Does a high saturated fat diet support high testosterone compared to a low-fat diet?
You might assume that the idea that a high saturated fat diet supports high testosterone originates with promoters of high-fat, animal-based diets, and you'd be wrong. In fact promoters of low-fat whole foods plant-based diets have embraced this idea and used it to promote abstention from saturated fats and animal products.
Research providing evidence that reducing total and saturated fat intake reduces testosterone levels OR makes androgens less available for action is not very difficult to find, because this has been proposed by proponents of low-fat diets as a mechanism by which low-fat and plant-based diets might prevent hormone-related cancers.
Many rank-and-file followers of low-fat whole foods plant-based diets appear unaware that leading medical advocates of such diets frankly assert that high-fat and animal-based diets support high testosterone levels in comparison to their proposed low-fat and plant-based diets.
For example, the Physician’s Committee for Responsible Medicine (PCRM), which promotes a low-fat vegan diet as a prevention for hormone-related cancers, asserts that a low-fat diet will reduce your sex hormone levels. Let's start with estrogen:
“Fatty foods affect the body in many ways and have a strong influence on hormonal activity in the body. First, high-fat diets increase the amount of estrogens, the female sex hormones, in the blood. It is known that many breast tumors are "fueled" by estrogens. Estrogens are normal and essential hormones for both women and men, but the more estrogen there is, the greater the driving force behind some kinds of breast cancer. On high-fat diets, estrogen levels increase. When women adopt low-fat diets, their estrogen levels drop noticeably in a very short time. Vegetarians have significantly lower estrogen levels than non-vegetarians, in part because of the lower fat content of their diet. In addition, they have more of certain carrier molecules, called sex hormone binding globulin, which circulate in the blood and have the job of holding onto sex hormones, keeping them inactive until they are needed. Fatty foods do the reverse: they increase estrogens and reduce the amount of the carrier molecule that is supposed to keep estrogens in check.”1
And now testosterone:
“Just as women on high-fat Western diets have more estrogens circulating in their blood and a higher risk of cancer of reproductive organs, a similar process occurs in men. High-fat diets alter the amounts of testosterone, estrogen, and other hormones in both men and women.
“Men who consume diets based on animal products tend to have higher levels of testosterone compared to men who eat plant-based diets. This increase may be due to overproduction of these hormones in the body. Also, fiber in the diet helps remove excess hormones with body wastes. Those who eat meats and dairy products miss out on a substantial amount of fiber, because animal products have no fiber at all. This hormonal boost can affect the prostate, and is likely the reason for increased cancer risk among those on meat-based diets.”2
[ Bold added.]
The PCRM further claims:
“A low-fat, high-fiber diet can help eliminate the hormonal aberrations that are known to be linked with prostate cancer, and may help improve survival among those who have the disease. Unfortunately, there has not been enough research in this area to know just how successful dietary change might be.”3
In other words, they believe that reducing your sex hormone levels by a low-fat vegan diet will be beneficial, but they don’t have any evidence for it yet.
Take note of their statement that vegetarians have higher level of “sex hormone binding globulin [SHBG], which circulate in the blood and have the job of holding onto sex hormones, keeping them inactive until they are needed.” This will be relevant later, when I discuss evidence linking higher SHBG in men to higher prostate cancer risk.
On another page, the PCRM states that “Low-fat, vegan diets lower cholesterol levels, but also raise SHBG, helping to mute testosterone effects.”4
Get that? I’ll repeat: A low-fat vegan diet helps to mute testosterone effects. “Mute” means: deaden, muffle, dampen, soften, quiet, hush; stifle, smother, suppress.
On another page,
“Changing your eating habits can help prevent prostate problems. The reason is not hard to imagine. The prostate is under hormonal control. In the prostate cells, testosterone is turned into a powerful hormone called DHT (dihydrotestosterone), and DHT is what drives prostate enlargement. This is the conversion that finasteride blocks.
