The Best & Worst Foods for Altering Testosterone | Muscular Development
The Best & Worst Foods for Altering Testosterone
Dietary strategies to promote natural testosterone production may seem meaningless to a person using anabolic steroids. As a matter of fact, they pretty much are, since androgen levels are controlled via syringe, rather than by the innate feedback system. The body monitors testosterone levels and adjusts production of the hormone within the testes by altering output of stimulatory hormones released from the hypothalamus and pituitary (glands in the brain). If the circulating (blood) testosterone concentration is low, the hypothalamus detects this and signals the pituitary gland to release a hormone that stimulates the testes called LH.
LH travels through the blood to the testes and drives testosterone production to increase output. As testosterone concentration rises in the blood, the hypothalamus detects the elevation and reduces the pituitary’s demand.1 In the case of a person using anabolic steroids, androgen levels are kept higher than the cut-off chronically, so the testes do not need to function (relative to producing testosterone) and atrophy (shrivel) as they do not receive a LH signal from the pituitary. However, when the cycle is finished, close attention needs to be paid to promoting the restoration of natural testosterone production.
Of course, the system is not as simple as one switch that is either ‘off’ or ‘on.’ In an anabolic, steroid-free environment, a person’s testosterone concentration is affected by conditions such as: sleep, physical demand, available rest, amount and quality of food, and presence of certain nutrients.2,3 While there is no scientific evidence that any one food or even the most selective diet will make a difference in regard to testosterone level and subsequent muscle growth over time (since no one has ever studied the demographics of strength and muscularity), the discriminating bodybuilder or fitness enthusiast will pay close attention to what he/she consumes. After all, it does no good to struggle to build muscle in the gym if a fad-diet lifestyle is sabotaging the anabolic response. Also, informal observations are fairly convincing in suggesting that vegans have a difficult time putting on muscle and the chronically undernourished live on the threshold of catabolism.
Before plunging into the buffet of knowledge ahead, this does not imply that other hormones that are modulated by the diet are not equally important. For the sake of clarity and brevity, this article will focus solely on the testosterone-diet associations.
Testosterone is a cholesterol-based chemical and many industrial sources (pharmaceutical companies) synthesize testosterone using steroid-ring precursors. However, testosterone is not created from dietary cholesterol in the body to a great degree. The starting chemical for endogenous production (natural testosterone production) appears to be acetyl-CoA, which is produced as sugar (glucose) and burned for calories. The body produces sugar in times of need, so even if one is on a strict ketogenic diet, acetyl-CoA should still be available. Acetyl-CoA goes through a series of reactions to become a molecule called hydroxymethylglutary-CoA, or HMG-CoA.4 Fortunately for the ketogenic dieters, HMG-CoA is also produced during ketogenesis, so the starting blocks for steroid production are well-provided.
HMG-CoA is then shuttled into another series of reactions to form squalene. A key reaction responsible for changing HMG-CoA is called the rate-limiting step. It is like the slowest walker on a prison chain gang. No matter how fast the rest of the crew is, they cannot move faster than the slowest moving prisoner. The top-selling cholesterol-lowering drugs, called statins (e.g., Lipitor®), work by making the slowest, rate-limiting reaction move even slower.5 Ironically, dieticians and drug companies worked for years on limiting dietary cholesterol, but it is the body’s own cholesterol-making machinery that is the cause of most cholesterol-related health problems.
Squalene is converted to a primitive steroid called lanosterol; this is the steroid equivalent of a cave man. Lanosterol is finally processed to form cholesterol; cholesterol can be processed to the more readily-recognized steroid hormones, such as: testosterone, androstenedione, DHEA, estradiol, progesterone, cotisol, etc.6 It is difficult to keep track of the number of chemical reactions involved, but it is a complicated process. This very brief introduction into steroidogenesis is provided to illustrate that the body doesn’t make testosterone simply and there really is no way to directly consume something that will directly convert into testosterone— at least not a food product. This revelation will likely disappoint fans of Rocky Mountain oysters and participants at Testicle Festival eating contests. Certainly, several products have been introduced into the sports nutrition market that are steroid precursors, or prohormones. However, these are not chemicals that are common in the food chain and some are thinly-veiled drugs.
The reactions in creating a steroid backbone (let alone the specific androgens, estrogens, glucocorticoids, etc.) require a great deal of energy. Additionally, the processes are predominantly oxidizing reactions. The pressure in Western society has long been to promote antioxidant consumption. Antioxidants suppress oxidizing reactions; this is beneficial in many situations, as free radicals can damage structural proteins in the cell or the DNA. However, the body burns calories and generates bio-molecules through oxidizing reactions as well, so the question must be asked, “Can you have too much of a good thing (antioxidants)?” In exploring this many, many years ago, I learned of reductive stress, but it appears to be a neglected area of research.
The foods that promote testosterone production primarily offer certain minerals which help form the metalloproteins and metalloenzymes involved in the chemical reactions to create cholesterol and eventually testosterone.7,8 Additionally, B vitamins are important co-factors (helpers); total calories and protein quality is also important.8 The most commonly referred foods that promote testosterone production are: oysters, eggs, beef, garlic, and broccoli. These foods are high in zinc, cholesterol, B vitamins, and arachidonic acid (AA).
