Testosterone deficiency: what is really behind it when drive becomes quieter
Causes, integrative medicine and holistic paths for men between 30 and 55.
There is a problem hardly anyone talks about.
Not because it is rare. But because it has become so normal that we overlook it.
I do not mean the men who come into my practice exhausted and say: "I think I have testosterone deficiency." I mean the men who do not come at all. Who think it is just everyday life. The stress. The age. Life itself.
The body functions. But without pressure. The mind thinks. But without fire. Daily life runs. But it no longer carries.
This connection is rarely talked about, even though it has been studied well. That the hormone system may also be involved does not occur to many people.
Not because doctors do something wrong. But because our system is trained to recognize illness. Not the loss of liveliness.
1. A decline that concerns whole generations
Now comes the part that really lands. Not as alarmism. As fact.
Testosterone does not only sink with age. It apparently also sinks from birth cohort to birth cohort. That means: in the groups studied, values were lower in men born later than in men of the same age from earlier cohorts.
Travison and colleagues published in 2007 in the Journal of Clinical Endocrinology & Metabolism one of the most important studies on this topic. They analyzed three survey waves of the Massachusetts Male Aging Study over almost two decades. The result: in men of the same age, testosterone values were lower in the later survey waves, on the order of about 1 percent per year and independent of age. A fall of the mean value from 501 to 391 ng/dL is reported. Even after adjustment for BMI, smoking and illness, the decline persisted. For context: the men studied were between 45 and 79 years of age, in the greater Boston area. Nothing can be derived directly from this for younger men.
Travison TG et al. A population-level decline in serum testosterone levels in American men. J Clin Endocrinol Metab. 2007;92(1):196–202. DOI: 10.1210/jc.2006-1375Similar observations exist from Denmark and Finland. Perheentupa and colleagues found in a Finnish cohort study, in men between 60 and 69 years of age, a difference from 21.9 to 13.8 nmol/l between the birth cohorts 1913 to 1922 and 1942 to 1951, so around 37 percent. This value applies explicitly to that age group and not to younger men. It was notable that gonadotropins (LH/FSH) did not rise along with it. That may point to the regulation at the hypothalamic-pituitary level being involved, and not only the testes themselves.
Make this tangible, without drama, but honestly:
If values are about 1 percent lower per calendar year, that would arithmetically be nearly one third over 30 years compared with the reference generation. That is an extrapolation, not a measurement. Whether the trend continues that way, and whether it also applies to men under 45, is open.
A Danish study showed that after adjustment for BMI, the decline became less marked. Obesity is a substantial mediator. The decline is real, but its causes are complex: endocrine disruptors from the environment, sleep deprivation, lack of movement, processed foods, chronic stress. There is no single cause and no single solution.
On frequency: depending on the diagnostic criterion, between 2 and 38 percent of men over 45 have testosterone deficiency. The huge difference is explained by the measurement threshold. If you apply purely biochemical thresholds, you find many. If you combine biochemical criteria with real symptoms, you find fewer. Reality lies in between: many men have functionally relevant values that formally lie within the "normal range".
2. Testosterone is not a muscle hormone. It is a life hormone.
May I ask you a question before I explain what testosterone does in the body?
What do you associate with it? Aggression? The gym? Potency?
Those are clichés that completely miss the actual point.
Testosterone is like the calorific value of a stove. Not the wood. Not the flame. But the question: how much warmth arises from what is there?
Low testosterone values are consistently associated in the scientific literature with insulin resistance, metabolic syndrome, visceral fat accumulation, loss of muscle and bone mass, reduced stress resilience, exhaustion, sleep disorders, depressive episodes and reduced cognition. This is no moral judgment. This is biochemistry.
Bianchi and Locatelli published in 2018 in Obesity Reviews a systematic review on the connection between testosterone and metabolic syndrome. The core finding: low testosterone and insulin resistance form a bidirectional loop. The authors themselves note that the evidence is primarily correlational. The strength of the association is nevertheless clinically relevant.
