Story
Andropause · Late-Onset Hypogonadism
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In one pass The word andropause equates two things that are not the same.
Educational content, not medical advice — consult a clinician.
Story path
Chapter 1
Not a male version of menopause
The word andropause equates two things that are not the same.
Menopause is a cliff: the ovaries shut down within a few years, there is a clear endpoint, and every woman goes through it. The male side is a gentle slope. The cells in the testes that make testosterone thin out slowly with age and answer the pituitary's prompting less briskly, so testosterone falls a little each year and is still measurable in very old men — there is no day you could call "switched off".
The biggest contrast is in how many men are affected. EMAS, a large population study of middle-aged and older men in Europe, required low testosterone and three sexual symptoms at the same time; by that standard, true late-onset hypogonadism (LOH) affects only about 2% of men aged 40–79. The tiredness, low drive and stubborn weight that get filed under "low T" mostly have little to do with testosterone, and cause and effect often run the other way: obesity, sleep apnea, long-term opioid painkillers and depression push testosterone down first.
So this story answers two questions: what testosterone does in your body, and when its decline is worth acting on.
Menopause is a cliff: the ovaries shut down within a few years, there is a clear endpoint, and every woman goes through it. The male side is a gentle slope. The cells in the testes that make testosterone thin out slowly with age and answer the pituitary's prompting less briskly, so testosterone falls a little each year and is still measurable in very old men — there is no day you could call "switched off".
The biggest contrast is in how many men are affected. EMAS, a large population study of middle-aged and older men in Europe, required low testosterone and three sexual symptoms at the same time; by that standard, true late-onset hypogonadism (LOH) affects only about 2% of men aged 40–79. The tiredness, low drive and stubborn weight that get filed under "low T" mostly have little to do with testosterone, and cause and effect often run the other way: obesity, sleep apnea, long-term opioid painkillers and depression push testosterone down first.
So this story answers two questions: what testosterone does in your body, and when its decline is worth acting on.
Mechanism · Where testosterone comes from and what it does
Everything in this story hangs on one chain. See the chain first: who places the order for testosterone, and once it is made, where it goes and what it does.The brain places the order, not the testes
Every so often the hypothalamus, at the base of the brain, releases a small pulse of signal — gonadotropin-releasing hormone (GnRH) — knocking on the pituitary like a door. The pituitary answers by releasing two hormones into the blood: (LH) and (FSH). LH travels in the bloodstream to the testes and settles on a cell type called Leydig cells; those cells are the actual workshop. They take cholesterol as raw material and reshape it, step by step, into testosterone. FSH works on a separate line: it acts on the Sertoli cells in the testes, the seedbed where sperm develop.
The testosterone that is made turns back and holds the upstream down
Testosterone in the blood, and the it is converted into around the body, turn back and lower both how often the hypothalamus releases its signal and how strongly the pituitary responds. That is negative feedback. This loop is the key to the whole story: phenomena that look unrelated — why obesity lowers testosterone, why testosterone from outside shuts down sperm production, why a man who wants children should not simply inject testosterone — all run through this same loop.
How it gets into a cell and does its work
Testosterone is fat-soluble. It does not queue at the cell door; it crosses the membrane directly, and inside the cell it meets a docking protein waiting for it, the androgen receptor. Once the two bind, the receptor changes shape, carries testosterone into the nucleus, parks on specific stretches of DNA and switches a set of genes on.
So testosterone does not give you energy; it changes what a group of cells will produce over the next few days. That is also why its effects are never immediate: between genes switching on, proteins being made and tissue changing, there are days to weeks.
In muscle: the receptor opens the production line for contractile proteins, and it also wakes the satellite cells that sit beside each muscle fiber on standby, so they fuse into the fiber and add new nuclei. When testosterone stays low for a long time, that production line runs a notch lower: the same amount of training holds on to muscle with more effort, and muscle is lost faster.
In bone: bone tissue has an enzyme called aromatase that converts arriving testosterone into estradiol on the spot. Estradiol holds back the osteoclasts, the cells that dismantle old bone. When supply from upstream falls, the dismantling side releases its handbrake and bone is taken apart bit by bit. Notice the contrast: the same enzyme converting testosterone to estradiol is bad news in fat, and in bone it is exactly what protects your bone mass. The same chemical reaction means something completely different depending on where it happens.
