Concerning Ethnic Differences of Testosterone in Men
by Kangster · December 9, 2013 test If you live in a diverse country, then you have probably noticed the variations in the body structure between ethnic groups. While individuals within an ethnic group can vary widely in terms of body composition, you can probably still pick out some commonalities among each ethnic group. I’ll state my observations bluntly: African Americans on average seem to be more muscular than the norm, while those of Asian descent on average seem to be less muscular than the norm (I’m not advocating racism; it is a fact of life that people of the same ethnic group are more genetically similar than those of different ethnic groups). This observation is in fact reinforced by findings of researchers. Asian Indian adults were found to have more fat and less skeletal muscle than Europeans and Polynesians [1]. Another study focused on the Fat-free mass index, a measurement of Fat-free mass in relation to fat mass and height, of Caucasians, African Americans, Hispanics, and Asians. Fat-free mass includes everything in your body that is not fat mass and is thus correlated with skeletal muscle mass. The study found that the FFMI was greatest in African Americans and the least in Asians [2]. ffmi
One of the most important factors in regulating muscle mass, is the hormone that we relate to all things masculine, testosterone. It is the reason why men are men. In fact, those that are genetically male (carry a Y chromosome) and display complete androgen receptor insensitivity (meaning they can’t respond to testosterone) develop as women [3]. However, if we were to look at our supposed culprit, we would find that there is no statistical difference in free testosterone levels between ethnic groups [4]. It should be noted that this study is limited by its small sample size for Asians. TestEthnicity
One study even showed Asian men to have slightly higher testosterone levels than whites and African-Americans [5].
Although plasma testosterone levels are an important factor in sex hormone-dependent features, they obviously cannot explain the ethnic differences in these features. These differences seem to be mediated instead by differential enzyme and androgen receptor activity [6]. Specifically, 5a-reductase, the enzyme that converts testosterone into DHT, activity seems to vary among ethnic groups. DHT is an androgenic hormone whose affinity to the androgen receptor is multitudes times greater than testosterone. A study recorded the DHT:testosterone ratio, an indicator of 5a-reductase activity[7], among ethnic groups and found levels to be highest in African-Americans, intermediate in Caucasians, and lowest in Asian-Americans [5]. Tissue-specific coactivators of the androgen receptor also play a role in differences in tissue-specific androgenicity. Different levels of these coactivators are found in different tissues(heart, skeletal muscle, and liver), and help determine the responsiveness of these receptors by binding to the androgen-androgen receptor complex [8-12].
The genetic differences in the gene encoding the androgen receptor itself contributes greatly to its ability to respond to testosterone and other androgens [13-15]. One of the most distinctive and important genetic differences found is called the CAG repeat polymorphism. This refers to the glutamine-tag attached to the androgen receptor becomes the sequence CAG is translated into the amino acid glutamine. The number of CAG repeats an individual has in his or her androgen receptor gene determines how effective his or her androgen receptor is at binding testosterone; those with less repeats are more sensitive to testosterone and those with a greater amount of repeats are less sensitive [16-21]. It has been found that those with short CAG repeats have the same symptoms of men with high testosterone levels, increased skeletal muscle mass, lower good cholesterol (HDL), and have an earlier onset of prostate cancer [21]. Those born with too many repeats (>38) may be at risk for certain genetic disorders [22]. The inverse association between the number of CAG repeats in the AR gene and functionality of the AR protein. Longer CAG tracts result in lower transcription of target genes and, thus, lower androgenicity. Expansion of the encoded polyglutamine stretch to beyond probably 38 leads to the neuromuscular disorder X-linked spinal bulbar muscular atrophy (XSBMA), a condition in which defective spermatogenesis and undervirilization are observed. Conversely, low numbers of CAG repeats are associated with increased androgenicity of susceptible tissues.
The inverse association between the number of CAG repeats in the AR gene and functionality of the AR protein. Longer CAG tracts result in lower transcription of target genes and, thus, lower androgenicity. Expansion of the encoded polyglutamine stretch to beyond probably 38 leads to the neuromuscular disorder X-linked spinal bulbar muscular atrophy (XSBMA), a condition in which defective spermatogenesis and undervirilization are observed. Conversely, low numbers of CAG repeats are associated with increased androgenicity of susceptible tissues. The mechanism behind the weaker transactivation of androgen receptors with longer CAG repeats was found in a study done in 1999. A coactivator of the androgen receptor, ARA24, was discovered which bound differentially with the polyglutamine region of the androgen receptor. ARA24 was found to bind more weakly to androgen receptors with longer repeats and thus allowed for weaker signalling for the transcription of androgen-related genes [11].
Small but significant differences in the average CAG repeat length were found between different ethnic groups. Men of African descent were found to have the lowest number of repeats at 18-20, caucasians at 21-22, and east asians at 22-23[21]. Not only does this information reinforce our observations about body composition and androgenicity among different ethnic groups, but it also offers us some clinical value. The differences in enzyme, coactivator and androgen receptor activity may explain why certain individuals respond to testosterone therapy more strongly than others. It seems, however, that there is no clear winner in the roulette of testosterone sensitivity; one group may see greater strength in the earlier years of life, while the other gains vitality in the later years.
Sources: 1. Rush EC, Freitas I, Plank LD. Body size, body composition and fat distribution: comparative analysis of European, Maori, Pacific Island and Asian Indian adults. Br J Nutr. 2009;102(4):632-641. 2. Hull HR, Thornton J, Wang J, et al. Fat-free mass index: changes and race/ethnic differences in adulthood. Int J Obes (Lond). 2011;35(1):121-7. 3. Oakes MB, Eyvazzadeh AD, et al. Complete androgen insensitivity syndrome–a review. J Pediatr Adolesc Gynecol, 2008 Dec;21(6):305-10. 4. Ellis L, Nyborg H. Racial/ethnic variations in male testosterone levels: a probable contributor to group differences in health. Steroids. 1992;57(2):72-5. 5. Wu AH, Whittemore AS, Kolonel LN, John EM, Gallagher RP,West DW et al. Serum androgens and sex hormone-binding globulins in relation to lifestyle factors in older African- American, white and Asian men in the United States and Canada. Cancer Epidemiology Biomarkers and Prevention 1995 4 735±741. 6. Zitzmann M, Nieschlag E. Testosterone levels in healthy men and the relation to behavioural and physical characteristics: facts and constructs. Eur J Endocrinol. 2001;144(3):183-97. 7. Horton, R. Dihydrotestosterone is a peripheral paracrine hormone. J. Androl., 13: 23-27, 1992.
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