“Foods can strongly influence sex hormones, including testosterone. Could it be that cutting out meats and dairy products and adding more vegetables to our plates could turn down the hormonal stimulation of the prostate and prevent prostate problems? That is, in fact, exactly what researchers have found....
“By the way, the enzyme (5-alphareductase) that turns testosterone into DHT is also found in the scalp, where it works mischief of a different sort. DHT plays a critical role in baldness. Without it, men will not lose their hair, no matter what their genetics may dictate. DHT activity in the scalp may be subject to dietary manipulation.”5
So, there you have it. According to the PCRM, eating animal products and saturated fats will support a high testosterone level, and the high testosterone will poison your prostate and make your hair fall out. Who needs that? Time to nutritionally castrate yourself, don’t you think?
DHT is the main metabolite of testosterone that exerts its androgenic effects. DHT binds more tightly to androgenic receptors and is the main nutrient essential for development and maintenance of the seminal vesicles and prostate gland, where the DHT concentration is naturally 10 times greater than testosterone. DHT is biologically required for sexual differentiation of male genitalia during embryogenesis, pubertal maturation of the penis and scrotum, growth of facial, body and pubic hair, and sebum production. Boys (46 XY karyotype) with a congenital deficiency of 5AR type 2, the enzyme that converts testosterone to DHT, are born with apparent female genitalia, show developmental delay of male characteristics, have rudimentary prostate development and scanty facial hair.6
Metabolites of DHT have antidepressant, anxiolytic, hedonic, anti-stress and pro-cognitive anti-dementia effects.7, 8
This raises the question: Could reducing high testosterone or blocking DHT, whether by diet or drugs, be detrimental to men’s health and even their masculinity?
It is also interesting to note that the PCRM is on the one hand claiming that a low-fat vegan diet will reduce high testosterone and this will be beneficial, yet it is also eager to assure men that eating soy rich in phytoestrogens “has no effect on men’s testosterone.”9
Does the PCRM want to have their cake and eat it too?
Dr. John McDougall, another low-fat plant-based diet promoter, also asserts that low-fat diets reduce sex hormone including high testosterone levels, which he considers a positive, supposedly protective against several hormone-dependent conditions.10
Dr. McDougall also maintains that high-fat diets cause male pattern baldness by supporting high testosterone levels. He states:
“Prostate enlargement, like prostate cancer, is related to the levels of the sex hormones in a man’s body throughout his life. These levels are a direct consequence of the foods he chooses to eat. More specifically, a diet high in fat results in elevated levels of these hormones, and is the primary factor in the cause of both conditions.”11
Notice how this passage goes directly from asserting first a relationship between hormones and prostate enlargement and cancer, to asserting that this relationship is causal, such that the hormones cause the enlargement or the cancer.
I will discuss that relationship later. For now I will only note that even if there does exist a correlation between diet, hormone levels and cancer, such that elevated hormones are found in people who have cancer, that doesn't itself prove that the diet or hormone levels cause the cancer.
There exists a correlation between burning buildings and fire trucks and hoses; this doesn't mean that fire trucks and hoses cause buildings to burn. Just as fire trucks and hoses correlate with burning buildings because the trucks and hoses are called to combat the fire, elevated hormone levels might be one of the body's ways of combatting the disease or its causes or effects.
It is also possible that enlarged prostates or tumors produce sex hormones, in which case high sex hormones would not be a cause of the tumors but caused by the tumors. I mention these possibilities just to underscore the fact that even if there exists a correlation between high sex hormones and certain cancers, this would not justify in itself a conclusion that the high hormones caused the cancer.
In fact, as I will show below, the relationship between high testosterone and prostate cancer is very likely NOT EVEN CLOSE to what the PCRM or Dr. McDougall would have you believe.