In the brain: androgen receptors are densest around the hypothalamus and the limbic system, which run the central drive behind libido and the round of spontaneous erections during the night. When EMAS screened a long list of candidate symptoms, the ones that clustered with low testosterone were three sexual symptoms — which fits where the receptors are (a match inferred from the mechanism; the study itself did not measure receptors). Low energy and a foggy head depend more on sleep, mood and blood sugar; in testosterone trials, energy and memory did not clearly improve either. Keep this in mind: judging which symptoms are real depends on it.
In bone marrow: testosterone pushes up the signal that makes red blood cells, and it is part of why men's hemoglobin averages higher than women's. With this in mind, it is clear why people on have their hematocrit (the share of the blood made up of red cells) watched, and why some need blood taken off.
In skin and prostate: here testosterone is remade once more, by a reductase enzyme, into a stronger androgen, dihydrotestosterone (DHT), which drives beard, body hair, hair loss at the crown and prostate size. The same molecule, remade into different forms in different places, does different jobs — which is also why adding testosterone never affects only one thing.
Evidence · How true LOH is defined, and how rare
Female menopause (the Perimenopause story covers this side):A cliff: estrogen falls by more than 90% within a few yearsA clear endpoint: 12 months in a row without a periodUniversal: every woman goes through it
Male testosterone:
A slow decline: after age 30, testosterone falls by roughly 1–2% a yearNo clear endpoint: most men still have measurable testosterone at 80Not universal: only about 2% of men meet EMAS's clinical definition (Wu 2010, *NEJM*)
The two curves have different shapes because what wears out is different. On the female side, the store of follicles is used up — a finite inventory that can run out. On the male side there is no inventory: the testes are a workshop that makes to order, and aging only thins the workforce and blunts how it answers the order. Running out and going dull are two completely different curves.
How true late-onset hypogonadism (LOH) is defined: the EMAS study, a population study of middle-aged and older men in Europe, required both conditions at the same time — testosterone that is genuinely low (both total and free testosterone), and three sexual symptoms (reduced libido, fewer morning erections, weaker erectile function). With both present, only about 2.1% of men aged 40–79 qualified. The whole point is the words at the same time: low testosterone without symptoms does not count, and symptoms without low testosterone do not count either.
Why insist on both? Because each clue on its own is unreliable. Numbers alone: testosterone swings a long way within a single day, and an afternoon blood draw can make a perfectly normal man look low. Symptoms alone: libido and erections also depend on blood vessels, mood, medicines and sleep, and a problem with any one of them can produce exactly the same picture. Two clues that each fail for unrelated reasons, pointing the same way at once, are what rule out coincidence. Once the bar is set, the numbers collapse from "looks common" to a single-digit percentage — and most of what falls away is not missed diagnoses but symptoms with another cause.
Why this matters
In China and the US, clinics that specialize in testosterone, and anti-aging marketing, describe LOH as far more widespread than thisEven when testosterone really is low, the common causes (obesity, sleep apnea, long-term opioid use, depression) can mostly be reversed
Clinical · Which symptoms really track testosterone
The list of symptoms filed under "low T" is long, but most of them have only a weak link to testosterone.Clearly linked to testosterone (EMAS, Wu 2010):
Reduced libidoFewer or absent morning erectionsWeaker erectile function (erectile dysfunction, ED)
Two more are linked to testosterone but do not depend on it alone: loss of muscle (training and protein intake matter just as much) and lower (when testosterone is truly deficient).
Weakly linked, with many possible causes (often overstated by testosterone clinics):
Fatigue: poor sleep, depression, chronic illness, iron deficiency and an underactive thyroid are more likelyBrain fog: sleep, stress, nutritionTrouble losing weight: diet, exercise, sleep, metabolic healthLow mood: depression, anxiety, sleepPoor concentration: sleep, attention-deficit/hyperactivity disorder (ADHD), stress
Low testosterone first, or these conditions first?
