut from the consumption of probiotic yogurt containing Bifidobacterium animalis subsp. lactis LKM512

There is little evidence for a relationship between probiotic metabolites and host cytokine production. We investigated in the present study the possibility that anti-inflammatory metabolites can be produced in the gut by LKM512 yogurt consumption by using murine macrophage-like J774.1 cells and extracts prepared from the feces of elderly volunteers.

These volunteers' acute inflammation had been inhibited by LKM512 yogurt consumption in a previous test. The tumor necrosis factor (TNF)-alpha production elicited in J774.1 cells stimulated by lipopolysaccharide (LPS) and in the fecal extracts obtained during the period of

LKM512 yogurt consumption was significantly decreased (p<0.05) than the pre-consumption baseline level. These findings and previous data enable us to conclude that intestinal bacterial metabolites produced by LKM512 yogurt consumption contributed to suppressing the inflammatory cytokine produced by macrophages and that one of the anti-inflammatory metabolites in the fecal extracts was likely to have been a polyamine.


PMID: 16794305 [PubMed - indexed for MEDLINE]



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Biosci Biotechnol Biochem. 2006 Jun;70(6):1287-92

Authors: Matsumoto M, Benno Y


Influence of daily consumption of probiotic and conventional yoghurt on the plasma lipid profile in young healthy women

BACKGROUND

A number of studies have found conflicting results concerning the modulation of plasma lipids induced by probiotics. Therefore, the aim of this study was to verify and compare the effects of probiotic and conventional yoghurt on the plasma lipid profile of normocholesterolemic women.


METHODS

In this study, female volunteers consumed 100 g/day of probiotic (n = 17) or conventional yoghurt (n = 16) for 2 weeks (T1-T2) and 200 g/day for further 2 weeks (T2-T3). A washout phase lasting 2 weeks followed (T4). Total and HDL cholesterol and triglycerides were determined by enzymatic methods; LDL cholesterol was calculated using the Friedewald formula.


RESULTS

The average concentration of total cholesterol was consistent throughout the whole study in the control group, but decreased significantly (p < 0.01) in the probiotic group consuming 200 g yoghurt/day (T2-T3). During the period of daily yoghurt intake (T1-T3) the mean HDL cholesterol level increased significantly (p < 0.05) in the probiotic group, resulting in a significant (p < 0.05) improvement of the total/HDL cholesterol ratio. The significant (p < 0.01) reduction of the average plasma LDL cholesterol values found in this period (T1-T3) in the probiotic and the control groups was associated with a significant (p < 0.05) improvement of the LDL/HDL cholesterol ratios in both tested groups.


CONCLUSION

Although several lipid parameters changed during the study in both the probiotic and the control group, no significant differences between the groups were observed. Therefore, it can be concluded that the regular consumption of both probiotic and conventional yoghurt for 4 weeks had a positive effect on the lipid profile in plasma of healthy women.


PMID: 16816529 [PubMed - indexed for MEDLINE]



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Ann Nutr Metab. 2006;50(4):387-93

Authors: Fabian E, Elmadfa I


Survival of yogurt bacteria in the human gut

Whether Lactobacillus delbrueckii subsp. bulgaricus and Streptococcus thermophilus can be recovered after passage through the human gut was tested by feeding 20 healthy volunteers commercial yogurt.


Yogurt bacteria were found in human feces, suggesting that they can survive transit in the gastrointestinal tract.


PMID: 16820518 [PubMed - indexed for MEDLINE]



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Appl Environ Microbiol. 2006 Jul;72(7):5113-7

Authors: Elli M, Callegari ML, Ferrari S, Bessi E, Cattivelli D, Soldi S, Morelli L, Goupil Feuillerat N, Antoine JM


Assimilation (in vitro) of cholesterol by yogurt bacteria

A considerable variation is noticed between the different species studied and even between the strains of the same species, in the assimilation of cholesterol in synthetic media, in presence of different concentrations of bile salts and under anaerobiosis conditions.

The obtained results show that certain strains of Streptococcus thermophilus and Lactobacillus bulgaricus resist bile salts and assimilate appreciable cholesterol quantities in their presence. The study of associations shows that only strains assimilating cholesterol in a pure state remain active when they are put in associations, but there is no additional effect.

However, the symbiotic effect between Streptococcus thermophilus and Lactobacillus bulgaricus of yogurt, with regard to bile salts, is confirmed.

The lactic fermenters of yogurt (Y2) reduce the levels of total cholesterol, HDL-cholesterol and LDL-cholesterol, in a well-balanced way. In all cases, the assimilated quantity of HDL-cholesterol is lower than that of LDL-cholesterol. Moreover, yogurt Y2 keeps a significant number of bacteria, superior to 10(8) cells ml(-1), and has a good taste 10 days after its production.


PMID: 16841872 [PubMed - indexed for MEDLINE]


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Ann Agric Environ Med. 2006;13(1):49-53

Authors: Dilmi-Bouras A


Evaluation of yogurt effect on acute diarrhea in 6-24-month-old hospitalized infants

Yogurt helps in treatment and prevention of diarrhea.

The aim of this study was to determine the efficacy of consumption of local factory yogurt, which is made with pasteurized milk, on moderately dehydrated hospitalized infants aged 6-24 months with acute non-bloody and non-mucoid diarrhea.

Eighty moderately dehydrated breast-feeding children aged between 6-24 months with acute non-bloody and non-mucoid diarrhea for fewer than four days were included in the study. Patients were randomly separated into two groups according to their treatment. Infants in the case group received at least 15 ml/kg/day of pasteurized cow milk yogurt orally plus routine hospital treatment. Infants in the control group received routine hospital treatment as in the case group. Weight gains, period of hospitalization, and reduction in diarrhea frequency during hospitalization period of the two groups were compared.

Mean duration of hospitalization (days), weight gain, and reduction in diarrhea frequency were 2.7 +/- 0.91 vs 3.1 +/- 0.74 days, 435 +/- 89.20 vs 383 +/- 98.9 g, and 4.30 +/- 1.74 vs 3.60 +/- 1.23 times for case and control groups, respectively. Significant differences were observed in mean hospitalization days (p=0.035), reduction in diarrhea frequency (p=0.049) and weight gain (p=0.017).

This study recommends universal use of yogurt in acute non-bloody diarrhea.


PMID: 16848109 [PubMed - indexed for MEDLINE]



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Turk J Pediatr. 2006 Apr-Jun;48(2):115-8

Authors: Pashapour N, Iou SG


Kefir: a symbiotic yeasts-bacteria community with alleged healthy capabilities

Kefir is a fermented milk beverage. The milk fermentation is achieved by the of kefir grains, a cluster of microorganisms held together by a polysaccharide matrix named kefiran. Kefir grains are an example of symbiosis between yeast and bacteria. They have been used over years to produce kefir, a fermented beverage that is consumed all over the world, although its origin is Caucasian. A vast variety of different species of organisms forming the kefir grains, comprising yeast and bacteria, have been isolated and identified. Kefir is a probiotic food. Probiotics have shown to be beneficial to health, being presently of great interest to the food industry. Kefir has been accredited with antibacterial, antifungal and antitumoural activities among other beneficial attributes. This review includes a critical revision of the microbiological composition of kefir along with its beneficial properties to human health.

PMID: 16854180 [PubMed - indexed for MEDLINE]



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Rev Iberoam Micol. 2006 Jun;23(2):67-74

Authors: Lopitz-Otsoa F, Rementeria A, Elguezabal N, Garaizar J


Dietary deprivation of fermented foods causes a fall in innate immune response. Lactic acid bacteria can counteract the immunological effect of this deprivation

Extrinsic factors such as maternal microbiota, bacterial load of the environment, diet and medication modulate the intestinal microbiota. Maturation and function of the immune system is influenced by established gut microbiota. In this work we describe the immunological effects of the dietary deprivation of fermented foods of healthy volunteers.

Significant decreases in faecal lactobacillus and total aerobes counts and concentration of short chain fatty acids were observed following deprivation of fermented food of the normal diet. Moreover, a decrease in phagocytic activity in leukocytes was observed after two weeks of restricted diet.

Therefore, the dietary deprivation of fermented foods could induce a decrease in innate immune response that might affect the capacity to respond against infections.

The ingestion of a probiotic product containing the strains Lactobacillus gasseri CECT5714 and Lactobacillus coryniformis CECT5711 or a standard yogurt containing a conventional starter Lactobacillus delbrueckii sp. bulgaricus counteracted the fall in the immune response, although the probiotic product was more effective than the standard yogurt.


PMID: 16987435 [PubMed - indexed for MEDLINE]



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J Dairy Res. 2006 Nov;73(4):492-8

Authors: Olivares M, Paz Díaz-Ropero M, Gómez N, Sierra S, Lara-Villoslada F, Martín R, Miguel Rodríguez J, Xaus J


Improvement of cholesterol levels and reduction of cardiovascular risk via the consumption of phytosterols

Hypercholesterolaemia is one of the main factors contributing to the appearance and progression of CVD, which is the main cause of death in the adult population of industrialized societies. By 2020, projections suggest that it will continue to hold first place, by then causing 37 % of all deaths.

Therapeutic life-style changes to reduce cardiovascular risk include dietary modifications, such as the inclusion of phytosterols or plant sterols (known since the 1950s to reduce cholesterol levels). These help prevent the absorption of cholesterol and thus condition a reduction in total cholesterol and LDL-cholesterol levels, and ultimately in cardiovascular mortality.

The fat-soluble nature of these sterols rendered margarine one of the best vehicles by which to supply them in the diet. Indeed, margarine was the first food to contain cholesterol-reducing phytosterols to be approved by the EU (in agreement with its regulations on new foods and food ingredients, 258/97/CE).

Presently, phytosterols can be emulsified with lecithin and thus delivered in non-fat or low-fat foods and beverages. Margarine and dairy products (yoghurt and milk) enriched in phytosterols have proved better at lowering total cholesterol and LDL-cholesterol levels than have enriched cereals and their derivatives, although all can be of help, depending on the characteristics of each subject.

The reduction in carotenoid bioavailability caused by sterols is minimized by increasing fruit and vegetable consumption. Individuals who habitually consume phytosterols should also follow traditional advice such as eating less dietary fat and increasing their physical activity.

Phytosterols have been shown to be safe and effective in lowering cholesterol levels in many rigorous studies. In few areas of nutrition is there such consensus. Diet professionals should feel comfortable in prescribing phytosterols/stanols for the treatment of hypercholesterolaemia. They are safe whether taken alone or in combination with cholesterol-reducing drugs, such as statins and fibrates. Reinforcement counselling is essential, as therapy is effective only if compliance is good.


PMID: 16923260 [PubMed - indexed for MEDLINE]



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Br J Nutr. 2006 Aug;96 Suppl 1:S89-93

Authors: Ortega RM, Palencia A, López-Sobaler AM


Effect of skim milk and dahi (yogurt) on blood glucose, insulin, and lipid profile in rats fed with high fructose diet

In the present study, the effect of skim milk and the fermented milk product named dahi (yogurt) on plasma glucose, insulin, and lipid levels as well as on liver glycogen and lipid contents in rats fed with high fructose diet has been investigated.

Rats were fed with high fructose diet (21%) supplemented with skim milk, dahi (10 g/day each), or no milk product (control group) for 6 weeks.

After 6 weeks of high fructose diet administration, the plasma glucose became significantly higher in control animals (246 mg/dL), whereas it was lower in skim milk (178 mg/dL)- and dahi (143 mg/dL)-fed rats.

The glucose tolerance became impaired at the third week of feeding of high fructose diet in control animals, whereas in skim milk- and dahi-fed animals achievement of glucose intolerance was delayed until the fourth and fifth week, respectively.

Blood glycosylated hemoglobin and plasma insulin were significantly lower in skim milk (10% and 34%, respectively)- and dahi (17%, and 48%, respectively)-fed animals than those of the control group. Plasma total cholesterol, triglycerides, low-density lipoprotein-cholesterol, and very-low-density lipoprotein-cholesterol and blood free fatty acids were significantly lower in skim milk (13%, 14%, 14%, 19%, and 14%, respectively)- and dahi (22%, 33%, 30%, 33%, and 29%, respectively)-fed animals as compared with control animals. Moreover, the total cholesterol, triglyceride, and glycogen contents in liver tissues were also lower in skim milk (55%, 50%, and 36%, respectively)- and dahi (64%, 27%, and 4%, respectively)-fed animals as compared with control animals. In contrast, high-density lipoprotein-cholesterol in plasma was higher in skim milk (14%)- and dahi (29%)-fed animals as compared with control animals.

These results indicate that skim milk and its fermented milk product, dahi, delay the progression of fructose-induced diabetes and dyslipidemia in rats and that these may be useful as antidiabetic food supplements that can be included in daily meals of the diabetic as well as normal population.


PMID: 17004894 [PubMed - indexed for MEDLINE]



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J Med Food. 2006;9(3):328-35

Authors: Yadav H, Jain S, Sinha PR


Effects of a fermented milk drink containing Lactobacillus casei strain Shirota on the human NK-cell activity

Nine healthy middle-aged and 10 elderly volunteers drank fermented milk containing 4 x 10(10) live cells of Lactobacillus casei strain Shirota daily for 3 wk, and their natural killer (NK) activity and other immunological functions were examined. In the experiments with middle-aged volunteers, NK activity significantly increased (P<0.01) 3 wk after the start of intake, elevated NK cell activity remained for the next 3 wk, and this effect was particularly prominent in the low-NK-activity individuals. In the experiments with elderly volunteers, NK activity significantly decreased (P<0.01) in the control group 3 wk after the start of intake; however, the intake of Lactobacillus casei strain Shirota maintained the NK activity. These results suggest that daily intake of Lactobacillus casei strain Shirota provides a positive effect on NK-cell activity.


PMID: 17311976 [PubMed - indexed for MEDLINE]



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J Nutr. 2007 Mar;137(3 Suppl 2):791S-3S

Authors: Takeda K, Okumura K


Fluctuation of fecal microbiota in individuals with Japanese cedar pollinosis during the pollen season and influence of probiotic intake

BACKGROUND

We have previously reported the results of a randomized, double-blind, placebo-controlled trial that found the intake of yogurt supplemented with a probiotic strain, Bifidobacterium longum BB536, alleviates symptoms and affects blood parameters in individuals with Japanese cedar pollinosis (JCPsis) during the pollen season.


OBJECTIVE

In the present study, fecal microbiota were investigated to examine whether any changes occur during the pollen season and whether any influence is exerted by probiotic intake. METHODS: Yogurt either with BB536 (BB536 yogurt) or without BB536 (placebo yogurt) was administered for 14 weeks at 2 x 100 g per day to 40 subjects (17 men, 23 women) with a clinical history of JCPsis. Fecal samples were obtained from 23 subjects (placebo group, n=13; BB536 group, n=10) before and during the intervention (weeks 4, 9 and 13) and fecal microbiota were analyzed using terminal-restriction fragment length polymorphism and real-time polymerase chain reaction (PCR) methods.


RESULTS

From the fluctuation patterns of terminal-restriction fragments, the Bacteroides fragilis group and bifidobacteria were among the species that changed most with pollen dispersion. Real-time PCR analyses indicated that the cell numbers of the B fragilis group increased significantly along with pollen dispersion in both BB536 and placebo groups. Cell numbers of bifidobacteria were significantly higher in the BB536 group compared with the placebo group (P < .05 at weeks 4 and 9). The ratio of cell numbers of the B fragilis group to bifidobacteria increased significantly during the pollen season in the placebo group (P < .01 at weeks 9 and 14), but not in the BB536 group. An in vitro study using peripheral blood mononuclear cells from JCPsis subjects indicated that strains of the B fragilis group induced significantly more helper T cell (T(H)) type2 cytokines (interleukin [IL]-6) but fewer T(H)1 cytokines (IL-12 and interferon) compared with those of bifidobacteria.


CONCLUSIONS

These results suggest a relationship between fluctuation in intestinal microbiota and pollinosis allergy. Furthermore, intake of BB536 yogurt appears to exert positive ihfluences on the formation of anti-allergic microbiota.


PMID: 17460947 [PubMed - indexed for MEDLINE]




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J Investig Allergol Clin Immunol. 2007;17(2):92-100

Authors: Odamaki T, Xiao JZ, Iwabuchi N, Sakamoto M, Takahashi N, Kondo S, Iwatsuki K, Kokubo S, Togashi H, Enomoto T, Benno Y


Extraction of lead, cadmium and zinc from overglaze decorations on ceramic dinnerware by acidic and basic food substances

Dinnerware decorated with overglaze designs can release toxic metals into food substances in amounts high enough to constitute health hazards.

When dishes made in the US before 1970 were filled with 4% acetic acid for 24 h, lead concentrations of up to 610 micrograms/ml and cadmium concentrations of up to 15 micrograms/ml were measured.

Acetic acid leachates from more than half the dishes tested for lead (78 of 149) contained levels exceeding the US Food and Drug Administration (FDA) allowable concentration of 3.0 micrograms/ml.

One-fourth of dishes tested for cadmium (26 of 98) exceeded the FDA limit of 0.5 microgram/ml.

High concentrations of lead, cadmium and zinc were also released into 1% solutions of citric and lactic acids.

Significant amounts of these metals were extracted by basic solutions of sodium citrate and sodium tripolyphosphate, as well as by commercial food substances including sauerkraut juice, pickle juice, orange juice, and low-lactose milk.

Relative concentrations of lead, zinc and cadmium released depend on the leaching agent used.

Citric acid leachates contain higher lead: cadmium and zinc:cadmium (but lower lead:zinc) ratios than do acetic acid leachates from nominally identical dishes.

Repeated extractions with acetic acid show that even after 20 consecutive 24-h leachings many dishes still release lead in concentrations exceeding FDA limits.


PMID: 9151439 [PubMed - indexed for MEDLINE]




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Sci Total Environ. 1997 Apr 30;197(1-3):167-75

Authors: Sheets RW


Soy isoflavone intake and estrogen excretion patterns in young women: effect of probiotic administration

BACKGROUND


Soy isoflavones may lower breast cancer risk through altered hepatic estrogen metabolism, leading to increased urinary excretion ratios of 2-hydroxyestrone (20HE1) to 16a-hydroxyestrone (16alphaOHE1).


MATERIALS AND METHODS

Urinary excretion of 20HE1/16alphaOHE1 was measured in 36 healthy, pre-menstrual women before and after ingestion of a soy-protein formula containing 120 mg of isoflavone daily for one month. Since isoflavone absorption and metabolism depends on intestinal bacteria, effects of co-administration of Lactobacillus GG (2 x 10(12)) on estrogen ratios and isoflavone excretion were studied. Urinary isoflavone excretion measurements assessed compliance.


RESULTS

Soy isoflavone ingestion induced quantitative differences in urinary excretion of estrogen metabolites and isoflavones but failed to alter 20HE1/16alphaOHE1 ratios. Co-administration of Lactobacillus GG with soy reduced excretion of total and individual isoflavones by 40% (p=0.08), without altering 2OHE1/16alphaOHE1 ratios.


CONCLUSION

Isoflavone-rich soy protein administration alone, or with probiotic supplement, did not alter urinary excretion of estrogen metabolites in premenopausal women. However, adding concentrated probiotics may alter isoflavone bioavailability.


PMID: 17591361 [PubMed - indexed for MEDLINE]



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In Vivo. 2007 May-Jun;21(3):507-12

Authors: Cohen LA, Crespin JS, Wolper C, Zang EA, Pittman B, Zhao Z, Holt PR


Consumption of soy foods and the risk of breast cancer: findings from the Japan Collaborative Cohort (JACC) Study

OBJECTIVE

The association between a lower incidence of breast cancer within the Asian population and the consumption of a diet high in soy has recently been the subject of much attention. To examine whether soy foods really have protective effects against breast cancer and how their influence on breast cancer is modified according to menopausal status, we conducted a population-based, prospective cohort study in Japan.


METHODS

We analyzed the data from the Japan Collaborative Cohort (JACC) Study. From 1988 to 1990, 30,454 women aged 40-79 years, completed a questionnaire on diet and other lifestyle features. Hazard ratios (HRs) were computed to examine the association between soy intake and the risk of breast cancer.


RESULTS

During the mean follow-up of 7.6 years, 145 cases of breast cancer were documented. We found no significant association between the risk of breast cancer and consumption of tofu, boiled beans, and miso soup; the multivariate HRs (95% CI) in the highest category of consumption were 1.14 (0.74-1.77), 0.77 (0.47-1.27) and 1.01 (0.65-1.56), respectively. Only among postmenopausal women, we found no significant associations between soy foods and the risk of breast cancer.


CONCLUSIONS

This prospective study suggests that consumption of soy food has no protective effects against breast cancer. Further large-scale investigations eliciting genetic factors may clarify different roles of various soybean-ingredient foods on the risk of breast cancer.


PMID: 17619154 [PubMed - in process]



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Cancer Causes Control. 2007 Oct;18(8):801-8

Authors: Nishio K, Niwa Y, Toyoshima H, Tamakoshi K, Kondo T, Yatsuya H, Yamamoto A, Suzuki S, Tokudome S, Lin Y, Wakai K, Hamajima N, Tamakoshi A


Dietary fatty acids and cholesterol differentially modulate HDL cholesterol metabolism in Golden-Syrian hamsters

Dietary fatty acids alter HDL cholesterol concentrations, presumably through mechanisms related to reverse cholesterol transport. The effect of dietary fats (coconut oil, butter, traditional stick margarine, soybean oil, canola oil) differing in fatty acid profile on this antiatherogenic process was assessed with respect to plasma lipids; exogenous and endogenous lecithin-cholesterol acyltransferase (LCAT), cholesterol ester transfer protein (CETP), phospholipid transfer protein (PLTP) activities; and LCAT, apolipoprotein (apo) A-I and scavenger receptor B class-1 (SR-B1) mRNA abundance.


Golden-Syrian hamsters were fed a nonpurified (6.25 g/100 g fat) diet containing an additional 10 g/100 g experimental fat and 0.1 g/100 g cholesterol for 6 wk.


Canola and soybean oils significantly lowered serum HDL cholesterol concentrations relative to butter. Canola oil, relative to butter, resulted in higher exogenous LCAT activity, and both soybean and canola oils significantly increased hepatic apo A-I and SR-B1 mRNA abundance. Butter, relative to margarine, coconut and soybean oils, significantly increased serum non-HDL cholesterol concentrations. Endogenous and exogenous LCAT, CETP, and PLTP activities did not differ in hamsters fed margarine or saturated fat diets, despite lower hepatic LCAT, apo A-I, and SR-B1 mRNA abundance, suggesting that changes in available substrate and/or modification to the LCAT protein may have been involved in lipoprotein changes.


These results suggest that lower HDL cholesterol concentrations, as a result of canola and soybean oil feeding, may not be detrimental due to increases in components involved in the reverse cholesterol transport process in these hamsters and may retard the progression of atherosclerosis.


PMID: 15735083 [PubMed - indexed for MEDLINE]



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J Nutr. 2005 Mar;135(3):492-8

Authors: Dorfman SE, Wang S, Vega-López S, Jauhiainen M, Lichtenstein AH


Successful treatment of acute aluminium phosphide poisoning: possible benefit of coconut oil

Aluminium phosphide is used to control rodents and pests in grain storage facilities. It produces phosphine gas, which is a mitochondrial poison. Unfortunately, there is no known antidote for aluminium phosphide intoxication, but our recent experience with a case showed that rapid prevention of absorption by coconut oil might be helpful.

In the present case, we used the same protocol in a 28-year-old man who had ingested a lethal amount (12 g) of aluminium phosphide with suicidal intent and was admitted to hospital approximately 6 hours postingestion. The patient had signs and symptoms of severe toxicity, and his clinical course included metabolic acidosis and liver dysfunction. Treatment consisted of gastric lavage with potassium permanganate solution, oral administration of charcoal and sorbitol suspension, intravenous administration of sodium bicarbonate, magnesium sulphate and calcium gluconate, and oral administration of sodium bicarbonate and coconut oil. Conservative and supportive therapy in the Intensive Care Unit was also provided.

The patient survived following rapid treatment and supportive care.

It is concluded that coconut oil has a positive clinical significance and can be added to the treatment protocol of acute aluminium phosphide poisoning in humans.


PMID: 15957538 [PubMed - indexed for MEDLINE]




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Hum Exp Toxicol. 2005 Apr;24(4):215-8

Authors: Shadnia S, Rahimi M, Pajoumand A, Rasouli MH, Abdollahi M


Influence of dietary fats on weight gain in albino rats

Carbon-chain length and degree of saturation of dietary fat may influence weight gain.

To examine this hypothesis we randomly allotted 100 male, 30-day old, albino rats to each of four groups. Each group was fed, ad libitum, a diet containing, as the only source of fat, either lard (L) or safflower oil (SO) (representing saturated and polyunsaturated fat respectively) or groundnut oil (GO) or coconut oil (CO) (representing long-chain and medium-chain triglycerides respectively).

At the end of 90 days it was found that rats fed SO consumed more food than those fed L enriched diet (P < 0.001) but the weight gain was similar in the two groups. Similarly rats fed GO-containing diet ate more than those fed diet containing CO (P < 0.001), yet weight gain was similar.

Thus it appears that carbon-chain length and degree of saturation of dietary fat does not influence weight gain in rats fed an ad libitum diet.



PMID: 16170990 [PubMed - indexed for MEDLINE]



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Indian J Physiol Pharmacol. 2005 Apr;49(2):206-12

Authors: Pereira N, Monteiro F, Abraham ME


Different palm oil preparations reduce plasma cholesterol concentrations and aortic cholesterol accumulation compared to coconut oil in hypercholesterolemic hamsters

Several studies have reported on the effect of refined, bleached and deodorized palm oil (RBD-PO) incorporation into the diet on blood cholesterol concentrations and on the development of atherosclerosis. However, very little work has been reported on the influence of red palm oil (RPO), which is higher in carotenoid and tocopherol content than RBD-PO. Thus, we studied the influence of RPO, RBD-PO and a RBD-PO plus red palm oil extract (reconstituted RBD-PO) on plasma cholesterol concentrations and aortic accumulation vs. hamsters fed coconut oil.

Forty-eight F1B Golden Syrian hamsters (Mesocricetus auratus) (BioBreeders, Watertown, MA) were group housed (three/cage) in hanging polystyrene cages with bedding in an air-conditioned facility maintained on a 12-h light/dark cycle. The hamsters were fed a chow-based hypercholesterolemic diet (HCD) containing 10% coconut oil and 0.1% cholesterol for 2 weeks at which time they were bled after an overnight fast and segregated into four groups of 12 with similar plasma cholesterol concentrations. Group 1 continued on the HCD, Group 2 was fed the HCD containing 10% RPO in place of coconut oil, Group 3 was fed the HCD containing 10% RBD-PO in place of coconut oil and Group 4 was fed the HCD with 10% reconstituted RBD-PO for an additional 10 weeks.

Plasma total cholesterol (TC) and non-high-density lipoprotein-cholesterol (HDL-C) (very low- and low-density lipoprotein) concentrations were significantly lower in the hamsters fed the RPO (-42% and -48%), RBD-PO (-32% and -36%) and the reconstituted RBD-PO (-37% and -41%) compared to the coconut oil-fed hamsters. Plasma HDL-C concentrations were significantly higher by 14% and 31% in hamsters fed the RBD-PO and RPO compared to the coconut oil-fed hamsters. Plasma triglyceride (TG) concentrations were significantly lower in hamsters fed RBD-PO (-32%) and the reconstituted RBD-PO (-31%) compared to the coconut oil-fed hamsters. The plasma gamma-tocopherol concentrations were higher in the coconut oil-fed hamsters compared to the hamsters fed the RPO (60%), RBD-PO (42%) and the reconstituted RBD-PO (49%), while for plasma alpha-tocopherol concentrations, the coconut oil-fed hamsters were significantly higher than only the RPO-fed hamsters (21%). The coconut oil-fed hamsters also had significantly higher plasma lipid hydroperoxide concentrations compared to RBD-PO (112%) and the reconstituted RBD-PO (485%). The hamsters fed the coconut oil diet excreted significantly more fecal total neutral sterols and cholesterol compared to the hamsters fed the RBD-PO (158% and 167%, respectively). The coconut oil-fed hamsters had significantly higher levels of aortic total, free and esterified cholesterol compared to the hamsters fed the RPO (74%, 50% and 225%, respectively), RBD-PO (57%, 48% and 92%, respectively) and the reconstituted RBD-PO (111%, 94% and 94%, respectively). Also, aortic free/ester cholesterol ratio in the aortas of hamsters fed RPO was significantly higher than in those fed the coconut oil (124%).

In conclusion, hamsters fed the three palm oil preparations had lower plasma TC and non-HDL-C and higher HDL-C concentrations while accumulating less aortic cholesterol concentrations compared to hamsters fed coconut oil.



PMID: 16081272 [PubMed - indexed for MEDLINE]



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J Nutr Biochem. 2005 Oct;16(10):633-40

Authors: Wilson TA, Nicolosi RJ, Kotyla T, Sundram K, Kritchevsky D


Dietary coconut oil increases conjugated linoleic acid-induced body fat loss in mice independent of essential fatty acid deficiency

Conjugated linoleic acid (CLA) induces a body fat loss that is enhanced in mice fed coconut oil (CO), which lacks essential fatty acids (EFA).

