Ian Spohn, ND, is a staff naturopathic doctor for Energique who enjoys challenging the dogmas of both conventional and alternative medicine. He is a passionate supporter of the paleo diet and classical homeopathy.
It has been known for quite some time now that testosterone levels in modern men are falling, a phenomenon which, while unexplained, still has important implications for men’s health. Despite the fact that testosterone replacement therapy remains a controversial subject in medicine, men’s health clinics are popping up everywhere that do essentially nothing more than prescribe testosterone to aging men. There is a very fine and still disputed line between treating a legitimate endocrine disorder presenting as hypogonadism with testosterone replacement therapy and medicalizing such common concerns as fatigue, weight gain, and generalized feelings of inadequacy as “low T” in order to secure an aegis under which to essentially sell people legalized steroids, profiting from humanity’s universal vanity and fear of its own mortality. Yet, evidence suggests that testosterone therapy might actually confer benefits far beyond such anti-aging concerns as a softly ripening physique and declining sexual vigor. In men over 40, for instance, testosterone levels are inversely related to all-cause mortality.[i] All chest-thumping and braggadocio aside, being less likely to die from literally everything would actually seem a fairly compelling reason for seeking to boost one’s testosterone level. Testosterone therapy has also been shown to increase walking distance in men with chronic heart failure[ii] and may even be an effective treatment for men’s depression.[iii] There seems to be a surprisingly intimate link between a man’s testosterone level and his overall health and sense of well-being, highlighting the importance of supporting testosterone levels at least into the normal range, which if previous generations are any indication is a figure actually exceeding the supposed average range today.[iv]
Several theories have been put forth to explain the worrying decline in men’s average testosterone level, none of which have stood up to scrutiny or proven sufficient to explain the decline. For instance, it has been noted that while average testosterone levels are decreasing, the average age of the population, including the male population, is increasing. Since circulating testosterone levels are expected to fall as a man ages, this might explain why the overall average is lower today. The problem with this theory is that studies have accounted for it and still revealed a true secular decline,[v] in other words, an effect independent of age. A fifty-year-old man today actually has less testosterone than a fifty-year-old man did twenty years ago, and, in fact, research has found that each year, testosterone levels in an age-matched population fell three times faster than would be expected by normal aging alone, suggesting an unknown environmental factor to be responsible.[vi].
Another interesting idea is that the decline in average testosterone levels might simply be due to the rising rate of obesity. It has been shown that testosterone levels decline as body mass index increases,[vii] possibly due to the capacity of adipose tissue to aromatize testosterone to estrogen.
Another interesting, though somewhat unsettling, theory has to do with cigarette smoking, the prevalence of which has obviously declined precipitously over the past few decades. Nicotine is actually a potent aromatase inhibitor with the capacity to thereby slightly raise testosterone levels, providing an intriguing rational basis for the Marlboro man, Joe Camel, and the various other stereotypes once used so effectively to advertise cigarette smoking on the basis of manliness. So rising obesity rates and less smoking would in theory account for a certain degree of lost testosterone since the 1950s, and yet research has revealed these trends insufficient to explain the actual magnitude of the decline.[viii] Even when controlling for these variables, there remains an additional, unknown lifestyle factor at play.
Among the theorized factors to blame for this mysteriously unaccountable decline are xenobiotic estrogens found in plastics, like bisphenol A, the phthalates used in common cosmetic products, and phytoestrogens in the diet, especially soy isoflavones. Soybeans have been much maligned for their reputed emasculating effects, but there may be another, even more serious, consequence of soy consumption currently threatening men’s health. Just as the clinical approach to men’s health has been dominated by testosterone replacement therapy, the search for what may be responsible has been dominated by a witch hunt for xenobiotic estrogens. Yet while soy consumption has been increasing, no one has been considering in what form it has been increasing. Most of the massive rise in soy consumption has not come from our eating more tofu, miso, natto, or drinking more soymilk; rather, today we mostly consume soy in the form of soybean oil, which is heavily processed and not actually a source of phytoestrogens. Instead, the final product is full of something which likely poses an even greater threat to its consumer’s manliness, a threat which might explain declining testosterone levels all over the world: a high content of polyunsaturated fatty acids.