Anyway, as already noted, rank-and-file proponents of low-fat and vegan diets who think their plant-based diets have no effect on their testosterone levels are flatly contradicted by leaders in their cause, who claim that reduction of high testosterone levels and activity (through elevation of SHBG and suppression of DHT, and blocking of androgen receptors) is one of the main ‘benefits’ of a low-fat vegan or whole foods plant-based diet.
Now let's see what evidence exists to support the claim that high dietary fat intake – and particularly, high saturated fat intake – supports high testosterone levels.
Far from being either without basis, or a contentious claim made only by promoters of high-fat, animal-based diets, considerable research, some apparently done by advocates of low-fat diets, supports the conclusion that diets high in total and saturated fat support high testosterone and other sex hormone levels.
Ingram et al. sought to test “the hypothesis that dietary fat acts as a promotional agent for the development of breast cancer by influencing sex hormone levels.”12 They randomly allocated 33 healthy women to consume either higher (40% of energy) or lower (20% of energy) fat diets in a cross-over study. They reported that in premenopausal women, the low-fat diet reduced levels of cholesterol, non-protein-bound estradiol and non-protein-bound testosterone. Cholesterol levels were significantly associated with estradiol, testosterone, and dehydroepiandrosterone (DHT). Levels of HDL were associated with estradiol and prolactin (i.e. higher HDL correlated with higher estradiol). In postmenopausal women the low-fat diet reduced cholesterol and HDL levels but did not have the same associations with the hormones. Ingram et al. concluded that their findings “add weight to the concept that attention to diet may be a means of reducing the incidence of breast cancer in our community” by providing evidence that a low-fat diet can reduce sex hormone levels.
In a study cited by the PCRM as support for their claim that low-fat diets reduce sex hormone levels, Rose et al studied the effect of dietary fat reduction on sex hormones in 16 patients with cystic breast disease. They reported that reducing dietary fat from 35% of energy at baseline to 21% of energy over 3 months, without increasing dietary fiber intake, produced significant reductions in luteal-phase serum total estrogens, estrone, and estradiol.13
In a study cited by McDougall, Adlercreutz et al. studied 27 postmenopausal women, 9 vegetarians, 10 omnivores, and 8 “apparently healthy women with breast cancer” (?). They reported:
“Androstenedione (A), testosterone (T), free T (FT), and SHBG were higher in omnivores than in vegetarians. In multiple correlation analysis, intakes of protein and fat were positively correlated with A, T, and FT, whereas the intakes of carbohydrate, grain, total fiber, and grain fiber showed the opposite correlations. Protein intake was positively correlated with percentage FT (%FT) and negatively with SHBG. BC patients had a similar pattern to omnivores with even higher levels of A and T (significant compared with vegetarians) and they showed significantly higher FT and lower SHBG than both control groups. We conclude that a Western-type diet in postmenopausal women is associated with high A, T, %FT, FT, and low SHBG and this pattern was apparent in the BC patients.”14 [Bold added.]
