This blog refutes that reasoning. There is a lack of evidence that eating animal products prevents the most common birth defects. There is also a lack of evidence that dietary omnivores have a lower overall risk of birth defects than vegans. In fact, in the U.S., the vast majority of birth defects occur among babies born to women who are dietary omnivores.
Prevalence of Birth Defects
The CDC states that "Major structural or genetic birth defects affect approximately 3% of births in the United States."[1 ]
According to the CDC, the U.S. fertility rate is about 63 births per 1000 women, and 3,952,841 babies were born in the United States in 2012.
Since the rate of birth defects is 3%, that means that about 118,585 babies were born with birth defects in 2012 in the U.S.. Does anyone believe that these birth defects are a problem unique to people who eat plant-based diets?
According to a 2012 Gallup Poll, 2% of respondents identified themselves as "vegan." 
However, in the Gallup Poll the question did not define "vegan." This means that the Gallup Poll relies on personal definitions of "vegan" which are notoriously variable. A 2006 poll by the Vegetarian Resource Group found that 1.4% of respondents agreed that they never eat meat, poultry, fish/seafood, dairy products, or eggs.
According to a Vegetarian Times poll, 59% of vegetarians are women.
For the sake of argument, I will assume that 59% of vegans are women as well. If 1.4% of the U.S. population is vegan (i.e. about 4 million people), then there are about 2.36 million vegan women.
|Source: Mother's Delight|
This would mean that the total number of births annually to vegan women in the U.S. would be 148,680.
This means that vegan women are producing only 4% of all U.S. births. Yet 3% of all U.S. births have birth defects.
If the rate of birth defects among vegans equals that of the general population, this would mean that 4505 vegan births will have birth defects.
If birth defects only occurred among vegans, then 118,585 out of 148,680 babies born to vegans would have birth defects. That would be a birth defect rate of 80%! But that is not what is happening. Just as the vast majority of people in the U.S. eats meat, the vast majority of babies born with birth defects are born to women who eat meat, eggs, and dairy.
Birth Defects Among Meat-Eaters
Based on some small studies contaminated with confounders, some people have claimed that the removal of animal products from the diet causes women to give birth to baby boys with a penile defect cause hypospadias. However, according to the largest study conducted so far, hypospadias occurs just as often among children of meat-eaters as it does among children of women who abstain from eating meat. In this study, only one percent of case mothers ate no meat nor fish (but still consumed dairy and eggs), and only one case mother and one control mother ate no meat, fish, eggs, or dairy products (a proxy for vegan diet). Based on this, the odds are even. The number of 'vegan' mothers giving birth to boys with hypospadias was identical to the number without, giving evidence that one can prevent hypospadias without eating animals during pregnancy.
But I want to emphasize this point: In this study, about 97% of cases of hypospadias were born to women who were eating meat, fish, dairy, and eggs. That is, neither meat-eating, fish-eating, dairy-eating, or egg-eating during pregnancy served as a universal preventive for hypospadias.
What if I put a headline above: "Animal Products Associated With 97% of Hypospadias Cases." It is a true statement. Would women then decide to abandon the consumption of animal products during pregnancy? Why do people ignore this fact, and decide to try to blame "the vegan diet" for hypospadias?
People trying to scare women away from vegan diets during pregnancy are blinded by and blinding others with the carnist ideology. Since hypospadias occurs in babies born to dietary omnivores, we can conclude that eating animal products does not prevent hypospadias. In addition, since not all vegan baby boys are born with hypospadias, we can conclude that if there is any nutrient that can prevent hypospadias, it is available in plant foods. If hypospadias does have a nutritional deficiency as a cause, it lies in the absence of some plant-based nutrient that both some meat-eaters and some vegans fail to consume.
Since in fact one is just as likely to have a baby with hypospadias on a meat-rich diet as on a vegan diet, there is no rational basis for taking up meat eating during pregnancy in order to prevent this defect. It may be just as likely that by replacing some plant foods with meat, you will be deficient in some plant-based nutrient necessary for preventing this defect.
According to the CDC, Trisomy 21, or Down Syndrome, is one of the most common birth defects in the U.S., with more than 6000 cases per year in 2004-2006. Advanced maternal age is the only generally accepted risk factor for this disorder, with no established nutritional link. People who eat diets rich in animal products give birth to babies with Trisomy 21 every single day of the year.