Arachidonic acid is a fatty acid that sits in the membrane of cells lining the Leydig cells of the testes (the actual site of testosterone production from cholesterol). Under the influence of LH from the pituitary, released when testosterone levels are registered as being low, enzymes pull AA from the membrane and form messenger chemicals that go to the nucleus (the control center of the cell where the DNA is located) and turn on the production of StAR (steroidogenic acute regulatory protein).9 Interestingly, AA can go down three pathways in the Leydig cell; two promote StAR production, but the third suppresses it. This third pathway is the cyclo-oxygenase pathway and research into promoting testosterone production via cyclo-oxygenase 2 inhibition is underway.10 Many people are familiar with Celebrex®, a drug used to treat the symptoms of arthritis, this is a cyclo-oxygenase 2 inhibitor. At this time, only animal studies have been performed to investigate the effect of Celebrex® on testicular function. Some protection of steroidogenesis during inflammatory challenge has been recorded, but no real increase in baseline testosterone production.11
Another common drug class, the statins (e.g. Lipitor®), may reduce testosterone by reducing the available pool of cholesterol to use in steroidogenesis. Data are conflicting at this time, but it appears that while total testosterone may be reduced, bioavailable testosterone is not affected.12,13 Men started on statins who experience symptoms of androgen deficiency may wish to be more diligent in monitoring testosterone concentrations through their physicians.
The dietary attention really needs to be paid to foods that may lower testosterone production— either through antioxidant suppression of the oxidizing reactions, promoting the conversion of testosterone to estrogen, or by acting as an estrogen directly. Research has shown that several foods, many of which are increasing in popularity in the U.S., suppress testosterone production. Some of this data is based on test-tube experiments, others from animal studies and the majority of the remainder from epidemiologic studies (observing trends in large groups).
Green tea— a beverage so healthy that the only worries are about the water added to the tea bags— or is there more to consider? Green tea is full of antioxidants, leading to the health claims about promoting health and prolonging life. Yet, recall that testosterone production is dependent upon oxidizing reactions. Recently studies looking at the effect of green tea, specifically the polyphenol compounds (antioxidant), on testosterone levels have reveal a dark side to green tea— at least for the muscle-building athlete.
Green tea has been shown in the lab to inhibit certain effects of testosterones, apparently by inhibiting the conversion of testosterone to the more potent androgen, DHT.14,15 Green tea, specifically EGCG, may also affect aromatase— the enzyme that converts testosterone to estrogen; in some studies aromatase is suppressed, in others it is increased.16,17 Animal studies and epidemiologic studies have shown that green tea consumption is associated with lower androgen and estrogen levels in Asians.18 Green tea appears to be protective against cancers that respond to sex hormones (prostate, breast).19
Yet, what about testosterone? If estrogen and DHT are lower because testosterone is not being converted into those metabolites, then testosterone levels should be higher. However, tissue studies suggest otherwise. Rats treated with green tea had a much lower response to hCG, the hormone used to stimulate testosterone at the end of an anabolic steroid cycle.20 Interestingly, when the tissue cultures were provided with androstenedione, the steroid that immediately precedes testosterone in the natural production sequence, normal testosterone response to hCG was seen. This suggests that the inhibition of green tea occurs earlier in the steroid production sequence and may affect other steroid classes.
Another Asian staple that has entered Western diets is soy. Soy is a protein-rich vegetable that also contains other bioactive components. Among these are genistein and isoflavones. Soy intake has also been shown to decrease testosterone, making the use of it as the primary protein source of questionable value for male athletes— but this has been challenged.21,22 Available soy products include protein powders and ready-to-drink shakes. A number of products contain soy protein to attract female members of the gym, as the isoflavones have estrogenic-support properties.
Another diet trend, also supported by observations of Asian societies, is food restriction. Certain communities in Japan are known for their longevity; often attributed to green tea, low saturated fat, soy and other habits, the basis for much of this longevity is life-long caloric restriction.23,24 These people consume less than the maintenance calories daily, much less than the average American. Caloric restriction has been shown to prolong life in lab rats. Yet, this same life-extending diet also suppresses testes function, resulting in lower testosterone. Remember, the body does not want to support any more muscle than it uses because muscle uses energy, and the body is designed to preserve calories to survive winters/famine/etc.
Even short-term fasting suppresses testosterone levels. Men fasting for 3½ days saw a 30-50 percent decrease in testosterone, which was due to changes in the pituitary signal, rather than the testes function.25 It is important to realize that supporting testosterone function is more than offering the building blocks used by the testes.