Our objective was to determine if CO enhancement of CLA-induced body fat loss is due to the lack of EFA. The CLA-EFA interaction was tested by feeding CO and fat free (FF) diets for varying times with and without replenishment of individual EFA.

Mice fed CO during only the 2-week CLA-feeding period did not differ from control mice in their adipose EFA content but still tended (P=0.06) to be leaner than mice fed soy oil (SO). Mice raised on CO or FF diets and fed CLA were leaner than the SO+CLA-fed mice (P<0.01). Mice raised on CO and then replenished with linoleic, linolenic, or arachidonic acid were leaner when fed CLA than mice raised on SO (P<0.001). Body fat of CO+CLA-fed mice was not affected by EFA addition. In summary, CO-fed mice not lacking in tissue EFA responded more to CLA than SO-fed mice. Also, EFA addition to CO diets did not alter the enhanced response to CLA.

Therefore, the increased response to CLA in mice raised on CO or FF diets appears to be independent of a dietary EFA deficiency.


PMID: 16216548 [PubMed - indexed for MEDLINE]



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Biochim Biophys Acta. 2005 Oct 15;1737(1):52-60

Authors: Hargrave KM, Azain MJ, Miner JL


Friday, July 27, 2007

Coconut fats

In many areas of Sri Lanka the coconut tree and its products have for centuries been an integral part of life, and it has come to be called the "Tree of life". However, in the last few decades, the relationship between coconut fats and health has been the subject of much debate and misinformation.

Coconut fats account for 80% of the fat intake among Sri Lankans. Around 92% of these fats are saturated fats. This has lead to the belief that coconut fats are 'bad for health', particularly in relation to ischaemic heart disease.

Yet most of the saturated fats in coconut are medium chain fatty acids whose properties and metabolism are different to those of animal origin. Medium chain fatty acids do not undergo degradation and re-esterification processes and are directly used in the body to produce energy. They are not as 'bad for health' as saturated fats.

There is the need to clarify issues relating to intake of coconut fats and health, more particularly for populations that still depend on coconut fats for much of their fat intake. This paper describes the metabolism of coconut fats and its potential benefits, and attempts to highlight its benefits to remove certain misconceptions regarding its use.


PMID: 17180807 [PubMed - indexed for MEDLINE]



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Ceylon Med J. 2006 Jun; 51(2):47-51

Authors: Amarasiri WA, Dissanayake AS


Dietary omega-3-polyunsaturated fatty acids prevent the development of metastases of colon carcinoma in rat liver

BACKGROUND

Fish oil consisting of omega-3 polyunsaturated fatty acids (PUFA) seems to reduce the incidence of colon cancer. The effect of PUFAs on metastasis of colon carcinoma is still unclear. AIM: The study was designed to examine the effects of a diet rich in omega-3-PUFAs on a model of colorectal metastasis.


METHODS

Thirthy animals (WAG/Rij) were randomly assigned to receive an omega-3 diet or a control diet to evaluate their effect on tumor growth. The target male rats (WAG/Rij) were fed a diet containing 15% omega-3-fatty acids three days before and 28 days after intervention and the control rats received 15% coconut oil at the same time points. CC 531 cells, a moderately differentiated colon adenocarcinoma, were injected into the spleen of each rat. After 28 days of diet, animals were sacrificed. The tumor growth was evaluated macroscopically and microscopically in liver tissue. The tissue was examined after immunostaining and the use of monoclonal antibodies.


RESULTS

PUFAs decreased the index of tumor load from 1.54 in the controls to 0.79 in the treatment group (P = 0.036). While 69.2% of the control animals were tumor positive, only 21.4% of the target animals showed tumor after omega-3-fatty acid (P < 0.05).


CONCLUSION

We could show that omega-3-fatty acids may decrease malignant metastatic tumor growth in the liver.




PMID: 17593466 [PubMed - in process]



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Eur J Nutr. 2007 Aug;46(5):279-85

Authors: Gutt CN, Brinkmann L, Mehrabi A, Fonouni H, Müller-Stich BP, Vetter G, Stein JM, Schemmer P, Büchler MW


DIETARY FLAXSEED INHIBITS ATHEROSCLEROSIS IN THE LDL RECEPTOR DEFICIENT MOUSE IN PART THROUGH ANTI-PROLIFERATIVE AND ANTI-INFLAMMATORY ACTIONS

Dietary flaxseed has been shown to have potent anti-atherogenic effects in rabbits. The purpose of the present study was to investigate the anti-atherogenic capacity of flaxseed in an animal model that more closely represents the human atherosclerotic condition, the LDL receptor deficient mouse (LDLrKO), and to identify the cellular mechanisms for these effects.

LDLrKO mice were administered a regular diet (RG), a 10% flaxseed supplemented diet (FX), or an atherogenic diet containing 2% cholesterol, alone (CH) or supplemented with 10% flaxseed (CF), 5% flaxseed (CF5), 1% flaxseed (CF1), or 5% coconut oil (CS) for 24 weeks.

LDLrKO mice fed a cholesterol supplemented diet exhibited a rise in plasma cholesterol without a change in triglycerides, and an increase in atherosclerotic plaque formation. The CS mice exhibited elevated levels of plasma cholesterol, triglycerides and saturated fatty acids, and an increase in plaque development. Supplementation of the cholesterol-enriched diet with 10% wt/wt ground flaxseed lowered plasma cholesterol and saturated fatty acids, increased plasma ALA and inhibited plaque formation in the aorta and aortic sinus as compared to mice supplemented with only dietary cholesterol.

The expression of proliferating cell nuclear antigen (PCNA) and the inflammatory markers IL-6, mac-3, and VCAM-1 was increased in aortic tissue from CH and CS mice. This expression was significantly reduced or normalized when flaxseed was included in the diet.

Our results demonstrate that dietary flaxseed can inhibit atherosclerosis in the LDLrKO mouse through a reduction of circulating cholesterol levels and, at a cellular level, via anti-proliferative and anti-inflammatory actions. Key words: linseed, alpha-linolenic acid, nutrition, atherosclerosis, inflammation.


PMID: 17616740 [PubMed - as supplied by publisher]



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Am J Physiol Heart Circ Physiol. 2007 Jul 6;

Authors: Dupasquier CM, Dibrov E, Kostenuk AL, Cheung PK, Lee KG, Alexander HK, Yeganeh BK, Moghadasian MH, Pierce GN


Effects of coconut oil on testosterone-induced prostatic hyperplasia in Sprague-Dawley rats.

Benign prostatic hyperplasia (BPH) is the benign uncontrolled growth of the prostate gland, leading to difficulty with urination. Saw palmetto lipid extracts (SPLE), used to treat BPH, have been shown to inhibit prostate 5a-reductase, and some major components, such as lauric, myristic and oleic acids also inhibit this enzyme.

Coconut oil (CO) is also rich in fatty acids, mainly lauric and myristic acids. We investigated whether CO prevents testosterone-induced prostate hyperplasia (PH) in Sprague-Dawley rats. Animals were distributed into seven groups (10 rats each).

A negative control group were injected with soya oil; six groups were injected with testosterone (3 mg kg(-1)) to induce PH: a positive control group, and five groups treated orally with SPLE (400 mg kg(-1)), CO or sunflower oil (SO) (400 and 800 mg kg(-1)). Treatments were given for 14 days. Rats were weighed before treatment and weekly thereafter. Rats were then killed and the prostates were removed and weighed.

CO (400 and 800 mg kg(-1)), SPLE (400 mg kg(-1)) and SO at 800 mg kg(-1), but not at 400 mg kg(-1), significantly reduced the increase in prostate weight (PW) and PW:body weight (BW) ratio induced by testosterone (% inhibition 61.5%, 82.0%, 43.8% and 28.2%, respectively). Since CO and SPLE, but not SO, contain appreciable concentrations of lauric and myristic acids, these results could be attributed to this fact. In conclusion, this study shows that CO reduced the increase of both PW and PW:BW ratio, markers of testosterone-induced PH in rats.


PMID: 17637195 [PubMed - in process]



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J Pharm Pharmacol. 2007 Jul;59(7):995-9

Authors: de Lourdes Arruzazabala M, Molina V, Más R, Carbajal D, Marrero D, González V, Rodríguez E


In vitro antimicrobial properties of coconut oil on Candida species in ibadan, Nigeria.

The emergence of antimicrobial resistance, coupled with the availability of fewer antifungal agents with fungicidal actions, prompted this present study to characterize Candida species in our environment and determine the effectiveness of virgin coconut oil as an antifungal agent on these species.


In 2004, 52 recent isolates of Candida species were obtained from clinical specimens sent to the Medical Microbiology Laboratory, University College Hospital, Ibadan, Nigeria. Their susceptibilities to virgin coconut oil and fluconazole were studied by using the agar-well diffusion technique.

Candida albicans was the most common isolate from clinical specimens (17); others were Candida glabrata (nine), Candida tropicalis (seven), Candida parapsilosis (seven), Candida stellatoidea (six), and Candida krusei (six). C. albicans had the highest susceptibility to coconut oil (100%), with a minimum inhibitory concentration (MIC) of 25% (1:4 dilution), while fluconazole had 100% susceptibility at an MIC of 64 mug/mL (1:2 dilution).

C. krusei showed the highest resistance to coconut oil with an MIC of 100% (undiluted), while fluconazole had an MIC of > 128 mug/mL. It is noteworthy that coconut oil was active against species of Candida at 100% concentration compared to fluconazole. Coconut oil should be used in the treatment of fungal infections in view of emerging drug-resistant Candida species.


PMID: 17651080 [PubMed - in process]



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J Med Food. 2007 Jun;10(2):384-7

Authors: Ogbolu DO, Oni AA, Daini OA, Oloko AP


Energy Intelligence: Amber Waves Of Green

Once upon a time, a century ago, Americans competed with their transportation for food. Back then, almost 30% of the nation's verdant farm land was used to grow food for fuel--feeding horses, of course, our bio-chemical transportation infrastructure, instead of today's thermo-mechanical horsepower. Those days are gone.

America actually has less land under irrigation today and produces stunningly larger quantities of food, for people. As Yogi Berra famously said, "it's déjà vu all over again." As of right now, we're on the way "back to the future" to devour a third of America's amber waves of corn (the dominant grain crop) to make money, er, ethanol to fuel our cars.

Global oil production is straining to meet the voracious appetite of 21st century transportation, hence the high prices. So a lot of people, including those in our government, think relief can be found in alcohol, specifically, grain ethanol.

The Energy Policy Act of 2005 has a Renewable Fuel Standard (RFS) increasing U.S. fuel ethanol to 7.5 billion gallons per year by 2012, up from today's 4 billion. But, does using grain alcohol as a major transportation fuel make any sense?

Farmers, and fuel pundits, not to mention some investors, are enjoying the enthusiasm for corn-based alcohol. Good for them. With corn selling at $2 to $3 a bushel more than it did a few years ago, no wonder farmers are eagerly planting corn; total corn acreage is the highest since 1944.

For every extra dollar per bushel, a middling 500-acre farm sees $100,000 flow right to the bottom line. Even though corn prices have softened a skosh recently, no one is predicting a price collapse any time soon.

Collaterally, construction is at a sizzling pace for alcohol breweries--called ethanol refineries, of course, borrowing the language of the hydrocarbon economy. There are already 120 of them, with some 80 more under construction, concentrated in the Corn Belt but stretching all the way to Florida.

Current U.S. ethanol capacity is nearly 6 billion gallons a year. Under-construction capacity will add another 7 billion gallons. At this pace, assuming the incentive policies continue, U.S. ethanol production will easily exceed the policy target of 8 billion gallons by 2011. (For scale context; Americans consume annually about a half-billion gallons of alcohol in the form of beer, wine and spirits, and about 200 billion gallons of petroleum in our internal combustion engines.)

Grain ethanol technology, aka. fermentation, is well established. It can be traced back to ancient Egypt. Think of it as a basic form of solar energy (photosynthesis) and biotechnology (yeast-based fermentation). There is little doubt that America has the land and economic and political muscle to make even more alcohol than is currently planned. Aside from the fact that America is huge with lots of fertile acreage, grain yields per acre are seven times what they were in the 1920s, and will get better yet. Per-acre yields are up 20% in the past decade alone.

Sounds good until one takes a sobering reality check. Even if every cob of corn (and all domestic sugar cane) were converted to fuel, that would displace just 10% of the current U.S. gasoline demand. And, already, ethanol is sparking a food-vs.-fuel fight. Record corn crops are seeing higher corn prices, rather than lower. The price ripples through the entire food chain since, from tortillas to beef, one in four products in the supermarket derives from corn, directly or indirectly.

Don't get me wrong. I like alcohol as much as the next guy (though preferably well aged in an oak cask first) but we'll have to undertake quite an expansion of food-to-fuel agriculture to make a meaningful dent in our transportation sector. And, to coin the phrase, some of my best friends are farmers--not to mention my father who grew up on his dad's grain farm in northern Manitoba.

A cynic might conclude this is more of political food fight. Just look at the U.S. Department of Agriculture map (below) showing Iowa at the epicenter of the location of America's ethanol capacity. You could be excused for concluding this particular gold rush has as much to do with presidential politics as oil alternatives.


072607_chartroom.jpg


It is the case, nonetheless, that we do need to find lots of options to feed the nation's gargantuan liquid fuel appetite. Fuel demand is just not going away, or even down, regardless of efficiency or conservation measures. The Energy Information Administration sees transportation fuel demand more than 50% higher by 2030.

Any and all viable sources of liquid fuels are of interest. Of course, we're setting aside the question of whether it may be just cheaper to drill for more domestic oil from the Gulf of Mexico to the Rocky Mountains, from California to Alaska; or whether our billions-of-barrels-equivalent in coal-to-liquids might make as much economic and geopolitical sense. All subjects for another time.

So what's the beef with a major expansion in corn alcohol? The big issues with using even more corn, or any grain-based ethanol, boil down to land and water use.

Let's start with water, the one "hidden" resource that's just now perking to the top of national environmental concerns. Nearly 1,000 gallons of irrigation water are used to grow enough corn to produce one gallon of ethanol.

And then there's the nitrogen fertilizer run-off carried by the irrigation (and rain) water into the local waterways. Switching crops over to corn, or planting more corn, substantially increases the run-off. And while nutrient pollution also comes from sewage treatment plants, golf courses and lawns, it is worth noting that the federal regulations that exist for those sources of pollutants don't apply to farm run-off.

The second issue, the land requirements, highlights a bit of an irony. Some of the same folks unhappy about sprawling urban areas and roads in particular have eagerly embraced the orders-of-magnitude greater land sprawl an ethanol-based transportation system would require. A point of statistical context is illustrative: The total aggregate use of land today for oil fields, pipelines, refineries, and including all our roads and highways, is about than one-tenth the land that would be required just to make the ethanol to fuel our transportation.

Still, America does have a lot of land. And there's a whole lot of it not essential or productive for food agriculture, or much of anything else for that matter. Ideally, rather than growing water-, fertilizer- and land-intensive crops like corn for fuel, we could use the billions of tons of biomass--weeds, grass and trees--that grow on the vast plains.

Unbeknownst to most, America has more acres of trees today than at the time of the Pilgrims. Over the long run, perhaps not that long either, it's a much better bet that the source of carbohydrates to make the ethanol won't come from our food supply, but from wood and weeds (and from the biotrash associated with food crops).

Since humans can't eat this cellulosic biomass of wood and grass, and since those wild crops grow abundantly with little irrigation or fertilizer (and the crop biotrash is a free byproduct), the negative impacts are dramatically mitigated. For those counting carbon emissions: where the total fuel-cycle corn-ethanol yields a modest 20% net reduction in green-house emissions, cellulosic ethanol reduces emissions 80%.

There's a rub though. We don't have any effective way to convert weeds and trees to alcohol. Understanding why calls for a modest understanding of the biology and chemistry here; knowledge that points to sustainable ethanol bets for both investors and policy makers.

Start with the easy-to-make ethanol. The starch in corn converts easily to a form of glucose (as if most of us haven't noticed … given our eating habits). Glucose is easy for enzymes to break down, and also easy for natural yeasts to ferment in to ethanol (which is why that's the source of beer and bourbon, and alternative automotive fuel).

On the other hand, the abundant and low-cost sources of biomass from trees, grass and corn stalks are made from more robust and literally hard-to-digest and ferment celluose, xylose and lignin. So the technology race that's on today is to find cost-effective techniques to: a) break down the hardy cellulose; and then b) find a way to ferment it. If the latter were easy, the illicit alcohol makers in back-woods stills in days of yore would have been using the forest to make the booze, not just to hide from the long arm of the law.

There are existing and natural processes that do break down cellulose and ferment it; but they're either not cost effective or commercially viable--yet. There are plenty of inter-related and nontrivial challenges in this bio-engineering race. One core challenge for the genetic engineers is to come up with a bug that can both manage to ferment the highly resistant cellulosic bio-glop, and yet is hardy enough to survive ethanol poisoning. The new bugs, so far, die off when the ethanol they produce reaches concentrations of 5% or 6%.

Inconvenient, to say the least, since the purpose of the fermentation is to produce 100% pure ethanol. DuPont claims to have a bug that can live up to a 10% concentration--in effect their bugs die around wine-grade alcohol. Still a long way to go to fuel-grade. So not surprisingly, cellulosic alcohol costs north of $2 a gallon to make, over twice the cost of corn alcohol.

There are some very smart genetic engineers trying crack the cellolosic code. One keeps an eye on the big traditional grain-ethanol and food companies like Archer Daniels Midland and Pacific Ethanol who have announced cellulosic projects. Then there are companies making (credible) bullish claims on advancing the key enzyme technology like Genencor, a division of Denmark's Danisco, one of the world's largest producers of food ingredients.

Notable amongst the rapidly growing field of smaller, leaner (and often more technologically aggressive) cellulosic players are companies like Novozymes which is one of the DOE favorites (having received federal funding) who properly highlights their collaboration with Abengoa. Abengoa itself is building the world's first commercial scale cellulosic ethanol biorefinery in Babilafuente, Spain, and plans to convert their Nebraska corn-ethanol plant to run on straw and corn stalk waste.

Add to the short list (given my family's western Canadian farming roots), Lignol Energy, which will process Canadian forest waste using proven technology pioneered by a General Electric subsidiary.

Finally, perhaps most tantalizing in the public domain is the newly minted Verenium formed by the merger of Diversa, an enzyme powerhouse, with Celunol, a cellulosic ethanol leader with the nation's first ethanol pilot facility in Jennings, La.

Given the size of the prize, there is a rapidly growing fleet of private companies chasing cellulosic technology. Companies like Synthetic Genomics (derivative from genetic pioneer J. Craig Venter and Nobel Laureate Hamilton O. Smith), Iogen (where Shell Oil owns 50%) with an operating demonstration facility, and funded by the VC community's premier biofuel-enthusiast Vinod Khosla, Range Fuels (building a plant in Georgia).

One intriguing dark horse in this genetic race--"dark" only because they're so far away--is a clever Australian team at Microbiogen. The bio brainiacs at Microbiogen have eschewed complex modern genetic engineering, and are instead using a souped-up version of the venerable approach to breeding. They are selectively culling an existing natural yeast that's already pretty happy fermenting cellulosic glop. This latter technique is, of course, how humans have been genetically engineering--breeding--for centuries and how we obtained most of today's grains, cattle and flowers.

But don't think cellulosic ethanol will dethrone king oil for transportation. The most optimistic federal study estimates at most 30% of U.S. transportation fuel could come from such sources, and not until mid-21st century. Still, even half that goal is worth pursuing--for both strategic reasons and for investors. It is a very big market. And it will happen.

All these smart bio-engineers will stumble deliberately on an elegant solution, or two--likely sooner than most suspect. In which case the epicenter of fuel crops will shift to bio-trash and the vast prairie and forested states--and not incidentally, put to rest the needless food-fuel conflict.

Written by Mark P. Mills, a physicist and a co-founding partner in Digital Power Capital, an energy tech venture fund. Mills is also co-author of The Bottomless Well: The Twilight of Fuel, the Virtue of Waste, and Why We Will Never Run Out of Energy (Basic Books, 2005). Mills may hold positions in companies discussed in this column, and may provide technology assessment services for firms that have interests in the companies. He can be contacted at inquiries@digitalpower.com .

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Mark P. Mills 07.26.07, 11:54 AM ET

Stock Of The Week: Taking A Fresh Bite Into Apple

Dan Sullivan is a guy who doesn't mind buying stocks that look expensive, as long as he can sell them later when they're even more expensive.

Sullivan, editor since 1969 of The Chartist investment newsletter, has been making picks based on chart strength, and one of his favorite stocks right now is Apple. He recommends buying the shares, which have more than doubled since last fall, and have added 50% in a little more than two months.

Apple's impressive earnings report after the close of trading on Wednesday encouraged investors to bid AAPL shares to fresh 52-week highs above $150 in after-hours action.

What most impressed Sullivan, however, was how Apple broke out to new highs above $130 earlier in July. Sullivan and other chart watchers know that stocks that make new highs many times continue to make new highs until some sort of sell-off on large volume shows that big money investors are getting out of the stock. That is not happening with Apple.

"While we would not be surprised to see some corrective activity and profit-taking from these levels, the stock looks like a winner," says Sullivan, who recommends using a "mental stop" of $115 on Apple long positions.



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John Dobosz 07.26.07, 11:24 AM ET

Ascendas India Trust launches Singapore IPO of 423.38m shares at SGD1.18

SINGAPORE (Thomson Financial) - Ascendas India Trust, which owns business parks in India, will launch Wednesday its initial public offering here of 423.38 million shares priced at 1.18 Singapore dollars apiece, the trust said Tuesday.

The trust is owned and sponsored by industrial landlord Ascendas Pte Ltd, a unit of Singapore government-owned industrial landlord JTC Corp.

The IPO comprises an international placement tranche of 392.10 million shares and a retail tranche of 31.28 million.

Ascendas India Trust's initial portfolio includes information technology business parks in the Indian cities of Bangalore, Chennai and Hyderabad with a combined built-up area of 3.6 million square feet.

The group is developing another 1.1 million square feet of business parks and has sites with a potential built-up area of 4.2 million square feet.

Jonathan Yap, the chief executive of the trust's trustee-manager, said: 'We believe that Ascendas India Trust represents the best of two worlds. The existing income-producing portfolio offers investors stable income distributions. It also provides upside growth potential from the higher development component possible from a business trust structure and land already within the portfolio.'

Yap said: 'Strong demand for quality business space in the key IT centers presents Ascendas India Trust with a platform to expand its product offering and diversify its tenant base.'

Ascendas India Trust's IPO closes on July 30 and trading in its units is expected to begin on Aug 1.

The IPO will raise gross proceeds of 549.50 million dollars, assuming the underwriters exercise their over-allotment option to issue up to 42.34 million shares to satisfy excess demand.

The proceeds will be used to repay debt and fund certain acquisitions.

(1 US dollar = 1.50 Singapore dollars)

TFN.Singapore@thomson.com



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AFX News Limited
07.24.07, 4:58 AM ET

Micromolar fluoride alters ameloblast lineage cells in vitro

Fluorosed enamel is caused by exposure to fluoride during tooth formation. The objective of this study was to determine whether epithelial ameloblast-lineage cells, derived from the human enamel organ, are directly affected by micromolar concentrations of fluoride.

Cells were cultured in the presence of fluoride, and proliferation was measured by BrdU incorporation. The effect of 0, 10, or 20 microM fluoride on apoptosis was determined by the flow cytometry apoptotic index. The effects of fluoride on gene expression were investigated by SuperArray microarray analysis and real-time PCR.

Fluoride had a biphasic effect on cell proliferation, with enhanced proliferation at 16 microM, and reduced proliferation at greater than 1 mM F. Flow cytometry showed that both 10 microM and 20 microM NaF significantly increased the apoptotic index of ameloblast-lineage cells.

There was no general effect of fluoride on gene expression. These results indicate multiple effects of micromolar fluoride on ameloblast-lineage cells.


PMID: 17384028 [PubMed - in process]


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J Dent Res. 2007 Apr;86(4):336-40.

Yan Q, Zhang Y, Li W, Denbesten PK.

Department of Orofacial Sciences
University of California at San Francisco
513 Parnassus Ave. S-704
San Francisco
CA 94143-0422, USA.


Animal health problems attributed to environmental contamination in lake Nakuru National Park, Kenya: a case study on heavy metal poisoning in the Waterbuck Kobus ellipsiprymnus defassa (Ruppel 1835)

A study was conducted in which samples of soil, forage, as well as serum, bone, kidney, and liver of waterbuck were collected from Lake Nakuru National Park.

The objective was to determine the ecosystem health status in order to establish the causes of animal health problems previously recorded in some sections of the Park.

Trace element analysis in serum indicated occurrence of copper (Cu) deficiency in the north and eastern sections of the Park where mean values were marginal (range: 0.36-0.81, mean: 0.62 mg/l) compared to concentrations recorded in the western part of the Park (range: 0.69-1.48, mean: 1.22 mg/l).

Bone analysis on dry matter basis (DM) indicated higher (p < 0.01) levels of cadmium (Cd, 0.437 mg/kg), fluoride (F, 3178 mg/kg), and lead (Pb, 20.62 mg/kg) in animals from the east compared to those from the west (0.002, 1492, 4.87 mg/kg, respectively), suggesting heavy exposure. In addition, samples from the east had much lower than normal calcium (Ca)-to-phosphorus (P) ratios (mean: 1.9:1) compared to those recorded in the west (2.2:1), suggesting poor bone mineralization.

There was a higher concentration of Cd in the kidney (16.24 mg/kg, p < 0.05) and Pb in the liver (58.3 mg/kg, p < 0.01) in animals from the east compared to those in the west (12.92 and 36.2 mg/kg, respectively), but the converse was true of Cu.

The liver Cu status was better in animals from the west with, concentrations (mean: 21.7 mg/kg) being about twice those recorded in the east (11.9 mg/kg DM). Forage analysis revealed prospects of Ca, P, and Cu deficiencies in the entire Park.

However, in the northeastern section of the Park (measuring 50 ha) where waterbuck residence times are high, forage concentrations of Cd (0.31 mg/kg DM), molybdenum (Mo, 7.20 mg/kg DM), Pb (2.88 mg/kg DM), and zinc (Zn, 126 mg/kg DM) were an order of magnitude greater (p < 0.01) than the levels recorded in the rest of the Park (ranges: 0.133-0.165, 3.69-5.61, 0.485-0.621, 11.6-17.4 mg/kg DM, respectively).

These disparities were attributed to a higher soil concentration of Cd (2.77 mg/kg DM), Pb (85.1 mg/k DM) and Zn (1414 mg/kg DM) in this section compared to the rest of the Park (ranges: 0.10-0.15, 5.02-6.26, 1.49-5.44 mg/kg DM, respectively), and strongly suggest heavy metal contamination as the source of animal health problems in the Park.


PMID: 17160492 [PubMed - indexed for MEDLINE]




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Arch Environ Contam Toxicol. 2007 Feb;52(2):270-81. Epub 2006 Dec 7.


Jumba IO, Kisia SM, Kock R.

Department of Chemistry, College of Biological and Physical Sciences, University of Nairobi, P.O. Box 30197 00100 Nairobi, Kenya. ijumba@uonbi.ac.ke


Animal health problems attributed to environmental contamination in lake Nakuru National Park, Kenya: a case study on heavy metal poisoning in the Waterbuck Kobus ellipsiprymnus defassa (Ruppel 1835).

A study was conducted in which samples of soil, forage, as well as serum, bone, kidney, and liver of waterbuck were collected from Lake Nakuru National Park.

The objective was to determine the ecosystem health status in order to establish the causes of animal health problems previously recorded in some sections of the Park.

Trace element analysis in serum indicated occurrence of copper (Cu) deficiency in the north and eastern sections of the Park where mean values were marginal (range: 0.36-0.81, mean: 0.62 mg/l) compared to concentrations recorded in the western part of the Park (range: 0.69-1.48, mean: 1.22 mg/l).

Bone analysis on dry matter basis (DM) indicated higher (p < 0.01) levels of cadmium (Cd, 0.437 mg/kg), fluoride (F, 3178 mg/kg), and lead (Pb, 20.62 mg/kg) in animals from the east compared to those from the west (0.002, 1492, 4.87 mg/kg, respectively), suggesting heavy exposure. In addition, samples from the east had much lower than normal calcium (Ca)-to-phosphorus (P) ratios (mean: 1.9:1) compared to those recorded in the west (2.2:1), suggesting poor bone mineralization.

There was a higher concentration of Cd in the kidney (16.24 mg/kg, p < 0.05) and Pb in the liver (58.3 mg/kg, p < 0.01) in animals from the east compared to those in the west (12.92 and 36.2 mg/kg, respectively), but the converse was true of Cu.

The liver Cu status was better in animals from the west with, concentrations (mean: 21.7 mg/kg) being about twice those recorded in the east (11.9 mg/kg DM). Forage analysis revealed prospects of Ca, P, and Cu deficiencies in the entire Park.