Bianchi VE, Locatelli V. Testosterone a key factor in gender related metabolic syndrome. Obesity Reviews. 2018;19(4):557–575. DOI: 10.1111/obr.12633And still: testosterone is not routinely measured. When it is, often only once, without context, without looking at the free fraction, without considering the time of day of the measurement. Many men walk around for years with a real deficit, without anyone taking the smoke alarm seriously.
3. The orchestra: how testosterone is actually made
Testosterone does not just fall from the sky. It is produced. And by a system that only delivers when the framework conditions are right.
Imagine this system as an orchestra.
The brain sets the tempo. The testes play. The metabolism delivers energy. The immune system decides whether peace or alarm reigns. When one of these musicians is permanently off, the music becomes quieter.
The HPG axis, the precise hormone system
In the normal state it runs like this: the hypothalamus, a small region in the brain, releases GnRH in pulses. This stimulates the pituitary to release LH and FSH. LH activates the Leydig cells in the testis to produce testosterone. Testosterone then inhibits both the hypothalamus and the pituitary via negative feedback. A precise, wonderful system.
A common assumption is: "My testes produce too little testosterone." In my consulting room I more often see a regulation problem than damage to the testis itself. That is an observation from practice, not a statistic. Organic causes do occur and have to be excluded, for example a disease of the pituitary, an iron storage disease or Klinefelter syndrome. With a regulation problem, the brain no longer clearly sends the signal: produce. It is safe. There is enough energy here.
Why this is so, the next section explains.
4. Anthroposophically considered: when the will no longer reaches the body
I would like to switch the frame here briefly. Not away from science, but to add a different lens.
Anthroposophically considered, testosterone is no isolated molecule. It is an expression of how strongly the human being is present in their own body.
Testosterone stands for embodiment of will. Inner uprightness. Creative and decision-making power. Warmth in the metabolism. Assertion outward, without hardness.
Many men with low testosterone live permanently in the nerve-sense pole: thinking, planning, controlling, screen, pressure, responsibility. Little grounding, little warmth, little rhythm. The counter-pole, the metabolic-limb pole, is short-changed: regular nourishing meals, movement with load, sleep rhythm, warmth, embodiment instead of constant thinking.
The will gets "stuck in the head". Biologically this shows up as a quiet metabolism. Hormonally as lower testosterone.
This is not a question of guilt. It is a diagnosis of our time. Chronic cognitive load, digital omnipresence, sleep deprivation and lack of movement are structural conditions of modern work. Testosterone deficiency is no personal failure. It is a physiological signal in response to a lifestyle that has moved too far from what the body needs.
Physiologically parallel to this, there is solid knowledge about the circadian rhythm as a hormonal basic condition. Testosterone follows a robust daily rhythm with peak values around 6 to 8 in the morning and a fall of 50 to 63 percent by evening. A disturbance of this rhythm, as in shift work, jet lag or chronic sleep deprivation, can throw hormone homeostasis off balance. Rhythm is no wellness recommendation. It is the language the body understands.
I know this pattern very well. Picture a man in his early forties who does not come because of testosterone, but because of exhaustion and concentration problems. What he says amounts to: I still function, but I used to have more energy for the things that mattered to me. In the background the same picture often stands: too little sleep, irregular times, screens until late, constant deadline pressure. No classical hypogonadism in the strict sense. But a hormone system that may have become quieter under the regulatory pressure of everyday life.
All details here are composite and describe no individual patient. I deliberately give no lab values and no course over time. How one person responds to changes cannot be predicted, and no cause can be derived from a single case.
5. Chronic stress: the factor that works most quietly
When I ask patients whether they are stressed, many say: "No, not really." And then they tell me about 55-hour work weeks, children who have to be made ready in the morning, sleep under seven hours and an inner monologue that keeps running at 11 in the evening.
That is stress. Even if you do not experience it as such.