A final example of the need for a suitable diet was demonstrated in a study looking at wrestlers who lost weight rapidly to meet the weight restrictions of their class. During a two- to three-week training regimen, wrestlers’ average testosterone concentration dropped approximately 30 percent.26 An earlier study even demonstrated that during a two-day tournament, resting testosterone concentration dropped.27
The body needs to know that the environment is safe for adding on metabolically demanding tissue, such as muscle. This includes consuming sufficient calories to avoid muscle wasting, eating a quality diet including animal-based protein, focusing on foods that are high in zinc and B vitamins. Men striving to lose weight, consuming soy-based foods and drinking green tea should be aware that one consequence is a probable reduction in testosterone concentration that will make building and maintaining muscle much more difficult. Of course, it is unwise to overdo any diet, as obesity is not the goal of most readers and the increase in adipose tissue will lead to elevations in estrogens. Further, the health benefits of green tea and soy, possibly flaxseed as well, need to be weighed against sports or physique goals.
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4. Päivä H, Thelen KM, et al. High-dose statins and skeletal muscle metabolism in humans: a randomized, controlled trial. Clin Pharmacol Ther, 2005 Jul;78(1):60-8.
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8. Jana K, Samanta PK, et al. Protective effect of sodium selenite and zinc sulfate on intensive swimming-induced testicular gamatogenic and steroidogenic disorders in mature male rats. Appl Physiol Nutr Metab, 2008 Oct;33(5):903-14.
9. Castilla R, Maloberti P, et al. Arachidonic acid regulation of steroid synthesis: new partners in the signaling pathway of steroidogenic hormones. Endocr Res, 2004 Nov;30(4):599-606.
10. Wang X, Shen CL, et al. Cyclooxygenase-2 regulation of the age-related decline in testosterone biosynthesis. Endocrinology, 2005 Oct;146(10):4202-8.
11. Winnall WR, Muir JA, et al. Effects of chronic celecoxib on testicular function in normal and lipopolysaccharide-treated rats. Int J Androl, 2008 Jun 2. [Epub ahead of print].
12. Stanworth RD, Kapoor D, et al. Statin therapy is associated with lower total but not bioavailable or free testosterone in men with type 2 diabetes. Diabetes Care, 2009 Apr;32(4):541-6.
13. Kocum TH, Ozcan TI, et al. Does atorvastatin affect androgen levels in men in the era of very-low LDL targeting therapy? Exp Clin Endocrinol Diabetes, 2009 Feb;117(2):60-3.
14. Liao S, Hiipakka RA. Selective inhibition of steroid 5 alpha-reductase isozymes by tea epicatechin-3-gallate and epigallocatechin-3-gallate. Biochem Biophys Res Commun, 1995 Sep 25;214(3):833-8.
15. Hiipakka RA, Zhang HZ, et al. Structure-activity relationships for inhibition of human 5alpha-reductases by polyphenols. Biochem Pharmacol, 2002 Mar 15;63(6):1165-76.
16. Satoh K, Sakamoto Y, et al. Inhibition of aromatase activity by green tea extract catechins and their endocrinological effects of oral administration in rats. Food Chem Toxicol, 2002 Jul;40(7):925-33.
17. Monteiro R, Assunção M, et al. Chronic green tea consumption decreases body mass, induces aromatase expression, and changes proliferation and apoptosis in adult male rat adipose tissue. J Nutr, 2008 Nov;138(11):2156-63.
18. Goh VH, Tong TY, et al. Interactions among age, adiposity, bodyweight, lifestyle factors and sex steroid hormones in healthy Singaporean Chinese men. Asian J Androl, 2007 Sep;9(5):611-21.
19. Zhou JR, Li L, et al. Dietary soy and tea combinations for prevention of breast and prostate cancers by targeting metabolic syndrome elements in mice. Am J Clin Nutr, 2007 Sep;86(3):s882-8.
20. Figueiroa MS, César Vieira JS, et al. Green tea polyphenols inhibit testosterone production in rat Leydig cells. Asian J Androl, 2009 May;11(3):362-70.
21. Goodin S, Shen F, et al. Clinical and biological activity of soy protein powder supplementation in healthy male volunteers. Cancer Epidemiol Biomarkers Prev, 2007;16:829-33.
22. Kalman D, Feldman S, et al. Effect of protein source and resistance training on body composition and sex hormones. J Int Soc Sports Nutr, 2007 Jul 23;4:4.
23. Rehm S, White TE, et al. Effects of food restriction on testis and accessory sex glands in maturing rats. Toxicol Pathol, 2008;36(5):687-94.
24. Chen H, Luo L, et al. Aging and caloric restriction: effects on Leydig cell steroidogenesis. Exp Gerontol, 2005 Jun;40(6):498-505.
25. Aloi JA, Bergendahl M, et al. Pulsatile intravenous gonadotropin-releasing hormone administration averts fasting-induced hypogonadotropism and hypoandrogenemia in healthy, normal weight men. J Clin Endocrinol Metab, 1997 May;82(5):1543-8.
26. Karila TA, Sarkkinen P, et al. Rapid weight loss decreases serum testosterone. Int J Sports Med, 2008 Nov;29(11):872-7.
27. Kraemer WJ, Fry AC, et al. Physiological and performance responses to tournament wrestling. Med Sci Sports Exerc, 2001 Aug;33(8):1367-78.
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