However, in the northeastern section of the Park (measuring 50 ha) where waterbuck residence times are high, forage concentrations of Cd (0.31 mg/kg DM), molybdenum (Mo, 7.20 mg/kg DM), Pb (2.88 mg/kg DM), and zinc (Zn, 126 mg/kg DM) were an order of magnitude greater (p < 0.01) than the levels recorded in the rest of the Park (ranges: 0.133-0.165, 3.69-5.61, 0.485-0.621, 11.6-17.4 mg/kg DM, respectively).

These disparities were attributed to a higher soil concentration of Cd (2.77 mg/kg DM), Pb (85.1 mg/k DM) and Zn (1414 mg/kg DM) in this section compared to the rest of the Park (ranges: 0.10-0.15, 5.02-6.26, 1.49-5.44 mg/kg DM, respectively), and strongly suggest heavy metal contamination as the source of animal health problems in the Park.


PMID: 17160492 [PubMed - indexed for MEDLINE]




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Arch Environ Contam Toxicol. 2007 Feb;52(2):270-81. Epub 2006 Dec 7.


Jumba IO, Kisia SM, Kock R.

Department of Chemistry, College of Biological and Physical Sciences, University of Nairobi, P.O. Box 30197 00100 Nairobi, Kenya. ijumba@uonbi.ac.ke


Radon and lung cancer risk: an extension of the mortality follow-up of the Newfoundland fluorspar cohort

Radon is a well-recognized cause of lung cancer, and studies of underground miners have provided invaluable insights on the mechanisms of radon carcinogenesis.


Given the dramatic decreases in occupational exposures and the latent interval between the time of exposure and the development of lung cancer, continued follow-up of these cohorts is needed to address uncertainties in risk estimates. Here, we report on the relationship between radon and lung cancer mortality in a cohort of 1,742 Newfoundland fluorspar miners between 1950 and 2001; follow-up has been extended 11 y from previous analyses. The standardized mortality ratio (SMR) was used to compare the mortality experience of the cohort to similarly aged Newfoundland males.

Poisson regression methods were used to characterize the radon-lung cancer relationship with respect to: age at first exposure, attained age, time since last exposure, interactions with cigarette smoking, and exposure rate. In total, 191 lung cancers were observed among underground miners (SMR = 3.09; 95% CI = 2.66, 3.56). ERR/WLMs decreased with attained age and time since last exposure. An inverse dose-rate effect was observed, while age at first exposure was not associated with lung cancer risk. An important strength of this study is that the effects of gamma radiation, thoron, and radioactive dust, common exposures in other miner studies, can be ruled out because the source of radon was from water running through the mine.

However, the results should be interpreted cautiously due to uncertainties associated with the estimation of radon exposure levels before ventilation was introduced into the mine, and the relatively small number of lung cancer deaths that precluded joint modeling of multiple risk factors.


PMID: 17220717 [PubMed - indexed for MEDLINE]




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Health Phys. 2007 Feb;92(2):157-69.

Villeneuve PJ, Morrison HI, Lane R.

Department of Public Health Sciences, University of Toronto, Toronto, Ontario, Canada. paul.villeneuve@utoronto.ca



Confirmation of and explanations for elevated blood lead and other disorders in children exposed to water disinfection and fluoridation chemicals.

Silicofluorides (SiFs), fluosilicic acid (FSA) and sodium fluosilicate (NaFSA), are used to fluoridate over 90% of US fluoridated municipal water supplies.


Living in communities with silicofluoride treated water (SiFW) is associated with two neurotoxic effects:

(1) Prevalence of children with elevated blood lead (PbB>10mug/dL) is about double that in non-fluoridated communities (Risk Ratio 2, chi(2)p<0.01). SiFW is associated with serious corrosion of lead-bearing brass plumbing, producing elevated water lead (PbW) at the faucet. New data refute the long-prevailing belief that PbW contributes little to children's blood lead (PbB), it is likely to contribute 50% or more.

(2) SiFW has been shown to interfere with cholinergic function. Unlike the fully ionized state of fluoride (F-) in water treated with sodium fluoride (NaFW), the SiF anion, [SiF6]2- in SiFW releases F- in a complicated dissociation process. Small amounts of incompletely dissociated [SiF6]2- or low molecular weight (LMW) silicic acid (SA) oligomers may remain in SiFW.

A German PhD study found that SiFW is a more powerful inhibitor of acetylcholinesterase (AChE) than NaFW. It is proposed here that SiFW induces protein mis-folding via a mechanism that would affect polypeptides in general, and explain dental fluorosis, a tooth enamel defect that is not merely "cosmetic" but a "canary in the mine" foretelling other adverse, albeit subtle, health and behavioral effects.

Efforts to refute evidence of such effects are analyzed and rebutted. In 1999 and 2000, senior EPA personnel admitted they knew of no health effects studies of SiFs. In 2002 SiFs were nominated for NTP animal testing. In 2006 an NRC Fluoride Study Committee recommended such studies. It is not known at this writing whether any had begun.


PMID: 17420053 [PubMed - as supplied by publisher]




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Neurotoxicology. 2007 Mar 1

Coplan MJ, Patch SC, Masters RD, Bachman MS.

Intellequity Technology Services Natick, Massachusetts, United States.


Protective effects of vitamins C and e against endometrial damage and oxidative stress in fluoride intoxication.

1. Fluoride (F) is an essential trace element that has protective effects against bone mineral loss. However, it becomes toxic at higher doses and induces some adverse effects on a number of physiological functions, including reproduction. The aims of this study were to examine F-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of vitamins C and E against possible F-induced endometrial impairment in rats.

2. Rats were divided into three groups: control, F and F plus vitamins. The F group was given 100 mg/L orally for 60 days. Combined vitamins were also administered orally. Fluoride administration to control rats significantly increased endometrial malondialdehyde (MDA) but decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities. Endometrial glandular and stromal apoptosis were investigated by DNA nick end-labelling (TUNEL) method on each sample and the mean endometrial apoptotic index (AI) was calculated.

3. Vitamin administration with F treatment caused endometrial MDA to decrease, but SOD, GSH-Px and CAT activities to increase, all to significant levels. Vitamins showed a histopathological protection against F-induced endometrial damage. There was a significant difference in the AI between the groups. Lymphocyte and eosinophil infiltration in stroma in F-treated rats were more than those in the control and F + Vit groups.

4. It can be concluded that oxidative endometrial damage plays an important role in F-induced endometrial toxicity, and the modulation of oxidative stress with vitamins reduces F-induced endometrial damage both at the biochemical and histological levels.



PMID: 17439417 [PubMed - in process]




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Clin Exp Pharmacol Physiol. 2007 May-Jun;34(5-6):467-74.

Guney M, Oral B, Demirin H, Karahan N, Mungan T, Delibas N.

Department of Obstetrics and Gynecology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.


Effect of fluoride on expression of telomerase reverse transcriptase expression and proliferating cell nuclear antigen in germ cells of rats' testes

OBJECTIVE

To study the damages of fluoride on the male reproductive system in rat testes.


METHODS

A total of 30 male SD rats were randomly divided into control group, high, low dose fluorine treated groups, which were given normal saline, 20 mg/kg sodium fluoride, and 10mg/kg sodium fluoride respectively. After 39 days the change of the weight of rats and the number of sperms were observed. The change of telomerase reverse transcriptase(TERT) and proliferating cell nuclear antigen (PCNA) were observed by using in situ hybridization and radioimmunoassay respectively.


RESULTS

The weight was (273.39 +/- 20.68), (240.00 +/- 21.39) g in NaF treated groups, which was lower than that in control group(P < 0.05); The rate of TERT expression in germ cells of testes in NaF treated groups was (13.89 +/- 4.86)% and (6.33 +/- 4.42)% respectively, which was significantly lower than that in control group (P < 0.05). The rate of PCNA expression in germ cells of tests in NaF treated groups was (0.71 +/- 0.05)%, (0.60 +/- 0.08)% respectively, which also was significant lower than that in control group(P < 0.05). The number of sperms was (18.31 +/- 1.20)10(10)/L, (9.17 +/- 1.38)10(10)/L, which was lower than that in control group (P < 0.05).


CONCLUSION

Fluorine possibly damages the male reproductive system by reducing the expression of TERT and PCNA.



PMID: 17456401 [PubMed - in process]



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Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2007 Feb;25(2):96-9.

Jiang Q, Song XK, Cui QH, Chen LJ.

Zhengzhou Prevention and Treatment Institute for Occupational Disease Zhengzhou 450053, China.


Oxidative stress induced by fluoride in adult mice and their suckling pups

To assess renal and liver damages in pregnant and lactating mice as well as in their suckling pups, Wistar female mice were given 500 ppm NaF (226 ppm F-) in drinking water from the 15th day of pregnancy until day 14 after delivery. All mice were sacrificed on day 14 after parturition.

In the present work, we evaluated the effects of sodium fluoride on histopathological aspects of kidney, antioxidant status, lipid peroxidation levels and on the expression of four stress proteins (namely, the cytosolic heat shock proteins: HSP72, 73, 90 and the reticulum-associated GRP94).

Histological studies have shown many abnormalities in mothers and their pups. Biochemical results showed that lipid peroxidation increased in NaF-treated mice, as evidenced by high kidney and liver thiobarbituric acid reactive substance (TBARS) levels.

Alteration of the antioxidant system was confirmed by the significant decline of serum total antioxidant status and of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in red blood cells. Besides, fluoride treatment induced a decrease in serum levels of non-enzymatic antioxidants such as uric acid and of some oligoelements: zinc and copper, known to be cofactors of superoxide dismutase (SOD-Cu–Zn). Compared to control group, the 72 kDa protein was found to be overexpressed in kidney of 14-day-old mice only. HSP90 expression in liver appeared moderately inhibited in mothers, but decreased significantly in their pups.
No significant changes were detected in the expression of 94 kDa protein in both liver and kidney.

Results showed that fluoride given to dams led to an oxidative stress in mothers as well as in offspring able to induce enhanced lipid peroxidation levels and protein conformational changes, as suggested by stress protein (HSP, GRP) expression changes.



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Experimental and Toxicologic Pathology, Volume 58, Issue 5, 26 April 2007, Pages 339-349

Hanen Bouaziz (a), Françoise Croute (b), Tahia Boudawara (c), Jean Pierre Soleilhavoup (b) and Najiba Zeghal (a), Corresponding Author Contact Information, E-mail The Corresponding Author

a) Laboratoire de Physiologie Animale, Département des Sciences de la Vie, Faculté des Sciences de Sfax, Route de la Soukra-Km 3.5, 3018 Sfax BP 802, Tunisie

b) Laboratoire de Biologie Cellulaire et Pollution, Faculté de Médecine Purpan, Université Toulouse III, 37 Allées Jules Guesde, 31073 Toulouse, France

c) Laboratoire d’Histopathologie, CHU Habib Bourguiba – Sfax, Tunisie

Arsenic and Fluoride Exposure in Drinking Water: Children's IQ and Growth in Shanyin County, Shanxi Province, China.

BACKGROUND

Recently, in a cross-sectional study of 201 children in Araihazar, Bangladesh, exposure to arsenic (As) in drinking water has been shown to lower the scores on tests that measure children's intellectual function before and after adjustment for sociodemographic features.

OBJECTIVES
We investigated the effects of As and fluoride exposure on children's intelligence and growth.

METHODS
We report the results of a study of 720 children between 8 and 12 years of age in rural villages in Shanyin county, Shanxi province, China. The children were exposed to As at concentrations of 142 +/- 106 mug/L (medium-As group) and 190 +/- 183 mug/L (high-As group) in drinking water compared with the control group that was exposed to low concentrations of As (2 +/- 3 mug/L) and low concentrations of fluoride (0.5 +/- 0.2 mg/L). A study group of children exposed to high concentrations of fluoride (8.3 +/- 1.9 mg/L) but low concentrations of As (3 +/- 3 mug/L) was also included because of the common occurrence of elevated concentrations of fluoride in groundwater in our study area. A standardized IQ (intelligence quotient) test was modified for children in rural China and was based on the classic Raven's test used to determine the effects of these exposures on children's intelligence. A standardized measurement procedure for weight, height, chest circumference, and lung capacity was used to determine the effects of these exposures on children's growth.

RESULTS
The mean IQ scores decreased from 105 +/- 15 for the control group, to 101 +/- 16 for the medium-As group (p < 0.05), and to 95 +/- 17 for the high-As group (p < 0.01). The mean IQ score for the high-fluoride group was 101 +/- 16 and significantly different from that of the control group (p < 0.05).
Children in the control group were taller than those in the high-fluoride group (p < 0.05); weighed more than the those in the high-As group (p < 0.05); and had higher lung capacity than those in the medium-As group (p < 0.05).

CONCLUSIONS: Children's intelligence and growth can be affected by high concentrations of As or fluoride. The IQ scores of the children in the high-As group were the lowest among the four groups we investigated. It is more significant that high concentrations of As affect children's intelligence. It indicates that arsenic exposure can affect children's intelligence and growth.


PMID: 17450237 [PubMed - as supplied by publisher]



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Environ Health Perspect. 2007 Apr;115(4):643-647. Epub 2007 Jan 9.

Wang SX, Wang ZH, Cheng XT, Li J, Sang ZP, Zhang XD, Han LL, Qiao XY, Wu ZM, Wang ZQ.

Shanxi Institute for Prevention and Treatment of Endemic Disease, Linfen, Shanxi Province, People's Republic of China.


Thursday, July 26, 2007

Eye Damage from MSG

Controversy surrounding food additive MSG (monosodium glutamate-a common flavor enhancer) was re-ignited when a Japanese researcher suggested that consuming too much of the ingredient could make you go blind.

Researchers at Hirosaki University in Japan have found that rats fed diets high in MSG suffer vision loss and have thinner retinas than those in the control group. Glutamate, a group of chemicals that includes MSG, is an amino acid that acts as a neurotransmitter. It has already been shown to cause nerve damage in experiments where it is injected directly into the eye.

MSG, a sodium salt of the amino acid glutamic acid and a form of glutamate, is used as a flavor enhancer in a variety of foods prepared in restaurants and by food processors. While technically MSG is only one of several forms of free glutamate used in foods, consumers frequently use the term MSG to mean all free glutamate.

Its use has become controversial in the past 30 years because of reports of adverse reactions in people who have eaten foods that contain MSG. According to the U.S. Food and Drug Administration (FDA), research on the role of glutamate in the nervous system has also raised questions about the chemical's safety.

According to lead researcher Hiroshi Ohguro, his is the first study to show that eye damage can be caused by eating food that contains MSG. A report in the New Scientist this week explains that in the study, rats were fed three different diets for six months, containing either high or moderate amounts of MSG, or none. In rats on the high-MSG diet, some retinal nerve layers thinned by as much as 75 percent, and tests that measured retinal response to light showed they could not see as well. Rats on the moderate MSG diet also had damage, to a lesser extent.

The researchers found high concentrations of MSG in the vitreous fluid, which bathes the retina. MSG binds to receptors on retinal cells, destroying them and causing secondary reactions that reduce the ability of the remaining cells to relay electrical signals.

Ohguro acknowledged that large amounts of MSG were used-20 percent of the total diet in the highest group. "Lesser amounts should be OK," he said, "but the precise borderline amount is still unknown."

He said the findings might explain why in eastern Asia, there is a high rate of normal-tension glaucoma, a form of the eye disease that leads to blindness without the usual increase in pressure inside the eyeball. The higher rate, however, could also be due to genetics.

The New Scientist report continues that Peng Tee Khaw, a glaucoma specialist at Moorfields Eye Hospital in London, said the amounts of MSG in the highest diet are "a lot, lot higher than you'd eat. But if you're a sodium glutamate junky, then you could potentially run into problems with your retina."

And while the amount of glutamate in the rats' diets was extremely high, lower dietary intakes could produce the same effects over several decades.

With such persuasive evidence it is clear that food processors must brace themselves for another wave of anti-MSG activity from global consumer associations. In a bid to reassure these same campaigners, food scientists must continue to investigate the impact of MSG, and free glutamates, on human health, as well as looking into alternatives.

One step toward finding alternatives was reported by FoodNavigator.com in April of this year. New research into the use of human taste and smell receptors in functional assays to screen for novel receptor activators and blockers was reported. Senomyx, the U.S. company that carried out the research, is hoping that their research will lead them to discover alternatives to MSG, as well as enhancers of sweet and umami (the taste conveyed by several substances naturally occurring in foods, including glutamate) tastes.

Most are aware that MSG is something that is wise to avoid due to its negative health effects. Most are not aware that MSG is added to most infant formulas. Soy formulas in particular are loaded with MSG.

This table displays some hidden sources of MSG:

These ingredients ALWAYS contain MSG:

Glutamate Glutamic acid Monosodium glutamate
Textured protein Hydrolyzed protein Monopotassium glutamate
Calcium caseinate Sodium caseinate Gelatin
Yeast extract Yeast food Autolyzed yeast

These ingredients OFTEN contain MSG or create MSG during processing:

Flavors & Flavorings Seasonings Natural flavors and flavorings
Natural pork flavoring Natural beef flavoring Natural chicken flavoring
Soy sauce Soy protein isolate Soy protein
Bouillon Stock Broth
Malt extract Malt flavoring Barley malt
Whey protein Carrageenan Maltodextrin
Pectin Enzymes Protease
Corn starch Citric acid Powdered milk
anything Protein fortified anything Enzyme modified anything Ultra-pasteurized

Some unexpected sources of MSG:

Salad dressings Frozen meals Packaged and restaurant soups
Cheese Reduced fat milk Chewing gum
Ice cream Cookies Vitamin enriched foods
Beverages Candy Cigarettes
Medications I.V. Materials Supplements, particularly minerals


Experimental Eye Research September, 2002 75: 307

Food Navigator.com October 23, 2002




How to Find Hidden MSG on Food Labels

MSG (monosodium glutamate) is used as a flavor enhancer in countless processed foods. But while it works enhancing your food’s flavors it is also at work doing potential damage to your brain and body.

MSG is an excitotoxin, a type of chemical transmitter that allows brain cells to communicate. The problem is that excitotoxins can literally excite your brain cells to death. Aside from harming your brain, MSG has also been linked to eye damage, headaches, fatigue, disorientation and depression.

It is very difficult to really know whether MSG is in your food because it has so many aliases. To avoid ingesting this toxic additive, you’re best off choosing fresh, unprocessed foods or becoming very familiar with the hidden names for MSG. Here is just a sampling of ingredients that contain MSG (the link below has a full list):
  • Gelatin
  • Hydrolyzed Vegetable Protein (HVP)
  • Yeast Extract
  • Malted Barley
  • Rice Syrup or Brown Rice Syrup
Also, many restaurants add MSG to their menu items, so when eating out always be sure to tell your server that you don't want MSG added to your food.

The Danger of MSG and How it is Hidden in Vaccines

The glutamate industry and companies, including pharmaceutical firms, that wish to use processed free glutamic acid (MSG) in their products, improperly claim that the term "MSG" only applies to the food ingredient "monosodium glutamate."

They pretend not to realize that "monosodium glutamate" is nothing more than glutamic acid that has been freed from protein through a manufacturing process (processed free glutamic acid), salt (sodium), and moisture. It is the processed free glutamic acid that MSG-sensitive people react to, providing that they ingest amounts that exceed their tolerances for the substance.

Consumers may react to processed free glutamic acid that is contained in any food ingredient or product, including AuxiGro, regardless of the name of the ingredient or product.

Because MSG-sensitive people may react to all ingredients and products that contain processed free glutamic acid, they refer to such ingredients and products as containing "MSG."

In August, 1995, the Food and Drug Administration (FDA) noted in a document entitled the "FDA Backgrounder" that consumers frequently refer to all [free] glutamic acid as "MSG." The "FDA Backgrounder" is still in use by the FDA and can likely be found on their Web site.

Based on peer reviewed studies, there is no question that glutamic acid is neurotoxic. This can be easily confirmed by accessing MEDLINE retrieval service for studies dating from 1966 to the present, using the words "glutamic acid" in combination with the words "brain lesions" and then "neurotoxicity." I would also suggest that you look up the words besity," " and "seizures" combination with the words "glutamic acid."

There is also no question that the young are most at risk from MSG. To confirm this, you might start by reviewing the work of John W. Olney, MD and look up the words "glutamic acid" in combination with the words "blood brain barrier" and "placental barrier."

You will learn that the blood brain barrier is not fully developed in the young to protect against toxins that enter the blood, and that glutamic acid can also penetrate the placental barrier.

Disregarding the blood brain barrier and the placental barrier issues, the literature clearly indicates that, based on the amount of MSG used in the 1970s, over 25% of the population react to MSG.

Although we have not reviewed all vaccines used on infants, we have found one or two sources of processed free glutamic acid (MSG) in those that we have information on. In discussion with a retired executive of a company that produces vaccines, he suggested to me that all viral vaccines would have free glutamic acid, used to feed the live virus.

The glutamic acid in vaccines are often described as "stabilizers," i.e., ingredients to keep the virus alive. We describe them as a hidden source of processed free glutamic acid (MSG).

An example for you would be the Chickenpox Vaccine by VariVax -- Merck & Co., Inc. (Merck). This vaccine includes "L-monosodium glutamate" and "hydrolyzed gelatin."

Another example would be Merck's M-M-R vaccine. The product insert states that the growth medium for measles and mumps includes "amino acids" and "glutamate." It is also stated that the medium for rubella included "amino acids" and "hydrolyzed gelatin." Finally, it states that the "reconstituted vaccine" for subcutaneous administration includes hydrolyzed gelatin.

We have no way of knowing which amino acids are used in Merck's vaccines, but we do know that the amino acids "glutamic acid," "aspartic acid," and "L-cysteine" are neurotoxic.

We also know that any hydrolyzed protein, such as the hydrolyzed gelatin will contain some processed free glutamic acid (MSG), some aspartic acid, and some L-cysteine, all considered to be neurotoxic by neuroscientists. Even without hydrolyzing gelatin, gelatin contains over 11% processed free glutamic acid (MSG) and some aspartic acid and L-cysteine. It is present as a result of the manufacturing process that results in gelatin.

The product insert for M-M-R vaccine by Merck provides a contraindication that states, in part: "Hypersensitivity to any component of the vaccine, including gelatin." It is footnoted to the following reference.

I cannot help but wonder if at least some of the subjects in the study above reacted to gelatin. Most reactions to processed free glutamic acid (MSG), as contained in gelatin, are not IgE mediated. They are best described as a sensitivity to a toxic substance.

If you wish to determine more about Merck vaccines, I would suggest you call their National Service Center at (800) NSC-MERCK. Do not ask about the presence of "MSG" in vaccines. Rather, ask about the presence of "free glutamic acid." You will have a better chance of getting a reliable answer.

Not long ago, a vaccine for Rotavirus came to market. The product, which contained some processed free glutamic acid (MSG), carried a warning in the product insert that it not be used for individuals who had a hypersensitivity to MSG. Shortly after the Rotavirus came to market, it was found that the vaccine resulted in digestive blockages, and the product was withdrawn from the market.

One last comment regarding the exposure of infants to processed free glutamic acid (MSG): the presence of processed free glutamic acid (MSG) in infant formulas.

We have found that major brands of infant formula, if not all infant formulas, contain some processed free glutamic acid (MSG). The hypoallergenic soy formulas contain very high levels of MSG. See www.truthinlabeling.org/formulacopy.html for further detail.

It might be worthwhile for someone to do a study of people who were raised on hypoallergenic formulas to determine if they have experienced a higher incidence of obesity, learning disabilities, and/or ADHD, in childhood and/or endocrine disorders later in life, as compared with people who were breast fed, and then as compared with people who were raised on milk based infant formulas.

If I can be of any further help to anyone on this important subject, they should not hesitate to write or call. If anyone receives a list of ingredients from vaccine producers, I would be pleased to go over the ingredients and advise them of the ingredients that contain processed free glutamic acid (MSG).


Jack Samuels
Phone: (858) 481-9333
E-mail: adandjack@aol.com

Making and using coconut milk

To make coconut milk from fresh coconut, put 4 cups freshly grated coconut (the yield from 1 medium coconut) in a blender. Add just enough boiling water, or boiling water mixed with reserved coconut water, to make a slurry that blends freely, probably 1 cup or a little more. Blend for at least 30 seconds to extract as much flavor as possible. Let the mixture stand until cool enough to handle. Set a sieve over a bowl and line the sieve with a muslin cloth or a triple thickness of cheesecloth. Add the contents of the blender, then gather the edges of the cloth into a bag and wring hard to extract as much liquid as you can.

Put the liquid in a tall glass container, such as a drinking glass or 1-quart jar. You will probably have 2 to 2 1/2 cups. Refrigerate for about 1 hour to allow it to separate into thick and thin layers. It is difficult to predict how much of each you will get. It depends on the fat content of your coconut, the efficiency of your blender, and how vigorously you squeezed. A ratio of one-third thick milk to two-thirds thin milk would be respectable.

If you are pressed for time, you can make acceptable coconut milk with frozen unsweetened grated coconut, preferably from Thailand. Thaw it first, then proceed as for fresh coconut. Dave Bayer, for one, believes it is richer than most of the fresh coconut available here.

Coconut milk quickly loses its sweet, fresh taste. Keep any unused milk in a plastic container in the refrigerator and use within three to four days.

50 Reasons to Oppose Fluoridation

Abstract

Water fluoridation is the practice of adding compounds containing fluoride to the water supply to produce a final concentration of fluoride of 1 part per million in an effort to prevent tooth decay. Trials first began in the US in 1945, but before any of these trials were complete, the practice was endorsed by the US Public Health Service in 1950. Since then fluoridation has been enthusiastically and universally promoted by US health officials as being a "safe and effective" for fighting tooth decay. However, even though most countries worldwide have not succumbed to America's enthusiasm for this practice, their teeth are just as good, if not
better, than those countries that have. The "50 Reasons" offered in this article for opposing fluoridation are based on a thorough review of the scientific literature as regards both the risks and benefits of being exposed to the fluoride ion. Documentation is offered which indicates that the benefits of ingested fluoride have been exaggerated, while the numerous risks have been downplayed or ignored.


1) Fluoride is not an essential nutrient (NRC 1993 and IOM 1997). No disease has ever been linked to a fluoride deficiency. Humans can have perfectly good teeth without fluoride.

2) Fluoridation is not necessary. Most Western European countries are not fluoridated and have experienced the same decline in dental decay as the US (See data from World Health Organization in Appendix 1, and the time trends presented graphically at http://www.fluoridealert.org/who-dmft.htm ). The reasons given by countries for not fluoridating are presented in Appendix 2.)

3) Fluoridation's role in the decline of tooth decay is in serious doubt. The largest survey ever conducted in the US (over 39,000 children from 84 communities) by the National Institute of Dental Research showed little difference in tooth decay among children in fluoridated and non-fluoridated communities (Hileman 1989). According to NIDR researchers, the study found an average difference of only 0.6 DMFS (Decayed Missing and Filled Surfaces) in the permanent teeth of children aged 5-17 residing in either fluoridated or unfluoridated areas (Brunelle and Carlos, 1990). This difference is less than one tooth surface! There are 128 tooth surfaces in a child's mouth. This result was not shown to be statistically significant. In a review commissioned by the Ontario government, Dr. David Locker concluded:

"The magnitude of [fluoridation's] effect is not large in absolute terms, is often not statistically significant and may not be of clinical significance" (Locker 1999).

4) Where fluoridation has been discontinued in communities from Canada, the former East Germany, Cuba and Finland, dental decay has not increased but has actually decreased (Maupome 2001; Kunzel and Fischer,1997,2000; Kunzel 2000 and Seppa 2000).

5) There have been numerous recent reports of dental crises in US cities (e.g. Boston, Cincinnati, New York City) which have been fluoridated for over 20 years. There appears to be a far greater (inverse) relationship between tooth decay and income level than with water fluoride levels.

6) Modern research (e.g. Diesendorf 1986; Colquhoun 1997, and De Liefde, 1998) shows that decay rates were coming down before fluoridation was introduced and have continued to decline even after its benefits would have been maximized. Many other factors influence tooth decay. Some recent studies have found that tooth decay actually increases as the fluoride concentration in the water increases (Olsson 1979; Retief 1979; Mann 1987, 1990; Steelink 1992; Teotia 1994; Grobleri 2001; Awadia 2002 and Ekanayake 2002).

7) The Centers for Disease Control and Prevention (CDC 1999, 2001) has now acknowledged the findings of many leading dental researchers, that the mechanism of fluoride's benefits are mainly TOPICAL not SYSTEMIC. Thus, you don't have to swallow fluoride to protect teeth. As the benefits of fluoride (if any exist) are topical, and the risks are systemic, it makes more sense, for those who want to take the risks, to deliver the fluoride directly to the tooth in the form of toothpaste. Since swallowing fluoride is unnecessary, there is no reason to force people (against their will) to drink fluoride in their water supply. This position was recently shared by Dr. Douglas Carnall, the associate editor of the British Medical Journal. His editorial appears in Appendix 3.