Aldercreutz did an intervention study with Hämäläinen et al., in which the customary 40% fat diet of the male subjects was replaced for 6 weeks by a practically isocaloric experimental diet providing only 25% of energy from fat, and having a high ratio of polyunsaturated-to-saturated fats (0.15 on the higher fat diet, 1.22 on the lower fat diet). According to their report, serum total and free testosterone and 4-androstenedione decreased, which in their words suggested “a possible change in biological activity.” They concluded that their results indicated that in men “a decrease in dietary fat content and an increase in the degree of unsaturated of fatty acids reduces the serum concentrations of androstenedione, testosterone, and free testosterone.”15
Dorgon et al conducted a controlled feeding study with a cross-over design to evaluate the effects of fat and fiber consumption on plasma and urine sex hormones in 43 men aged 19-56 years. The men were initially randomly assigned to either a low-fat, high-fiber or a high-fat, low-fiber diet. The low-fat diet provided 18.8% of energy from fat and had a polyunsaturated to saturated (P:S) ratio of 1.3, whereas the high-fat diet provided 41% of energy from fat with a P:S ratio of 0.6. The low-fat diet had 2.3 times as much fiber as the high-fat diet, deemed significant because dietary fiber may bind hormones in the gut and remove them from the body. Mean plasma concentrations of total and sex-hormone-binding-globulin (SHBG)-bound testosterone were, respectively, 13% and 15% higher on the high-fat, low-fiber diet. Men’s daily urinary testosterone was also 13% higher on the high-fat, low-fiber diet. On the other hand, their urinary excretion of estradiol and estrone and their metabolites were 12-28% lower during the high-fat, low-fiber diet. This means that the high-fat, low-fiber diet produced a significantly greater testosterone:estrogen ratio compared to the low-fat, high-fiber diet. They concluded that their results “suggest that diet may alter endogenous sex hormone metabolism in men.”16
Bélanger et al undertook a study of the levels of unconjugated steroids, steroid glucuronides, and SHBG in normal adult men who were either vegetarians or omnivores. They reported:
“Vegetarian group showed a higher levels of sex hormone-binding globulin (SHBG) while the free androgen index (FAI; calculated by the ratio testosterone/SHBG) was lower in this group. Although the concentrations of androsterone glucuronide were higher in vegetarian group, the vegetarians had a 25-50% lower level of androstane-3 alpha, 17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide. Our data further indicate that both, androstane-3 alpha,17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide concentrations are significantly correlated with SHBG levels and with the FAI values. The increases in androstane-3 alpha,17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide levels in the omnivorous group are probably a consequence of the elevation of the FAI. Our data suggest that in a vegetarian group, less testosterone is available for androgenic action.”17 [Bold added]
As noted earlier, the PCRM and other doctors who promote low-fat whole foods plant based diets consider elevations of SHBG to be ‘good’ because this binds more sex hormones, rendering them less or in- active, reflected in reductions of the free androgen index. Bélanger et al.’s finding is one of those which McDougall, the PCRM, and others base their hypothesis that eating a low-fat whole foods plant based diet will reduce the risk of hormone-related cancers. But, to repeat, Bélangeret al. claim to have found evidence that vegetarians may have "less testosterone available for androgenic activity" than non-vegetarians.
Key et al. reported that in comparison with male omnivores, male vegans had 7% higher total T, 23% higher SHBG, 3% lower free T, and 11% higher estradiol (E2). They concluded that “a vegan diet causes a substantial increase in SHBG but has little effect on total or free T or on E2.”18
If Key et al.’s results were to refute all the previous studies on this topic, they bring the PCRM et al to an impasse. You can’t hold to the idea that vegetarian low fat diets have no effect on testosterone activity, and yet also assert that vegetarian diets protect against hormone-related cancers by reducing testosterone levels or activity. However, Table 4 of the Key et al. paper shows that the mean fat intake of vegans was 33% of energy, while that of the omnivores was 38% of energy. In other words, this was not a comparison of distinctly low- vs. high- fat intakes as in the previously cited studies. The vegans in this study were consuming about 50% more total fat than the target levels of the trials already discussed. Their higher fat intakes may have brought their testosterone levels up closer to those of the omnivores. There exists evidence that diets high in olive oil, for example, may produce higher testosterone levels.44
Further, the omnivores in the Key et al. study consumed 35 g/d of fiber, compared to 57 g/d for the vegans. The previously cited studies the high- and low- fat groups also were either, respectively, low- and high- fiber groups, or both low-fiber. The omnivores in the Key et al. study had fiber intakes more than double the mean of about 15 g/d in the U.S. population.19 Perhaps this reduced the omnivores' testosterone levels significantly through enteric binding, one of the mechanisms proposed for explaining the reduction of high testosterone produced in other studies by feeding low-fat, high-fiber diets.
