Table of Contents
- Sidebar: Dioxins: Some Background
- Exposure to Dioxins
- Sidebar: A Modern Threat?
- Dioxin and Cancer: “Sufficient Evidence” Not Required
- Sidebar: Dioxins in Pastured Animal Products?
- Non-Cancer Effects of Dioxins
- Dioxins: It’s Not Just about the Meat
- Factors Affecting Dioxin Toxicity
- Dioxin Toxicity and Vitamin A
- Dioxins, Vitamin A, and Cancer
- Dioxins, Vitamin A, and Non-Cancer Toxicity
- Dioxin Toxicity, Free Radicals, and Antioxidants
- Dioxin Toxicity: Vegetarian Versus Traditional Diets
- Dioxin Shmioxin: It All Comes Back to Weston Price
- Abbreviations Used in this Review
- About the Author
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 natives 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 indigenous 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 indigenous 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.
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.
Table 2. Dioxin Concentration in Foodstuffs, Finland, 2004.
Data are reported assuming a non-detect is equal tozero.
Table 3. Dioxin Concentration in Foodstuffs, The Netherlands, 1999.
Data are reported assuming a non-detect is equal to zero.
Table 4. Dioxin Concentration in Foodstuffs, Greece, 2002.
Data are reported assuming a non-detect is equal to the limit of detection.
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.
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
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 indigenous 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 indigenous 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 ReviewAA – 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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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Fall 2005.