Most of the time it runs the other way: obesity, depression and sleep apnea push testosterone down, rather than low testosterone causing them.
Obesity: aromatase in fat converts testosterone into estrogen, and leptin released by fat also presses on the axis; when weight comes down, testosterone comes back up somewhatObstructive sleep apnea (): low oxygen and chopped-up sleep lower testosterone productionDepression and chronic stress: persistently high cortisol holds down the hypothalamic-pituitary-gonadal axis (HPG axis)Long-term opioid painkillers: they hold down the very top of this axis, causing central low testosteroneMetabolic syndrome and type 2 diabetes: the protein that carries testosterone in the blood () falls, so total testosterone looks low while free testosterone may still be normal
In practice
An assessment starts with symptoms, a physical exam and lifestyle; blood tests come afterIf you do test: draw in the morning, repeat the test, and measure , , SHBG, and (PSA) at the same timeDon't jump straight to "test testosterone, and start if it's low" — that is how testosterone clinics sell, not evidence-based medicine
Numbers · Normal range, and when decline is disease
How to use these numbers: they are for ruling out, not for diagnosing. A value inside the range mostly lets you set testosterone aside and look for other causes; a value outside it only tells you to keep looking — on its own it has not proved anything yet.Testosterone ranges for healthy adult men
Total testosterone: 264–916 ng/dL (varies slightly between labs). The range was set in healthy, non-obese young men, and the Endocrine Society's 2018 guideline adopts itFree testosterone: 9–30 ng/dL (calculated with the Vermeulen formula)A blood draw at 7–10 am catches the day's peak; a single low reading does not countTest at least 2 times, 4–6 weeks apart, to rule out a passing dip
The width of the range is itself information: among healthy men of the same age, the high end can be several times the low end, and neither man is ill. So "I'm lower than someone else" is not a diagnosis. The questions that matter are whether you have dropped from your own earlier level, and whether matching symptoms are there.
Is a slow decline in testosterone a disease?
Not necessarily. Compared with age 35, a healthy 65-year-old man's testosterone is on average 25–50% lower; that is normal physiology. Treatment is considered only when symptoms and lab results agree:
Low testosterone without symptoms: watch it, no treatment neededSymptoms with testosterone in the middle band (300–400 ng/dL): change lifestyle firstClear LOH (low testosterone plus the three sexual symptoms): see an endocrinologist or urologist
Read the three lines together and one logic holds: treatment targets symptoms, and the lab value is only there to confirm whether a symptom is worth blaming on the hormone. Topping up a low number in someone with no symptoms leaves nothing to get better; topping up a symptomatic man whose number is normal only makes the upstream turn its own output down. That is why the guideline states both conditions together instead of a single threshold.
Chapter 2
Why testosterone tests mislead
The testosterone number on a lab slip is far more slippery than most people think.
It slips at the blood draw: testosterone secretion follows sleep. Early morning is the day's high point, and the level drops clearly by afternoon and evening; a cold, major surgery or an extreme training session can also hold it down for a while. Draw blood from the same man on two different days and the numbers can be far apart. So a single low value often measured the timing, not the body.
It slips in what the number means: only about 2% of the testosterone in blood is fully free. The rest is held in two batches — about 44% gripped tightly by a transport protein, (SHBG), and about 54% hanging loosely on albumin. Albumin holds loosely and lets go as blood passes through tissue, so that batch plus the free 2% is the part the body can actually use. Obesity and insulin resistance lower SHBG, so total testosterone looks low while the working share may have barely moved.
The level above that is the real point: obesity, sleep apnea, long-term opioid use, depression and chronic disease are often the cause that pushes testosterone down, not its result — and most of them can be released.
It slips at the blood draw: testosterone secretion follows sleep. Early morning is the day's high point, and the level drops clearly by afternoon and evening; a cold, major surgery or an extreme training session can also hold it down for a while. Draw blood from the same man on two different days and the numbers can be far apart. So a single low value often measured the timing, not the body.
It slips in what the number means: only about 2% of the testosterone in blood is fully free. The rest is held in two batches — about 44% gripped tightly by a transport protein, (SHBG), and about 54% hanging loosely on albumin. Albumin holds loosely and lets go as blood passes through tissue, so that batch plus the free 2% is the part the body can actually use. Obesity and insulin resistance lower SHBG, so total testosterone looks low while the working share may have barely moved.