Polyunsaturated fatty acids, or PUFAs, were once an extremely minor contributor to the average person’s diet. Fatty foods of animal origin and even many traditionally consumed plant-based oils like olive oil are relatively low in PUFAs, being primarily comprised of fully saturated or monounsaturated fats. Though PUFAs are actually essential to the body in small quantities (all of the essential omega fats are PUFAs), most edible substances only contain them in small quantities. Even foods that are “high” in the omega-unsaturated fats, like oily fish, are only relatively high – they have more of these than most other foods, but PUFAs still represent an almost negligible portion of their overall fat content. Two notable exceptions to this rule are canola (rapeseeds) and soybeans, which of course in their raw form are only edible to humans in the loosest sense of the word but have increasingly been added to the food supply in the form of highly processed, PUFA-rich oils. To put this recent trend in perspective, between 1909 and 1999 the United States witnessed an estimated 16,700 percent increase in canola oil consumption.[ix] Even more shockingly, it witnessed an estimated 116,300 percent increase in its soybean oil consumption.[x] Even excluding other forms of soy, soybean oil itself is now the fourth leading source of calories in the American diet (following grains, added sugars, and dairy, in that order). Consumption of soybean oil really took off in the late 1960s, back when the average testosterone level was still much higher than it is today. To quote an exhaustive analysis of 20th century dietary trends[xi]:
“The most striking modification of the US food supply during the 20th century was the >1000 fold increase in the estimated per capita consumption of soybean oil….
“The majority of the increase in soybean oil consumption occurred in the latter half of the 20th century.”
How could the soybean’s oil, as opposed to its phytoestrogen-containing fractions, be lowering testosterone levels and possibly also causing the massive decline in fertility that is affecting both sexes all over the world? From a nutritional perspective, the most salient feature of soybean oil is its extremely and disproportionately high PUFA content, to the extent that an increase in soybean oil consumption can be considered a de facto increase in PUFA consumption. Compared to all other fats, PUFAs are extremely vulnerable to oxidation due to their multiple unsaturated bonds, a health-destroying process which the body normally mitigates with a family of fat-soluble antioxidants collectively known as vitamin E. When vitamin E was originally discovered, it was named “anti-sterility factor X” due to the fact that animals went sterile shortly after it was experimentally excluded from their diets. People wonder why fertility rates are declining all over the world: is it possibly because we are consuming less vitamin E? It might actually be one step more complicated than that. The pieces of the declining testosterone puzzle begin to fit together when one realizes that vitamin E requirements are highly variable and actually depend in large part on one’s diet. It has been shown, in fact, that the vitamin E requirement of one’s diet, that is the amount necessary to prevent a deficiency, increases in direct proportion to the PUFA content of one’s diet; researchers were actually able to quantify this requirement as 0.6 mg of vitamin E for every gram of PUFA consumed.[xii] Basically, the more PUFAs you eat the more their inevitable oxidation depletes your body’s vitamin E stores, and the more vitamin E you therefore need to consume to avoid becoming deficient. And yet soybean oil, the main source of PUFAs in the diet, is not considered an adequate dietary source of vitamin E.[xiii] While processed soybean oil admittedly does contain some vitamin E, it’s not very much and it’s mostly in the form of gamma-tocopherol, which is not nearly as active as alpha-tocopherol and whose relative preponderance at the expense of alpha-tocopherol is apparently somewhat peculiar to soy.[xiv]
Soy is quite an excellent food on the basis of its protein content, but it turns out a horrendous food on the basis of its fat content. Basically the more soybean oil you eat (and almost everyone is eating more), especially if it has been exposed to the pro-oxidant effects of frying heat (which it often has), the lower your vitamin E levels will be. If increased PUFA consumption from soy was the real unexplained factor accounting for lower testosterone levels, all that is missing would be a putative mechanism and evidence proving that supplementing vitamin E can raise testosterone levels. An interesting fact is that while testosterone levels typically decline with age, luteinizing hormone (LH) levels do not decline with age and sometimes actually rise in aging men as testosterone levels fall.[xv] LH normally stimulates testosterone production in the testes, allowing the process to be controlled through negative feedback. If the so-called “andropause” was real, and men were actually intended to lose testosterone as they age, one would expect the brain’s central control mechanisms to be responsible or at the very least involved, when in fact a rise in LH would suggest the opposite, that the aging body is aware of its declining testosterone levels and trying to restore them by increasing pituitary stimulation of the testes. Experiments conducted with rodent testes have found that as they age, the glands themselves become less responsive to normal pituitary stimulation by a mechanism believed to involve the effects of free radical oxidation.[xvi] The process of synthesizing steroid hormones itself actually generates free radicals, and the fact that sterility is among the first effects of vitamin E deficiency underscores the critical relationship of antioxidants, especially fat-soluble antioxidants, to the health and longevity of the gonads. Also, as expected, supplemental vitamin E has been proven to raise testosterone levels,[xvii] and this far more inexpensively than testosterone replacement therapy, growth hormone injections, deer antler velvet, or the scores of other dubious methods which have been tried.
