Testosterone is a reproductive hormone present in both males and females, regulating muscle mass, bone density, mood, and sex drive. Maintaining adequate levels of this hormone depends on consistent energy availability from food intake. An insufficient supply of energy, whether from intentional dieting or involuntary deprivation, triggers an immediate physiological response that prioritizes survival over reproduction. Not eating definitively lowers testosterone levels, as the body’s endocrine system is highly sensitive to changes in energy balance. This suppression is a protective adaptation, signaling that the environment is not suitable for reproductive processes.
The Observed Effect of Energy Restriction
Restricting caloric intake has a direct and measurable suppressive effect on circulating testosterone levels. The degree of this reduction is proportional to the severity of the energy deficit, a relationship known as dose-response. This rapid suppression can begin within hours or days of initiating a significant energy deficit, impacting the pulse frequency of luteinizing hormone.
The effect is particularly pronounced in healthy individuals who maintain a normal body weight or in lean athletes. Studies show that calorie restriction results in significant decreases in total testosterone concentrations. Conversely, in men with overweight or obesity, a moderate calorie deficit may sometimes lead to an increase in testosterone, as weight loss reduces the amount of body fat that converts testosterone into estrogen.
Hormonal Signaling and the HPG Axis
The mechanism linking low energy intake to reduced testosterone involves the Hypothalamic-Pituitary-Gonadal (HPG) axis. This axis acts as the body’s reproductive thermostat, constantly monitoring metabolic signals before authorizing hormone production. When the brain detects energy scarcity, it initiates a cascade that downregulates the entire reproductive system.
The process begins with sensing molecules that circulate throughout the body, providing real-time metabolic feedback to the brain. Leptin, a hormone produced by fat cells, decreases sharply when energy stores are low, signaling depletion. Conversely, Ghrelin, often called the hunger hormone, increases significantly during food restriction, reinforcing the signal of energy deficit.
The hypothalamus interprets these signals and adjusts the output of a neuropeptide called Kisspeptin. Kisspeptin neurons are considered the primary conduit through which metabolic status is relayed to the reproductive system. When Leptin is low and Ghrelin is high, Kisspeptin release is suppressed, translating the metabolic distress signal into a reproductive shutdown.
This suppression of Kisspeptin then leads to a reduced pulsatile release of Gonadotropin-Releasing Hormone (GnRH) from the hypothalamus. The reduced GnRH signal causes the pituitary to decrease its secretion of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). Since LH stimulates the gonads to produce testosterone, a diminished LH signal results in a significant reduction in circulating testosterone levels. This biological process is a highly conserved survival mechanism designed to conserve energy by halting non-essential functions like reproduction.
Differentiating Acute Fasting from Chronic Calorie Deficit
The impact on testosterone differs based on the duration and severity of the energy restriction. Acute fasting, such as a 24- to 48-hour period of intermittent fasting, can cause a temporary dip in testosterone due to immediate metabolic stress. During this short period, the body experiences a transient disruption in the LH pulse frequency, but the HPG axis has not fully committed to long-term suppression. These fluctuations are typically reversed quickly once feeding resumes.
The detrimental effects occur during chronic calorie deficit, which involves weeks or months of sustained energy restriction. In this prolonged state, the body undergoes a deep-seated adaptation by downregulating the entire HPG axis. This results in a sustained suppression of reproductive hormonal signaling. Studies on lean men practicing long-term calorie restriction have shown significantly lower total and free testosterone levels, even when their diets are nutritionally adequate.
For healthy, lean individuals, this chronic restriction results in a sustained suppression that can fall into a clinically low range. Research on intermittent fasting in individuals with obesity, however, has shown no change in testosterone over a 12-month period, likely reflecting that the metabolic benefits of losing excess fat outweigh the negative effect of brief fasting windows.
Recovery of Testosterone Levels and Practical Context
The suppression of testosterone caused by not eating is generally reversible once a positive or neutral energy balance is restored. Recovery time depends on the severity and duration of the deficit. For a short-term, moderate diet, recovery can be relatively fast, but a prolonged, severe deficit may require several weeks or months.
This hormonal suppression is a concern for specific populations, notably endurance athletes and individuals engaging in extreme dieting behaviors. Athletes who combine intense training with insufficient calorie intake risk developing Relative Energy Deficiency in Sport (RED-S), characterized by reproductive dysfunction. Adequate nutrition is necessary for recovery, involving not just increasing total calories but also ensuring sufficient intake of macronutrients, particularly healthy fats, which are precursors to steroid hormones. Restoring energy availability signals to the HPG axis, allowing Kisspeptin, LH, and testosterone production to normalize.