8) Despite being prescribed by doctors for over 50 years, the US Food and Drug Administration (FDA) has never approved any fluoride product designed for ingestion as safe or effective. Fluoride supplements are designed to deliver the same amount of fluoride as ingested daily from fluoridated water (Kelly 2000).

9) The US fluoridation program has massively failed to achieve one of its key objectives, i.e. to lower dental decay rates while holding down dental fluorosis (mottled and discolored enamel), a condition known to be caused by fluoride. The goal of the early promoters of fluoridation was to limit dental fluorosis (in its mildest form) to 10% of children (NRC 1993, pp. 6-7). A major US survey has found 30% of children in optimally fluoridated areas had dental fluorosis on at least two teeth (Heller 1997), while smaller studies have found up to 80% of children impacted (Williams 1990; Lalumandier 1995 and Morgan 1998). The York Review estimates that up to 48% of children in optimally fluoridated areas worldwide have dental fluorosis in all forms and 12.5% with symptoms of aesthetic concern (McDonagh, 2000).

10) Dental fluorosis means that a child has been overdosed on fluoride. While the mechanism by which the enamel is damaged is not definitively known, it appears fluorosis may be a result of either inhibited enzymes in the growing teeth (Dan Besten 1999), or through fluoride's interference with G-protein signaling mechanisms (Matsuo 1996). In a study in Mexico, Alarcon-Herrera (2001) has shown a linear correlation between the severity of dental fluorosis and the frequency of bone fractures in children.

11) The level of fluoride put into water (1 ppm) is up to 200 times higher than normally found in mothers' milk (0.005 – 0.01 ppm) (Ekstrand 1981; Institute of Medicine 1997). There are no benefits, only risks, for infants ingesting this heightened level of fluoride at such an early age (this is an age where susceptibility to environmental toxins is particularly high).

12) Fluoride is a cumulative poison. On average, only 50% of the fluoride we ingest each day is excreted through the kidneys. The remainder accumulates in our bones, pineal gland, and other tissues. If the kidney is damaged, fluoride accumulation will increase, and with it, the likelihood of harm.

13) Fluoride is very biologically active even at low concentrations. It interferes with hydrogen bonding (Emsley 1981) and inhibits numerous enzymes (Waldbott 1978).

14) When complexed with aluminum, fluoride interferes with G-proteins (Bigay 1985, 1987). Such interactions give aluminum-fluoride complexes the potential to interfere with many hormonal and some neurochemical signals (Strunecka & Patocka 1999, Li 2003).

15) Fluoride has been shown to be mutagenic, cause chromosome damage and interfere with the enzymes involved with DNA repair in a variety of cell and tissue studies (Tsutsui 1984; Caspary 1987; Kishi 1993 and Mihashi 1996). Recent studies have also found a correlation between fluoride exposure and chromosome damage in humans (Sheth 1994; Wu 1995; Meng 1997 and Joseph 2000).

16) Fluoride forms complexes with a large number of metal ions, which include metals which are needed in the body (like calcium and magnesium) and metals (like lead and aluminum) which are toxic to the body. This can cause a variety of problems. For example, fluoride interferes with enzymes where magnesium is an important co-factor, and it can help facilitate the uptake of aluminum and lead into tissues where these metals wouldn't otherwise go (Mahaffey 1976; Allain 1996; Varner 1998).

17) Rats fed for one year with 1 ppm fluoride in their water, using either sodium fluoride or aluminum fluoride, had morphological changes to their kidneys and brains, an increased uptake of aluminum in the brain, and the formation of beta amyloid deposits which are characteristic of Alzheimers disease (Varner 1998).

18) Aluminum fluoride was recently nominated by the Environmental Protection Agency and National Institute of Environmental Health Sciences for testing by the National Toxicology Program. According to EPA and NIEHS, aluminum fluoride currently has a "high health research priority" due to its "known neurotoxicity" (BNA, 2000). If fluoride is added to water which contains aluminum, than aluminum fluoride complexes will form.

19) Animal experiments show that fluoride accumulates in the brain and exposure alters mental behavior in a manner consistent with a neurotoxic agent (Mullenix 1995). Rats dosed prenatally demonstrated hyperactive behavior. Those dosed postnatally demonstrated hypoactivity (i.e. under activity or "couch potato" syndrome). More recent animal experiments have reported that fluoride can damage the brain (Wang 1997; Guan 1998; Varner 1998; Zhao 1998; Zhang 1999; Lu 2000; Shao 2000; Sun 2000; Bhatnagar 2002; Chen 2002, 2003; Long 2002; Shivarajashankara 2002a, b; Shashi 2003 and Zhai 2003) and impact learning and behavior (Paul 1998; Zhang 1999, 2001; Sun 2000; Ekambaram 2001; Bhatnagar 2002).

20) Five studies from China show a lowering of IQ in children associated with fluoride exposure (Lin Fa-Fu 1991; Li 1995; Zhao 1996; Lu 2000; and Xiang 2003a, b). One of these studies (Lin Fa-Fu 1991) indicates that even just moderate levels of fluoride exposure (e.g. 0.9 ppm in the water) can exacerbate the neurological defects of iodine deficiency.

21) Studies by Jennifer Luke (2001) showed that fluoride accumulates in the human pineal gland to very high levels. In her Ph.D. thesis Luke has also shown in animal studies that fluoride reduces melatonin production and leads to an earlier onset of puberty (Luke 1997).

22) In the first half of the 20th century, fluoride was prescribed by a number of European doctors to reduce the activity of the thyroid gland for those suffering from hyperthyroidism (over active thyroid) (Stecher 1960; Waldbott 1978). With water fluoridation, we are forcing people to drink a thyroid-depressing medication which could, in turn, serve to promote higher levels of hypothyroidism (underactive thyroid) in the population, and all the subsequent problems related to this disorder. Such problems include depression, fatigue, weight gain, muscle and joint pains, increased cholesterol levels, and heart disease.

It bears noting that according to the Department of Health and Human Services (1991) fluoride exposure in fluoridated communities is estimated to range from 1.6 to 6.6 mg/day, which is a range that actually overlaps the dose (2.3 - 4.5 mg/day) shown to decrease the functioning of the human thyroid (Galletti & Joyet 1958). This is a remarkable fact, particularly considering the rampant and increasing problem of hypothyroidism in the United States (in 1999, the second most prescribed drug of the year was Synthroid, which is a hormone replacement drug used to treat an underactive thyroid). In Russia, Bachinskii (1985) found a lowering of thyroid function, among otherwise healthy people, at 2.3 ppm fluoride in water.

23) Some of the early symptoms of skeletal fluorosis, a fluoride-induced bone and joint disease that impacts millions of people in India, China, and Africa , mimic the symptoms of arthritis (Singh 1963; Franke 1975; Teotia 1976; Carnow 1981; Czerwinski 1988; DHHS 1991). According to a review on fluoridation by Chemical & Engineering News, "Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed" (Hileman 1988). Few if any studies have been done to determine the extent of this misdiagnosis, and whether the high prevalence of arthritis in America (1 in 3 Americans have some form of arthritis - CDC, 2002) is related to our growing fluoride exposure, which is highly plausible. The causes of most forms of arthritis (e.g. osteoarthritis) are unknown.

24) In some studies, when high doses of fluoride (average 26 mg per day) were used in trials to treat patients with osteoporosis in an effort to harden their bones and reduce fracture rates, it actually led to a HIGHER number of fractures, particularly hip fractures (Inkovaara 1975; Gerster 1983; Dambacher 1986; O’Duffy 1986; Hedlund 1989; Bayley 1990; Gutteridge 1990. 2002; Orcel 1990; Riggs 1990 and Schnitzler 1990). The cumulative doses used in these trials are exceeded by the lifetime cumulative doses being experienced by many people living in fluoridated communities.

25) Nineteen studies (three unpublished, including one abstract) since 1990 have examined the possible relationship of fluoride in water and hip fracture among the elderly. Eleven of these studies found an association, eight did not. One study found a dose-related increase in hip fracture as the concentration of fluoride rose from 1 ppm to 8 ppm (Li 2001). Hip fracture is a very serious issue for the elderly, as a quarter of those who have a hip fracture die within a year of the operation, while 50 percent never regain an independent existence (All 19 of these studies are referenced as a group in the reference section).

26) The only government-sanctioned animal study to investigate if fluoride causes cancer, found a dose-dependent increase in cancer in the target organ (bone) of the fluoride-treated (male) rats (NTP 1990). The initial review of this study also reported an increase in liver and oral cancers, however, all non-bone cancers were later downgraded – with a questionable rationale - by a government-review panel (Marcus 1990). In light of the importance of this study, EPA Professional Headquarters Union has requested that Congress establish an independent review to examine the study's results (Hirzy 2000).

27) A review of national cancer data in the US by the National Cancer Institute (NCI) revealed a significantly higher rate of bone cancer in young men in fluoridated versus unfluoridated areas (Hoover 1991). While the NCI concluded that fluoridation was not the cause, no explanation was provided to explain the higher rates in the fluoridated areas. A smaller study from New Jersey (Cohn 1992) found bone cancer rates to be up to 6 times higher in young men living in fluoridated versus unfluoridated areas. Other epidemiological studies have failed to find this relationship (Mahoney 1991; Freni 1992).

28) Fluoride administered to animals at high doses wreaks havoc on the male reproductive system - it damages sperm and increases the rate of infertility in a number of different species (Kour 1980; Chinoy 1989; Chinoy 1991; Susheela 1991; Chinoy 1994; Kumar 1994; Narayana 1994a, b; Zhao 1995; Elbetieha 2000; Ghosh 2002 and Zakrzewska 2002). While studies conducted at the FDA have failed to find reproductive effects in rats (Sprando 1996, 1997, 1998), an epidemiological study from the US has found increased rates of infertility among couples living in areas with 3 or more ppm fluoride in the water (Freni 1994), and 2 studies have found a reduced level of circulating testosterone in males living in high fluoride areas (Susheela 1996 and Barot 1998).

29) The fluoridation program has been very poorly monitored. There has never been a comprehensive analysis of the fluoride levels in the bones, blood, or urine of the American people or the citizens of other fluoridated countries. Based on the sparse data that has become available, however, it is increasingly evident that some people in the population – particularly people with kidney disease - are accumulating fluoride levels that have been associated with harm to both animals and humans, particularly harm to bone (see Connett 2004).

30) Once fluoride is put in the water it is impossible to control the dose each individual receives. This is because 1) some people (e.g. manual laborers, athletes, diabetics, and people with kidney disease) drink more water than others, and 2) we receive fluoride from sources other than the water supply. Other sources of fluoride include food and beverages processed with fluoridated water (Kiritsy 1996 and Heilman 1999), fluoridated dental products (Bentley 1999 and Levy 1999), mechanically deboned meat (Fein 2001), teas (Levy 1999), and pesticide residues on food (Stannard 1991 and Burgstahler 1997).

31) Fluoridation is unethical because individuals are not being asked for their informed consent prior to medication. This is standard practice for all medication, and one of the key reasons why most of western Europe has ruled against fluoridation (see appendix 2).

As one doctor aptly stated, "No physician in his right senses would prescribe for a person he has never met, whose medical history he does not know, a substance which is intended to create bodily change, with the advice: 'Take as much as you like, but you will take it for the rest of your life because some children suffer from tooth decay.’ It is a preposterous notion."

32) While referenda are preferential to imposed policies from central government, it still leaves the problem of individual rights versus majority rule. Put another way -- does a voter have the right to require that their neighbor ingest a certain medication (even if it's against that neighbor's will)?

33) Some individuals appear to be highly sensitive to fluoride as shown by case studies and double blind studies (Shea 1967, Waldbott 1978 and Moolenburg 1987). In one study, which lasted 13 years, Feltman and Kosel (1961) showed that about 1% of patients given 1 mg of fluoride each day developed negative reactions. Can we as a society force these people to ingest fluoride?

34) According to the Agency for Toxic Substances and Disease Registry (ATSDR 1993), and other researchers (Juncos & Donadio 1972; Marier & Rose 1977 and Johnson 1979), certain subsets of the population may be particularly vulnerable to fluoride's toxic effects; these include: the elderly, diabetics and people with poor kidney function. Again, can we in good conscience force these people to ingest fluoride on a daily basis for their entire lives?

35) Also vulnerable are those who suffer from malnutrition (e.g. calcium, magnesium, vitamin C, vitamin D and iodide deficiencies and protein poor diets) (Massler & Schour 1952; Marier & Rose 1977; Lin Fa-Fu 1991; Chen 1997; Teotia 1998). Those most likely to suffer from poor nutrition are the poor, who are precisely the people being targeted by new fluoridation programs. While being at heightened risk, poor families are less able to afford avoidance measures (e.g. bottled water or removal equipment).

36) Since dental decay is most concentrated in poor communities, we should be spending our efforts trying to increase the access to dental care for poor families. The real "Oral Health Crisis" that exists today in the United States, is not a lack of fluoride but poverty and lack of dental insurance. The Surgeon General has estimated that 80% of dentists in the US do not treat children on Medicaid.

37) Fluoridation has been found to be ineffective at preventing one of the most serious oral health problems facing poor children, namely, baby bottle tooth decay, otherwise known as early childhood caries (Barnes 1992 and Shiboski 2003).

38) The early studies conducted in 1945 -1955 in the US, which helped to launch fluoridation, have been heavily criticized for their poor methodology and poor choice of control communities (De Stefano 1954; Sutton 1959, 1960 and 1996; Ziegelbecker 1970). According to Dr. Hubert Arnold, a statistician from the University of California at Davis, the early fluoridation trials "are especially rich in fallacies, improper design, invalid use of statistical methods, omissions of contrary data, and just plain muddleheadedness and hebetude." In 2000, the British Government’s “York Review” could give no fluoridation trial a grade A classification – despite 50 years of research (McDonagh 2000, see Appendix 3 for commentary).

39) The US Public Health Service first endorsed fluoridation in 1950, before one single trial had been completed (McClure 1970)!

40) Since 1950, it has been found that fluorides do little to prevent pit and fissure tooth decay, a fact that even the dental community has acknowledged (Seholle 1984; Gray 1987; PHS 1993; and Pinkham 1999). This is significant because pit and fissure tooth decay represents up to 85% of the tooth decay experienced by children today (Seholle 1984 and Gray 1987).

41) Despite the fact that we are exposed to far more fluoride today than we were in 1945 (when fluoridation began), the "optimal" fluoridation level is still 1 part per million, the same level deemed optimal in 1945! (Marier & Rose 1977; Levy 1999; Rozier 1999 and Fomon 2000).

42) The chemicals used to fluoridate water in the US are not pharmaceutical grade. Instead, they come from the wet scrubbing systems of the superphosphate fertilizer industry. These chemicals (90% of which are sodium fluorosilicate and fluorosilicic acid), are classified hazardous wastes contaminated with various impurities. Recent testing by the National Sanitation Foundation suggest that the levels of arsenic in these chemicals are relatively high (up to 1.6 ppb after dilution into public water) and of potential concern (NSF 2000 and Wang 2000).

43) These hazardous wastes have not been tested comprehensively. The chemical usually tested in animal studies is pharmaceutical grade sodium fluoride, not industrial grade fluorosilicic acid. The assumption being made is that by the time this waste product has been diluted, all the fluorosilicic acid will have been converted into free fluoride ion, and the other toxics and radioactive isotopes will be so dilute that they will not cause any harm, even with lifetime exposure. These assumptions have not been examined carefully by scientists, independent of the fluoridation program.

44) Studies by Masters and Coplan (1999, 2000) show an association between the use of fluorosilicic acid (and its sodium salt) to fluoridate water and an increased uptake of lead into children's blood. Because of lead’s acknowledged ability to damage the child’s developing brain, this is a very serious finding yet it is being largely ignored by fluoridating countries.

45) Sodium fluoride is an extremely toxic substance -- just 200 mg of fluoride ion is enough to kill a young child, and just 3-5 grams (e.g. a teaspoon) is enough to kill an adult. Both children (swallowing tablets/gels) and adults (accidents involving fluoridation equipment and filters on dialysis machines) have died from excess exposure.

46) Some of the earliest opponents of fluoridation were biochemists and at least 14 Nobel Prize winners are among numerous scientists who have expressed their reservations about the practice of fluoridation (see appendix 4).

47) The recent Nobel Laureate in Medicine and Physiology, Dr. Arvid Carlsson (2000), was one of the leading opponents of fluoridation in Sweden, and part of the panel that recommended that the Swedish government reject the practice, which they did in 1971. According to Carlsson:

"I am quite convinced that water fluoridation, in a not-too-distant future, will be consigned to medical history...Water fluoridation goes against leading principles of pharmacotherapy, which is progressing from a stereotyped medication - of the type 1 tablet 3 times a day - to a much more individualized therapy as regards both dosage and selection of drugs. The addition of drugs to the drinking water means exactly the opposite of an individualized therapy" (Carlsson 1978).

48) While pro-fluoridation officials continue to promote fluoridation with undiminished fervor, they cannot defend the practice in open public debate – even when challenged to do so by organizations such as the Association for Science in the Public Interest, the American College of Toxicology, or the US Environmental Protection Agency (Bryson 2004). According to Dr. Michael Easley, a prominent lobbyist for fluoridation in the US, "Debates give the illusion that a scientific controversy exists when no credible people support the fluorophobics' view" (See appendix 5).

In light of proponents’ refusal to debate this issue, Dr. Edward Groth, a Senior Scientist at Consumers Union, observed that "the political profluoridation stance has evolved into a dogmatic, authoritarian, essentially antiscientific posture, one that discourages open debate of scientific issues" (Martin 1991).

49) Many scientists, doctors and dentists who have spoken out publicly on this issue have been subjected to censorship and intimidation (Martin 1991). Most recently, Dr. Phyllis Mullenix was fired from her position as Chair of Toxicology at Forsythe Dental Center for publishing her findings on fluoride and the brain; and Dr. William Marcus was fired from the EPA for questioning the government’s handling of the NTP’s fluoride-cancer study (Bryson 2004). Tactics like this would not be necessary if those promoting fluoridation were on secure scientific ground.

50) The Union representing the scientists at US EPA headquarters in Washington DC is now on record as opposing water fluoridation (Hirzy 1999). According to the Union’s Senior Vice President, Dr. William Hirzy:

"In summary, we hold that fluoridation is an unreasonable risk. That is, the toxicity of fluoride is so great and the purported benefits associated with it are so small - if there are any at all - that requiring every man, woman and child in America to ingest it borders on criminal behavior on the part of governments."

Conclusion

When it comes to controversies surrounding toxic chemicals, invested interests traditionally do their very best to discount animal studies and quibble with epidemiological findings. In the past, political pressures have led government agencies to drag their feet on regulating asbestos, benzene, DDT, PCBs, tetraethyl lead, tobacco and dioxins. With fluoridation we have had a fifty year delay. Unfortunately, because government officials have put so much of their credibility on the line defending fluoridation, and because of the huge liabilities waiting in the wings if they admit that fluoridation has caused an increase in hip fracture, arthritis, bone cancer, brain disorders or thyroid problems, it will be very difficult for them to speak honestly and openly about the issue. But they must, not only to protect millions of people from unnecessary harm, but to protect the notion that, at its core, public health policy must be based on sound science not political expediency. They have a tool with which to do this: it's called the Precautionary Principle. Simply put, this says: if in doubt leave it out. This is what most European countries have done and their children's teeth have not suffered, while their public's trust has been strengthened.

It is like a question from a Kafka play. Just how much doubt is needed on just one of the health concerns identified above, to override a benefit, which when quantified in the largest survey ever conducted in the US, amounts to less than one tooth surface (out of 128) in a child's mouth?

For those who would call for further studies, I say fine. Take the fluoride out of the water first and then conduct all the studies you want. This folly must end without further delay.


APPENDIX 1.
World Health Organization Data

DMFT (Decayed, Missing & Filled teeth) Status for 12 year olds by Country

DMFTs Year Status*
Australia 0.8 1998 More than 50% of water is fluoridated
Zurich, Switzerland 0.84 1998 Water is unfluoridated, but salt is fluoridated
Netherlands 0.9 1992-93 No water fluoridation or salt fluoridation
Sweden 0.9 1999 No water fluoridation or salt fluoridation
Denmark 0.9 2001 No water fluoridation or salt fluoridation
UK (England & Wales) 0.9 1996-97 11% of water supplies are fluoridated
Ireland 1.1 1997 More than 50% of water is fluoridated
Finland 1.1 1997 No water fluoridation or salt fluoridation
Germany 1.2 2000 No water fluoridation, but salt fluoridation is common
US 1.4 1988-91 More than 50% of water is fluoridated
Norway 1.5 1998 No water fluoridation or salt fluoridation
Iceland 1.5 1996 No water fluoridation or salt fluoridation
New Zealand 1.5 1993 More than 50% of water is fluoridated
Belgium 1.6 1998 No water fluoridation, but salt fluoridation is common
Austria 1.7 1997 No water fluoridation, but salt fluoridation is common
France 1.9 1998 No water fluoridation, but salt fluoridation is common

Data from WHO Oral Health Country/Area Profile Programme Department of Noncommunicable Diseases Surveillance/Oral Health WHO Collaborating Centre, Malmö University, Sweden
http://www.whocollab.od.mah.se/euro.html


APPENDIX 2.
Statements on fluoridation by governmental officials from several countries

Germany: "Generally, in Germany fluoridation of drinking water is forbidden. The relevant German law allows exceptions to the fluoridation ban on application. The argumentation of the Federal Ministry of Health against a general permission of fluoridation of drinking water is the problematic nature of compuls[ory] medication." (Gerda Hankel-Khan, Embassy of Federal Republic of Germany, September 16, 1999). www.fluoridealert.org/germany.jpeg

France: "Fluoride chemicals are not included in the list [of 'chemicals for drinking water treatment']. This is due to ethical as well as medical considerations." (Louis Sanchez, Directeur de la Protection de l'Environment, August 25, 2000). www.fluoridealert.org/france.jpeg

Belgium: "This water treatment has never been of use in Belgium and will never be (we hope so) into the future. The main reason for that is the fundamental position of the drinking water sector that it is not its task to deliver medicinal treatment to people. This is the sole responsibility of health services." (Chr. Legros, Directeur, Belgaqua, Brussels, Belgium, February 28, 2000). www.fluoridation.com/c-belgium.htm

Luxembourg: "Fluoride has never been added to the public water supplies in Luxembourg. In our views, the drinking water isn't the suitable way for medicinal treatment and that people needing an addition of fluoride can decide by their own to use the most appropriate way, like the intake of fluoride tablets, to cover their [daily] needs." (Jean-Marie RIES, Head, Water Department, Administration De L'Environment, May 3, 2000). www.fluoridealert.org/luxembourg.jpeg

Finland: "We do not favor or recommend fluoridation of drinking water. There are better ways of providing the fluoride our teeth need." (Paavo Poteri, Acting Managing Director, Helsinki Water, Finland, February 7, 2000). www.fluoridation.com/c-finland.htm

"Artificial fluoridation of drinking water supplies has been practiced in Finland only in one town, Kuopio, situated in eastern Finland and with a population of about 80,000 people (1.6% of the Finnish population). Fluoridation started in 1959 and finished in 1992 as a result of the resistance of local population. The most usual grounds for the resistance presented in this context were an individual's right to drinking water without additional chemicals used for the medication of limited population groups. A concept of "force-feeding" was also mentioned.

Drinking water fluoridation is not prohibited in Finland but no municipalities have turned out to be willing to practice it. Water suppliers, naturally, have always been against dosing of fluoride chemicals into water." (Leena Hiisvirta, M.Sc., Chief Engineer, Ministry of Social Affairs and Health, Finland, January 12, 1996.) www.fluoridealert.org/finland.jpeg

Denmark: "We are pleased to inform you that according to the Danish Ministry of Environment and Energy, toxic fluorides have never been added to the public water supplies. Consequently, no Danish city has ever been fluoridated." (Klaus Werner, Royal Danish Embassy, Washington DC, December 22, 1999). www.fluoridation.com/c-denmark.htm

Norway: "In Norway we had a rather intense discussion on this subject some 20 years ago, and the conclusion was that drinking water should not be fluoridated." (Truls Krogh & Toril Hofshagen, Folkehelsa Statens institutt for folkeheise (National Institute of Public Health) Oslo, Norway, March 1, 2000). www.fluoridation.com/c-norway.htm

Sweden: "Drinking water fluoridation is not allowed in Sweden...New scientific documentation or changes in dental health situation that could alter the conclusions of the Commission have not been shown." (Gunnar Guzikowski, Chief Government Inspector, Livsmedels Verket -- National Food Administration Drinking Water Division, Sweden, February 28, 2000). www.fluoridation.com/c-sweden.htm

Netherlands: "From the end of the 1960s until the beginning of the 1970s drinking water in various places in the Netherlands was fluoridated to prevent caries. However, in its judgement of 22 June 1973 in case No. 10683 (Budding and co. versus the City of Amsterdam) the Supreme Court (Hoge Road) ruled there was no legal basis for fluoridation. After that judgement, amendment to the Water Supply Act was prepared to provide a legal basis for fluoridation. During the process it became clear that there was not enough support from Parlement [sic] for this amendment and the proposal was withdrawn." (Wilfred Reinhold, Legal Advisor, Directorate Drinking Water, Netherlands, January 15, 2000). www.fluoridation.com/c-netherlands.htm

Northern Ireland: "The water supply in Northern Ireland has never been artificially fluoridated except in 2 small localities where fluoride was added to the water for about 30 years up to last year. Fluoridation ceased at these locations for operational reasons. At this time, there are no plans to commence fluoridation of water supplies in Northern Ireland." (C.J. Grimes, Department for Regional Development, Belfast, November 6, 2000). www.fluoridealert.org/Northern-Ireland.jpeg

Austria: "Toxic fluorides have never been added to the public water supplies in Austria." (M. Eisenhut, Head of Water Department, Osterreichische Yereinigung fur das Gas-und Wasserfach Schubertring 14, A-1015 Wien, Austria, February 17, 2000). www.fluoridation.com/c-austria.htm

Czech Republic:"Since 1993, drinking water has not been treated with fluoride in public water supplies throughout the Czech Republic. Although fluoridation of drinking water has not actually been proscribed it is not under consideration because this form of supplementation is considered as follows:

(a) uneconomical (only 0.54% of water suitable for drinking is used as such; the remainder is employed for hygiene etc. Furthermore, an increasing amount of consumers (particularly children) are using bottled water for drinking (underground water usually with fluor)

(b) unecological (environmental load by a foreign substance)

(c) unethical ("forced medication")

(d) toxicologically and phyiologically debateable (fluoridation represents an untargeted form of supplementation which disregards actual individual intake and requirements and may lead to excessive health-threatening intake in certain population groups; [and] complexation of fluor in water into non biological active forms of fluor." (Dr. B. Havlik, Ministerstvo Zdravotnictvi Ceske Republiky, October 14, 1999).
www.fluoridealert.org/czech.jpeg


APPENDIX 3.
Statement of Douglas Carnall, Associate Editor of the British Medical Journal, published on the BMJ website (http://www.bmj.com ) on the day that they published the York Review on Fluoridation.

See this review on the web at http://bmj.bmjjournals.com/cgi/content/full/321/7265/904/a

British Medical Journal, October 7, 2000, Reviews, Website of the week: Water fluoridation

Fluoridation was a controversial topic even before Kubrick's Base Commander Ripper railed against "the international communist conspiracy to sap and impurify all of our precious bodily fluids" in the 1964 film Dr Strangelove. This week's BMJ shouldn't precipitate a global holocaust, but it does seem that Base Commander Ripper may have had a point. The systematic review published this week (p 855) shows that much of the evidence for fluoridation was derived from low quality studies, that its benefits may have been overstated, and that the risk to benefit ratio for the development of the commonest side effect (dental fluorosis, or mottling of the teeth) is rather high.

Supplementary materials are available on the BMJ 's website and on that of the review's authors, enhancing the validity of the conclusions through transparency of process. For example, the "frequently asked questions" page of the site explains who comprised the advisory panel and how they were chosen ("balanced to include those for and against, as well as those who are neutral"), and the site includes the minutes of their meetings. You can also pick up all 279 references in Word97 format, and tables of data in PDF. Such transparency is admirable and can only encourage rationality of debate.

Professionals who propose compulsory preventive measures for a whole population have a different weight of responsibility on their shoulders than those who respond to the requests of individuals for help. Previously neutral on the issue, I am now persuaded by the arguments that those who wish to take fluoride (like me) had better get it from toothpaste rather than the water supply (see www.derweb.co.uk/bfs/index.html and www.npwa.freeserve.co.uk/index.html for the two viewpoints).

Douglas Carnall
Associate Editor
British Medical Journal


APPENDIX 4.
List of 14 Noble Prize winners who have opposed or expressed reservations about fluoridation.