The central mechanism: CRH inhibits GnRH
Chronic stress can inhibit the HPG axis at the central nervous level. CRH (corticotropin-releasing hormone) can dampen GnRH pulsatility in the hypothalamus. That can mean less LH, and less LH can mean less testosterone from the Leydig cells. In addition, kisspeptin neurons, the main activators of GnRH, can be inhibited by chronically elevated glucocorticoids. The underlying idea: the brain prioritizes survival before reproduction. A large part of these mechanisms has been described in animal models. In humans the direction is plausible, but not documented to the same depth.
Rivier and Rivest described as early as 1991 in a review that stress can influence the HPG axis on multiple levels: CRH can inhibit GnRH neurons directly, glucocorticoids can reduce pituitary GnRH sensitivity, and cortisol can impair Leydig cell responsiveness. This review rests overwhelmingly on rodent data. In the animal model, GnIH/RFRP-3 was additionally described as a further stress-dependent inhibitor of GnRH neurons, in Kirby and colleagues 2009, in male rats. In humans this is not yet documented in the same way. I list it here as a hypothesis, not as an established finding.
Rivier C, Rivest S. Effect of stress on the activity of the hypothalamic-pituitary-gonadal axis: peripheral and central mechanisms. Biol Reprod. 1991;45(4):523–532. DOI: 10.1095/biolreprod45.4.523You may have read somewhere that stress "steals" the pregnenolone needed for testosterone. That sounds plausible. But by current knowledge it is not correct. The three zones of the adrenal cortex produce pregnenolone in separate cell populations with their own enzymes. There is no known intercellular transfer. Gonadal testosterone is produced fully separately from the adrenal cortex under LH control. The better documented mechanism runs at the central nervous level: CRH can inhibit GnRH. Assuming a stolen pregnenolone does not fit what we know about these cells.
The saber-toothed tiger back then. The presentation tomorrow morning. The 57 unanswered emails. For your nervous system, alarm equals alarm. It releases cortisol without asking questions. That was brilliant, because the saber-toothed tiger was gone after a few minutes. The problem today: the alarm does not run for minutes. It runs for months. For years. And at some point the body starts saving. First on things that are not about survival.
6. Sleep: the lever no one takes seriously enough
If there is a single factor that is non-negotiable for testosterone, it is sleep.
Not "good sleep would be nice". But: too little sleep can markedly disturb nocturnal testosterone production.
Testosterone is not produced evenly across the day. The major part arises at night, coupled to the first deep sleep and REM phases. Axelsson and colleagues documented a rise that begins with sleep onset and reaches its daily peak with waking. Sleep is the production window, not a recovery break.
Leproult and Van Cauter conducted a crossover study in 2011 with 10 healthy young men. After 3 nights of 10 hours in bed followed 8 nights with only 5 hours of sleep. The result: daytime testosterone fell by 10 to 15 percent (from about 18.4 to about 16.5 nmol/L). The authors compared this effect with that of 10 to 15 years of aging. Cortisol was unaffected, which shows: the mechanism is not mediated through the stress axis, but through the sleep-wake rhythm itself.
Leproult R, Van Cauter E. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA. 2011;305(21):2173–2174. DOI: 10.1001/jama.2011.710Sleep apnea: poor sleep despite enough hours
Many men with low testosterone do not have too little sleep, but bad sleep. Sleep apnea means repeated breathing pauses, oxygen drops, stress reactions in the brain, alarm mode all night long.
Luboshitzky and colleagues found in 2002 that men with obstructive sleep apnea had lower nocturnal LH and testosterone values than controls (67.2 vs. 113.3 nmol/L · h, p<0.003), even after adjustment for BMI. The study is small: 10 patients against 5 controls. It shows an association, not a cause.
Luboshitzky R et al. Decreased pituitary-gonadal secretion in men with obstructive sleep apnea. J Clin Endocrinol Metab. 2002;87(7):3394–3398. DOI: 10.1210/jcem.87.7.8663Hints of sleep apnea: loud snoring, daytime sleepiness despite long sleep duration, morning headaches, abdominal fat, high blood pressure. With suspicion, diagnostics is worthwhile.