Thus the populations studied by Key et al. may not have been disparate enough to detect a strong effect of diet on serum hormones. Nevertheless, Key et al. did find that the male vegans had higher estrogen and SHBG levels, and slightly lower free (that is, active) testosterone levels than omnivores, hence likely a lower active testosterone:estrogen level than the omnivores, which is broadly consistent with the previously cited studies.
Habito et al found that replacing meat with soyabean in the diet resulted in an increase in SHBG, and a decline of the free androgen index and the testosterone: estradiol ratio on the tofu diet, which they suggested “could influence prostate cancer risk.”20
In summary of the above, the research broadly provides evidence that low-fat, high-fiber, and high-soy diets increase SHBG, and decrease the free androgen index and testosterone:estrogen ratio. And, as documented, neither the PCRM nor McDougall dispute this, in fact they consider this reduction of testosterone activity to be one of the benefits of eating a low-fat whole foods plant-based diet. This data was not first exploited by promoters of high-fat diets. It was darling to promoters of low-fat diets.
Conversely, the data also provides evidence that increasing total protein, dietary fat and saturated fat and reducing carbohydrate and fiber will support high testosterone levels compared to a low-fat, low-protein, carbohydrate-rich, high-fiber plant-based diet.
Now you might say, Don, maybe that’s all good, if as claimed by the PCRM and McDougall high testosterone and/or DHT causes or promotes prostate cancer.
But is this hypothesis that high testosterone causes or promotes prostate disease well supported by evidence?
The hypothesis that high testosterone and DHT cause prostate cancer was counter-intuitive from the get-go, as it would suggest that young males aged 18-30 would have the highest prostate cancer risk due to their having very high testosterone levels compared to older men. A more reasonable hypothesis that better fits the evidence is that prostate cancer arises due to andropause and testosterone deficiency, as noted by Abraham Morgentaler of Harvard Medical School:
“A critical shortcoming of the focus on high T is that it utterly fails to account for the high prevalence of PCa at an age when men are older and their T levels have declined and the absence of clinical PCa when men are young and have their highest lifetime T levels. I believe if a Martian scientist landed on Earth, was provided with this epidemiologic data, and was asked to investigate the relationship between T and PCa, he would immediately begin research into the effects of low T on PCa. If he did so, he would discover a fascinating literature that began in the mid-1990s and that has largely been overlooked by the scientific community. However, the accelerating accumulation of new studies demonstrating a worrisome association between low T and PCa can no longer be ignored....
“More recently, we reported biopsy results in a larger series of 345 hypogonadal men with PSA less than 4.0 ng/ml. The overall cancer rate was similar at 15%, but the most significant finding was that the risk of a positive biopsy increased with severity of testosterone deficiency. Men with a T level <250 ng/dl had a cancer rate of 21% compared with 12% for men with a T level >250 ng/dl. And the probability of cancer was more than doubled when men in the lowest tertile were compared to men in the highest tertile, for both total T and free T. In addition, the combination of low T and PSA value of 2.0–4.0 ng/ml was particularly worrisome, with a cancer rate of 30%.”21
A search of PubMed for studies confirming the low-fat doctors’ hypothesis that high testosterone causes or promotes prostate disease produces considerable contrary evidence. For example:
“In 1941 Huggins and Hodges reported that marked reductions in T by castration or estrogen treatment caused metastatic pCA [prostate cancer] to regress, and administration of exogenous T caused pCA to grow. Remarkably, this latter conclusion was based on results from only one patient. Multiple subsequent reports revealed no pCA progression with T administration, and some men even experienced subjective improvement, such as resolution of bone pain. More recent data have shown no apparent increase in pCA rates in clinical trials of T supplementation in normal men or men at increased risk for pCA, no relationship of pCA risk with serum T levels in multiple longitudinal studies, and no reduced risk of pCA in men with low T....This historical perspective reveals that there is not now-nor has there ever been-a scientific basis for the belief that T causes pCA to grow. “22
“There is no level-one quality evidence that confirms or refutes the relationship between either high or low serum testosterone levels and the subsequent development of prostate cancer.”23
Another team of researchers reported:
“The contention that high levels of testosterone or that the use of TTh [testosterone therapy] increases the risk of PCa doesn't seem to be supported from the literature.”24
“To date, as documented in many reviews on the subject, nothing has been found to support the evidence that restoring testosterone levels within normal range increases the incidence of prostate cancer... In fact, the incidence of prostate cancer in primary or secondary testosterone treated hypogonadal men is lower than the incidence observed in the untreated eugonadal population.”25
In fact I found a substantial body of reports supporting the hypothesis that low testosterone availability or high SHBG – as produced by low-fat, high-fiber diets, according to the PCRM – are risk factors for prostate cancer, particularly high-grade. Let's look at testosterone first.