There is some evidence suggesting that inadequate intake of folate could contribute to Trisomy 21.[8, 9] Folate is a plant-based nutrient named after foliage, i.e. leaves. Green leafy vegetables and legumes provide abundant folate. One can obtain the recommended 400 µg of folic acid/day by consuming 1.5 cups of legumes (about 400 kcal), or 1.5 cups of cooked spinach (about 60 kcal), or half a head of romaine lettuce (about 50 kcal), or some combination daily. Actually, many plant foods contain folate. I typically obtain more than 900 mcg folate daily from my plant-based diet.
|One of my folate-rich meals: Lentils and Romaine Lettuce|
Larsson and Johansson reported that teen-age female vegans consumed an average of 473 mcg folate daily, whereas age-matched omnivores consumed only 226 mcg. Schüpbach et al reported that among Swiss omnivores, 58% did not consume adequate folate.
Orofacial cleft (OFC) is also a more common defect, with cleft lip or palate cases totaling about 7088 per year. Folate deficiency may be a risk factor for this defect.[12, 13] However, some authors contend that the evidence for a protective effect of folate was inconsistent as of 2008.
Krapels et al.  studied maternal nutrition and orofacial cleft (OFC) defects and reported:
"The energy-adjusted intakes of vegetable protein, fiber, beta-carotene, ascorbic acid, alpha-tocopherol, iron, and magnesium were significantly lower in cases compared with controls. Increasing intakes of vegetable protein, fiber, ascorbic acid, iron, and magnesium decreased OFC risk. In conclusion, a higher preconceptional intake of nutrients predominantly present in fruits and vegetables reduces the risk of offspring affected by OFC..."Imagine that: Eating fruits and vegetables may prevent birth defects. Who would have thought? Apparently, not the folks at Weston A Price Foundation.
Krapels et al. found that in both cases and controls, the geometric mean dietary intake of energy, fiber, and iron were below the RDA. Adequate energy intake is very important for gestation and necessary for growth and development. In this population, women with increased fat intake would likely have greater energy intake and this alone may explain the positive association with fat.
Krapels et al. found that women with greater vegetable protein and specifically soy consumption had a lower risk of giving birth to babies with OFC.  Iron was also protective, but only at the level of the RDA, which is easily achieved on a plant-based diet.
"The most important risk reductions were observed for ascorbic acid and magnesium above the RDA and for fiber and iron equal to the RDA."Krapels et al. also found a link between increased intakes of cholesterol and saturated fats and a decreased risk of cleft palate only (CPO), but they considered the number of CPO cases was too small to provide any basis for strong conclusions. That probably wouldn't prevent the WAPF crew from making a mountain of this molehill. However, a look at their data on cholesterol and saturated fat intakes in the case and control populations reveals no basis for any claim that these nutrients prevented birth defects in this population.
In this population cases and controls both consumed an average of 15% of energy as saturated fat. Cases consumed and average of 35 g saturated fat daily, controls, 37 g.  There is no biological mechanism by which 2 grams of saturated fat would make the difference between cleft and no cleft defect. Moreover, cases had a saturated fat intake range of 19-53 g, and controls, 24-58 g.  The ranges overlap to such an extent, that their saturated fat intakes are practically indistinguishable. Some women who had saturated fat intakes of 50 g per day had babies with OFC, some did not. Some women who consumed as little as 24 g per day did not have babies with OFC, while some did.
Cases consumed an average of 191 mg cholesterol daily, and controls 208 mg, a difference of only 17 mg, which could not by any plausible biological mechanism account for the presence or absence of clefts. Further, among cases, cholesterol intake ranged from 112 to 311 mg/d, and among controls, 131 and 360 mg/d. This means that some women who consumed as much as 311 mg cholesterol daily gave birth to babies with clefts (while some did not), and some who consumed as little as 131 mg daily did not have babies with clefts (while some with that intake did). This makes it very unlikely that saturated fat and cholesterol were the actual protective factors. Probably these nutrients were associated with some other protective factor, such as taking multivitamins.
In this study, cases consumed an average of 47 g animal protein daily (range, 27-74), and controls, 49 g (range, 31-76).  There is no plausible biological mechanism by which these small differences in animal protein intake could account for the presence of clefts. Some women who ate 74 g animal protein daily had babies with OFC, some did not; some who consumed as little as 31 g per day had babies with OFC, some did not.
Regarding animal-source vitamin A (retinol), in this study, cases had an average intake of 583 mcg/d, and controls, 616 mcg/d, a difference of only 33 mcg/d. Moreover, the cases ranged from 238 to 1660 mcg/d, and controls, 266 to 1505 mcg/d. The people with the highest retinol intake were among the cases, but the average difference was practically insignificant.