Because testosterone is critical not just to men’s sexual health but to men’s overall health, it is tempting to justify the widespread use of testosterone replacement therapy as a panacea for the aging male. In reality, something as simple as losing weight, consuming a more traditional diet, and supplementing vitamin E might be a safer and more natural way to help male patients restore their testosterone to more youthful levels. Such an approach might also be critical to helping patients of both sexes who struggle with infertility.
[i] Goodale T, Sadhu A, Petak S, Robbins R. Testosterone and the Heart. Methodist Debakey Cardiovasc J. 2017;13(2):68-72. doi:10.14797/mdcj-13-2-68
[ii] Pugh PJ, Jones RD, West JN, Jones TH, Channer KS. Testosterone treatment for men with chronic heart failure. Heart. 2004;90(4):446-447. doi:10.1136/hrt.2003.014639
[iii] Walther A, Breidenstein J, Miller R. Association of Testosterone Treatment With Alleviation of Depressive Symptoms in Men: A Systematic Review and Meta-analysis. JAMA Psychiatry. 2019;76(1):31–40. doi:10.1001/jamapsychiatry.2018.2734
[iv] Thomas G. Travison, Andre B. Araujo, Amy B. O’Donnell, Varant Kupelian, John B. McKinlay, A Population-Level Decline in Serum Testosterone Levels in American Men, The Journal of Clinical Endocrinology & Metabolism, Volume 92, Issue 1, January 2007, Pages 196–202, https://doi.org/10.1210/jc.2006-1375
[vii] Diaz-Arjonilla, M., Schwarcz, M., Swerdloff, R. et al. Obesity, low testosterone levels and erectile dysfunction. Int J Impot Res 21, 89–98 (2009). https://doi.org/10.1038/ijir.2008.42
[viii] Thomas et al 2007
[ix] Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011;93(5):950-962. doi:10.3945/ajcn.110.006643
[xii] Raederstorff D, Wyss A, Calder PC, Weber P, Eggersdorfer M. Vitamin E function and requirements in relation to PUFA. Br J Nutr. 2015;114(8):1113-1122. doi:10.1017/S000711451500272X
[xiii] Grilo, Evellyn Câmara, Costa, Priscila Nunes, Gurgel, Cristiane Santos Sânzio, Beserra, Andressa Fernanda de Lima, Almeida, Fernanda Niéce de Souza, & Dimenstein, Roberto. (2014). Alpha-tocopherol and gamma-tocopherol concentration in vegetable oils. Food Science and Technology, 34(2), 379-385. Epub May 30, 2014.https://dx.doi.org/10.1590/S0101-20612014005000031
[xv] Zirkin BR, Tenover JL. Aging and declining testosterone: past, present, and hopes for the future. J Androl. 2012;33(6):1111-1118. doi:10.2164/jandrol.112.017160
[xvii] Umeda F, Kato K, Muta K, Ibayashi H. Effect of vitamin E on function of pituitary-gonadal axis in male rats and human subjects. Endocrinol Jpn. 1982;29(3):287-292. doi:10.1507/endocrj1954.29.287
Any homeopathic claims are based on traditional homeopathic practice, not accepted medical evidence. Not FDA evaluated.
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