Target setting for sleep: constant rise time also at the weekend, morning light to set the inner rhythm, evening reduction of stimuli from 9 in the evening. This is no wellness recommendation. In my view this is the basis, before thinking about anything else.
7. Belly fat and aromatase: a loop that can reinforce itself
Now it gets biochemically concrete. And important.
Visceral fat is no passive energy store. It is a hormonally active organ. And one of its favorite enzymes is called aromatase.
Aromatase (CYP19A1) converts testosterone to estradiol. This is a normal physiological function. Ahmed and colleagues found in 2025 in the Journal of Clinical Endocrinology & Metabolism that in men with obesity, aromatase expression in subcutaneous fat tissue was higher than in lean men, and that this was linked to insulin resistance and higher blood glucose. No association was found in that work between aromatase and circulating estradiol. The idea that more belly fat automatically means more conversion and therefore less testosterone is plausible. It is not yet that simply documented.
And then the loop begins:
More belly fat can mean more aromatase, that can mean less free testosterone, that can make muscle build-up harder, that can worsen insulin sensitivity, and that can again mean more belly fat. Each turn can make the next way out harder. This is no character problem. This is metabolism.
Dhindsa and colleagues described that about one third of men with type 2 diabetes have a hypogonadotropic hypogonadism. In a randomized controlled trial with 44 men over 24 weeks, insulin sensitivity improved by 32 percent under intramuscular testosterone compared with placebo (p=0.03). That speaks for the loop being able to run in both directions.
Dhindsa S et al. Insulin resistance and inflammation in hypogonadotropic hypogonadism. Diabetes Care. 2016;39(1):82–91. DOI: 10.2337/dc15-1518SHBG is another mediator: hyperinsulinemia suppresses hepatic SHBG production. Lower SHBG means that arithmetically more "free" testosterone is present, but at the same time total testosterone sinks, and the picture becomes confusing. Therefore measuring total testosterone alone is not enough.
8. Nervous system, HRV and breath work: easing off the gas pedal
Many men with low testosterone live permanently with a foot on the gas pedal. Not physically. But neurally.
The autonomic nervous system has two main modes: sympathetic (activation, performance, stress) and parasympathetic (regeneration, hormone production, build-up). Chronic stress means: the sympathetic system stays on. The parasympathetic system does not really get its turn.
Much speaks for the build-up metabolism needing parasympathetic phases. This is no mental training. This is a physiological consideration. An intervention study that has tested exactly this for testosterone does not exist.
What is HRV and why is it relevant?
Heart rate variability (HRV) describes how flexibly the heart responds to load and recovery. High HRV signals a good balance between sympathetic and parasympathetic. Low HRV can point to chronic stress and low resilience. There are indications that HRV may improve under testosterone therapy in hypogonadal men. That is not yet solid proof of a link between testosterone status and autonomic regulation.
Slow breathing measurably improves HRV
The evidence for slow breathing (about 6 breaths per minute) and HRV improvement is strong. Laborde and colleagues analyzed 223 studies in a 2022 meta-analysis and confirmed rises in vagally mediated HRV both acutely and after multi-week practice programs.
Laborde et al. (2022) analyzed 223 studies on heart rate variability biofeedback and showed consistent rises in vagally mediated HRV after short practice sessions (5 to 10 minutes daily) both acutely and after intervention periods.
Laborde S et al. Heart Rate Variability Biofeedback in Sport and Performance. Neurosci Biobehav Rev. 2022;138:104711. DOI: 10.1016/j.neubiorev.2022.104711Four seconds in. Six to seven seconds out. Twice a day, five minutes. That is the biochemical brake. Free of charge. Available everywhere. With well-documented effect on stress regulation.
9. Nutrition: several paths, no dogma
May I ask you an uncomfortable question?
What did you eat for breakfast this morning?