1) Adolf Butenandt (Chemistry, 1939)
2) Arvid Carlsson (Medicine, 2000)
3) Hans von Euler-Chelpin (Chemistry, 1929).
4) Walter Rudolf Hess (Medicine, 1949)
5) Corneille Jean-François Heymans (Medicine, 1938)
6) Sir Cyril Norman Hinshelwood (Chemistry, 1956)
7) Joshua Lederberg (Medicine, 1958)
8) William P. Murphy (Medicine, 1934)
8) Giulio Natta (1963 Nobel Prize in Chemistry)
10) Sir Robert Robinson (Chemistry, 1947)
11) Nikolai Semenov (Chemistry, 1956)
12) James B. Sumner (Chemistry, 1946)
13) Hugo Theorell (Medicine, 1955)
14) Artturi Virtanen (Chemistry, 1945)


APPENDIX 5.
Quotes on debating fluoridation from Dr. Michael Easley, Director of the National Center for Fluoridation Policy and Research, and one of the most active proponents of fluoridation in the US (Easley 1999). Easley’s quotes typify the historic contempt that proponents have had to scientific debate.

"A favorite tactic of the fluorophobics is to argue for a debate so that 'the people can decide who is right.' Proponents of fluoride are often trapped into consenting to public debates."

"Debates give the illusion that a scientific controversy exists when no credible people support the fluorophobics' view."

"Like parasites, opponents steal undeserved credibility just by sharing the stage with respected scientists who are there to defend fluoridation"; and,

"Unfortunately, a most flagrant abuse of the public trust occasionally occurs when a physician or a dentist, for whatever personal reason, uses their professional standing in the community to argue against fluoridation, a clear violation of professional ethics, the principles of science and community standards of practice."


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McClure F. (1970). Water fluoridation, the search and the victory. US Department of Health, Education, and Welfare, Washington DC.

McDonagh M, et al. (2000). A Systematic Review of Public Water Fluoridation. NHS Center for Reviews and Dissemination,. University of York, September 2000.

Meng Z, Zhang B. (1997). Chromosomal aberrations and micronuclei in lymphocytes of workers at a phosphate fertilizer factory. Mutation Research 393: 283-288.

Mihashi,M. and Tsutsui,T.(1996). Clastogenic activity of sodium fluoride to rat vertebral body-derived cells in culture. Mutation Research 368: 7-13.

Moolenburgh H. (1987). Fluoride: The Freedom Fight. Mainstream Publishing, Edinburgh.

Morgan L, et al. (1998). Investigation of the possible associations between fluorosis, fluoride exposure, and childhood behavior problems. Pediatric Dentistry 20: 244-252.

Mullenix P, et al. (1995). Neurotoxicity of sodium fluoride in rats. Neurotoxicology and Teratology 17: 169-177.

Narayana MV, et al. (1994). Reversible effects of sodium fluoride ingestion on spermatozoa of the rat. International Journal of Fertility and Menopausal Studies 39: 337-46.

Narayana MV, Chinoy NJ. (1994). Effect of fluoride on rat testicular steroidogenesis. Fluoride 27: 7-12.

National Research Council. (1993). Health Effects of Ingested Fluoride. National Academy Press, Washington DC.

National Sanitation Foundation International (NSF). (2000) Letter from Stan Hazan, General Manager, NSF Drinking Water Additives Certification Program, to Ken Calvert, Chairman, Subcommittee on Energy and the Environment, Committee on Science, US House of Representatives. July 7. http://www.keepersofthewell.org/product_pdfs/NSF_response.pdf

National Toxicology Program [NTP] (1990). Toxicology and Carcinogenesis Studies of Sodium Fluoride in F344/N Rats and B6C3f1 Mice. Technical report Series No. 393. NIH Publ. No 91-2848. National Institute of Environmental Health Sciences, Research Triangle Park, N.C. The results of this study are summarized in the Department of Health and Human Services report (DHHS,1991) op cit.

O'Duffy JD, et al. (1986). Mechanism of acute lower extremity pain syndrome in fluoride-treated osteoporotic patients. American Journal of Medicine 80: 561-6.

Olsson B. (1979). Dental findings in high-fluoride areas in Ethiopia. Community Dentistry and Oral Epidemiology 7: 51-6.

Orcel P, et al. (1990). Stress fractures of the lower limbs in osteoporotic patients treated with fluoride. Journal of Bone and Mineral Research 5(Suppl 1): S191-4.

Paul V, et al. (1998). Effects of sodium fluoride on locomotor behavior and a few biochemical parameters in rats. Environmental Toxicology and Pharmacology 6: 187–191.

Pinkham, JR, ed. (1999). Pediatric Dentistry Infancy Through Adolescence. 3rd Edition. WB Saunders Co, Philadelphia.

Public Health Service (PHS). (1993). Toward improving the oral health of Americans: an overview of oral health status, resources, and care delivery. Public Health Reports 108: 657-72.

Retief DH, et al. (1979). Relationships among fluoride concentration in enamel, degree of fluorosis and caries incidence in a community residing in a high fluoride area. Journal of Oral Pathology 8: 224-36.

Riggs BL, et al. (1990). Effect of Fluoride treatment on the Fracture Rates in Postmenopausal Women with Osteoporosis. New England Journal of Medicine 322: 802-809.

Rozier RG. (1999). The prevalence and severity of enamel fluorosis in North American children. Journal of Public Health Dentistry 59: 239-46.

Schnitzler CM, et al. (1990). Bone fragility of the peripheral skeleton during fluoride therapy for osteoporosis. Clinical Orthopaedics (261): 268-75.

Seholle RH. (1984). Preserving the perfect tooth (editorial). Journal of the American Dental Association 108: 448.

Seppa L, et al. (2000). Caries trends 1992-98 in two low-fluoride Finnish towns formerly with and without fluoride. Caries Research 34: 462-8.

Shao Q, et al. (2000). [Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi 34(6):330-2.

Shashi A. (2003). Histopathological investigation of fluoride-induced neurotoxicity in rabbits. Fluoride 36: 95-105.

Shea JJ, et al. (1967). Allergy to fluoride. Annals of Allergy 25:388-91.

Sheth FJ, et al. (1994). Sister chromatid exchanges: A study in fluorotic individuals of North Gujurat. Fluoride 27: 215-219.

Shiboski CH, et al. (2003). The association of early childhood caries and race/ethnicity among California preschool children. Journal of Public Health Dentistry 63:38-46.

Shivarajashankara YM , et al. (2002). Brain lipid peroxidation and antioxidant systems of young rats in chronic fluoride intoxication. Fluoride 35: 197-203.

Shivarajashankara YM , et al. (2002). Histological changes in the brain of young fluoride-intoxicated rats. Fluoride 35: 12-21.

Singh A, Jolly SS. (1970). Fluorides and Human Health. World Health Organization. pp 239-240.

Singh A, et al. (1963). Endemic fluorosis: epidemiological, clinical and biochemical study of chronic fluoride intoxication in Punjab. Medicine 42: 229-246.

Sprando RL, et al. (1998). Testing the potential of sodium fluoride to affect spermatogenesis: a morphometric study. Food and Chemical Toxicology 36: 1117-24.

Sprando RL, et al. (1997). Testing the potential of sodium fluoride to affect spermatogenesis in the rat. Food and Chemical Toxicology 35: 881-90.

Sprando RL, et al. (1996). Effect of intratesticular injection of sodium fluoride on spermatogenesis. Food and Chemical Toxicology 34: 377-84.

Stannard JG, et al. (1991). Fluoride Levels and Fluoride Contamination of Fruit Juices. Journal of Clinical Pediatric Dentistry 16: 38-40.

Stecher P, et al. (1960). The Merck Index of Chemicals and Drugs. Merck & Co., Inc, Rathway NJ. p. 952.

Steelink C. (1992). Fluoridation controversy. Chemical & Engineering News (Letter). July 27: 2-3.

Strunecka A, Patocka J. (1999). Pharmacological and toxicological effects of aluminofluoride complexes. Fluoride 32: 230-242.

Sun ZR, et al. (2000). Effects of high fluoride drinking water on the cerebral functions of mice. Chinese Journal of Epidemiology 19: 262-263.

Susheela AK. (1993). Prevalence of endemic fluorosis with gastrointestinal manifestations in people living in some North-Indian villages. Fluoride 26: 97-104.

Susheela AK, Kumar A. (1991). A study of the effect of high concentrations of fluoride on the reproductive organs of male rabbits, using light and scanning electron microscopy. Journal of Reproductive Fertility 92: 353-60.

Sutton P. (1996). The Greatest Fraud: Fluoridation. Lorne, Australia: Kurunda Pty, Ltd.

Sutton P. (1960) Fluoridation: Errors and Omissions in Experimental Trials. Melbourne University Press. Second Edition.

Sutton, P. (1959). Fluoridation: Errors and Omissions in Experimental Trials. Melbourne University Press. First Edition.

Teotia M, et al. (1998). Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian Journal of Pediatrics 65: 371-81.

Teotia SPS, Teotia M. (1994). Dental caries: a disorder of high fluoride and low dietary calcium interactions (30 years of personal research). Fluoride 27: 59-66.

Teotia SPS, et al. (1976). Symposium on the non-skeletal phase of chronic fluorosis: The Joints. Fluoride 9: 19-24.

Tsutsui T, Suzuki N, Ohmori M, Maizumi H. (1984). Cytotoxicity, chromosome aberrations and unscheduled DNA synthesis in cultured human diploid fibroblasts induced by sodium fluoride. Mutation Research 139:193-8.

Waldbott GL, et al. (1978). Fluoridation: The Great Dilemma. Coronado Press, Inc., Lawrence, Kansas.

Waldbott GL. (1965). A Battle with Titans. Carlton Press, NY.

Wang C, et al. (2000). Treatment Chemicals contribute to Arsenic Levels. Opflow (a journal of the American Water Works Association). October 2000.

Wang Y, et al. (1997). [Changes of coenzyme Q content in brain tissues of rats with fluorosis]. Zhonghua Yu Fang Yi Xue Za Zhi 31: 330-3.

WHO (Online). WHO Oral Health Country/Area Profile Programme. Department of Noncommunicable Diseases Surveillance/Oral Health. WHO Collaborating Centre, Malmö University, Sweden. http://www.whocollab. od.mah.se/euro.html

Williams JE, et al. (1990). Community water fluoride levels, preschool dietary patterns, and the occurrence of fluoride enamel opacities. Journal of Public Health Dentistry 50: 276-81.

Wu DQ, Wu Y. (1995). Micronucleus and sister chromatid exchange frequency in endemic fluorosis. Fluoride 28: 125-127.

Xiang Q, et al. (2003a). Effect of fluoride in drinking water on children's intelligence. Fluoride 36: 84-94.

Xiang Q. (2003b). Blood lead of children in Wamiao-Xinhuai intelligence study. Fluoride 36: 138.

Zakrzewska H, et al. (2002). In vitro influence of sodium fluoride on ram semen quality and enzyme activities. Fluoride 35: 153-160.

Zhai JX, et al. (2003). [Studies on fluoride concentration and cholinesterase activity in rat hippocampus]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 21: 102-4.

Zhang Z, et al. (2001). [Effects of selenium on the damage of learning-memory ability of mice induced by fluoride]. Wei Sheng Yan Jiu 30: 144-6.

Zhang Z, et al. (1999). [Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice] [Article in Chinese]. Wei Sheng Yan Jiu 28:210-2.

Zhao XL, Wu JH. (1998). Actions of sodium fluoride on acetylcholinesterase activities in rats. Biomedical and Environmental Sciences 11: 1-6.

Zhao LB, et al (1996). Effect of high-fluoride water supply on children's intelligence. Fluoride 29: 190-192.

Zhao ZL, et al. (1995). The influence of fluoride on the content of testosterone and cholesterol in rat. Fluoride 28: 128-130.

Ziegelbecker R. (1970). A critical review on the fluorine caries problem. Fluoride 3: 71-79.

The 19 studies on the possible association of hip fracture and fluoridated-water.

a) Studies Reporting an Association between fluoridated water (1 ppm fluoride) & hip fracture.

1 a) Cooper C, et al. (1990). Water fluoride concentration and fracture of the proximal femur. Journal of Epidemiology and Community Health 44: 17-19.

1 b) Cooper C, et al. (1991). Water fluoridation and hip fracture. JAMA 266: 513-514 (letter, a reanalysis of data presented in 1990 paper).

2) Danielson C, et al. (1992). Hip fractures and fluoridation in Utah's elderly population. Journal of the American Medical Association 268: 746-748.

3) Hegmann KT, et al. (2000). The Effects of Fluoridation on Degenerative Joint Disease (DJD) and Hip Fractures. Abstract #71, of the 33rd Annual Meeting of the Society For Epidemiological research, June 15-17, 2000. Published in a Supplement of American Journal of Epidemiology P. S18.

4) Jacobsen SJ, et al. (1992). The association between water fluoridation and hip fracture among white women and men aged 65 years and older; a national ecologic study." Annals of Epidemiology 2: 617-626.

5) Jacobsen SJ, et al. (1990). Regional variation in the incidence of hip fracture: US white women aged 65 years and olders. JAMA 264(4): 500-2.

6 a) Jacqmin-Gadda H, et al. (1995). Fluorine concentration in drinking water and fractures in the elderly. JAMA 273: 775-776 (letter).

6 b) Jacqmin-Gadda H, et al. (1998). Risk factors for fractures in the elderly. Epidemiology 9(4): 417-423. (An elaboration of the 1995 study referred to in the JAMA letter).

7) Keller C. (1991) Fluorides in drinking water. Unpublished results. Discussed in Gordon, S.L. and Corbin, S.B,(1992) Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis International 2: 109-117.

8) Kurttio PN, et al. (1999). Exposure to natural fluoride in well water and hip fracture: A cohort analysis in Finland. American Journal of Epidemiology 150(8): 817-824.

9) May DS, Wilson MG. (1992). Hip fractures in relation to water fluoridation: an ecologic analysis. Unpublished data, discussed in Gordon SL, and Corbin SB. (1992). Summary of Workshop on Drinking Water Fluoride Influence on Hip Fracture on Bone Health. Osteoporosis International 2:109-117.

b) Studies reporting an association between water-fluoride levels higher than fluoridated water (4 ppm+) & hip fracture.

Li Y, et al. (2001). Effect of long-term exposure to fluoride in drinking water on risks of bone fractures. Journal of Bone and Mineral Research 16: 932-9.

Sowers M, et al. (1991). A prospective study of bone mineral content and fracture in communities with differential fluoride exposure. American Journal of Epidemiology 133: 649-660.

c) Studies Reporting No Association between water fluoride & hip fracture:

(Note that in 4 of these 8 studies, an association was actually found between fluoride and some form of fracture – e.g. wrist and hip. See notes and quotes below.)

Cauley J. et al. (1995). Effects of fluoridated drinking water on bone mass and fractures: the study of osteoporotic fractures. Journal of Bone and Mineral Research 10: 1076-86.

Feskanich D, et al. (1998). Use of toenail fluoride levels as an indicator for the risk of hip and forearm fractures in women. Epidemiology 9: 412-6.

While this study didn't find an association between water fluoride and hip fracture, it did find an association - albeit non-significant 1.6 (0.8-3.1) - between fluoride exposure and elevated rates of forearm fracture.

Hillier S, et al. (2000). Fluoride in drinking water and risk of hip fracture in the UK: a case control study. The Lancet 335: 265-2690.

Jacobsen SJ, et al. (1993). Hip Fracture Incidence Before and After the Fluoridation of the Public Water Supply, Rochester, Minnesota. American Journal of Public Health 83: 743-745.

Karagas MR, et al. (1996). Patterns of Fracture among the United States Elderly: Geographic and Fluoride Effects. Annals of Epidemiology 6: 209-216.

As with Feskanich (1998) this study didn't find an association between fluoridation & hip fracture, but it did find an association between fluoridation and distal forearm fracture, as well as proximal humerus fracture. "Independent of geographic effects, men in fluoridated areas had modestly higher rates of fractures of the distal forearm and proximal humerus than did men in nonfluoridated areas."

Lehmann R, et al. (1998). Drinking Water Fluoridation: Bone Mineral Density and Hip Fracture Incidence. Bone 22: 273-278.

Phipps KR, et al. (2000). Community water fluoridation, bone mineral density and fractures: prospective study of effects in older women. British Medical Journal 321: 860-4.

As with Feskanich (1998) and Karagas (1996), this study didn't find an association between water fluoride & hip fracture, but it did find an association between water fluoride and other types of fracture - in this case, wrist fracture. "There was a non-significant trend toward an increased risk of wrist fracture."

Suarez-Almazor M, et al. (1993). The fluoridation of drinking water and hip fracture hospitalization rates in two Canadian communities. American Journal of Public Health 83: 689-693.

While the authors of this study conclude there is no association between fluoridation and hip fracture, their own data reveals a statistically significant increase in hip fracture for men living in the fluoridated area. According to the authors, "although a statistically significant increase in the risk of hip fracture was observed among Edmonton men, this increase was relatively small (RR=1.12)."




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Paul Connett, PhD
April 12, 2004
Professor of Chemistry
St. Lawrence University
Canton, NY 13617

Fluoridation: The Fraud of the Century

Fluoridation is not about "children’s teeth," it is about industry getting rid of its hazardous waste at a profit, instead of having to pay a fortune to dispose of it.

Only calcium fluoride occurs naturally in water; however, that type of fluoride has never been used for fluoridation. Instead what is used over 90 percent of the time are silicofluorides, which are 85 times more toxic than calcium fluoride.
They are non-biodegradable, hazardous waste products that come straight from the pollution scrubbers of big industries. If not dumped in the public water supplies, these silicofluorides would have to be neutralized at the highest rated hazardous waste facility at a cost of $1.40 per gallon (or more depending on how much cadmium, lead, uranium and arsenic are also present). Cities buy these unrefined pollutants and dump them--lead, arsenic and all--into our water systems. Silicofluorides are almost as toxic as arsenic, and more toxic than lead.1, 2

The EPA has recently said it is vitally important that we lower the level of both lead and arsenic in our water supplies, and their official goal is zero parts per million. This being the case, why would anyone recommend adding silicofluorides, which contain both of these heavy metals?3

On July 2, 1997, EPA scientist, J. William Hirzy, PhD, stated, "Our members’ review of the body of evidence over the last eleven years, including animal and human epidemiology studies, indicate a causal link between fluoride/fluoridation and cancer, genetic damage, neurological impairment and bone pathology. Of particular concern are recent epidemiology studies linking fluoride exposure to lowered IQ in children."4

The largest study of tooth decay in America (by the National Institute of Dental Research in 1987) proved that there was no significant difference in the decay rates of 39,000 fluoridated, partially fluoridated and non-fluoridated children, ages 5 to 17, surveyed in 84 cities. The media has never disclosed these facts. The study cost us, the taxpayers, $3,670,000. Surely, we are entitled to hear the results.5

Newburgh and Kingston, both in the state of New York, were two of the original fluoridation test cities. A recent study by the New York State Department of Health showed that after 50 years of fluoridation, Newburgh’s children have a slightly higher number of cavities than never-fluoridated Kingston.5

The recent California fluoridation study, sponsored by the Dental Health Foundation, showed that California has only about one quarter as much water fluoridation as the nation as a whole, yet 15-year-old California children have less tooth decay than the national average.6

From the day the Public Health Service completed their original 10-year Newburgh and Kingston fluoridation experiment, fluoride promoters have repeatedly claimed that fluoride added to drinking water can reduce tooth decay by as much as 60 to 70 percent.

Adding fluoride to the water has never prevented tooth decay, it merely delays it, by provoking a genetic malfunction that causes teeth to erupt later than normal. This delay makes it possible to read the statistics incorrectly without lying. Proponents count teeth that have not yet erupted as "no decay." Therefore, they claimed that the fluoridated Newburgh children age 6 had 100 percent less tooth decay; by age 7, 100 percent less; by age 8, 67 percent less; age 9, 50 percent less; and by age 10, 40 percent less.

Obviously, the only reduction that really counted was the 40 percent by age 10, but the Public Health Service totaled the five reductions shown, then divided by 5 to obtain what they called "an over-all reduction of 70 percent."

Had the Health Department continued their survey beyond age 10, they would have found that the percentage of reduction continued down hill to 30, 20, 0, and eventually the children drinking fluoridated water had more cavities--not less. The rate of decay is identical, once the children’s teeth erupt. In other words, this "65 percent less dental decay" is just a statistical illusion. It never happened!7

EPA scientists recently concluded, after studying all the evidence, that the public water supply should not be used "as a vehicle for disseminating this toxic and prophylatically useless. . . substance." They felt there should be "an immediate halt to the use of the nation’s drinking water reservoirs as disposal sites for the toxic waste of the phosphate fertilizer industry." Unfortunately, the management of the EPA sides not with their own scientists, but with industry on this issue.8

There is less tooth decay in the nation as a whole today than there used to be, but decay rates have also dropped in the non-fluoridated areas of the United States and in Europe where fluoridation of water is rare. The Pasteur Institute and the Nobel Institute have already caused fluoride to be banned in their countries (France and Sweden). In fact, most developed countries have banned, stopped or rejected fluoridation.9

Several recent studies, here and abroad, show that fluoridation is correlated with higher rather than lower rates of caries. There has been no study that shows any cost-saving by fluoridation. This claim has been researched by a Rand corporation study and found to be "simply not warranted by available evidence."10In fact, dentists make 17 percent more profit in fluoridated areas as opposed to non-fluoridated areas.11 There are no savings.

Meanwhile, the incidence of dental fluorosis has skyrocketed. It is not just a "cosmetic effect." Webster’s Encyclopedic Unabridged Dictionary says: "Fluorosis is poisoning by fluorides." Today, in North America, there is an increased prevalence of dental fluorosis, ranging from about 15 percent to 65 percent in fluoridated areas and 5 percent to 40 percent in non-fluoridated areas.12 African-American children experience twice the rate of dental fluorosis as white children and it tends to be more severe.13 The widespread and uncontrolled use of fluoride in our water, dental products, foods and beverages (grown and processed in fluoridated communities) is causing pervasive over-exposure to fluoride in the U.S. population.

A 1995 American Dental Association (ADA) chart shows that a certain fluoride drug should not be given to children under six months of age. It also shows that if fluoride is put into water, all children under six years of age will be getting an overdose.14

The FDA states that fluoride is a prescription drug, not a mineral nutrient. Who has the right to put a prescription drug in the water supply where there can be no control of dosage? People who drink a lot of water, like diabetics and athletes, will be overdosed, and studies have proven that 1 percent of the people are allergic to fluoridated water. Today, an unusual number of children in non-fluoridated areas are developing dental fluorosis!

Even if fluoride were good for teeth, shouldn’t the water be as safe as possible for everyone? Why should those who are against it be forced to drink it? What has happened to "Freedom of Choice?" We all know that fluoride is not "just one of forty chemicals used to treat water," it is the only chemical added to treat the people! It is compulsory medication, which is unconstitutional. There are other alternatives that do not infringe on the rights of all consumers to choose their own form of medication.16

When the people have been given a chance to vote on this issue, more often than not, they have voted "no." In the majority of cases, nationwide, it is the local city council that has forced it on the people. Fluoride promoters find it much easier to convince a few city council members than the general public. Here in America, we shouldn’t have to fight to keep a hazardous waste out of our water supply!

Bottom line: There are no benefits to fluoridation. We actually pay the phosphate fertilizer industries for their crude hazardous waste. Fluoridation contributes to many health problems and hither dental bills, and causes more (not less) suffering. Only big business wins with fluoridation--not our children (or us).

On Nov. 24, 1992, Robert Carton, PhD, a former EPA scientist, made this statement: Fluoridation is the greatest case of scientific fraud of this century, if not of all time. Impossible? No, it’s not--look at how many years millions of Americans were fooled by the tobacco industries!


-
Anita Shattuck

working to oppose the fluoridation of water supplies in Escondido, California.

can be reached at (760) 752-1621.

Other fluoridation battles are currently taking place in Santa Monica,CA and in the state of Ohio.

For further information contact Citizens for Safe Drinking Water (800)-728-3833, GreenJeff@home.com.

For "50 Reasons to Oppose Fluoridation," by Dr. Paul Connett, Professor of Chemistry, St. Lawrence University, NY 13617

Health Hazards of Mercury

In Greek mythology, Mercury is the fleet-footed messenger of the Gods. He was the cleverest of the Olympians, patron of translators and interpreters. He ruled over wealth, good fortune, commerce, fertility. . . and thievery. He brought the souls of the dead to the underworld, and was honoured as a god of sleep. As a physical substance in the living organism, however, mercury is the antithesis of the fleet-footed messenger's finer qualities. In the body, mercury disrupts cellular function at all levels, robbing the body of health and escorting the victim to the underworld of neurological dysfunction.

Mercury is a powerful poison. Published research has shown that mercury, even in small amounts, is more toxic than lead, cadmium and even arsenic. Some of the most common signs and symptoms of mercury exposure include irritability, fits of anger, lack of energy, fatigue, low self-esteem, drowsiness, decline of intellect, low self-control, nervousness, memory loss, depression, anxiety, shyness/timidity and insomnia.

Mercury, the Element

Mercury is a dense liquid metal that gives off a colorless, odorless, tasteless vapor at relatively low temperatures. The three most commonly encountered forms are the vapor form (Hg), the ionic form, (Hg2+) and the organic family of forms, principally methyl mercury (Cl-Hg0-CH3). Each has its own effects, routes of absorption and tissue specificity.1

In spite of its well recognized toxicity, mercury in its various forms is released into the environment at the rate of 11,000 tons annually, supposedly for the "benefit" of mankind. Cinnabar (mercuric sulphite), for instance, continues to be used for red pigment in many tattoo salons; calomel (mercurous chloride) is a common treatment for diaper rash; mercury vapour lamps provide enhanced indoor and outdoor lighting; and elemental mercury has many uses including thermostat regulation and the manufacture of plastics, mirrors and thermometers.

Although a natural component of the earth's crust, mercury does not have a role in the human body. Yet humans are constantly exposed to mercury, primarily through large fish (terrestial animals are negligible sources),2 thimerosol (a preservative added to vaccinations and many other pharmaceuticals) and "amalgam" or mercury-based dental fillings. Adverse health effects, particularly of a neurological nature, have resulted from low exposure levels, especially to the foetus in pregnant women.

Mercury vapor released from mercury dental fillings is absorbed very rapidly and thoroughly by your body, primarily by inhalation and swallowing.3 This elemental mercury also adds to the environment in significant amounts when dental wastes are not disposed of properly,4 and through cremation, which vaporizes the mercury in the amalgams. Although crematoriums now often use mercury vapor collectors to prevent this, they are not mandatory. Mercury vapor collectors are also used in some dental surgeries but a better solution is the immediate cessation of the use of amalgam fillings.

Mercury released into the atmosphere is indestructible; it merely hides or changes its form, being truly fleet-footed. Mercury is incorporated into the food chain as methyl mercury, primarily through the action of bacteria and other microbes transforming elemental or inorganic forms. Even mercury from amalgams is readily methylated by bacteria in the mouth.5 Organic mercury is the most deadly of the mercury compounds, probably due to its ability to enter the cells almost effortlessly. Within the cell it can destroy the various components selectively or in total by releasing lysosomes, damaging DNA and by rupturing the cell membrane. Its effects upon the neurological and reproductive system have been extensively documented.6

Methyl mercury accumulates in living organisms because it has a strong affinity for protein sulfhydryl groups. As lower-order organisms are eaten by higher-order organisms, the mercury concentration is increased along the food chain.7 This process of accumulation at each trophic level is called biological magnification. As humans are at the highest trophic levels, mercury can have a very destructive effect on individuals and on the entire gene pool.8 Most poison molecules that enter the body are processed by the liver or kidney and broken down into smaller components, then excreted in relatively less toxic forms than they were originally. Heavy metals are different. They cannot be broken down, so unless they are excreted immediately after they are ingested, these absolutely indestructible elements accumulate and continue as a source of potential damage.

The toxicity of mercury came into world prominence in the 1950s as a result of mercury dumping in the Minamata Bay in Japan. Consumption of seafood from the bay led to widespread neurological damage and teratogenic effects. After all the cats in the neighbourhood died--some found committing suicide--and birds began falling from the sky, the government began an investigation. They brought in new cats and followed them around to see what was killing them. Even when the source was known--the bay and subsequently the wildlife there--the chemical plant continued to pollute and fishermen continued to sell their catch. By 1997, 2,200 people were certified as having Minamata disease and qualified for compensation. More than 8,000 suffered from some degree of physical and psychological symptoms, such as muscle and joint pain, forgetfulness, memory loss, fatigue and tremors.9,10

Mercury Hot Spots

Scientists investigating mercury buildup in wildlife have looked closely at two locations where mercury concentrations are particularly high: the Mediterranean basin and the island of Madeira in the Atlantic.

Marine animals found in the Mediterranean Basin have high mercury concentrations compared to similar species from most parts of the Atlantic because of the natural presence of mercury from volcanic activity. About half of world mercury resources are located in the Mediterranean area.11 Mining in the area has increased the release of mercury into the environment.

