When young men take a high dose of testosterone while eating very few calories, their body starts making more iron available to produce red blood cells, but their metabolism and how they burn food don’t change.

In young men (18–30 years) in severe caloric deficit (≤15 kcal/kg/day), compare supraphysiological testosterone (200 mg/week IM) versus placebo over 8 weeks, measuring serum hepcidin, soluble transferrin receptor, ferritin, hemoglobin, energy expenditure via indirect calorimetry, and substrate oxidation via respiratory quotient.

In the same group of young men, compare two 6-week phases: one with supraphysiological testosterone (200 mg/week) and one with placebo, both during severe caloric deficit, separated by a 4-week washout. Measure hepcidin, soluble transferrin receptor, energy expenditure, and substrate oxidation at the end of each phase.

Observe young men undergoing intentional severe caloric deficit (e.g., athletes or military trainees) who are either receiving exogenous testosterone (200 mg/week) or not, and compare changes in hepcidin, sTfR, energy expenditure, and substrate oxidation over 6–8 weeks.

Measure temporal changes in hepcidin, sTfR, iron parameters, and metabolic markers in young men receiving 200 mg/week testosterone during caloric deficit, with frequent sampling (e.g., days 0, 3, 7, 14, 28) to establish kinetics and causal sequence.

Test whether supraphysiological testosterone directly suppresses hepcidin expression in human hepatocytes and enhances sTfR expression in erythroid precursors under low-nutrient conditions mimicking caloric deficit.