I am not asking to judge. I ask because in my practice I keep experiencing the same surprise: a man who considers himself well-nourished wears a blood-glucose sensor for three days. And the curve looks like a rollercoaster ticket.
The basic condition: energy and fat as building material
Testosterone is a steroid hormone. It is synthesized from cholesterol. For production, the body needs three basics: sufficient total energy, sufficient dietary fat as building material, sufficient protein for enzymes and transport proteins. Chronic calorie deficit, aggressive diets or constant "clean eating" without calories are testosterone-hostile. Not morally. Physiologically.
Whittaker and Wu published in 2021 in Journal of Steroid Biochemistry and Molecular Biology a meta-analysis of 6 crossover studies (206 participants). Low-fat diets lowered total testosterone (SMD −0.38, p=0.04) and free testosterone (SMD −0.37, p=0.005) compared with higher-fat diets. The effect size is statistically significant and clinically moderate. Nothing changed for SHBG and LH. The authors themselves write that further randomized trials are needed to confirm the effect.
Whittaker J, Wu K. Low-fat diets and testosterone in men: Systematic review and meta-analysis of intervention studies. J Steroid Biochem Mol Biol. 2021;210:105878. DOI: 10.1016/j.jsbmb.2021.105878Ketogenic: a strong tool, with one important limitation
Several studies describe testosterone rises under very-low-calorie ketogenic diet (VLCKD) in obese men. But the effect is more likely due to weight loss and the better insulin situation than to ketosis itself.
A ketogenic diet can raise SHBG (sex-hormone-binding globulin). In a small crossover study with 11 participants, five of them men, total testosterone in the men was unchanged, while SHBG rose and the free androgen index fell. That means: the freely available fraction can fall, even when the total value looks the same. The sample is small, the clinical significance is open. In my view, ketogenic is not a permanent state, but a time-limited tool with a clear indication and a clean exit.
Paleo: the most stable basis for many men
For many men, a paleo-like diet is the physiologically calmest path: unprocessed foods, sufficient protein and fat, moderate carbohydrates, high micronutrient density, low inflammation load. Jönsson and Lindeberg found in 2009, in a small randomized crossover pilot study with 13 people with type 2 diabetes, better HbA1c values, lower triglycerides and lower weight on a paleo diet than on a diabetes diet. A connection with testosterone would at most be indirect, via less visceral fat and therefore possibly less aromatase. That was not directly measured there.
Blood sugar stability: underestimated, extremely effective
For many men, the solution is not low carb, but stable glucose. Strong blood-sugar swings can raise cortisol, inflammation and mitochondrial load. The strategy: protein first. Then fat. Then carbohydrates targeted. This can buffer the blood-sugar rise and dampen the cortisol counter-regulation.
Carnivore: honest classification
There are no controlled studies on carnivore and testosterone. No randomized trials, no comparison groups, no hormone measurements. Only case reports and a survey study without endpoint measurements. Theoretical mechanisms exist (high zinc and cholesterol intake), but unproven. Whoever wants to try this: with medical supervision, time-limited, with a clear indication.
The most important message: there is no single diet. What is decisive is the fit. No dogma, but test, measure, adjust.
10. Movement: testosterone needs load, not chronic stress
Muscle is no decorative tissue. Muscle is an endocrine organ.
Active skeletal muscle releases myokines, signaling molecules like IL-6, irisin and FSTL-1, which communicate with fat tissue, liver, pancreas and brain and can improve insulin sensitivity. This is indirectly relevant for testosterone, via the known loop: better insulin sensitivity, less visceral fat, less aromatase.
Kraemer and colleagues measured in 1998, in 8 younger and 9 older men, significant rises of total and free testosterone after heavy compound exercises with large muscle groups (for example 4 x 10RM squats), measured over 30 minutes after the load. The work contains no statement about the resting level. Whether the acute response results in a higher resting value is open. Strength training is worth it anyway, above all via muscle mass and insulin sensitivity.