The process of biomagnification in the Mediterranean basin is evident. High levels of mercury are found in Mediterranean tuna compared to similar species in most parts of the Atlantic, as well as in smaller species such as anchovy and sardines, and also in local marine birds and their eggs. An investigation of fishermen and their families in coastal villages on the north Tyrrhenian Sea found a correlation between the number of seafood meals and the mercury levels from hair samples. Those consuming one or fewer seafood meals per month averaged about 1 mcg/g while those who consumed four or more seafood meals per week had an average of 36 mcg/g. Levels over 50 mcg/g of mercury in hair were found in a few fishermen, who then underwent a cytogenetic monitoring study to evaluate DNA damage. A positive correlation was found between mercury concentration in blood and chromosomal aberration, findings that have been confirmed by several authors.

A study of women in the village of Camara de Lobos in the island of Madeira, where sea currents cause a concentration of mercury in local sea life, found that average values of total mercury in hair and blood were about 10 mcg/g and 32 mcg/L respectively. These levels have been associated with risk for fetal brain development.

Mercury from Amalgams

The largest exposure to mercury among adults comes comes from a source that is completely avoidable--amalgam fillings--primarily in the form of vapor of metallic, elemental mercury. Elemental mercury forms a monatomic gas that is highly volatile and readily inhaled.12

Whether inhaled from an industrial process or from mercury amalgam fillings, mercury vapor is readily absorbed across the pulmonary membranes. It then dissolves in plasma, persisting as a dissolved gas for a period sufficient to cross most of the diffusion barriers in the body including the blood-brain barrier.

Once it enters cells, whether the brain or red blood cells, or any other body cell, mercury undergoes an oxidation reaction to the inorganic ionic form--often referred to as divalent mercury (Hg2+). Through this route Hg2+ does indeed accumulate in the body from the metallic mercury vapor given off by dental amalgam fillings. In addition, methyl mercury, the highly toxic organic compound, can be formed from inorganic mercury by the action of bacteria in the mouth.

A study carried out by M. J. Vimy in 1990,13 brought to light the highly absorbable nature of mercury out-gassed by amalgam fillings. He placed twelve occlusal amalgams containing radioactively tagged mercury (that does not occur in nature) in the molars of pregnant sheep. Radioactivity measurements determined that by the third day mercury was found in the amniotic fluid and foetal blood, and that by the 26th day most foetal tissues (especially the liver, bile, bone marrow, blood and brain) had a higher mercury level than that within three days found in maternal tissues. During lactation mercury levels in the milk were eight times greater than those in the maternal blood serum, thereby causing great risk of mercury exposure to the neonate. Even after the 73rd day the mercury level in the foetal tissues was still rising, prompting Vimy's team to conclude that placing amalgam during pregnancy unquestionably places the foetus at undue risk and endangers the health of our children.

Vimy also found that the labelled mercury concentrated within three days in the sheeps' kidneys and caused a significant reduction in the glomerular filtration rate. In a second animal study of monkeys, whose digestive tract is much more closely related to that of humans, a team of microbiologists from the University of Georgia working with Vimy found that mercury from dental amalgam promoted the development of mercury-resistant bacteria in both the mouth and in the intestine, a finding of far-reaching significance.14

Mercury in Breast Milk

Studies carried out during the mid 1990s found a correlation between the mercury concentrations in the kidneys of newborn babies and the number of amalgam fillings of the mother.15 As a result, the Federal Institute of Medicines and Medical Products (an agency of the German government) officially advised against the use of amalgam as a filling material during pregnancy and breast feeding.16

These studies found that the mercury concentration in the urine of pregnant and lactating women positively correlated with the number and surfaces of amalgam fillings and with frequency of fish consumption.17 Levels of mercury in breast milk taken at day 2 of lactation also depended on the number and surfaces of amalgam fillings and with frequency of fish consumption. Mercury levels in the second breast milk sample, taken after two months of breastfeeding, were found to depend only on fish consumption. Investigators believed the lower concentrations of mercury in the milk at 2 months were due to higher amounts of milk being produced.

Mercury is excreted predominantly in the faeces, but also in sweat and urine. Five percent will be excreted in breast milk. By the time of parturition, a baby's levels can be 30 percent higher to 100 percent higher than that of the mother. Mercury passes readily across the placenta, and binds to the red blood cells and tissues in the foetus. Since the foetus is not sweating, making bile or having bowel movements, the mercury accumulates. Also, foetal haemoglobin has a greater affinity for mercury than the mother's haemoglobin.18

On January 12, 2001, the FDA press office released a statement advising pregnant women, women of childbearing age who may become pregnant, nursing mothers, and young children not to eat shark, swordfish, tilefish and king mackerel. The statement also warned against two servings of any other fish per week. Government agencies in Australia and New Zealand have issued similar recommendations.

The FDA report cited swordfish that routinely tested over the 1 mcg/g "action level," above which fish should not be sold. Some swordfish contained greater than 3 ppm of mercury. Thus, the EPA and FDA advises expectant mothers to reduce or eliminate their intake of seafood due to the possibility that the amount of methyl mercury contained in fish might adversely affect their unborn offspring. The question is, why aren't the EPA and FDA clamoring for the elimination of mercury amalgam restorations--a much greater source of mercury than swordfish--at least in pregnant women, women of child bearing age and children? As long ago as 1991, a panel of experts convened by the World Health Organization determined that mercury amalgam fillings were the primary source of mercury exposure in the non-occupationally exposed population.19

Thimerosal

In spite of well-established health risks, organic mercurials are still added to prescription and non-prescription drugs, such as medicines for haemorrhoids (Preparation H), as well as in formulations for the treatment of bacterial and fungal infections. Because mercury has antifungal properties, it is used in indoor paints.20

Until recently, nearly all contact lens solutions contained thimerosal as an antibacterial agent. Thimerosal is ethyl mercury, an organic mercurial (sometimes called merthiolate). In some patients, thimerosal caused visible accumulation of mercury in the retina and chronic eye irritation. In a few highly sensitive people, the mercury-based additive caused loss of sight. Nevertheless, manufacturers continued to add it to contact lense solution for many years. The ban on thimerosal in contact lens solutions did little to eliminate its use in other products, such as eardrops and nose drops. Thimerosal continues to be used today in a variety of health-related products: for preserving vaccines and intramuscular injections, cosmetics, and some drugs that must be kept in solution.

It is the thimerosal used in childhood vaccines that gives the greatest cause for concern. Investigators evaluating doses of mercury in the form of thimerosal used as a preservative in childhood immunizations found that they exceeded US federal safety guidelines. The analysis showed increased risks for neurodevelopment disorders, autism and heart disease with increasing exposure to thimerosal in vaccines. The US Environmental Protection Agency (EPA) safety of exposure standard is .1 microgram per kilogram of body weight per day equating to 7 micrograms for a 70 kilogram adult. Fully vaccinated children receive as much as 237.5 micrograms of mercury from vaccines in doses of up to 25 micrograms each. According to studies carried out by the research team of Geier and Geier, thimerosal in a single vaccine greatly exceeds the EPA adult standard.21

The epidemiological evidence is compelling and statistically conclusive. Geier and Geier found that the prevalence of speech disorders, autism and heart arrest was a function of the mercury dose that the children received. Autism is now epidemic in the United States, rising from 1 in 2500 children in the mid 1980s to 1 in about 300 children in 1996. There has been a steady increase to the childhood vaccination schedule since the late 1970s.

Mercury and Heart Disease

Mercury exposure may also contribute to heart disease in adults. In a study involving over 1000 men aged 42-60, the "The Kuopio Ischemic Heart Disease Risk Factor Study" (KIHD), researchers from the University of Kuopio, Kuopio, Finland, noted that lipid peroxidation and excess risk of myocardial infarction (MI) could be best related to high mercury levels in the hair.22 At the four-year follow-up point of the KIHD study, the same research team noted that high hair mercury levels were related to increased arterial wall thickness and growth in the carotid arteries.23 The team concluded: "Accumulation of mercury in the body is associated with accelerated atherosclerotic progression in men."

A Case History

I have a busy, biologic dental practice in the Queensland area of Australia, which specializes in patients suffering from mercury toxicity. The typical patient is a female with numerous dental amalgams in her mouth and who has followed the advice of the Australian Heart Foundation, consuming a low-protein, low-fat, low-cholesterol diet that includes fish as the chief animal food, often eaten several times per week.

Nervanne was such a patient. She originally consulted our practice in November of 2001 with a multiplicity of symptoms including migraines three times per week; tremors (both internal and visible external) with associated tingling in the hands and feet; poor memory and decline of cognitive function; chronic unrelenting fatigue and depression; tinnitus; painful joints; night urination; a metallic taste in her mouth; and abdominal bloating with a history of diarrhoea and now constipation. She was also on thyroid medication due to a bout of autoimmune thyroid disease, and suffered recurrent yeast and bacterial infections. An MRI revealed no sign of angiopathy in the carotid and vertebral arteries but did reveal evidence of deep white matter disease, demyelination and possible multiple sclerosis.

Nervanne had many mercury amalgams and gum disease as revealed by bleeding upon flossing and oral examination. She also had three root-filled teeth, one with obvious apical pathology. Her children suffered from dental malocclusions and attention behavioral problems. One of her sons was autistic.

Detoxification

The body deals with toxins in a very ordered fashion:

  • Protective barriers and secretions (skin, mucus, tears, saliva)
  • Immunologically (inflammation, immunoglobulin response)
  • Biotransformation (activation of cytochrome P450 enzyme detoxification systems)
  • Raising blood lipids (HDL, LDL and VLDL cholesterol and tryglycerides.)24,25

By doing a comprehensive blood chemistry, based on the principles of Free Radical Therapy,26 we can gain a fairly accurate idea of which toxin or combination of toxins we are dealing with, where the toxin is located, how much is there and how it is being transported, and thereby gain some idea of how best to neutralize the toxins and get them out.

The protocol we use to help the patient get rid of mercury is a multi-step process. The first step involves changing the diet to enhance the body's ability to handle contaminant materials. The next step adds specific supplementation and chelation therapy. We then do a comprehensive survey of the mouth to determine the best order for removal of amalgams and the most compatible type of dental material with which to replace them. Only then do we proceed with the removal of amalgam fillings.

Upon examining Nervanne's blood results the following findings were of particular interest: her total serum cholesterol was very low at 150 mg/dl with HDL-cholesterol at 48 mg/dl; and her total protein and albumin levels were low, the globulin was high normal.

Nervanne's total cholesterol, HDL-cholesterol and total protein levels had never before been this low. So I asked her what sort of dietary regimen she had been following. Nervanne had not eaten eggs, red meat or dairy products (except skim milk or soy milk on her cereal) for several years prior to her devastating decline in health. She had reduced her diet to salads, pasta, fruits, an occasional serving of skinless chicken and frequent canned tuna due to convenience and her desire to increase her omega-3 intake. She regularly consumed "cholesterol-free" crackers with margarine and "lite" cheese as a snack. She also consumed many other sources of trans fatty acids--margarine, pastries, breads, cereals and chocolate.

Did Nervanne's health fail as a result of her new eating habits, or was it mere coincidence that her recent health decline followed the adoption of an extremely low-fat, low-cholesterol, low-animal-protein diet? I believe it was the latter and the scientific literature confirms my beliefs.

Nervanne's reduction in cholesterol and total serum protein had made her vulnerable to bacterial and viral infection by promoting T-cell suppression. This is especially so in the presence of mercury, which has been shown to reduce resistance to viruses, cancer and autoimmune disease.27,28 Low levels of cholesterol also make T-cell proliferation more difficult,29,30,31,32 and the excretion of mercury nearly impossible.

The onset of emotional depression and irritability is frequently reported in people who suddenly lower their cholesterol levels. These symptoms have occurred in all of the longer-term studies on cholesterol lowering, but rarely do physicians link their patients' depressive symptoms with the sudden change in diet or cholesterol level.

Neurotoxins are transported throughout the body attached to protein components of lipoproteins, and therefore require cholesterol for their transport and elimination. These neurotoxins also have a strong affinity for lipoidal tissue of the nervous system and brain. A rise in cholesterol levels and triglycerides in response to neurotoxins protects by preventing permanent attachment of the neurotoxin to the nerve and brain cells. Symptoms of neurotoxicity are most likely to occur when the cholesterol is lowered suddenly or when the affected patient goes on a low-fat, low-cholesterol, low-protein diet.

In a human trial, a high-protein, low-carbohydrate diet was compared to a low-protein, high-carbohydrate diet. The researchers found greater clearance of toxins with the high-protein, low-carbohydrate diet and diminished clearance when the ratio was reversed.33,34 To utilise the protein correctly, the fat on the "lamb" needs to be eaten. The use of additional butter or lard in cooking is of paramount importance. By having adequate fat, bile production is stimulated, absorption of minerals increased and the excretion of mercury facilitated as long as constipation is avoided.

In my practice, I have found that people who are sturdy in structure recover more quickly and have less reactivity during their treatment, compared with people who are extremely thin or who lose the most weight or undergo ill-advised fasting procedures concurrently while having been exposed to toxins such as mercury.35 This observation is supported by recent studies published in the Journal of Obesity.36

A correct cholesterol response is fundamental to move mercury and other neurotoxins to sites where they can be excreted. A Danish study of 50,318 users of statin (cholesterol-lowering) drugs revealed a higher risk of peripheral neuropathy related to the percentage of drop in total cholesterol. In other words, lowering cholesterol increases risk of reactivity to nerve toxins37 resulting in pain, paraesthesia, numbness and demyelinating effects. Six additional studies since 1994 have indicated the same rise in polyperipheral neuropathy symptoms for users of statin drugs,38,39,40,41,42,43 supporting our clinical findings that low cholesterol levels in the presence of a potent neurotoxin such as mercury found in amalgam fillings or any other source, is a recipe for disaster. Nervanne's history was characteristic of this pattern.

Therapy

Our treatment for Nervanne involved a radical change in her diet followed by the careful removal of her amalgam fillings (as well as her root-filled teeth). Proper diet is fundamental to clearing toxins, as well as to regaining the best of health. We advised Nervanne to eliminate tuna and other seafoods from her diet, but to incorporate a variety of meats, eggs and whole milk dairy products. The only seafood allowed is cod liver oil to provide vitamins A and D.

Protein deprivation has been shown to decrease the liver content of several of the cytochrome P450 enzymes, the enzyme system the body calls upon to remove toxins.44 Mercury also blocks the P450 system.45 Trans fats also interfere with the P450 detoxification enzyme system, according to research carried out by Dr. Mary Enig, so these must also be eliminated from the diet.46

The proteins in the diet must be animal proteins, providing a complete specturm of amino acids. A study of Asian vegetarians with incomplete amino acid intake showed reduced clearing of xenobiotics.47 Low levels of hydrochloric acid have an adverse impact on the availability of dietary amino acids, even in a higher protein diet, so stimulating the pancreas using lacto-fermented foods is crucial. Our protocol makes the use of cultured dairy products rich in whey protein. Not only will whey provide the complete protein needed for metabolization of xenobiotics and mercury, it has also been shown to increase glutathione content in the liver.48,49 We recommend sheep's milk yoghurt, rich in lauric acid, whey and glutathione.

By April of 2002, Nervanne's migraines had completely ceased and her gastrointestinal symptoms had abated. For the first time in many years, she can string a sentence together without stuttering. Her inability to cope, internal irritability and feelings of helplessness had resolved and she was now able care for her family and support her husband's efforts.The children's behaviors were also improving and the parents were ready to commence a program for the child with autism.

Conclusions

Most individuals can protect themselves against mercury by avoiding unnecessary exposure. That means using only composite dental fillings--never amalgam--and avoiding vaccines and pharmaceuticals that may contain thimerosal. Occasional fish consumption is fine in a healthy person who also consumes a diet rich in animal protein and fat, but tuna, swordfish and larger predatory species should be consumed only on rare occasions.

The pregnant and nursing woman represents a special case. The foetus has no way to eliminate mercury that may cross the placental barrier and is therefore very vulnerable. It has been clearly documented that mercury in the developing infant and foetus can lead to permanent and irreversible brain damage. Thus, it is highly recommended that all amalgam fillings be removed before conception and imperative that none be put in place during pregnancy and lactation. Pregnant and lactating women should avoid consumption of tuna, swordfish and similar species completely. RH-negative women should insist on vaccines that are thimerosal-free.

Many unnecessary uses of mercury combined with the burning of coal and other fossil fuels (the most significant source of air-borne mercury) can contaminate our food chain and pollute our environment to an extent that threatens the health of everyone. Mercury is the most toxic of the heavy metals. Thus, if we are to protect our own health as well as that of future generations, it's imperative that we and the scientific community pass legislation soon at the state, local, federal and international levels for reducing or halting the indiscriminate use of mercury in all of its various forms; especially the conscious act of implanting mercury directly into people like you and your child by using mercury dental fillings and mercury-containing vaccines.


REFERENCES

  1. Queen HL. Chronic Mercury Toxicity: New Hope Against An Endemic Disease, Queen and Company Health Communications, Inc., Colorado Springs, Colorado, 1998.
  2. Renzoni A, Zino F, Franchi E. Mercury Levels Along the Food Chain and Risk for Exposed Populations. Environmental Research, 1998;77(2):68-72.
  3. Drexler H, Schaller KH. The Mercury Concentration in Breast Milk Resulting from Amalgam Fillings and Dietary Habits. Environmental Research, 1998;77(2):124-129.
  4. Arenholt-Bindslev D, Larsen, AH. Mercury Levels and Discharge in Waste Water from Dental Clinics. Water Air Soil Pollution, 1996;86(1-4):93-9.
  5. Leistevuo J, Leistevuo T, Helenius H, Pyy L, Osterblad M, Huovinen P, Tenovuo J. Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res May-June 2001;35(3):163-6.
  6. Geier MR, Geier DA 2003, Thimerosal in Childhood Vaccines, Neurodevelopment Disorders, and Heart Disease in the United States. Journal of American Physicians and Surgeons, 2003;8(1):6-11.
  7. Renzoni, op cit.
  8. Heintze U, Edwardsson S, Derand T, Birkhed D. Methylation of Mercury from Dental Amalgam and Mercuric Chloride by Oral Streptococci in vitro. Scand. J. Dental Research 1983;91(2) 150-152.
  9. Harda M. Minamata Disease: Methylmercury Poisoning in Japan Caused by Environmental Pollution. Crit Rev Toxicol 1995;25(1):1-24.
  10. Fukuda Y, Ushijima K, Kitano T, Sakamoto M, Futatsuka M. An Analysis of Subjective Complaints in a Population Living in a Methylmercury-Polluted Area. Environ Res 1999;81(2):100-107.
  11. Renzon1, op cit.
  12. Vimy MJ, Lorscheider, FL. Intra-Oral Air Mercury Released from Dental Amalgam. J Den Res 1985;64:1069-71.
  13. Vimy MJ and others. Maternal-fetal Distribution of Mercury203 Released from Dental Amalgam Fillings. J Am Physiol 1990, R939-45.
  14. Vimy MJ, Lorscheider FL. Dental Amalgam Mercury Daily Dose Estimated from Intra-oral Vapor Measurements: a Predictor of Mercury Accumulation in Human Tissues. J Trace Elem Exp Med 1990;3: 111-23.
  15. Drasch G, Roider G. Zahnamalgam und Schwanger-schaft. Geburtsh. und Frauenheilk, 1995;55:M63-M65.
  16. Drexler, op cit.
  17. Drexler, op cit
  18. Mahafey KR, Rice GE. Environmental Protection Agency Office of Air Quality Planning and Standards. Mercury Study Report to Congress. Govt Reports Announcements and Index (GRA and I), Issue 09,1998. Also Dec, 1999. www.epa.gov/ttnuatw1/112nmerc/mercury.html.
  19. World Health Organization, Environmental Health Criteria 118: Inorganic Mercury, Geneva, 1991.
  20. Geier, op cit.
  21. Geier, op cit.
  22. Salonen JT and others. Circulation 1995;91:645-55.
  23. Salonen JT and others. Circulation October 15, 1995;(Suppl) 92(8):abstract 1040.
  24. Queen, HL, Cholesterol-Lowering Drugs Should Carry A Warning: The Mercury Connection. Heart Talk 7(2): 9-15, November 1988
  25. Queen HL, Health Realities Journal, Number 1,Volume 19, 2003.
  26. www.healthrealities.org
  27. Hayes RB. The carcinogenicity of metals in humans. Cancer Causes & Control May 1997;8(3): 371-85.
  28. Whitekus MJ and others. Protection Against CD95-Mediated Apoptosis By Inorganic Mercury In Jurkat T Cells. J Immunol June 15, 1999;162(12): 7162-70.
  29. Hui DY, Harmony AK. Biochem J, 1980;192:91.
  30. Miller M. Science News, November 1988, p.348.
  31. Meydani M. Dietary effects on detoxification processes. In: Hathcock JN, ed. Nutritional Toxicology Vol. 2. San Diego, CA: Academic Press; 1987;1-40.
  32. Brodie MJ, Boobis AR, Toverud EL and others. Drug metabolism in white vegetarians. Br J Clin Pharmacol 1980;9:523-525.
  33. Kappas A, Anderson KE, Conney AH, Alvares AP. Influence of dietary protein and carbohydrate on antipyrine and theophylline metabolism in man. Clin Pharmacol Ther 1976;20:643-653.
  34. Anderson KE, Kappas A. Dietary regulation of cytochrome P450. Annu Rev Nutr 1991;11:141-167.
  35. Stevens J, Juhaeri M, Cai J. Am J Epidemiol May 15, 2001;153(10):946-953.
  36. Allison DB and others. Internat J Obesity & Related Metabol Disorders March 2002;26(3):410-416.
  37. Gaist D and others. Statins and risk of polyneuropathy. Neurol May 1, 2002;58:1333-1337.
  38. Jacobs MB. Ann Intern Med 1994;120:970.
  39. Ahmed S. Lovastatin and Peripheral Neuropathy. Am Heart J 1995;130:1321.
  40. Phan T and others. Peripheral Neuropathy Associated with Simvastatin. J Neurol Neurosurg Psy 1995;58:625-28.
  41. Ziajka PE. South Med J 1998;91:667-68.
  42. Jeppesen U and others. Eur J Clin Pharmacol 1999;54:835-38.
  43. Gaist D and others. Eur J Clin Pharmacol 2001;56:931-33.
  44. Meydani M. Dietary effects on detoxification processes. In: Hathcock JN, ed. Nutritional Toxicology Vol. 2. San Diego, CA: Academic Press; 1987;1-40.
  45. Anderson, op cit.
  46. Enig MG. Modification of Membrane Lipid Composition and Mixed-Function Oxidases in Mouse Liver Microsomes by Dietary Trans Fatty Acids. Doctoral Thesis, University of Maryland, 1984.
  47. Brodie MJ, Boobis AR, Toverud EL and others. Drug metabolism in white vegetarians. Br J Clin Pharmacol 1980;9:523-525.
  48. Bounous G, Gervais F, Amer V and others. The influence of dietary whey protein on tissue glutathione and the diseases of aging. Clin Invest Med 1989;12:343-349.
  49. McIntosh GH, Regester GO, Le Leu RK and others. Dairy proteins protect against dimethylhydrazine-induced intestinal cancers in rats. J Nutr 1995;125:809-816.


NOTES

Symptoms of Mercury Toxicity

  1. Local Oral Cavity: Excessive salivation; metallic taste; swollen tongue with scalloped edges; periodontal disease; bleeding gums; stomatitis; loosening of teeth; foul breath; white patches in mouth; bone loss around teeth; ulcers of gums, palate, tongue; burning of mouth; gum pigmentation.
  2. Psychological: Irritability and unreasonable anger; inability to make decisions; insomnia; lack of concentration; low self-confidence; drowsiness; decline of intellect; low self-control; nervousness; memory loss; depression; anxiety; shyness /timidity.
  3. Neurological: Headaches, including migraines; tremors (hands, feet, eyelids, tongue); muscular weakness; diffuse myalgia (muscular rheumatism); tinnitus (ringing in the ears); paraesthesia (abnormal skin sensations); impaired visual fields and visual acuity; depression; memory loss.
  4. Cardiovascular and Respiratory: Tachyarrhythmia (irregular heart beat); chest pain; changes in blood pressure; feeble or irregular pulse; pain or pressure in chest; persistent cough; emphysema; shallow or irregular breathing.
  5. Gastrointestinal: Abdominal pain (often mimicking ulcers); colitis; constipation; diarrhoea; irritable bowel.
  6. Immunological: Allergies; rhinitis; swollen lymph nodes in neck; asthma; sinusitis.
  7. Endocrinological: Chronic fatigue; subnormal temperature; excessive perspiration; edema; weight loss; cold, clammy hands and feet; muscle weakness; hypoxia (oxygen deficiency in the tissues); loss of appetite; joint pain; thyroid dysfunction; infertility.
  8. Urinogenital: Frequent urination; night urination; loss of libido.
  9. Integumentary: Unexplained rashes.

Average Daily Intake of Mercury Per Source

Dental amalgam fillings (mercury vapor), according to the American Dental Association: 1.0-2.0 mcg/day

Dental amalgam fillings (mercury vapor), according to the World Health Organization: 3.0-17.5 mcg/day (average 10 mcg/day, extreme 100 mcg/day)

Fish (methylmercury): 2.4 mcg/day

Non-fish food (inorganic mercury): 0.3 mcg/day

Air, water and food: 3.09 mcg/day (absorbed 2.26 mcg/day)

Other sources: negligible



-
Eric Davis, DDS

Principal physician of a large and busy dental practice and is well known in the Health Care Industry as a leader in the field of Biological Dentistry.

Clinical director of Nutrition Diagnostics. He has pursued post-graduate studies in the areas of clinical nutrition, medical acupuncture, neural therapy, homotoxicology and electro-acupuncture.

Founding member and past president of the Australian Society of Oral Medicine and Toxicology.

In 1996 Dr. Davis was made a fellow of the Australian College of Nutritional and Environmental Medicine.

Lectured in the areas of Biological Dentistry and Nutrition both nationally and internationally.

Dioxins in Animal Foods: A Case for Vegetarianism?

Introduction

The research of Dr. Weston A. Price, documented in his classic volume Nutrition and Physical Degeneration, demonstrated the absolute necessity of certain fatty animal foods for good health. However, a challenging argument against eating animal foods--especially animal fat--arises from vegetarian circles. This argument focuses on a class of chemicals called dioxins, and suggests that in the modern world, overburdened by pollutants, these fat-soluble chemicals accumulate specifically in the fatty tissue of animal products, making a vegetarian--even vegan--diet a necessity for those living in the modern world.

For example, one vegetarian website argues that "nearly 95 percent of our dioxin exposure comes in the concentrated form of red meat, fish, and dairy products, because when we eat animal products, the dioxin that animals have built up in their bodies is absorbed into our own," and that eating dioxin-laced animal products will make us vulnerable to "a wide range of effects, including cancer, depressed immune response, nervous system disorders, miscarriages, and birth deformities."1

The same argument appears in environmentalist circles as well. For example, the Pennsylvania-based environmental organization ActionPA's "Dioxin Homepage" argues that "[t]he best way to avoid dioxin exposure is to reduce or eliminate your consumption of meat and dairy products by adopting a vegan diet."2

Thus, this argument for vegetarianism essentially builds on a series of three points:

  • Dioxins are potent human carcinogens, endocrine disruptors, reproductive disruptors and immune disruptors;
  • Animal products are uniquely high in dioxins;
  • Avoiding the harmful effects of dioxins is primarily dependent upon minimizing dioxin intake, and therefore avoiding animal products.

The assertion that dioxins accumulate specifically in animal products is simplistic and inaccurate, and in fact a diet rich in pastured animal products provides protective nutrients, especially vitamin A, that directly oppose the toxic actions of dioxins in animal experiments, while a diet rich in most plant fats provides compounds that enhance the actions of dioxin. The argument that we should avoid animal products because of their dioxin concentration is thus no less flawed than the argument that we should avoid animal products because they contain saturated fat and cholesterol.


Dioxins: Some Background

The prototypical dioxin compound is 2,3,7,8 tetrachlorodibenzo-p-dioxin, abbreviated as "TCDD." The word "dioxin," however, refers more broadly to dioxin-like compounds from three classes: polychlorinated dibenzo-p-dioxins (PCDDs, including TCDD), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs). Not all PCDDs, PCDFs, and PCBs are considered dioxins. Only 17 out of 210 PCDDs and PCDFs are considered dioxin-like, and only 11 out of 209 PCBs are considered dioxin-like. The precise positioning pattern of chlorine atoms on the molecule determines whether or not it is dioxin-like, and it is important not to confuse the PCBs classified as dioxins with other PCBs that are believed to be toxic through non-dioxin-like mechanisms.3

The relative toxicity of dioxins is expressed in relation to the toxicity of TCDD, the most potent dioxin. A "toxicity equivalency factor" (TEF) relates the degree of toxicity of a specific PCDD, PCDF or PCB to the toxicity of the prototypical TCDD, and the TEF is then multiplied by the number of molecules of that particular dioxin compound in a food to yield a "toxicity equivalent quantity" (TEQ). The sum of TEQs from all dioxin compounds within a given foodstuff estimates the presumed degree of toxicity contained within that foodstuff.3

A higher amount of TEQs doesn't necessarily mean that there is a greater absolute quantity of dioxins in the food, since the TEQ gives greater weight to the more potent dioxins. So, a food with a smaller total amount of dioxins but a more potent specific compound could have a higher TEQ value than a food with a higher quantity of dioxins but less potent specific types of dioxins. However, the TEQ is not necessarily an indicator of how toxic the food is, simply because some dioxins, such as PCBs, also have toxicity that is non-dioxin-like.