The level above that is the real point: obesity, sleep apnea, long-term opioid use, depression and chronic disease are often the cause that pushes testosterone down, not its result — and most of them can be released.
Mechanism · Five measurement traps and why each exists
Measuring testosterone looks simple, but there are several traps; any one of the five below can make a normal man test low.Trap 1 · Timing
Testosterone has a clear daily rhythm: it peaks at 7–10 am and can be 30–40% lower by afternoon and evening (most marked in young men; the rhythm flattens with age)So the blood should be drawn in the morningBoth the Endocrine Society 2018 guideline and the American Urological Association (AUA) 2018 guideline require this
The daily rhythm is set by the upstream beat. The hypothalamus releases its signal in small pulses, densest during night-time sleep; the pituitary follows with waves of , so the testes produce the most from the second half of the night into early morning. After a full day awake and moving, the pulses thin out and the number falls on its own. So an afternoon draw has not caught a truer you; it has caught the trough of this rhythm. This also explains why chronically poor sleep pulls testosterone down: the day's highest-output window has been torn up.
Trap 2 · A single test
Testosterone varies a lot on its own; the same man may test at 600 ng/dL one day and 350 ng/dL the nextGuidelines require at least 2 draws, 4–6 weeks apart, both low, before it counts
Trap 3 · Acute states
Acute illness (flu, a cold, after major surgery): testosterone drops for a whileHard training combined with rapid weight loss: testosterone also drops temporarilyA diagnosis should not be made at these times
The acute drop has a reason. When the body is dealing with infection or injury, it pulls resources away from long-term building, and testosterone is the very signal that directs building, so it is turned down first. The low value at that moment faithfully shows that you are ill; it cannot tell you where your baseline will sit once you recover.
Trap 4 · Total versus free testosterone ( decides)
Total testosterone has three parts: about 44% bound tightly to sex hormone-binding globulin (SHBG), about 54% hanging loosely on albumin, and about 2% freeThe free share is biologically active; free plus albumin-bound testosterone together are called bioavailable testosteroneWhen SHBG is high (low insulin levels, more estrogen, an overactive thyroid), total testosterone looks high while free testosterone may be merely normalWhen SHBG is low (insulin resistance, type 2 diabetes, obesity, an underactive thyroid), total testosterone looks low while free testosterone may still be normalThere is a mirror image in women: in polycystic ovary syndrome (), insulin resistance lowers SHBG, free testosterone rises, and signs of androgen excess appear (the chapter How insulin drives up androgens in the Polycystic Ovary Syndrome story)The Endocrine Society's 2018 guideline advises that when total testosterone is near the lower limit of normal, or a condition that alters SHBG is present, free testosterone should be obtained, either measured directly by equilibrium dialysis or estimated with an accurate formula (the Vermeulen formula is the common one) from total testosterone and SHBG
Why doesn't the SHBG-held share count? To do its work, testosterone has to cross the cell membrane and find its receptor inside, and the share bound to SHBG is held too tightly to get in. The albumin batch is different: it holds loosely and lets go as blood passes through tissue, so it is counted with the free 2% as the bioavailable share — which is why "only the free fraction counts" is a widespread error. Think of SHBG as porters with a tight grip and albumin as porters who put things down easily: the first group's cargo rarely reaches the shelf, while the second group unloads as they pass. Change the number of SHBG porters and the total-inventory reading moves, while the stock on the shelf may not have moved at all. That is why total and free testosterone can point to opposite conclusions, and why heavier men are especially easy to misread as low on total testosterone.