Kraemer WJ et al. Acute hormonal responses to heavy resistance exercise in younger and older men. Eur J Appl Physiol. 1998;77(3):206–211. DOI: 10.1007/s004210050323The other side: too much endurance training
Hackney coined the term "Exercise-Hypogonadal Male Condition" (EHMC): chronically trained endurance athletes show baseline testosterone values of 50 to 85 percent of the level of comparable sedentary men. The mechanism is presumed to be central, that is hypothalamic. The phenomenon is associated with years of high-volume training and possibly with relative energy deficit.
Not training more. Training more correctly. Load plus recovery is the equation. Daily maximum load without regeneration can raise cortisol chronically and lower testosterone in the long term. Three to four strength training sessions per week with heavy compound exercises, combined with sufficient sleep and recovery phases, is in my view the most sensible foundation.
Hormesis: a dosed stimulus can strengthen
The body needs stimuli, but dosed ones. Hormesis means: a brief stress stimulus that has a long-term adaptive effect.
Warmth can promote circulation and signal safety to the nervous system. Sauna combines an acute stimulus with parasympathetic recovery afterward. That is likely the decisive mechanism. Cold can be an effective tool, but only adaptive, brief and voluntary. Cold as chronic stress can work against you. The testes sit outside the body for good reason: sperm production needs it cooler than core body temperature. For testosterone production the effect is less clear. Long sitting phases without movement breaks are unfavorable anyway, for other reasons.
11. Supplements: supportive, never replacing
Supplements do not replace sleep, movement or meaning. But they can compensate for a limiting factor, if one truly exists. And that is the only sensible frame in which to talk about them.
Here is an overview of the study situation. It is a scientific classification, not a purchase and not an intake recommendation.
| Supplement | Claim | Evidence | Limitation |
|---|---|---|---|
| Zinc | Deficiency can lower T; compensating a deficiency might help | Indications from very small studies in deficiency (Prasad 1996) | Very small samples (4 and 9 men respectively). With normal zinc status no effect is shown. High doses over longer periods can displace copper. |
| Vitamin D | Might raise T in deficiency (about 25% in the within-group comparison) | Weak (Pilz 2011, n=54) | Secondary analysis of a weight-reduction program, significant was the within-group comparison. The authors themselves write only "might increase" and call for confirming trials. Overdosing can drive up the calcium level. |
| Magnesium | Might raise free testosterone | Weak (Cinar 2011, in athletes) | No real RCT, small sample; with normal magnesium status unclear |
| Ashwagandha | Cortisol down and testosterone up (both together not documented) | Partly, contradictory | No single paper shows both significantly at the same time. Lopresti, Medicine 2019: cortisol down significantly, testosterone not (p=0.158). Lopresti, Am J Mens Health 2019: salivary testosterone +14.7% (p=0.010), cortisol not significant. Risks: liver injury has been described in individual cases, an effect on the thyroid is possible, in pregnancy it is off limits. |
| Boron | Might lower SHBG and raise free testosterone | Weak (Naghii 2011) | n=8, no placebo group, no blinding, not replicated. I deliberately give no dose here: the tolerable total intake of boron is narrowly limited. |
| Shilajit | Might influence Leydig cell function and raise T | Weak (Pandit 2016) | Testosterone rise present in the RCT. Leydig cell function is not directly measured in the study, this claim comes from in-vitro data. Risk: shilajit preparations can be contaminated with heavy metals. Without a certificate of analysis I keep my hands off them. |
| Omega-3 | Can lower inflammation, a testosterone effect is not shown | Anti-inflammation well documented (Calder 2015) | Calder 2015 does not address testosterone. The connection is indirect: less inflammation, better HPG function. No direct testosterone effect documented in the study. |
For zinc there is an officially authorised claim: zinc can contribute to the maintenance of normal testosterone levels in the blood. For all other substances in this overview there is no authorised health claim relating to testosterone. I present the study situation here only as a scientific discussion, not as a promise of effect and not as a purchase recommendation.
12. Social biology and meaning: what testosterone also needs
The human being is a social being. Hormonally too.