Tu et al. reported that in comparison to a normal testosterone group of men, men with low testosterone had 2.9-fold, 5.6-fold, and 72.4-fold increased risk of having intermediate-risk, high-risk, and metastatic prostate cancer, respectively. Low testosterone levels were also significantly associated with a 10.7-fold increased risk of prostate cancer (PCa) specific mortality. They concluded that "low levels of total serum testosterone at diagnosis are associated with aggressive PCa and predict poor PCa-specific survival.26
Park et al. reported that low testosterone level is an independent risk factor for high-grade prostate cancer detection at biopsy, and concluded that checking for low testosterone levels could help to determine whether a prostate biopsy is indicated.27
Garcia-Cruz et al. reported:
“Patients with PCa and lower testosterone levels have poor prognosis factors and higher tumour burden before treatment onset. These findings reinforce the idea that low testosterone levels pretreatment are related to a poor prognosis in PCa.”28
Llukani et al. reported that among men aged 45-64 years, low pretreatment serum free testosterone and total testosterone predicted more aggressive prostate cancer found on biopsy.29
Pichon et al. reported that low serum testosterone is an independent risk factor for discovery of high-grade prostate cancer after radical prostatectomy, and for upgrading from low- to high- grade between biopsies and radical prostatectomy.30
Yassin et al. reported that among hypogonadal men, those who were receiving testosterone replacement therapy (TRT) had the lowest incidence of positive prostate biopsies and significantly lower severity of prostate cancer staging and grading. They concluded "These results suggest that TRT might have a protective effect against high-grade PCa."31
Algarté-Génin et al. reported:
“Several studies analyzing the role of testosterone for prostatic epithelial cells evidenced that testosterone acts in prostatic cell differentiation but does not have a direct role for induction of cell proliferation. Moreover, clinical studies have shown that low free testosterone levels in serum is associated with aggressive prostate cancer, like that has been observed in men with prostate cancer under prostate cancer chemoprevention by finasteride. These data suggest that an androgen pathway disruption in prostate is responsible of cell deregulations that may be associated not only with apoptosis of differentiated prostatic cells but also with potential cell transformation. The effects of androgens withdrawal for prostate cancer therapy induced in a short time the tumor arrest growth. However with time, cells adapt to low levels of androgens leading to the evolution of an androgen-independent tumor, which is more aggressive and most often fatal.”32 [Bold added.]
If testosterone is necessary for prostatic cell differentiation, then it would make sense that low testosterone would create an environment that would favor proliferation of undifferentiated cells, such as tumor cells. Conversely high testosterone as found among young men and really healthy elders would protect against prostate disease by creating an environment that favors prostatic cell differentiation.
Thus, it seems there is significant evidence casting serious doubt on the hypothesis, held by advocates of low-fat plant-based diets, that high testosterone or its derivatives, including DHT, are responsible for causing or promoting prostate cancer. It appears on the contrary that low testosterone levels, availability or activity are more likely to create an environment favorable to prostate cancer. Yet advocates of low-fat plant-based diets apparently believe that such diets will reduce prostate cancer risk by reducing levels, availability or activity of testosterone, in part by increasing levels of SHBG.