Trap 5 · Test method
Direct immunoassays are cheap but inaccurate, especially at low valuesLiquid chromatography–tandem mass spectrometry (LC-MS/MS) is the gold standard and agrees well between labsUse LC-MS/MS where possible; do not diagnose on a single low immunoassay result
Line the five traps up and they point to the same thing: a testosterone number only means something once its conditions are stated — when it was drawn, how many times, what state the body was in, which method was used, and whether SHBG was measured alongside. Without those, the number is just a number.
mulhall-2018-aua-testosterone
Clinical · Five reversible causes and where each acts
Even when the number is measured correctly, the low value usually does not mean the testes themselves have failed. More often one of the things below is pressing the brake upstream. Each one can potentially be released.Five reversible causes to check before any evaluation
1. Obesity
In population data, every 5 points higher on body mass index () goes with total testosterone about 100 ng/dL lower on average (an observed association)Aromatase in visceral fat converts testosterone into Follow-up data from EMAS (Camacho 2013, an observational cohort) show that men who lost more weight had a larger rise in testosterone. A commonly quoted figure is "lose 5–10% of body weight, gain about 15–25% in testosterone", but the paper's abstract gives only the direction and a proportional relationship, not this number, so treat it as a rough order of magnitude
Read this as a circle, not a line. Fat tissue contains aromatase, which converts passing testosterone into estradiol on the spot; and estradiol is the most sensitive brake in the negative-feedback loop, turning back to lower how often the hypothalamus signals and how much the pituitary sends. Less LH means fewer orders reaching the testes, so testosterone falls further; lower testosterone makes muscle harder to keep and visceral fat easier to gain; a little more fat means a little more aromatase, and the brake goes down further. So weight loss here is not a side benefit. It takes the foot off that brake.
2. Obstructive sleep apnea ()
In observational studies, men with moderate to severe OSA had testosterone 20–30% below men of the same ageWhat to do: screen yourself first with the STOP-BANG questionnaire (a screening questionnaire for snoring and breathing pauses), confirm with an overnight sleep study () if needed, and once diagnosed, use a breathing machine ()
Following on from the daily rhythm: testosterone's production peak depends on unbroken night-time sleep. People with OSA are woken over and over through the night as the airway collapses, so sleep is cut into fragments, with bout after bout of low oxygen on top — the day's highest-output window has effectively been taken apart. By the mechanism, opening the airway should bring the window back and the number with it; but in studies of CPAP treatment, the change in testosterone has been inconsistent. Treating OSA is well worth doing for its own sake; just do not count on it as a way to raise testosterone.
3. Long-term opioid use
Opioids directly hold down the release of GnRH, causing central low testosteroneSome reports put the share of long-term opioid users with low testosterone as high as about 75%What to do: discuss reducing the dose or switching with the pain team
Opioids act at the very top: they hold down the pulse generator in the hypothalamus. The command is never sent, the pituitary does not release LH, and the testes, fully intact, never receive an order. That is what "central" means: the workshop is not broken; the order never arrived. How can you tell? Look at LH: in this situation LH does not rise (the chapter Whether to test, when to see a doctor explains how LH separates the two roads).
4. Depression and chronic stress
Cortisol rises and holds down the HPG axisWhat to do: psychotherapy (such as cognitive behavioral therapy, ) and, where needed, antidepressants (, )
Stress takes a road close to the opioid one: chronically high cortisol also holds down the hypothalamic pulse generator. The body's logic is blunt — in a state of ongoing threat, reproduction and building muscle are not urgent, so the whole axis is turned down. This is also why these men's testosterone often comes back on its own once the source of stress is removed, without needing to be topped up.
5. Chronic disease (type 2 diabetes, chronic liver disease, HIV infection, chronic kidney disease)
What to do: control the underlying disease
This group moves the reading in more than one direction. Insulin resistance, type 2 diabetes and fatty liver lower , so total testosterone looks low while free testosterone may not be; cirrhosis and HIV infection, by contrast, often raise SHBG, so total testosterone can look normal while free testosterone is already low. Only by measuring SHBG and calculating free testosterone can you tell which is happening.
Line the five up and they sit on different links of the same chain: obesity works on the negative-feedback brake, OSA on the production time window, opioids and stress on the pulse generator at the top, and chronic disease on the transport protein in the blood. None of them is the testicular workshop itself breaking down — which is exactly why they are reversible.
In practice: before considering , it is advisable to deal with these five causes for 6–12 months first. Quite a lot of "low testosterone" returns to the normal range once they are dealt with.