Exposure to Dioxins

Although 95 percent of human exposure to dioxins is believed to come from food,3 this fact deceptively overestimates the impact of foodbased dioxins, because industrially exposed populations have been exposed to 10-1000 times higher concentrations of dioxin than the general population.4 And even at these high exposures the evidence of dioxin-induced harm is inconclusive at best.

Since the 1970s, after an historical peak in the 1950s and 1960s, sources of dioxins released into the environment have changed, and the levels have dramatically declined,4 due to government regulations and to the advancement of technology. The US and other countries have banned the use of pesticides and herbicides such as 2,4,5-trichlorophenoxyacetic acid and hexachlorophene, the production of which was once a primary source of dioxin contamination. Alternatives to the bleaching of paper with free chlorine have further reduced or eliminated dioxin production. The dioxin contribution of municipal and medical waste incineration has decreased by over 90 percent because of technological advances in waste disposal.5

Open barrel burning of trash is now the primary source of dioxin released through human agency, while modern incinerators make a comparatively negligible contribution. Certain metal refining processes also lead to dioxin generation. The other major contributors are natural, including volcanoes5 and forest fires.6

Human body burdens of TCDD, the most potent dioxin, in the US have decreased 10-fold, and total dioxin TEQs have decreased 4-fold to 5-fold between 1972 and 1999. Given the typical half-life of dioxins in the body, this means that dioxin exposure during this period has decreased by a full 95 percent!6 Similar observations have been found in other countries. For example, dioxin concentration in the breast milk of Japanese mothers declined by 87 percent between 1974 and 1998.7 Dioxin intake declined about 90 percent in the Netherlands between 1978 and 1999,8 and in Finland dioxin exposure declined 50 percent over the course of the 1990s alone.9

We will never know exactly what level of dioxins Price's healthy primitives or other premodern societies were exposed to. However, since natural sources of dioxins like volcanoes and, more significantly, forest fires, are now primary sources of dioxins, and since pre-modern populations would be expected to have additional exposure through the direct inhalation of fumes from the incineration of heating and cooking materials (living, for example, in thatched houses without chimneys, as Price described the primitive Gaelics), as well as the use of incinerated materials as soil fertilizer (such as slash-and-burn techniques or the use of smoke-impregnated thatch as a fertilizer, both described by Dr. Price), it is not unreasonable to conclude that we are now approaching a level of dioxin exposure similar to that of pre-industrial populations.

Even by conservative estimates, no one in the US is currently consuming a level of dioxins that would be expected to exert physiological harm. The World Health Organization (WHO) developed what is called a "tolerable daily intake" (TDI) for dioxins based on the intake levels that produce decreased sperm count, immune suppression and genital malformations in the offspring of exposed rats, and neurobehavioral effects and endometriosis in the offspring of exposed monkeys.4 However, since the WHO's TDI is supposed to assume the greatest degree of sensitivity, in order to yield the safest and most conservative estimate, the harm done to male rats exposed during gestation is the primary basis for the TDI.6

Using this estimate, taken from the most sensitive individual rats, the WHO then added a "safety factor" of 10 to yield a TDI of 2 picograms (pg) TEQ per kilogram of body weight.4 (A picogram is a trillionth of a gram or a billionth of a milligram.) This means that a human whose intake of dioxins meets the WHO's TDI is consuming only one-tenth of the concentration required to yield, after a lifetime of exposure, body burdens with concentrations that were required to produce the minimum physiological effect not in the most sensitive adult or child rat, but in the most sensitive rat during gestation, the critical period where a developing organism would be much more sensitive than at any other time.

According to a 2005 study covering the years 1999 through 2002, only 1 percent of 2-year-olds in the United States exceeded the TDI in 1999 and 2000, and this excess of the TDI was very small. The risk to children is probably overestimated since the TDI is based on body weight alone and does not take into account the fact that children have higher fecal excretion rates of dioxin, nor does it take into account the fact that, since we are experiencing a decline in dioxin exposure, current exposures will overestimate the cumulative body burden that will be reached over time. In 2001 and 2002, no intakes at any age in the US were estimated to exceed the TDI.6


A Modern Threat?

Dioxins are not merely a modern industrial phenomenon. Chlorinated organic compounds are produced naturally, by biological and abiotic means, have been found in coal samples dating back 300 million years, and are produced by cyanobacteria, which have existed for billions of years.a

There are 4,519 known naturally ocurring organohalogens, 2,320 of which are organochlorines. Bleach, chlorine gas, and organochlorines are naturally produced in the human body. Brominated dioxins are produced biologically by sponges as a defense mechanism, while chlorinated dioxins are naturally produced by the decay of plant matter in peat bogs, the incineration of wood in forest fires, or in gases released from volcanos.a

The smoke of fires--to which primitive peoples, unlike moderns, were exposed on a daily basis--contains between 10 and 40 nanograms of chlorinated dioxins per gram of smoke.b A single gram of smoke thus contains between 125 and 500 times the amount of dioxin that a 80 kg adult consumes from food per day.

Wood naturally contains chloride compounds that are oxidized under high heat, producing chlorine that readily reacts with organic compounds to form organochlorines, including dioxins. Although chlorine released into the atmosphere by industry makes a very small contribution to the chlorine available for this reaction, of the 4 million tons of methyl chloride --the most abundant atmospheric form of chlorine--produced each year, only 10,000 tons originate from industry.a

Therefore the healthy pre-modern groups that Price studied, who thrived on diets rich in animal products, probably consumed some level of dioxins in their food, possibly rivaling our own consumption. What has changed in the modern era is not the introduction of chemical pollutants, but the disappearance of protective factors abundant in traditional diets -- which have protected us from pollutants throughout history--from the modern menu.

  1. Gribble, Gordon W., "Amazing Organohalogens," American Scientist Online, Vol 92 No.621 (2004) 342-349
  2. US EPA, "A Summary of the Emissions Characterizations and Noncancer Respiratory Effects of Wood Smoke." EPA-453/R-93-036, as cited in Citizens for Safe Water Around Badger, "Fact Sheet: Open Burning at Ravenna Arsenal," http://www.cswab.org/ravenna.html Accessed October 2, 2005.


Dioxin and Cancer:
"Sufficient Evidence" Not Required

Although the World Health Organization's (WHO) International Agency for Research on Cancer (IARC) designated TCDD (but not the other dioxins) as carcinogenic to humans (Group 1) in 1997, TCDD does not actually pass the test for carcinogenicity.

For decades, sufficient evidence of carcinogenicity to humans was a necessary criterion for classification of a substance as a Group 1 carcinogen. TCDD was the second chemical whose classification utilized the IARC's 1990 change of criteria, by which a substance could be judged carcinogenic to humans even if ". . . evidence in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent . . . acts through a relevant mechanism of carcinogenicity." [emphasis added]10

Dioxins do not initiate the transformation of a normal cell to a cancerous cell in any species. TCDD has been shown, however, to be a very powerful promoter of cancers that are first initiated by another carcinogen, and is thus considered a "non-genotoxic carcinogen." For example, one study using mouse fibroblasts in cell culture found TCDD to enhance the carcinogenic effect of N-methyl-N'-nitro-N-nitrosoguanidine over 3-fold, and to enhance the carcinogenic effect of 3-methylcholanthrene almost 4-fold. Yet in the absence of these carcinogens, TCDD could not initiate cancer foci even at doses 1000 times higher than those used for its promoting effect and 1000 times higher than the dose of the genotoxic carcinogens used for initiation of cancer.11

The cancer-promoting effects of dioxin are not consistent across species or across tissues. In fact TCDD has been used to inhibit estrogen-dependent breast cancer in rodent models and cultured human cells, leading researchers to look into development of anti-cancer drugs from this dioxin.12 The fact remains, however, that TCDD can be a powerful cancer-promoter in certain tissues of certain species.

The mechanism by which TCDD exerts its toxic effects is believed to be mediated by its binding to the aryl hydrocarbon receptor (AhR), a receptor that is also involved in mediating responses to polynuclear aromatic hydrocarbons, combustion products and numerous phytochemicals such as flavanoids and indole-3-carbinol. Once bound, the TCDD-AhR complex then moves into the nucleus, where it binds to the aryl hydrocarbon receptor nuclear translocator (Arnt) protein. Finally, this TCDD-AhR-Arnt complex then binds to DNA to induce the expression of the cytochrome P-450 1A1 gene.5 Less is known about precisely how this activation of the cytochrome P-450 system leads to toxicity and carcinogenesis, but the toxic effects of TCDD are usually correlated with its activation of this system and appear to be dependent upon it.

The WHO's argument for TCDD's inclusion as a Group 1 carcinogen despite its failure to fulfill the criterion of sufficient evidence of carcinogenicity in humans relies on the following reasoning:

  • TCDD is a multi-site carcinogen in animals acting through the AhR;
  • The AhR is highly conserved across species and acts in a similar way in humans as it does in animals;
  • Tissue concentrations in humans where epidemiological studies have observed increased risk of cancer are similar to those of rats exposed to carcinogenic doses in the laboratory.13

Yet, although the AhR is highly conserved across species, the carcinogenicity and toxicity of TCDD is not. For example, the lethal dose of TCDD varies 5000-fold across species.5 Activation of the AhR cannot be sufficient to induce cancer, because the effect of indole-3-carbinol, a substance found in cruciferous vegetables, is also mediated by the AhR, yet is used to inhibit cancer.14 TCDD's use of inhibiting estrogen-dependent breast cancer in rodent and human mammary cells is also mediated through the AhR.12

In a major review on dioxins published in 2003, Phillip Cole and his co-workers point out that TCDD acts as a carcinogen in certain tissues in certain species, not many tissues in one species. The variation across species as to which tissues are vulnerable to carcinogenicity is not an argument for multi-site carcinogenicity in humans, but an argument against generalizing from species to species. The types of cancer induced in animals by TCDD "bear little correspondence to those reported among humans exposed to TCDD," and, while the tissue concentrations of TCDD are similar in animals who develop cancer and humans observed to have an increased risk of cancer, "even the few positive epidemiological studies of TCDD-exposed populations generally report at most a minimal increase of total cancer, while in rats the increase is much greater."13

The fact that activation of the AhR is not consistently linked to cancer, that the response of animals varies widely to TCDD, and that the types of cancer and magnitude of increased risk observed in humans bear little resemblance to the types of cancer and magnitude of increased risk in rats is sufficient to refute the WHO's inclusion of TCDD as a Group 1 carcinogen by its own criteria.

A question remains: Do humans exposed to high concentrations of dioxins really exhibit an increased risk for cancer? The Cole review refutes this hypothesis, showing that the WHO used its evidence selectively, and that researchers failed to appropriately adjust for exposure to other carcinogens.13

The WHO's argument rests on epidemiological evidence from industrial and occupational exposure, populations that have been exposed to 10-1000 times the concentrations of TCDD compared to the general population.4 While admitting the absence of a strong case for the elevation of any specific cancer, they have compiled four major cohort studies to find a 40 percent increased risk for all cancers combined for "highly exposed" workers, the definition of which differed between studies.

Yet the WHO excluded from this compilation a study by Kogevinas that the very same monograph referred to as " . . . the largest overall cohort study of [TCDD]-exposed workers," and which included the data from the other four cohorts. The WHO argued that it had to be excluded because it included individuals with lower TCDD exposures; but, as Cole and his colleagues point out, the data were reported separately for those who were "highly exposed," and those with lower exposure. Therefore the Kogevinas study could--and should--have been included. The Kogevinas study found a 20 percent increased risk for all cancers with occupational dioxin exposure, but those who were most highly exposed (20 or more years of work experience) had an 8 percent decreased risk of all cancers.13

The Seveso cohort study described the highest exposure to TCDD ever documented in a population. Seveso was the site of a 1976 accident at a chemical manufacturing plant in which a dense cloud of TCDD was released from a reactor in quantities measured in kilograms over 10 square miles, necessitating the evacuation of 600 homes.15 Yet follow-up of the Seveso population reveals that "all-cause and all-cancer mortality did not differ significantly from those expected in any of the contaminated zones."13

Cole and his team also noted that in numerous studies, confounding factors were not taken into account:

  • The NIOSH cohort study used smoking information from industrial plants 1 and 2, where there was no lung cancer elevation, but did not record smoking data from plants 8 and 10, where lung cancer was elevated, which they attributed to dioxin exposure.
  • In the same study, two deaths from mesothelioma could have reflected exposure to asbestos, and workers were also exposed to the bladder carcinogen 4-amino-biphenyl, neither of which was taken into account, while cancers in those exposed to these known carcinogens were attributed to dioxin.
  • In the Zober study, 35 of 37 cancer cases were smokers, and 10 of 11 respiratory cancer cases were smokers, yet cancer risk was assumed attributable to TCDD.
  • The one study (Ott and Zober) "with even minimally adequate information on smoking" found no statistically significant relationship between respiratory cancer incidence or mortality and TCDD.
  • No attention was given to possible confounding of socioeconomic class, "even though the individuals most exposed to TCDD frequently are from the less privileged socio-economic groups that have high overall mortality, including mortality from all cancer."13

All of the epidemiologic studies published before 1997 that were not included in the WHO's IARC Monograph, found no association between TCDD exposure and increased risk for cancer or mortality, including those by Dalager and team concerning non-Hodgkin's lymphoma, Watanabe and team concerning overall mortality, Bullman and team concerning testicular cancer, and Dalager and team concerning Hodgkin's disease.13

After the WHO's IARC classified TCDD as a Group 1 carcinogen in 1997, subsequent reviews and studies began to rely on the IARC's interpretation of earlier study results, rather than the study results themselves. Of the follow-up studies since 1997, the data of Steenland and team show that longer follow-up decreased the magnitude of associations previously found in the same cohort, and caused loss of statistical significance; Pesatori and team found that non-cancer mortality in Seveso--where the highest exposure to dioxins ever documented occurred--did not differ from that of the general population, and Ketchum and team found 30 percent fewer deaths from cancer in US Air Force veterans who were highly exposed to dioxins.13

Thus, while TCDD is claimed to be a non-genotoxic multi-site carcinogen, the evidence suggests that the wide variation in responses to dioxins across species prevents generalization to humans, and that the failure of dioxin exposure to act as an independent risk factor for cancer, even in human populations exposed to concentrations 1000 times greater than the general population, would contradict claims of human carcinogenicity.


Dioxins in Pastured Animal Products?

A review published in 1995 suggested that pastured animal products would probably contain higher dioxin concentrations because of a higher rate of soil ingestion;3 however, newer research has revealed the fact that the primary sources of above-average dioxin concentration in beef samples are feeding troughs constructed with pentachlorophenol-treated wood and the inclusion of incinerator waste as a feed additive.6 Grass-fed beef is not exposed to these sources of dioxins.


Non-Cancer Effects of Dioxins

Dioxins are responsible for a wide range of different toxic effects in different species. Non-cancer effects observed in wildlife exposed to high concentrations of dioxins, experimentally induced in animals treated with dioxins, and observed in humans exposed to industrial concentrations of dioxins vary between species and between types of exposure. Like dioxins' carcinogenic effects, the non-cancer effects of dioxins are believed to be primarily mediated by their ability to bind to the aryl hydrocarbon receptor (AhR).5

Seals fed dioxin-contaminated fish had depressed blood levels of vitamin A and thyroid hormone, and depressed natural killer cell and T-cell activity (indicating immune suppression). Herring gulls have been found with decreased liver stores of vitamin A, but increased egg yolk vitamin A levels, when exposed to dioxins, while great blue herons have lower levels of vitamin A in their egg yolks. Exposed cormorants experience decreased levels of free thyroid hormone, herring gulls experience decreased vitamin A, and common terns experience both decreased vitamin A and thyroid hormone levels. In white suckerfish, the AhR-mediated dioxin-like activity of PCBs was associated with birth defects. Skin diseases (resembling vitamin A-deficiency skin diseases) and increased thyroid weight have been observed in response to organochlorines, which include, but are not limited to dioxins.16

One interesting experiment, demonstrating the variation of dioxin toxicity between species, fed goiter-bearing salmon exposed to high concentrations of dioxin-like and non-dioxin-like PCBs in the wild to rats and other salmon. Although every single one of the wild salmon (previously transferred from the Pacific to the Great Lakes) in the organochlorine-polluted Great Lakes had an enlarged thyroid gland and a high PCB body burden, the degree of thyroid enlargement had no relation to PCB burden. When these PCB-laden fish were fed to immature Coho salmon, the latter did not develop any thyroid enlargement. Yet, when the PCB-laden fish were fed to lab rodents, the rodents developed goiter in direct proportion to the dioxin-like activity induced by the dietary PCBs. It has been hypothesized that the reason the Great Lakes salmon developed goiter is because of a goitrogenic factor of bacterial metabolism in the Great Lakes, which has also proved goitrogenic to humans, while to rodents, on the other hand, the PCBs carried by the fish are the goitrogenic factor.16

Reduced female fertility and reduced male sperm production, as well as genital deformations, have been induced by dioxin exposure in rodents. Dioxins can cause calcium uptake in neurons of the rat hippocampus, and have species- specific effects on gene expression in the nervous system of zebrafish and rats, though it is unknown how these effects may or may not result in any type of neurotoxicity.5 TCDD, the most potent dioxin, acts as an anti-estrogen in rodent mammary and uterine tissues, as well as human mammary cells, where it exerts anti-carcinogenic effects.17

TCDD can induce wasting syndrome and death in chickens and rodents, though its lethal dose varies 5000-fold across species. TCDD can induce cleft palate and other deformities, reproductive failure and liver damage in birds,18 endometriosis in rhesus monkeys, growth of surgically induced endometriotic cysts in rats and mice, and various effects on metabolism and hormones in various species.4

In humans, the only conditions to which dioxins have been conclusively linked are a type of skin acne known as chloracne, and a temporary increase in liver enzymes. Other non-cancer phenomena have been associated with exposure to industrial concentrations of dioxins in some human epidemiological studies, but the evidence is inconclusive or contradicting.4

Effects on various thyroid-related hormones and proteins were found in the Ranch Hand cohort and the National Institute for Occupational Safety and Health (NIOSH) cohort, but they were mostly weak and non-significant, and not consistent between studies. In one sub-section of the NIOSH cohort, diabetes was not associated with TCDD, but the highest-exposed group did have the highest rate of diabetes. The NIOSH cohort as a whole found a negative correlation between TCDD exposure and diabetes mortality, while women, but not men, in zones A and B in Seveso had a greater risk of diabetes mortality with greater TCDD-exposure.4

Exposure to dioxins in breast milk was associated with tooth enamel defects in one study, and alterations in thyroid hormone levels have been associated with prenatal dioxin exposure in children. In one study, exposure to dioxins in breast milk was found to have no effect on psychomotor outcome of infants between three and seven months or after 18 months, but was associated with depressed psychomotor skills between seven and 18 months. Few studies have identified statistically significant effects of industrial-level dioxin exposure on spontaneous abortions, birth weight,or birth defects. However, the most TCDD-contaminated area of Seveso, which has the highest exposure of a population to TCDD ever documented, found a modification in the sex ratio in favor of females to be associated with the total dioxin exposure of both parents. This is an interesting finding, but there were only 13 couples and 15 children in this group, and the association was only found in the highest-exposed group and between the years 1977 and 1984.4

The failure of dioxins to be consistently and conclusively correlated with cancer in humans, or non-cancer effects in humans with the exception of chloracne and temporary increases in liver enzymes, even at industrial levels that exceed what the general population encounters by up to a factor of 1000, should give pause to those who advocate exchanging the proven health-promoting diets of our ancestors for modern vegetarian and vegan diets that do not provide the same type of nutrition. Although dioxins can experimentally induce a variety of endocrine-disrupting, immune-depressing or anti-reproductive effects in animals, the effects are generally species-specific and in a minority of cases--such as the anti-estrogenic effects in mammary and uterine tissues--apparently beneficial.

Even if we assume that the worst of these findings can be generalized to humans, the fact that dioxin exposure has declined 95 percent since the 1970s and continues to decline, and the fact that no one in the US is currently exposed to even one-tenth of the dosage that has produced an abnormality in the most sensitive gestational rat, should assure us of the safety of consuming animal products. Moreover, dioxins do not act in a vacuum, but their effects are subject to the influence of many other physiological and dietary factors, and it is a diet rich in traditionally valued animal products that offers the most protection against their effects.


Dioxins: It's Not Just about the Meat

The first leg of the dioxin-based argument for a vegetarian or vegan diet--that dioxins are potent human carcinogens, endocrine disruptors, reproductive disruptors, and immune disruptors--has been shown above to be either false or irrelevant at the level of dioxins currently consumed in the US. The second leg of the argument--that animal products are uniquely high in dioxins--likewise fails to sustain analysis. While the most contaminated foods in some studies have been animal products, other studies cite animal products as among the least contaminated foods. Variation between samples is usually much greater than any variation between animal and vegetable products, making any supposed trend inconsistent at best.

One 2003 study actually measured the intake of dioxins in humans, where fourteen subjects ate an omnivorous diet for two weeks, then ate a vegan diet for two weeks. Although exposure to dioxins on a TEQ basis was higher during the omnivorous phase than the vegan phase, the diets of some subjects were actually comparable in total PCBs in the vegan and omnivorous phases. The TEQ measurement weights the relative dioxin-like toxicity of each dioxin-like compound against the toxicity of TCDD, so that compounds with less dioxin-like activity (meaning less toxicity mediated by the aryl hydrocarbon receptor) will contribute less per weight to the total TEQ. However, since PCBs have non-dioxin-like toxicity, and since dioxin-like PCBs measured in the study could be indicators for the presence of non-dioxin-like PCBs, it's possible that total PCB-related toxicity of the vegan diets could have been comparable to that of the omnivorous diets. Most significantly, even on the higher-TEQ omnivorous diet, average TEQ intake was 1.09 pg/kg bodyweight, which is only about half of the WHO's tolerable daily intake (TDI), a hyperconservative estimate of toxicity risk.19

A 1995 review of the significance of animal products as sources of human exposure to dioxins claimed that the "major food sources [of dioxins] seem to be fat-containing animal products and some seafoods."3 Since data from the US was not available at the time, the authors used data from Germany and the Netherlands. Table 2 of this review, showing the contribution of selected food products in pg TEQ per day, shows no consistent role of animal products in exposure to dioxins. For example, in the Netherlands, leafy vegetables (4.4) contributed a quantity of TEQs roughly equivalent to pork (4.2), and poultry and eggs (4.8). In Germany, vegetable oils (3.8) contributed only half as many TEQs as pork (7.6), and only 20 percent as many as beef and veal (19), while in the Netherlands, vegetable oils (14) contributed 3.3 times as many TEQs as pork (4.2) and 7 percent more than beef (13). Not only did the contribution of TEQs in the same type of food vary widely between the two countries, but the relative contribution of animal and vegetable products also varied widely.3

More recently, data from a wider range of countries has become available, and the FDA provides data from the years 2000-2003 on its website. These results continually reaffirm the wide variation between regions and samples and the lack of any consistent trend between animal and vegetable products.

For example, in Finland, fish accounted for 94 percent of dioxin TEQ intake,9 while in Canada fish only accounted for 3 percent of TEQ intake.20 A Japanese study found fish intake to be an independent predictor of blood dioxin levels, while for all other animal products except pork the correlations were insignificant. Eggs, butter, cheese and pork were actually negatively associated with dioxin levels. Yet the variation of blood levels between regions was large, ranging from 13 TEQ per gram of lipid to 21 TEQ per gram of lipid. Despite the higher fish intake in Japan, the median blood levels of dioxin were still lower than those found in other industrialized countries, especially from earlier studies, probably reflecting both inter-regional differences and declining dioxin levels in the environment.21

Clearly, however, it would be more beneficial to look at the quantities in food rather than the contribution of foods to intake, since the former is independent of what the general population is eating. What we are interested in is whether a diet rich in traditional animal products is excessive in dioxins compared to a vegetarian diet, not which foods people eating a standard diet are getting their dioxins from.

Unfortunately, most of the studies available have relatively small sample sizes which, when combined with the large variance between the samples, make the data relatively useless for establishing trends among types of foods. For example, in Greece, five samples of fish oil varied by a factor of six (meaning the sample with the highest concentration had six times more dioxins than the sample with the lowest concentration); five samples of butter and seven samples of farmed fish both varied by a factor of five; eight samples of lamb varied by a factor of three; three samples of poultry, three samples of beef liver and three samples of rice all varied by a factor of two; four samples of wild fish had concentrations ranging from zero to amounts nearly approaching the median for farmed fish.22

The FDA's data for the United States only uses three samples for each item.23 Although the report does not give information indicating the variation between samples, we can infer that there is considerable variation between samples by comparing different specific food items within the same type of food. For example, expressed in pg TEQ per gram, ground beef contains 0.0425 while a fast food quarter-pound burger contains 0.0, and whole milk contains 0.0087 while half and half, which should concentrate the dioxins in the butterfat, contains 0.0.24

The FDA's report offers us another way to ascertain the type of variation found among samples because the FDA reports the data in three ways: the first, where a non-detect is assumed to be equal to zero; the second, where a non-detect is assumed to be equal to half the limit of detection; and a third, where a non-detect is assumed to be equal to the limit of detection. If there weren't any non-detects, we would expect all three figures to be the same. If there is one or more non-detect, we should expect a certain pattern: the second figure should be higher than the first, and the difference between the third and the first figures should be exactly double the difference between the second and the first figures.

In fact, this pattern is nearly ubiquitous among the items that showed any detectable contamination with dioxins. This fact allows us to conclude that some of the items contained at least one sample with no detected dioxin, including milk, beef, lamb, turkey, beef liver, butter and salmon.

The FDA's data show that some of the highest concentration of dioxin TEQs are found in animal products, but this finding hardly provides justification for adoption of a vegan diet. Of the few whole foods actually measured, pork loin, eggs, and shrimp were animal products containing no detectable dioxin. Even the highest-ranking animal products, such as butter, salmon, lamb and beef had at least one non-detect among three samples, which means that only one or two samples out of three are responsible for the high ranking, while one or two out of the three samples did not contain any detectable dioxin at all.

Table 1 shows selected items from the FDA's report.24 Animal products are scattered among the highest and lowest concentrations of dioxin TEQs, with some plant foods containing significant quantities of dioxins. Since the FDA's report contained little in the way of vegan protein foods, I estimated the dioxin concentration of tofu using the FDA's figures for the dioxin concentration of
vegetable oil (usually meaning soybean oil) and the USDA's25 data for the fat content of tofu. Every single item listed had at least one sample in which no dioxin was detected.

Since the US FDA's data rely on only three samples, and since the variation between samples appears to be large, it is necessary to look at other data to establish or refute a trend--and this data destroys the argument that dioxins are found primarily in animal foods.

Table 2 gives data from Finland.9 Although animal products have a tendency to be higher on the list, vegetables have higher concentrations than milk products, and cereal products have more than a 4-fold concentration of dioxins compared to milk products. Fish take the cake in Finland, with 163 times the dioxin concentration compared to their nearest competitor, fats. According to this data, avoiding meat in favor of cereals would have a negligible impact compared to avoiding fish in favor of meats. Unfortunately the Finnish data give us no information on vegan sources of protein.

Table 3 provides data from the Netherlands.8 Since animal products except fish were reported per gram of fat while the other data were reported per kilogram of product, I adjusted the animal product data by choosing at random a specific item from the USDA's database25 to represent each category, and multiplying the grams of fat per gram of product by the pg TEQ per gram fat to yield the adjusted figures. The data for fish and plant products were divided by 1000 to yield the adjusted figures. As in Finland, fish in the Netherlands are considerably higher in dioxins than any other food, having 10 times the dioxin concentration as beef. Still, vegetables have about a 50 percent greater concentration of dioxins than whole milk, and roughly the same concentration as pork.

The data from Greece,22 shown in Table 4, are particularly damning to the notion that dioxins exist primarily in animal products. In this compilation, since plant products were reported on the basis of product weight while animal products were reported on the basis of grams of fat, it was necessary to choose a specific food product to represent each category and adjust the animal product figures in the same way as the previous table. It is therefore possible that some of the items, such as "farmed sockeye salmon," were not actually sampled in Greece, but serve only as a model to adjust the figures for the purpose of comparison.

Amazingly, the Greek study found, with the exception of fish oil, which isn't consumed in significant quantities, that rice was the most concentrated source of dioxin TEQs! Like the FDA's data for the US, the Greek study found animal products to be distributed between both the highest and lowest sources of dioxins, but this study actually found plant products in general to be higher in concentration than most of the animal products. For example, vegetables had almost six times the dioxin concentration of beef liver.