Chronic isolation can raise cortisol and inflammation markers and dampen parasympathetic networks. Social connection, friendship, physical closeness and real conversations can act directly on stress regulation. This is no soft factor.
And then there is something that is harder to measure, but in practice keeps becoming relevant:
Testosterone follows not only calories. It also follows meaning. A body invests energy in muscle build-up, drive and reproductive readiness only when there is an inner "why". Chronic emptiness of meaning, constant conformity and missing perspective can dampen motivation, raise stress and through that lower testosterone indirectly. I know of no direct studies on this, I am describing a consideration and an observation. The will needs direction, otherwise it gets stuck in the head.
13. When is testosterone therapy really sensible?
I do not judge. I inform. Because the educational conversation around the question of TRT is often shockingly short, in both directions: either prescribed immediately or categorically rejected.
Testosterone therapy is no lifestyle tool. But it is also no taboo.
When TRT can be sensible
According to current guidelines of the Endocrine Society and the European Association of Urology, TRT indication requires: clinical symptoms of a deficit and consistently low testosterone values, confirmed by at least two morning measurements (7 to 11 in the morning) with a validated assay. The Endocrine Society orients itself to the lower limit of the harmonised reference range. In the 2018 guideline that is 264 ng/dL. In practice, 300 ng/dL is often used, which shows the discussion around the right threshold rather well. The EAU 2025 guidelines see the most reliable threshold at <12 nmol/L, with the greatest therapeutic benefit at <8 nmol/L.
Important: lifestyle, weight and accompanying conditions come first, TRT afterwards.
Contraindications
TRT is contraindicated in breast or prostate carcinoma, PSA >4 ng/mL without urological workup, hematocrit >50 percent, untreated severe sleep apnea, severe voiding complaints (IPSS >19), uncontrolled heart failure and active wish for children. TRT suppresses spermatogenesis as a rule, usually reversibly.
Anyone receiving TRT needs regular monitoring. That includes haematocrit and haemoglobin, because testosterone can raise the number of red blood cells, plus PSA and prostate findings as well as the symptoms themselves. Without this monitoring, a TRT should in my view not be started.
Lincoff and colleagues published in 2023 in the New England Journal of Medicine the largest RCT to date on TRT safety. It enrolled 5,246 men between 45 and 80 years of age with hypogonadism and pre-existing or high cardiovascular risk. For the main question, major adverse cardiac events, testosterone was non-inferior to placebo (MACE: 7.0% vs. 7.3%, HR 0.96). In the testosterone group, however, atrial fibrillation, acute kidney injury and pulmonary embolism occurred more often than under placebo. Both belong together in the informed consent conversation. The study was co-funded by the manufacturer.
Lincoff AM et al. Cardiovascular safety of testosterone-replacement therapy. N Engl J Med. 2023;389(2):107–117. DOI: 10.1056/NEJMoa2215025The question is not: "Do I need testosterone?" The question is: "Why does my body no longer produce it sufficiently itself? What has slowed it down?" If you understand that, you can often intervene before TRT becomes necessary. And if TRT is still indicated, then as a replacement for a failed function, not as a lifestyle upgrade. Controlled. Accompanied. Responsibly.
14. The seven levers. Today. Not next Monday.
I know how it is. You read something, nod inwardly, and a month later nothing happens. Because everything sounds somehow doable, but nothing is really anchored.
Therefore I ask you: choose right now while reading two levers. Only two. And start tomorrow morning.
01 Sleep routine before everything else
Constant rise time, also at the weekend. Morning light in the first 30 minutes after waking. Dim screens from 9 in the evening. This can set the circadian beat and protect nocturnal testosterone production. For sleep there is, in my view, the most convincing data among the lifestyle factors. That is why I start here with most men.
02 Protein first. Every morning.
Your breakfast sets the blood sugar and cortisol curve for the entire morning. Protein can buffer the glucose rise. Eggs, skyr, cottage cheese, nuts. First protein. Then the rest. Oats with fruit without protein in front: a rollercoaster ticket for your stress axis.
