A SCIENTIFIC REBUTTAL OF THE “SOY-BOY” INSULT

February 23, 2018 Adam Riva

TRANSCRIPT & SOURCES

Veganism is not a Leftist Ideology

The derogatory slur “soy-boy” is used to humiliate, discriminate, or otherwise ostracize a vegan based on the pre-conception that vegan males are frail and emasculated men who suffer from low testosterone. This ad hominem attack is deployed without actually disproving the superiority of the dietary and lifestyle choice through argumentation. When someone uses the insult “soy boy,” it is an admission of nutritional ignorance.

Unfortunately some of my favorite content creators on YouTube who I highly respect such as Paul Joseph Watson, Steven Crowder, Faith Goldy, and Stephan Molyneux use this pejorative to mock vegans because veganism is generally associated with the political left. Of course, not all vegans are social justice warriors.

The Medical Literature on Soy

Let us now rebut this ad hominem using peer-reviewed medical literature, as well as addressing the real causes of the feminization of western men as well as Japanese males. For anyone who has watched my Science Explained video series, this will not come as a surprise to you.

What does the scientific community conclude about excessive consumption of soy protein lowering testosterone in men? Thankfully, the medical literature is quite clear on this.

A 2010 meta-analysis by Hamilton-Reeves et al. published in the American Society for Reproductive Medicine’s journal Fertility and Sterility set out, in their own words,

“To determine whether isoflavones exert estrogen-like effects in men by lowering bioavailable T through evaluation of the effects of soy protein or isoflavone intake on T, sex hormone–binding globulin (SHBG), free T, and free androgen index (FAI) in men.”

The study was set up as follows.

“Fifteen placebo-controlled treatment groups with baseline and ending measures were analyzed. In addition, 32 reports involving 36 treatment groups were assessed in simpler models to ascertain the results.”

Finally, the team spelled out their conclusion in plain English.

“The results of this meta-analysis suggest that neither soy foods nor isoflavone supplements alter measures of bioavailable T concentrations in men.”

Also in 2010, Mark Messina published a meta-analysis concluding,

“The intervention data indicate that isoflavones do not exert feminizing effects on men at intake levels equal to and even considerably higher than are typical for Asian males.”

According to a peer-reviewed paper published in 2007 by Kalman et al., soy protein was shown to have no effect on the reproductive hormones of men. Soy was demonstrated to promote lean body mass in men, which also seems to contradict many people’s misconception about soy being a poor protein for anabolic muscle production. This was further corroborated 3 years later by two separate studies [1, 2].

It is worth pointing out that men have far less estrogen receptors than women and that men naturally produce estrogen in the testes, so even if men consume trace amounts of phytoestrogens as is the case with soy, this has little impact on hormonal homeostasis, as demonstrated by Dickson and Clarke in 1981.

To date, very few isolated studies found a disruption in male testosterone but these studies had the participants consuming over 16 servings of soy per day and it is entirely possible that genetic abnormalities played a role in these anomalous results.

MYTH: Soy Lowers Sperm Count

Another misconception about soy that has contributed to the “soy-boy” stereotype is that it lowers sperm count. This is categorically false and demonstrates how individuals can misinterpret data. The truth is that soy actually increases seminal fluid production resulting in lower sperm concentration but not lower sperm count. The overall sperm count remains the same. This is backed up by findings from Chavarro, Toth, Sadio, and Hauser in 2008.

According to their study,

“Soy food and soy isoflavone intake were unrelated to sperm motility, sperm morphology or ejaculate volume. These data suggest that higher intake of soy foods and soy isoflavones is associated with lower sperm concentration.”

Soy Consumption Safe for Infants and Children

A 2014 study conducted by Vandenplas and associates reported that when administering soy-based infant formulas, which were introduced over 100 years ago, they “did not find strong evidence of a negative effect on reproductive and endocrine functions.” Additionally, the researchers said, “Wherever possible, a meta-analysis was carried out.” Finally, they added,

“The patterns of growth, bone health and metabolic, reproductive, endocrine, immune and neurological functions are similar to those observed in children fed CMF (cow’s milk formula) or HM (human milk).”

This study mirrored identical results found 13 years prior in 2001 by Strom et al. The stated objective of the study was “To examine the association between infant exposure to soy formula and health in young adulthood, with an emphasis on reproductive health.” They concluded,

“Exposure to soy formula does not appear to lead to different general health or reproductive outcomes than exposure to cow milk formula. Although the few positive findings should be explored in future studies, our findings are reassuring about the safety of infant soy formula.”

So what about infant exposure to cow’s milk? In 1999, Vaarala and colleagues demonstrated,

“Cow’s milk feeding is an environmental trigger of immunity to insulin in infancy that may explain the epidemiological link between the risk of type 1 diabetes and early exposure to cow’s milk formulas.”

[Also see Gottlieb’s article summarizing the results in 2000.]

In 1992, researchers found that cow’s milk triggers an autoimmune response that attacks the pancreas.

Other Benefits of Soy Consumption

In 2003, researchers found that soy protein promotes bone and calcium homeostasis in postmenopausal women, effectively strengthening bones in a section of the population particularly at risk for osteoporosis, whereas milk protein was found responsible for leaching 33% more calcium compared to baseline levels thereby increasing women’s risk for bone loss.

And while we are on the subject, according to a 2006 study, consumption of soy decreases prostate cancer risk in men and breast cancer risk in women.