I just want to emphasize here that in this study, 182 women who were consuming large amounts of animal protein, cholesterol, and retinol vitamin A gave birth to babies with orofacial clefts. Again, people are claiming that women need to eat animal products to prevent birth defects, but women who eat large amounts of animal products do in fact give birth to babies with serious birth defects.
According to the Teratology Society, orofacial clefts are among the birth defects observed in animals given excess vitamin A in the form of retinol, the same as provided by animal products.
According to the CDC, about 1460 babies every year are born with spina bifida.
Spina bifida can be prevented by a diet rich in folic acid and B12.
"In September 1992, the U.S. Public Health Service (USPHS) recommended that all women capable of becoming pregnant should consume 400 µg of folic acid/day on an ongoing basis to reduce their risk for having a pregnancy affected by spina bifida and anencephaly (i.e., neural tube defects [NTDs])...
"...in 1998, the Food and Drug Administration began requiring the fortification of enriched cereal grain products with folic acid at the level of 140 µg/100 grams of grain (fortification was optional during March 1996--December 1997). This level of fortification was chosen to assist women of reproductive age in increasing their folic acid consumption by an average of 100 µg of folic acid daily."
Why was this fortification made mandatory? Because, as shown above, many meat-eaters don't consume enough folic acid to prevent spina bifida. In contrast, again as shown above, even teen-age vegan girls consume more than the recommended 400 mcg/d.
Meat is touted as a source of B12. However, despite widespread consumption of meat, eggs, and milk, B12 deficiency may be prevalent in the U.S.. Tufts University researchers report no association between meat consumption and B12 status:
"Oddly, the researchers found no association between plasma B12 levels and meat, poultry, and fish intake, even though these foods supply the bulk of B12 in the diet. “It’s not because people aren’t eating enough meat,” Tucker said. “The vitamin isn’t getting absorbed.”Vitamin B12 is not an animal product. All the vitamin B12 in the world is produced by microbes, not livestock raised for animal products. Since B12 is not an animal product, and we can get what we need by cultivating microbes, no one needs to eat animals to get it.
In fact, authorities are now calling for mandatory microbial B12 fortification of grain products to prevent neural tube defects:
"There was almost a tripling in the risk for NTD in the presence of low maternal B(12) status, measured by holoTC. The benefits of adding synthetic B(12) to current recommendations for periconceptional folic acid tablet supplements or folic-acid-fortified foods need to be considered. It remains to be determined what fraction of NTD cases in a universally folate-fortified environment might be prevented by higher periconceptional intake of B(12)." If animal foods are such awesome sources of B12, why would a population that consumes an average of 195 pounds of meat annually (22, USDA data) – one-half pound daily – need to fortify one of its plant foods (grain products) with B12 to prevent deficiency and neural tube defects? B12 in animal products is second-hand. Why not get this nutrient directly from the primary source which is according to research the most effective at serving human needs, and in addition the most economical choice? I am not going to settle for second hand, second best sources of B12.
"Mandatory vitamin B12 fortification of enriched grain products is long overdue in the United States and Canada. Fortification would help provide the 2.4 mug of synthetic vitamin B12 that the US Institute of Medicine recommends for all persons 50 years and older. The findings of Ray and colleagues in this issue suggest that B12 may also help to prevent neural tube defects."
A 2010 study found that low dietary levels of fructose and glucose and a low dietary glycemic index were significantly associated with anencephaly.
"For anencephaly, we observed reduced risk with high glycemic index and increased risk with low intake of fructose and glucose."Let me state this finding otherwise: Those women with high intakes of high glycemic carbohydrates were less likely to have brainless babies. Interesting, eh? Except for a very small amount of glucose in whole milk or yogurt, animal foods completely lack fructose and contain only negligible traces of glucose. If meat and animal fat are so good and necessary for building brains, why didn't these researchers find that meat or fat consumption was protective against being born brainless?
This same study reported:
"Some nutrients that contribute to one-carbon metabolism showed lowered risks (folate, riboflavin, vitamins B6 and B12); others did not (choline, methionine, zinc). Anti-oxidant nutrients tended to be associated with lowered risks (vitamins C, E, A, β-carotene, lutein)."The authors also reported an increased risk of anencephaly with "high intake of thiamin, zinc, and iron." Proponents of meat-eating for pregnant women – such as the Weston A Price Foundation – usually claim that these women need to eat meat to ensure adequate iron and zinc intake to prevent birth defects, but this study actually reported an increased risk of neural tube defects among women with high intakes of zinc and iron. Could excessive intakes of these nutrients due to meat-eating (as opposed to the adequate intakes that can be provided by whole foods plant based diets) actually be promoting birth defects?
