Testosterone, the primary androgen, is a steroid hormone produced mainly in the testes in males and in smaller amounts by the ovaries and adrenal glands in females. It is responsible for the development of male secondary sexual characteristics, such as deepening of the voice and growth of facial hair. Testosterone also regulates muscle mass, bone density, fat distribution, red blood cell production, mood, and sex drive in both sexes. Circulating levels arise from a complex interaction between inherited genetic makeup and external environment and lifestyle. Genetics establish a foundational predisposition, while environmental factors modify where an individual’s hormone level falls within that inherited range.
The Statistical Heritability of Testosterone Levels
Heritability quantifies the proportion of variation in a trait across a population attributable to genetic differences. Studies using twin and family data consistently show that testosterone levels are significantly genetically determined. For adult men, estimated heritability typically ranges between 40% and 70%. This means nearly half to two-thirds of the difference in testosterone levels observed between men can be linked to their genes.
For women, heritability estimates are also substantial, often ranging from 40% to 60% of the variance. These figures indicate a strong genetic component influences the baseline production and regulation of testosterone in both sexes. Heritability is a population-level statistic, however, meaning it describes the group, not the individual. The remaining variation is influenced by factors unique to an individual’s life, such as diet, exercise, and age.
The genetic baseline largely sets an individual’s capacity for testosterone production. For example, genetic effects accounted for approximately 50% of the variance in testosterone levels during early puberty in both boys and girls. This genetic framework allows non-genetic influences to act to raise or lower the circulating hormone concentration.
Key Genetic Pathways Controlling Testosterone Production and Action
The significant heritability of testosterone levels stems from genetic variations affecting hormone metabolism and signaling.
Hormone Production
Genetic influence begins with hormone production, which involves a cascade of enzymatic reactions. Genes coding for enzymes in the steroidogenesis pathway, such as CYP17A1 and HSD17B3, have variants that alter the efficiency of testosterone synthesis. Differences in these genes lead to variations in the rate at which the body manufactures the hormone.
Hormone Transport
Once produced, testosterone is transported through the bloodstream, where genetic factors affecting Sex Hormone Binding Globulin (SHBG) play a substantial role. The SHBG gene determines the production of this protein, which binds tightly to testosterone, making it biologically inactive. Variations in the SHBG gene can alter the quantity of the globulin produced, changing the proportion of “free,” or active, testosterone available to tissues. A high genetic predisposition for SHBG production can lower the amount of functional testosterone, even if total production is high.
Tissue Action
Genetic differences also affect how target tissues respond to the hormone through variations in the Androgen Receptor (AR). The AR gene contains a segment that varies in length, influencing the receptor’s sensitivity to testosterone. A receptor with lower sensitivity requires a higher concentration of the hormone to elicit the same biological effect. Genetic variants in the AR affect how effectively testosterone drives muscle growth, regulates mood, or maintains bone density.
Lifestyle and Environmental Modifiers
While genetics provides the blueprint, external factors exert considerable influence, explaining the remaining variance.
The most well-documented non-genetic factor is age, as testosterone levels naturally begin to decline in men starting around the third or fourth decade of life. This age-related decrease is a physiological process causing a predictable downward trend in hormone concentration over time, independent of the genetic baseline.
Nutritional status is a powerful modifier, with specific micronutrients playing a direct role in the endocrine system. Inadequate intake of zinc can impair enzymes involved in testosterone synthesis, and Vitamin D is associated with healthy testosterone levels. Deficiencies in these nutrients can lead to lower hormone output, even with a favorable genetic background.
Physical activity, particularly the type and intensity of exercise, significantly alters hormone balance. Resistance training and high-intensity interval training temporarily elevate testosterone levels, and consistent engagement supports a higher baseline. Conversely, a sedentary lifestyle contributes to increased body fat, which contains the enzyme aromatase that converts testosterone into estrogen, lowering the circulating androgen concentration.
Chronic psychological stress, leading to persistently elevated cortisol, can suppress testosterone production. Cortisol operates in an inverse relationship with reproductive hormones, and its prolonged elevation inhibits the hormonal axis responsible for testosterone release. Furthermore, the quality and duration of sleep are important; the body produces a significant portion of its daily testosterone during deep sleep cycles, meaning chronic sleep deprivation directly impairs production.