03 Three times a week strength training with heavy compound exercises
Squats, deadlifts, bench press, rows. Large muscle groups. Sufficient load. Sufficient recovery. Not daily at maximum. More correctly, not more. Shortly after heavy compound exercises, testosterone and free testosterone rise measurably. Whether this becomes a higher resting value is open. With cardiovascular pre-existing conditions, high blood pressure or disc problems, please clarify medically beforehand.
04 Address belly fat, not overnight, but consistently
More visceral fat can mean more aromatase and therefore less free testosterone. Every kilo less visceral fat can reduce the aromatase load. No crash diet, that can set the body into saving mode. A moderate deficit of about 10 to 15 percent can work, if protein and sleep are right. This is not for you if you are already lean or have an eating disorder in your history. Have it supervised. Patience is the active ingredient.
05 Two minutes of breath work, three times daily
4 seconds in. 6 to 7 seconds out. Slow breathing can measurably improve heart rate variability. Whether this affects your testosterone has never been examined directly. I recommend it because of stress regulation, not as a testosterone lever. Free of charge. Available everywhere.
06 Lab, complete and at the right time
In the morning, fasting, between 7 and 11. Two measurements on different days. Sensible are total testosterone, free testosterone, SHBG, LH, FSH, prolactin, ferritin and transferrin saturation, vitamin D, zinc, fT3/fT4 (not only TSH), hsCRP and fasting insulin. Prolactin and transferrin saturation explicitly belong in the lab. A low testosterone with low or normal LH can have a cause in the brain, for example a benign adenoma of the pituitary, or an iron storage disease. That is rare, but it has to be excluded before anyone talks about lifestyle. This workup belongs in medical hands and not in self-management.
07 Ask about the temporal connection
Did it begin after substantial weight gain? After a particularly stressful year? After chronic sleep deprivation? After stopping medications? These questions are no esoterics. They show where to look, and make the difference between symptom treatment and root-cause work.
15. Your self-check: who are you in this story?
Before you go to the doctor, before you order, before you change anything: ask yourself these questions.
Not for me. But so that you start to understand your own body as a system.
Block 1: your symptoms
- Do you have the feeling that your energy has become quieter over the last years, not suddenly, but gradually?
- Is it harder for you than before to build muscle or lose fat, despite similar effort?
- Do you notice changes in drive, libido, focus or recovery capacity?
- Do you regularly sleep less than 7 hours, with irregular times or with snoring or pause phases?
Block 2: your everyday life
- How many hours per day do you sit, and how much of that is real stress in your head?
- Do you eat carbohydrates first thing in the morning without protein? (Possible sign of an unfavorable glucose curve.)
- Do you have regular recovery phases, or does the sympathetic system also keep running in the evening?
- Do you regularly drink alcohol, even if "only" 2 to 3 glasses per day? (Regular alcohol consumption can impair testosterone production, above all in higher amounts and over longer periods.)
Block 3: your story
- When did your body last feel really awake, performant and present?
- Has something essential changed since then: weight, sleep, stress level, medications?
- Are there men in your family who had similar symptoms and were dismissed as "simply aging"?
Please seek prompt medical workup with:
- Severe symptoms that limit daily life (exhaustion, depression, loss of libido)
- Suspicion of sleep apnea (snoring, pauses, daytime sleepiness)
- Pronounced abdominal fat in combination with symptoms
- Wish for children and fertility questions (TRT excludes this)
- Known pre-existing conditions such as heart disease, prostate problems, polycythemia
Sources
- Travison TG et al. A population-level decline in serum testosterone levels in American men. J Clin Endocrinol Metab. 2007;92(1):196–202. DOI: 10.1210/jc.2006-1375
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This article does not replace medical advice, diagnosis or treatment. It describes general connections, not individual recommendations. Do not stop any medication and do not start any supplement without medical consultation. With acute complaints, please see a doctor promptly; in an emergency call 112.