Except for vitamin A (retinol) and B12, every one of the nutrients that this last study found associated with lower risk of birth defects occurs abundantly in whole plant foods. As already noted, it appears that everyone in the U.S. is best served by dietary B12 supplements or fortification, regardless of meat intake. With an adequate intake of ß-carotene, pregnant women do not need dietary retinol, and in fact, the Teratology Society states:
"Women in their reproductive years should be informed that the excessive use of vitamin A shortly before and during pregnancy could be harmful to their babies....It is important to determine the type of vitamin A consumed, since beta-carotene has not been associated with vitamin A toxicity in animals or man."Further, from the Teratology Society again:
"5. Is it biologically plausible that high doses of vitamin A may cause birth defects in the human?Looks like the society devoted to the study and prevention of birth defects has determined that plant foods are the best for preventing vitamin A-related birth defects.
Yes, isotretinoin is a known human teratogen. Since isotretinoin and vitamin A (retinol and retinyl esters) induce similar patterns of malformations in animals, it is probable that similar pathogenetic mechanisms are involved in inducing the malformations. Currently there is no evidence to suggest that vitamin A should act differently than isotretinoin in the human conceptus. Beta-carotene, a provitamin A, does not produce vitamin A toxicity nor does it produce teratogenicity in animals. All of these data are consistent with a specific vitamin A-related teratogenic response."
In Powered By Plants: Natural Selection & Human Nutrition I have a chapter devoted to discussing evidence regarding the effect of consumption of animal products on human fertility. To sum it up, we have evidence that consumption of animal products impairs ovulation in women and sperm production and quality in men.[For example, 24, 25, 26] Prior to the introduction of hormonal birth control, populations consuming diets low in animal protein had significantly greater fertility than those consuming diets high in animal protein, and it appeared that diets high in animal protein reduced fertility in a dose-response fashion.
We also have evidence that diets high in protein and EPA/DHA consumption are toxic to embryos. High protein intake increases embryo exposure to ammonium and this impairs implantation and fetal growth , and high protein intake has been found to increase the risk of neonatal death and small-for-gestational-age infants [for example, 28]. Regarding the omega-3 fats, Wakefield et al reported:
"...the exposure of oocytes to an environment high in n-3 PUFA during in vivo fertilization adversely affected the morphological appearance of the embryo and decreased developmental ability to the blastocyst stage. This study suggests that high maternal dietary n-3 PUFA exposure periconception reduces normal embryo development in the mouse and is associated with perturbed mitochondrial metabolism, raising questions regarding supplementation with n-3 PUFAs during this period of time."Could these findings help to explain the undeniable fact that in the U.S. population dietary omnivores give birth to a rather large number of and the vast majority of babies with birth defects?
1. In the U.S. and European nations, the vast majority of birth defects occur in babies whose mothers ate meat, fish, non-human milk, and eggs during their pregnancy.
2. We lack consistent evidence that omnivores have a lower risk of birth defects than vegetarians or vegans.
3. For some birth defects, there is a lack of solid evidence for any nutritional cause.
4. Where nutritional causes for birth defects have been studied, it appears that dietary omnivores are no less (and possibly more) prone to the relevant deficiencies than people who eat plant-based diets.
5. Retinol, the form of vitamin A found in animal products, has been demonstrated to cause birth defects in experimental animal studies and there is reason to believe these nutrients would also cause birth defects in humans.
6. For the most common birth defects, the nutrients that provide protection can be obtained from a plant-based diet supplemented with microbial vitamin B12.
7. For the prevention of neural tube defects, experts have recommended mandatory B12 fortification of all grain products sold in the U.S. despite the fact that per capita consumption of meat theoretically supplies adequate B12.
8. There is no one universally followed vegan diet. Some people who avoid animal products eat nutrient-dense diets, some do not. Therefore, it is to be expected that among any given random population of vegans or vegetarians, some will have nutrient deficiencies, while others will not. This is also the case with dietary omnivores.
9. So far, it appears that a conscientious vegan dieter can be at least as successful at preventing birth defects as any dietary omnivore, and may in fact have an advantage, as the nutrients most clearly associated prevention of birth defects can all be obtained from non-animal sources.
Therefore, if a vegan woman does give birth to a baby having birth defects, this does not provide evidence that the defects were caused by avoidance of animal products. Since the vast majority of birth defects occur among dietary omnivores, and many vegan mothers give birth to healthy babies, it logically follows that if there are any nutrients essential to prevention of birth defects, they are available from non-animal sources.