As mentioned above, low-fat, vegan and vegetarian diets have been shown to raise SHBG levels and thereby reduce availability of androgens. According to the PCRM, McDougall, and other proponents of low-fat whole foods plant based diets, raising your SHBG level by avoiding animal protein and fat will help prevent prostate cancer.
In contrast to this hypothesis, men with prostate cancer have been found to have significantly higher levels of SHBG than men without PCa. Garcia-Cruz et al. reported:
“T levels were comparable in men with and without PCa, but SHBG levels were significantly higher in men with PCa. In men with low T, the men with PCa had a lower serum T levels and a lower prostate volume than the men without PCa.”33 [Italics added]
The finding of lower prostate volume in men with prostate cancer is interesting given the basic fact that DHT is the primary nutrient for the prostate, suggesting the hypothesis that low testosterone bioavailability leads to low prostate DHT which leads to prostate atrophy and an environment that favors proliferation of undifferentiated cells, hence an increased susceptibility to cancer as suggested by Morgentaler's work cited above.
In another study, Garcia-Cruz et al. found:
“Low bioavailable testosterone levels and high SHBG levels were related to a 4.9- and 3.2-fold risk of detection of PCa on prostate biopsy owing to PSA elevation or abnormal DRE. This fact may be useful in the clinical scenario in counseling patients at risk for PCa."34
Let that sink in. The low testosterone bioavailability and high SHBG levels that the PCRM apparently correctly reports will be produced by a low-fat vegan diet increased the risk of detection of prostate cancer in men with elevated PSA by 4.9- and 3.2-fold respectively.
If as the studies previously cited evidence, and the PCRM agrees, low-fat plant-based diets raise SHBG, this raises the question: Could low-fat, high-fiber plant-based diets increase risk of prostate cancer in individuals who develop low testosterone or high SHBG when eating such diets? Obviously, we need more research to determine the answer to this question.
Proponents of low-fat whole foods plant-based diets are quick to assert that their favored diet has no harmful affect on male sexual function, despite also stating that their low-fat plant-based diets will reduce testosterone levels or mute testosterone effects. As noted above, the PCRM even has a page dedicated to convincing readers that soy consumption has no adverse effects on testosterone levels.
However, testosterone levels are not the only concern. Even if plant-based diets didn't reduce total or free testosterone levels, some plant-compounds have been found to block androgen actions through other mechanisms.
Soy and other plant foods have been proposed to prevent prostate disease precisely because they have anti-androgen effects.35 Phytoestrogens have been reported to block DHT’s androgen action,36 block the production of DHT by inhibiting 5-alpha reductase (the enzyme that converts testosterone to DHT),37 and suppress androgen receptor expression (making tissues less responsive to testosterone and DHT) without changing estrogen receptor expression.38
This means that when you eat a phytoestrogen-rich plant-based diet, even if the diet doesn't reduce your total or free testosterone level, or bind up the testosterone with SHBG, you may convert less testosterone to its most active form (DHT), and that DHT may have less effect on your tissues because the phytoestrogens block the androgen receptors without changing cellular receptivity to estrogens.
A possible result of these hormonal changes would be a feminized body. You may not believe that a plant-based diet could have this effect, but at least one case study argues otherwise. A 19-y-old male (i.e. at the peak of natural testosterone production) developed erectile dysfunction and loss of libido after eating a vegan-style diet with large quantities of soy products; his testosterone levels were very low and it took one year for him to regain full sexual function and testosterone levels after cessation of the vegan diet.39
If a phytoestrogen plant-based diet can have this effect on a 19-y-old male at the peak of his testosterone production, what effect might it have on a man past 40-y old, when testosterone levels tend lower?