“Suggestive evidence that soy-rich diets decrease prostate cancer risk, accords well with the observation that ERbeta appears to play an antiproliferative role in healthy prostate. In the breast, ERalpha promotes epithelial proliferation, whereas ERbeta has a restraining influence in this regard – consistent with the emerging view that soy isoflavones do not increase breast cancer risk, and possibly may diminish it.”

Additionally, they found that soy is negatively associated with blood clot-related disorders such as pulmonary embolisms or strokes.

“Hepatocytes do not express ERbeta; this explains why soy isoflavones, unlike oral estrogen, neither modify serum lipids nor provoke the prothrombotic effects associated with increased risk for thromboembolic disorders.” 

True Causal Factors in the Feminization of Men

Now that we have looked at what the medical literature has to say about soy, we will address how the paranoia around soy is a red herring for the truly feminizing dietary and environmental risk factors. These risk factors include consumption of poultry and beer, exposure to phthalates such as BPA and BPS, and lifestyle problems such as inadequate sleep, use of anabolic steroids, consumption of highly fatty foods, and obesity.

Contrary to popular belief, testosterone levels in males do not naturally decline after age 40. Kelsey et al. proved this when they published a peer-reviewed paper in 2014 entitled A Validated Age-Related Normative Model for Male Total Testosterone Shows Increasing Variance but No Decline after Age 40 Years.

Phthalates are both natural and manmade acids that can be found in fatty animal foods such as milk, butter, and meat. Poultry is the highest dietary source of phthalates. They have been shown to disrupt the endocrine system through antiandrogenic pathways and are often referred to as “gender-bender chemicals.”

A 2006 cross-sectional study of Americans found that phthalates are positively associated with obesity, insulin resistance, and type 2 diabetes.

There, you have a secondary risk factor as obesity has been linked repeatedly to lower testosterone levels, such as in this 2014 study by Fui, Dupuis, and Grossman entitled Lowered testosterone in male obesity: mechanisms, morbidity and management.

Moreover, high-fat meals have been shown to reduce testosterone concentrations without affecting luteinizing hormone.

Soy opponents often point out that testosterone has dropped dramatically in the west in the last 20 years, while the domestic soy industry has swelled from $200 million annually to $3 billion. However, correlation does not equal causation and this superficial evaluation ignores the fact that obesity has skyrocketed from 10% in 1960 to over 34% by 2012, according to the CDC.

In 2010, Colacino, Harris, and Schecter conducted a similar national review and found equally alarming trends primarily linked to the consumption of poultry and other types of meat, but, to be fair, also found phthalate metabolites in tomatoes and potatoes. However, phthalate metabolites are not as potent as phthalates.

Swan and associates found that prenatal phthalate exposure impairs testicular function, stunts growth of the penis later in life, and contributes to an overall physical feminization of men. Suddenly, eating meat doesn’t seem so manly anymore.

That same year, Swan, along with a different team, published another paper on the matter, demonstrating a behavioral abnormality expressed in boys with higher phthalate exposure, stating that they are less prone to play outdoors, physically, aggressively, to take risks, and other male-typical play behavior, suggesting an overall docility and lower levels of testosterone.

This was corroborated by parallel findings in 2010 where Cho et al. found that phthalate exposure adversely affects neurodevelopment in children, while citing earlier findings that it has a positive association with delayed development of the reproductive system, reduced birth weight, allergies, and asthma.

The detrimental effects of phthalate exposure are thoroughly documented, with its toxicity often referred to as the “phthalate body burden” because the body is struggling to develop properly despite environmental and dietary exposure.

In 2009, Maruyama, Oshima, and Ohyama traced consumption of bovine milk to decreased testosterone as a result of the exogenous estrogen inherent in cow’s milk.

Alcohol Consumption Lowers Testosterone

Beer contains hops which have isoflavones that behave more detrimentally in the body than those in soy. Hops contain a phytoestrogen named 8-PN which is thousands of times more potent than those found in soy, as pointed out by Possemiers et al. in the Journal of Agriculture and Food Chemistry in 2005.

This is partly due to the fact that 8-PN bonds with alpha receptors as pointed out by Schaefer et al. in 2003 whereas soy bonds with beta receptors as demonstrated by McCarty in 2006. It is this very reason that soy could potentially help prevent gynecomastia, or the development of “man boobs,” because when the isoflavones in soy bond with beta receptors in breast tissue it turns off cell proliferation. This is the same pathway by which soy prevents breast cancer. According to the study,

“In the breast, ERalpha promotes epithelial proliferation, whereas ERbeta has a restraining influence in this regard – consistent with the emerging view that soy isoflavones do not increase breast cancer risk, and possibly may diminish it.”

Compare this with findings by Durmaz et al. in 2009 that demonstrated phthalates, such as those found in poultry, cause pubertal gynecomastia, or the enlargement of male breasts in adolescence. Chicken consumption causes “man boobs” whereas soy prevents against it.

In 1979, Ellingboe and Varanelli found that ethanol inhibits testicular testosterone production.

That same year, Van Thiel and colleagues discovered that alcohol causes testicular atrophy in rodents, although this does not necessarily correlate in humans as rodent models are not directly indicative of human results.

Van Thiel also confirmed liver cirrhosis as a pathogenic mechanism for the feminization of men in human trials.

As early as 1983 in the journal Alcoholism: Clinical and Experimental Research, the doctors pointed out that,

“Male gonadal dysfunction produced by liver cirrhosis has been recognized for decades. The association of testicular atrophy, gynecomastia, and liver cirrhosis was described initially by Corda and Silvestrini.”

This journal has dozens of studies linking alcohol consumption to lower testosterone for those wishing to explore further.

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