In all of these analyses, in most cases the wide variation of dioxin concentrations between regions and between individual samples is wider than the variation between types of foods. Animal products tend to be distributed randomly among the highest and lowest concentrations, yielding no consistent trend of dioxin accumulation in animal products. In some cases, such as the Greek data, vegetable products dominate the higher-concentration readings, and animal products dominate the lower-concentration readings. In the United States, certain animal products like butter are found to have the highest concentrations, but the presence of at least one sample of butter out of three with no detectable dioxins and three out of three samples of half and half with no detectable dioxins makes it impossible to claim a consistent connection between butterfat and dioxin.

Thus, the second leg of the dioxin-based argument for vegetarianism, that animal products are uniquely high in dioxins, crumbles to pieces when subjected to critical analysis.


Table 1.
Dioxin Concentrations in Foodstuffs, United States, 2003.

Data are reported assuming a non-detect is equal to zero.

FOOD ITEM PG TEQ DIOXIN/G PRODUCT
Butter 0.2847
Salmon Steak/Fillet 0.1918
Lamb Chop 0.0714
Beef Roast, Chuck 0.0687
Beef Loin 0.0606
Olive Oil 0.0295
Tomato Sauce 0.0232
Beef liver 0.0207
Roasted Turkey Breast 0.0171
Vegetable Oil 0.0150
Whole Milk 0.0087
Margarine 0.0015
Chicken Leg, fried with skin 0.0014
Tofu, Firm 0.0006
White Beans 0.0001
Sunflower Seeds, roasted 0.0000
Peanuts, dry roasted 0.0000
Tuna, canned 0.0000
Shrimp, boiled 0.0000
Half and Half 0.0000
Eggs, scrambled or boiled 0.0000
Pork Loin 0.0000


Table 2.
Dioxin Concentration in Foodstuffs, Finland, 2004.

Data are reported assuming a non-detect is equal tozero.

FOOD ITEM PG DIOXIN TEQ/G PRODUCT
Fish 1.80000
Fats 0.01100
Meat and Eggs 0.00820
Cereal Products 0.00430
Solid Milk Products 0.00270
Vegetables 0.00120
Liquid Milk Products 0.000930
Fruits and Berries 0.000830
Beverages 0.000170
Potato Products 0.000031



Table 3.
Dioxin Concentration in Foodstuffs, The Netherlands, 1999.

Data are reported assuming a non-detect is equal to zero.

FOOD ITEM PG DIOXIN TEQ/G PRODUCT
Fatty Fish 3.1580
Crustaceans 1.3540
Butter 1.3305
Lean Fish 0.5930
Cheese 0.4253
80% Lean Ground Beef 0.3654
Chicken, Dark Meat 0.3230
Margarine 0.3000
Prepared Fish 0.2670
Vegetable Oil 0.1800
Pork Chop Loin 0.0614
Vegetables 0.0600
Whole Milk 0.0410
Nuts 0.0130



Table 4.
Dioxin Concentration in Foodstuffs, Greece, 2002.

Data are reported assuming a non-detect is equal to the limit of detection.

FOOD ITEM PG DIOXIN TEQ/G PRODUCT
Fish Oil 1.010
Rice 0.900
Butter 0.640
Fruit 0.470
Vegetable 0.430
Olive Oil 0.300
Lamb Shoulder 0.110
80% Lean Hamburger 0.098
Beef Liver 0.077
Pork Chop 0.051
Farmed Sockeye Salmon 0.050
Boiled Egg 0.039
Chicken Leg 0.017
Wild Sockeye Salmon 0.013


Factors Affecting Dioxin Toxicity

Although the first tenet of the dioxin-based argument for vegetarianism, that dioxins are potent human carcinogens, endocrine disruptors, reproductive disruptors, and immune disruptors appears to be false or irrelevant to humans at the levels at which they are exposed, it is still sensible for us to err on the side of caution and, ceteris paribus (all things being equal), opt for a lower dioxin intake over a higher one. However, the argument for vegetarianism does not use the ceteris paribus stipulation; rather, it argues that dioxin intake be minimized regardless of other factors.

The third and final leg of the dioxin-based argument for vegetarianism,-- that avoiding the harmful effects of dioxins is primarily dependent upon minimizing dioxin intake and therefore avoiding animal products--implicitly assumes that dioxin toxicity is merely a function of dioxin intake. On the contrary, a variety of dietary and other factors influence dioxin uptake from the intestines, excretion of dioxin, the half-life of dioxin in the body and the toxicity of dioxin at the cellular level. As it turns out, vegetarian diets tend to be lower in protective nutrients and higher in toxicity-enhancing compounds, whereas a traditional diet is highest in protective nutrients and lowest in toxicity-enhancing compounds.

Not all dioxin consumed in a food is actually absorbed. One human study found widely varying intestinal absorption rates, with a maximum of 63 percent. The study did find that a higher-fat meal produced a higher absorption rate; however, since protective compounds are also fat-soluble, it shouldn't be concluded that a lower-fat diet is preferable. The older individuals in this study actually had a net excretion of dioxins, excreting more dioxins in the feces than was present in the food. Apparently, dioxins are stored in the tissues when tissue levels are lower than blood levels, and released from the tissues when blood levels drop below tissue levels. Since dioxin levels have decreased so dramatically over the past few decades, older individuals who experienced the high peaks in environmental dioxin levels in earlier decades cannot eat high enough concentrations in food to prevent automatic tissue release and fecal excretion.26

Various vegetable fibers have been shown to increase fecal excretion of dioxin in animals. Chlorophyll compounds, especially copper chlorophyllin, were shown in one study to be the most effective compounds, increasing excretion rates by 144 percent over normal when fed as 1 percent of the diet by weight.27 This might indicate a modest benefit of chlorophyll-rich vegetables (which would supply a much lower concentration of chlorophyll than used in the study), which could be obtained from both a vegetarian and a meat-based diet.

Once absorbed from the diet or from other forms of exposure into the bloodstream, dioxins are stored in fatty tissues and slowly detoxified and excreted over long periods of time. The half-lives of dioxins are not consistent between individuals, however. Investigations into the halflives of dioxins in industrially exposed persons reveal that the variation between minimum and maximum half-lives in different individuals is often several times greater than the value of the median half-life. Kidney and thyroid disorders may inhibit detoxification of dioxins, though results for thyroid disorders are conflicting. Persons with a higher percentage body fat have a slower dioxin decay rate, while intermediate weight loss can increase the decay rate by a factor of 2.5. For some unknown reason, smoking increases the decay rate significantly, although when adjusted for age and percent body fat the association becomes lower and for TCDD it becomes non-significant. For certain dioxins, however, smoking decreases the half-life by up to 25 percent.28

The most important variations in diet that affect the potential for toxic effects of dioxins are antioxidants and factors that increase oxidative damage in the body, such as polyunsaturated fatty acids. Among the antioxidants, vitamin A has many other roles independent of its antioxidant activity and deserves special attention, since depletion of vitamin A and interference with vitamin A metabolism is central to the toxicity of dioxins.


Dioxin Toxicity and Vitamin A

Although relatively little is known about which factors tie the ability of dioxins to bind to the aryl hydrocarbon receptor (AhR) and the subsequent activation of the cytochrome P-450 system to their toxicity, it is clear that one of the missing links is vitamin A. Changes in vitamin A levels in wildlife are correlated with dioxin exposure, and TCDD is able to experimentally induce vitamin A depletion as well as resistance to vitamin A signaling, which is correlated with its toxic effects. Also, TCDD and vitamin A have opposing actions in certain tissues, and the addition of dietary vitamin A exerts a strong protective effect against a wide range of TCDD-induced effects.

The most consistent effects observed in wildlife in response to dioxin exposure are changes in vitamin A and thyroid hormone levels. Changes in liver or plasma vitamin A concentrations have occurred in captive harbor seals eating polluted fish, Great Lakes herring gulls and tree swallows, great blue herons and lake sturgeon of the St. Lawrence River, common terns of Belgium and the Netherlands and white suckerfish of Montreal. Typically, decreases in liver or plasma vitamin A are observed, or signs of increased mobilization of vitamin A from the liver. In several of these cases, decreased levels of thyroid hormone have also occurred, and in cormorants of the Netherlands, a decrease in free thyroid hormone was observed without changes in vitamin A.16

When rats were fed daily doses of dioxins roughly equivalent to one million times more than humans typically consume, major impacts on vitamin A and thyroid hormone levels occurred. TCDD increased blood levels of vitamin A by 21 percent, while all other dioxins decreased blood levels. All of the dioxins, including TCDD, depleted liver stores of vitamin A by 60-80 percent. This was considered a "very sensitive response" to dioxins, since even the lowest dose, only 70,000 times the equivalent of that which humans consume, produced a statistically significant effect. A dose-dependent reduction of thyroid hormone (T4) was induced, yielding a 76 percent reduction at a dose equivalent to two million times more than humans typically consume, and still yielding a significant 50 percent decrease even in the group fed only 70,000 times more than humans typically consume.29

The above study found the effect of TCDD at reducing thyroid hormone levels to be much less potent than that of the other dioxins, while it actually raised blood levels of vitamin A rather than lowering them. This is probably because some of the other dioxins produce metabolites that bind to transthyretin, the protein that transports both vitamin A and thyroid hormone in the blood. TCDD, however, does not have this effect. The study found the WHO's TEQ concept to have no predictive value with respect to these effects. This calls into question whether vegan diets that are lower in dioxin TEQs but comparable in absolute quantities of dioxin-like PCBs are truly lower in toxic elements.19

Dioxins, Vitamin A, and Cancer

It appears that the capacity of dioxins to produce both cancer and non-cancer toxicity relates to their ability to deplete vitamin A reserves and oppose the actions of vitamin A in the body. In cultured human skin cells incubated with TCDD, TCDD induces the expression of transforming growth factor alpha (TGF-a) and decreases the expression of transforming growth factor beta-2 (TGF-ß2), while incubation with retinoic acid, the hormone form of vitamin A, increases the expression of TGF-ß2. (TGF-a increases cellular proliferation, while TGF-ß2 has the opposite effect.) Since excessive cellular proliferation is a mechanism of cancer promotion--causing cells to multiply before they are able to fix DNA damage--this may explain part of the carcinogenic potential of dioxins and the protective effect of vitamin A.30

On the other hand, in human breast cancer cells where dioxins inhibit cancer, vitamin A enhances the anti-estrogenic effect of dioxins. Both retinoic acid and TCDD inhibit breast cancer in rodents by opposing the effects of estrogen. In cultured human cells, TCDD and retinoic acid inhibit estrogen-induced cell proliferation and the synthesis of estrogen receptors, and the effectiveness of each is enhanced when used together.31

Both the carcinogenic and non-carcinogenic toxicity of dioxins are believed to stem from the ability of dioxins to bind to the AhR and induce the formation of the cytochrome P-450 system. A recent study showed that vitamin A fed to rodents reduced the TCDD-induced expression of cytochrome P-450 by 68 percent.32 Other studies also show vitamin A to be effective, along with other antioxidants, in inhibiting the free radical products that are induced by dioxins and also believed to play a role in carcinogenesis, as well as many other toxic effects, discussed below.


Dioxins, Vitamin A, and Non-Cancer Toxicity

Many of the observed toxic effects of dioxins resemble those of vitamin A deficiency. Table 5 shows selected effects of dioxins in various species that are also widely accepted to be effects of vitamin A deficiency. Diseases such as cancer that are effectively treated with or prevented by vitamin A but are not considered deficiencies of vitamin A in standard literature are not included.

Many of the toxic effects induced by dioxins correlate with vitamin A depletion. TCDD can result in impaired growth and wasting disease, and in the guinea pig, rat, mouse and hamster, a dose-response relationship has been demonstrated between degree of vitamin A depletion and degree of depressed weight gain.38 Decreased vitamin A stores have been found along with hyperkeratotic skin diseases in elephant seals, decreased fertility and suppressed immune function in harbor seals, suppressed immune function in herring gulls, and increased birth defects in white suckerfish and lake sturgeon, all of which resemble the effects of vitamin A deficiency and were associated with exposure to dioxins or organochlorines in general.16

Thus, dioxins deplete vitamin A stores and are associated with many effects that seem to mimic vitamin A deficiency. But there is more to the story. Although liver reserves are depleted when vitamin A deficiency-like symptoms induced by dioxins arise, these symptoms usually occur when there are still significant tissue reserves remaining, whereas in simple vitamin A deficiency, symptoms usually do not occur until tissue reserves are almost entirely depleted. Dioxins appear not only to deplete vitamin A, but also to induce cellular resistance to retinoic acid, which is the hormone form of vitamin A.39

Many effects of dioxins can be reversed by vitamin A. Supplementation with vitamin A enabled 25 percent of rats fed a lethal dose of TCDD to survive, while supplementation with vitamin E enabled only 10 percent to survive.40 Injection of vitamin A into a fertile egg largely protected against the increase in mortality of chicks caused by injection of TCDD, while other antioxidants had no effect, and vitamin A also reduced the increase in birth defects by half.18 In rodents, vitamin A by itself reduces TCDD-induced reduction of body weight and thymus weight and reduces DNA damage following TCDD treatment by over 60 percent; in combination with vitamin E it reduces TCDD-induced increase in liver weight.41 TCDD-induced hyperkeratosis (psoriasis) and chloracne (a type of acne) are reversed by topical application of vitamin A.39

Thus, vitamin A appears to play a unique role in protecting against the toxicity of dioxins, and has some protective effects that other antioxidants do not have. A large part of vitamin A's protective role is attributable to its antioxidant effect. Other antioxidants have also been shown to confer a large degree of protection against dioxin toxicity, a fact that also has implications regarding the types of fats we should consume.


Table 5.
Effects Shared by Vitamin A Deficiency and Dioxin Toxicity

Information compiled from various sources.5, 16 , 33, 34, 35, 36, 37

EFFECT:
Decreased circulating androgens
Male and female infertility: Decreased sperm production in males; fetal loss in females
Genital malformations
Cleft palate and various birth defects
Immune suppression
Hyperkeratosis and other skin diseases
Growth retardation
Increased mortality



Dioxin Toxicity, Free Radicals, and Antioxidants

The aryl hydrocarbon receptor (AhR) is involved in the detoxification of many compounds. However, once this process is begun, hydrogen peroxide and other chemicals capable of free radical damage are formed. Ideally, free radical formation is intercepted by antioxidant systems, but when free radical production exceeds antioxidant capacity, oxidative damage occurs. Polyunsaturated fatty acids in the membrane of the cell are the preferred target of free radicals, which, when converted to lipid peroxides by free radicals, initiate a chain reaction of damage to the membrane.42

A wide array of antioxidant compounds play specific roles in forming a protective network against this damage, including vitamin A, which protects the integrity of membranes, vitamin E, which intercepts the lipid peroxide chain reaction, glutathione peroxidase, a selenium-dependent enzyme that converts hydrogen peroxide to water,41 and coenzyme Q1043 and vitamin C,44 both of which act as antioxidants themselves and help to regenerate vitamin E. While dietary antioxidants protect against oxidative damage, consuming polyunsaturated fatty acids raises lipid peroxide levels, which will be discussed further below.

TCDD treatments have been shown to increase lipid peroxidation up to 7-fold in rats, 2-fold in mice, and by 25 percent in chickens exposed during embryonic development.45 The powerful protective effect against carcinogenicity and toxicity by supplemental antioxidants provides a compelling argument for a role in lipid peroxidation and oxidative stress in general in the mechanisms of dioxin-related toxicity.

Vitamins A and E both offer roughly 61-66 percent protection to mice against free radical production and DNA damage induced by a single acute dose of TCDD roughly equivalent to 50 million times that which a human typically consumes in a day.41 A study of mouse fibroblasts in cell culture found TCDD to enhance the carcinogenic effect of two other carcinogens between 3.5 and 3.8-fold, but the addition of a mixture of vitamins E and C was found to considerably reduce the tumor-promoting effect of TCDD when tumors were initiated by N-methyl-N'-nitro-N-nitrosoguanidine, and to entirely abolish the tumor-promoting effect of TCDD when tumors were initiated by 3-methylcholanthrene. Amazingly, when the hydroxyl scavenger mannitol was used as the antioxidant there were actually fewer tumors in TCDD-mannitol-treated groups than in the control for either initiator!11

A protective role for the selenium-dependent antioxidant enzyme glutathione peroxidase has also been demonstrated. TCDD has been shown to lower glutathione peroxidase levels up to 68 percent. Vitamin A, but not vitamin E, inhibits TCDD-induced reduction of glutathione peroxidase. Stohs and his team found vitamin A to be 2.5 times more effective than vitamin E at enabling the survival of rats exposed to a lethal dose of TCDD, and protection to be associated with glutathione peroxidase levels.40 Some of the protective effects of vitamin A that are not shared by vitamin E, then, might be attributable to vitamin A's glutathione peroxidase-sparing activity.

To date, no studies examining the affect of coenzyme Q10, an important protector against lipid peroxidation, on susceptibility to dioxin toxicity has been indexed for Medline.


Dioxin Toxicity: Vegetarian vs. Traditional Diets

Although the second leg of the dioxin-based argument for vegetarianism, that animal products are uniquely high in dioxins, has been shown to be false, even were it true, traditionally raised animal products provide important protective nutrients that vegetarian diets do not provide in comparable amounts. The third leg of the argument, then, that avoiding the harmful effects of dioxins is primarily dependent upon minimizing dioxin intake, and therefore avoiding animal products, is independently false because dioxin toxicity is mediated by many other factors, and a diet rich in traditional animal products is rich in protective factors, while a vegetarian diet and especially a vegan diet enhances the toxicity of dioxin.

Children on vegetarian diets have been found to have lower blood levels of vitamins A and E.46 Although vitamin C levels tend to be higher in vegetarians, selenium and selenium-dependent glutathione peroxidase levels are lower in vegetarians.47 Vegetarians have also been found to have higher vitamin A and E levels48 than their non-vegetarian counterparts, but most meat-eaters do not consume traditional vitamin A-rich animal foods like organ meats and cod liver oil or traditionally pastured animal products rich in vitamin E. That meat-eaters tend to have lower levels of vitamin C is most likely a reflection of the fact that the average meat-eater does not consume sufficient quantities of fruits and vegetables.

Vitamin C, carotenes, and vitamin E-rich plant foods, however, are not exclusive to a vegetarian diet. A meat-inclusive diet can be rich in fruits and vegetables if it is low in refined foods, while vegetarian and vegan diets by definition restrict animal products. It is noteworthy that pasture-fed meats contain four times as much vitamin E as their grain-fed counterparts,49 which is likely to be at least as true for grass-fed milk and butter, but it is also true that adequate vitamin E can be easily obtained on a vegetarian diet.

Vitamin A, on the other hand, is a nutrient that occurs only in animal foods. Although carotenes from plant foods can be converted to vitamin A, the conversion rate is low, and is continually being revised downward.

While the World Health Organization had considered six units of beta-carotene to be equal to one unit of vitamin A, the US Institute of Medicine revised this downward in 2002, considering 12 units of carotene in foods on a mixed diet to be equal to one unit of vitamin A. However, even this revision was criticized by a review in the Journal of Nutrition, which reported field studies suggesting that it took 21 units of beta-carotene to equal one unit of vitamin A.50 While the Institute of Medicine's figure considered half of the carotene in oils to be converted to vitamin A, a much higher conversion rate than that for solid foods, a more recent study found that even when carotene is provided as a concentrated dose in the form of an oil, conversion factors range from a minimum of 2.4 to a maximum of 20.2.51 Additionally, several medical conditions interfere with the conversion of carotenes to vitamin A, children have lower conversion rates than adults, and infants cannot make this conversion at all, requiring an animal source of vitamin A.36

Table 6 compares the four animal foods richest in vitamin A and the four plant foods richest in carotenes. For the plant foods, the USDA's listing25 for "vitamin A" is shown in parentheses. The amount of true vitamin A yielded is shown in bold, using the US Institute of Medicine's conversion factor of 12. Even this figure is likely to overestimate the amount of vitamin A yielded by the plant foods.

Considering the inefficiency of carotene conversion to vitamin A, it appears nearly impossible for a plant-based diet to supply the levels of vitamin A found in a traditional diet. Using the figures in Table 6, a quarter pound of liver supplies 29,210 IU of vitamin A, while a half-cup of sweet potatoes supplies only 1,792 IU. In order to meet the vitamin A content of a mere teaspoon of high-vitamin cod liver oil, one would have to consume 1.6 pounds or 3 cups of sweet potatoes. Using the conversion factor of 21 that some studies have suggested as more appropriate, it would take 3.1 pounds of carrots to equal the amount of vitamin A in one teaspoon of high-vitamin cod liver oil and a full 13.4 pounds of spinach to match a tablespoon of high-vitamin cod liver oil.

Although these calculations demonstrate the dramatic inferiority of plant foods as a source of vitamin A, the truth is that even such massive doses of carotenes could not match the vitamin A activity of a diet emphasizing vitamin A-rich animal products, because excessive doses of carotenes depress the vitamin A activity of the portion of the carotene that is absorbed.58

While antioxidants protect against lipid peroxidation, consumption of polyunsaturated fatty acids (PUFA) raises lipid peroxides. PUFA levels can be low on a vegetarian diet if oils like olive oil or saturated coconut oil are staples, but cod liver oil, an animal product, is the only polyunsaturated oil that has been shown to provide essential fatty acids without raising lipid peroxide levels.

Polyunsaturated plant oils rich in essential fatty acids such as soybean oil,52 corn oil53 and the omega-3-rich perilla oil54 all raise lipid peroxide levels. It is not only heated polyunsaturated oils that raise lipid peroxides. Even fresh, unoxidized perilla oil stored at –20C and fresh, unoxidized, purified DHA and EPA--the omega-3 PUFAs found in fish oil and cod liver oil,--stored at –80C, mixed into the diets of rats immediately before feeding, raised lipid peroxide levels in tissues considerably--even when rats were fed adequate vitamin E.54

Cod liver oil, on the other hand, has been shown to inhibit lipid peroxidation. One study found that cod liver oil depressed drug-induced lipid peroxidation in mice under the same conditions by which soybean oil increased lipid peroxidation.52 Another study found that feeding cod liver oil entirely abolished the increased level of lipid peroxidation found in diabetic rats.55 In both studies, the depression of lipid peroxidation was related to a sparing effect on glutathione peroxidase activity, which was also the case in rats saved from a lethal dose of dioxin by vitamin A supplementation, suggesting that the protective effect of cod liver oil is due to its high vitamin A content.

The omega-3 and omega-6 PUFA in plant oils must be desaturated and elongated by the body to form the important fatty acids that have structural and hormone precursor value, such as DGLA and AA in the omega-6 family, and EPA and DHA in the omega-3 family. Since this conversion is relatively inefficient, especially in vegetarian diets that tend to be low in zinc, a larger amount of total PUFA must be consumed from plant oils to meet requirements for these fatty acids than from animal products that contain these fatty acids in their needed form. The increase in total PUFA consumption directly increases the risk of lipid peroxidation above that which is required on an animal product-inclusive diet.

It is possible for vegetarian diets to be relatively low in PUFA and for meat-inclusive diets to be excessive in PUFA, but maximal protection against lipid peroxidation is only possible on a diet utilizing organ meats and cod liver oil. Organ meats and butter can provide the omega-6 fatty acids DGLA and AA without an excess of total PUFA,56 while cod liver oil can supply the omega-3 fatty acids EPA and DHA without an excess of total PUFA. Liver and cod liver oil also provide the vitamin A required to protect these fatty acids from oxidation and boost the level of the protective enzyme glutathione peroxidase.

Coenzyme Q10's effect on susceptibility to dioxin toxicity has not been studied, but since it is a known inhibitor of lipid peroxidation and is necessary for vitamin E function43 it is highly likely to offer considerable protection. Coenzyme Q10 is produced in the body, but synthesis begins declining at the age of 20, after which dietary sources become more important. Although there are no studies of coenzyme Q10 levels in vegetarians indexed for Medline at the time of writing, Dr. Al Sears, MD, director of the south Florida Center for Health and Wellness, reports in The Doctor's Heart Cure that strict vegans tend to have "extremely low" levels of coenzyme Q10, based on several hundred patients whose blood levels he has measured. Coenzyme Q10 is a heat-sensitive nutrient primarily found in traditional foods like organ meats. According to Dr. Sears, the organs of wild and grass-fed animals have up to ten times the levels of coenzyme Q10 compared to the levels in the organs of grain-fed animals.57


Table 6.
Vitamin A Content of Animal Foods vs. Plant Foods

NIMAL FOODS VITAMIN A (IU/G) PLANT FOODS VIT. A EQUIVALENTS (IU/G)
High-Vitamin Cod Liver Oil 2,500 Sweet Potato 16.0 (192.2)
Turkey Giblets 357.9 Carrots 14.3 (172.0)
Beef Liver 260.9 Canned Pumpkin 13.0 (155.6)
Chicken Liver 133.3 Spinach 10.1 (120.6)


Dioxin Shmioxin:
It All Comes Back to Weston Price


The hysteria surrounding dioxins in some circles is difficult to understand considering the fact that exposure to dioxins has declined by 95 percent over the past three decades, a fact that is verified both by major declines in body burdens and in human breast milk concentrations. The simple fact is that dioxins do not exist in the environment at concentrations that warrant making dietary changes. Modifying antioxidant intake and fatty acid intake in the diet can produce major changes in lipid peroxidation, a major mechanism of dioxin toxicity, due not to the presence of dioxins, but to the direct impact of compounds that are present in our diets in much more relevant concentrations than dioxins.

The dioxin-based argument for vegetarianism stands upon three legs, each of which crumble under analysis, the failure of each being sufficient for the argument to fall. Dioxins have not been shown to be potent human carcinogens, endocrine disruptors, reproductive inhibitors or immune toxicants; dioxins do not occur primarily in animal foods, and in some cases, as in Greece, occur primarily in plant foods; and intake is not the only or even primary determinant of toxicity. Furthermore, vegetarian diets cannot provide the degree of protection conferred by a traditional diet compatible with the Weston A. Price Foundation's principles, and require the consumption of polyunsaturated plant oils to provide essential fatty acids, which enhance the type of toxicity exemplified by dioxins.

Ultimately, diets must be looked at in their entirety. If the goal of minimizing dioxin intake was truly more important than all other dietary considerations, then it would make sense to eat a diet comprised mostly of potatoes, which studies consistently show to be the lowest carriers of dioxins in all countries, and to use margarine as one's staple fat, which has been found to be lower in dioxin concentration than vegetable oil, olive oil and butter. Using the tortured logic of the dioxin-dreaders, smoking cigarettes would also be advisable, to increase the detoxification and excretion of stored dioxins.

The studies that compare vegetarians to meat-eaters on modern diets compare two relatively poor diets, both devalued by poor soil fertility and the absence of traditional foods like organ meats and cod liver oil. The reason Weston Price's research remains persistently relevant and continues to trump a multitude of conflicting research findings is because Price was able to document truly healthy populations rather than only those who suffered from disease.

Not all pre-modern peoples had the same robust health as those observed by Dr. Price. Price chose to document groups based on their immunity to degenerative disease and tooth decay, not merely their isolation from modern society, and Price did not note the presence or absence of any singular element to be responsible for the superior health he observed. A combination of numerous dietary factors, soil maintenance practices, and prenatal and lactational diets were all required together to confer superb health.

It is highly likely that the populations Price studied had at least some exposure to dioxins, produced from natural sources such as forest fires and volcanoes. Yet Price found that, without exception, certain animal products were considered necessary, sacred, protective and health-promoting. Of vegetarian diets, he noted: "As yet I have not found a single group of primitive racial stock which was building and maintaining excellent bodies by living entirely on plant foods. I have found in many parts of the world most devout representatives of modern ethical systems advocating restriction of foods to the vegetable products. In every instance where the groups involved had been long under this teaching, I found evidence of degeneration in the form of dental caries, and in the new generation in the form of abnormal dental arches to an extent very much higher than in the primitive groups who were not under this influence."59

Our focus should not be on any given compound which, when isolated and given to animals at thousands of times the concentration found in food, produces toxic effects, but on what type of diet as a whole is able to promote long, healthful and happy lives. Price demonstrated that the healthiest of humans have always included animal products as a valuable and important part of such a diet, a truth whose relevance persists today.


Abbreviations Used in this Review

AA – Arachidonic acid.
AhR – The aryl hydrocarbon receptor.
Arnt – The aryl hydrocarbon receptor nuclear translocator protein.
DGLA – Dihomo-gamma-linoleic acid.
DHA – Docosohexaenoic acid.
EPA – Eicosapentaenoic acid.
IARC – International Agency for Research on Cancer, an arm of the World Health Organization.
NIOSH – National Institute for Occupational Safety and Health.
PCB – Polychlorinated biphenyl. Some PCBs are dioxins; others are not. Non-dioxin PCBs are also believed to be toxic.
PCDD – Polychlorinated dibenzo-dioxins, a class of dioxins to which TCDD belongs.
PCDF – Polychlorinated dibenzo-furans, a class of dioxins.
PUFA – Polyunsaturated fatty acid
TCDD – 2,3,7,8-tetrachlorodibenzo-p-dioxin, the prototypical and most potent dioxin, also a PCDD.
TDI – Tolerable daily intake. A value determined by the World Health Organization.
TEF
– Toxic equivalency factor
TEQ – Toxic equivalent quantity.
WHO – World Health Organization


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