Apologists for the plant-based diet will often point out that this individual ate an unusually large amount of soy products. So? Soy is not the only plant food containing phytoestrogens. Phytoestrogens naturally occur in fruits (plum, pear, apple, grape, berries, …), vegetables (beans, sprouts, cabbage, spinach, soybeans, grains, hops, garlic, onion,…), seeds (flax, sesame, sunflower,...), wine, tea, and many herbs used as dietary supplements.40
Further, people will naturally vary in their tolerance for these chemicals. It is possible that some men have a low tolerance for these chemicals and will suffer adverse effects on their testosterone function even on plant-based diets that contain no soy foods at all.
There exists a body of evidence, produced by people who had some interest in promoting low-fat diets, indicating that reducing dietary total and saturated fats and increasing the polyunsaturated:saturated ratio will reduce testosterone levels in women and men (and estrogen levels in women). These studies support the converse conclusion that diets higher in total and saturated fats and lower in polyunsaturated (i.e. mostly plant-based) fats support higher sex hormone levels – including high testosterone – in men and women.
Promoters of low-fat and plant-based diets such as PCRM and John McDougall M.D. have cited these studies as evidence supporting their claim that such diets will reduce the risk of putatively hormone-dependent cancers (by reducing hormone levels or activity). If you are a follower of a low-fat plant-based diet believing that low-fat plant-based diets do not reduce testosterone levels, you might have missed that memo from the plant-based diet leadership.
Promoters of plant-based diets also point to the anti-androgen effects of phytoestrogens as support for their hypothesis that whole foods plant-based diets will reduce the risk of prostate disease by "muting" testosterone effects; yet the PCRM also is keen to assure you that these same phytoestrogens will have no adverse effect on your testosterone expression.
Promoters of low-fat and plant-based diets promote the idea that raising your SHBG level to bind up and render inactive more of your testosterone will protect you from prostate cancer. In fact, evidence seems to be pointing to elevated SHBG as a factor increasing the risk of prostate cancer.
The idea, promoted by advocates of low-fat and plant-based diets, that high testosterone levels put men at risk for prostate disease, has apparently not been adequately supported by evidence. In fact, a rather substantial and apparently growing body of evidence supporting the hypothesis that prostate disease is linked to and favored by low testosterone levels and/or low testosterone activity caused by high SHBG or poor conversion of testosterone to DHT, the main nutrient for a healthy prostate, or by blocking of androgen recptors by anti-androgens.
Which leads us back to high fat diets. If high testosterone and strong conversion of testosterone to DHT similar to a healthy young man protects against prostate disease, and diets high in total and saturated fat support high testosterone levels and promote conversion of T to DHT, then the question arises:
Do we have evidence to support the hypothesis that a high-fat, low-carbohydrate diet might provide protection against prostate disease?
The short answer is yes.41,42,43
2. PCRM. https://www.pcrm.org/health/cancer-resources/diet-cancer/facts/prostate-cancer
6. Marks LS. 5α-Reductase: History and Clinical Importance. Reviews in Urology. 2004;6(Suppl 9):S11-S21.<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472916/>
7. Pan W, Han S, Kang L, Li S, Du J, Cui H. Effects of dihydrotestosterone on synaptic plasticity of the hippocampus in mild cognitive impairment male SAMP8 mice. Experimental and Therapeutic Medicine. 2016;12(3):1455-1463. doi:10.3892/etm.2016.3470.<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4997989/>
8. McHenry J, Carrier N, Hull E, Kabbaj M. Sex Differences in Anxiety and Depression: Role of Testosterone. Frontiers in neuroendocrinology. 2014;35(1):42-57. doi:10.1016/j.yfrne.2013.09.001.<https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3946856/>
12. Ingram DM, Bennett FC, Willcox D, de Klerk N. Effect of low-fat diet on female sex hormone levels. J Natl Cancer Inst. 1987 Dec;79(6):1225-9. PubMed PMID:3480374.
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