Chapter 3
Start with lifestyle
For most men who do not meet the bar for LOH, changing lifestyle is more worth doing first than adding testosterone: what it moves is not the number on the lab slip but the machine upstream.
Losing belly fat means less of the enzyme in fat that converts testosterone into , so the brake in the negative-feedback loop eases and the pituitary is willing to send its commands again. Sleeping enough and getting snoring checked gives back to the body the night-time sleep window when testosterone output is highest. Strength training and eating enough protein catch testosterone's signal at the receptor end, so the building genes it switches on have raw material to work with. Bringing chronic stress down lifts the hand that cortisol presses on the same axis.
The four look unrelated, but each moves a different link of the same chain: the command at the top, the production time window, the execution downstream, and the brake that has been held down all along. By the mechanism, that is why they add up — and why no single one of them is enough.
Losing belly fat means less of the enzyme in fat that converts testosterone into , so the brake in the negative-feedback loop eases and the pituitary is willing to send its commands again. Sleeping enough and getting snoring checked gives back to the body the night-time sleep window when testosterone output is highest. Strength training and eating enough protein catch testosterone's signal at the receptor end, so the building genes it switches on have raw material to work with. Bringing chronic stress down lifts the hand that cortisol presses on the same axis.
The four look unrelated, but each moves a different link of the same chain: the command at the top, the production time window, the execution downstream, and the brake that has been held down all along. By the mechanism, that is why they add up — and why no single one of them is enough.
Numbers · Five interventions and how much each moves
1. Losing weight, especially belly fatThe more weight men lose, the more their testosterone rises (observational data; for the size of the effect, see the chapter Why testosterone tests mislead)Waist size is more worth watching than body mass index (): 5 cm off the waist says more than a small drop in BMIMechanism: less aromatase in visceral fat, less leptin resistance, better insulin sensitivityHow: any calorie deficit you can sustain, while eating enough protein to keep muscle
2. Strength training (resistance training)
2–3 sessions a week, built on big compound lifts, with the load raised graduallyAfter a session testosterone rises briefly by 15–30% and soon falls back; the long-term gain is keeping muscleThere is no need to follow online "testosterone-boosting workout" marketing; standard strength training is enoughIt works together with protein: leucine starts muscle protein synthesis through a signaling pathway called (the chapter Muscle protein synthesis in the Protein & Amino Acids story)
3. Sleep
In a small experiment, healthy young men who slept only 5 hours a night for a week had daytime testosterone 10–15% lowerFor people diagnosed with obstructive sleep apnea (), a breathing machine () is the single most effective treatment for it7–9 hours a night is the baseline
4. Managing stress
Chronically high cortisol holds down the HPG axisMindfulness, belly breathing, exercise and time with other people all help bring cortisol downCounseling (such as cognitive behavioral therapy, ) helps with stress and depression, and testosterone may rise indirectly as a result
5. Drinking less, not smoking
Long-term heavy drinking (more than 21 units of alcohol a week, as the UK counts them): testosterone falls and estrogen risesSmoking may nudge testosterone up in the short term, but overall it harms the heart and blood vessels and raises cancer risk
On nutrition: there is no "miracle food for testosterone", but a few things are worth checking:
Enough zinc: the US Recommended Dietary Allowance () for men is 11 mg a day; supplement only if you are deficient (oysters, red meat, pumpkin seeds)Enough vitamin D: a serum of at least 20 ng/mL (50 nmol/L) is adequate for most people; correct a deficiencySome healthy fat (olive oil, fish, nuts): a very low-fat diet lowers testosteroneProtein at 1.2–1.6 g/kg (the Protein & Amino Acids story)There is no need to go keto for testosterone; no evidence supports it
A few places in these numbers are worth pausing on.
The rise after training is not your everyday level. It lasts a short time and is the stress response of the session itself. What is actually worth something is the muscle kept through long-term training — more muscle, better insulin sensitivity, less visceral fat, and a lighter aromatase brake in the fat. So strength training helps testosterone the long way round, not through that spike.
Why a very low-fat diet lowers testosterone is not mysterious either: testosterone starts as cholesterol, and the Leydig cells in the testes reshape cholesterol into testosterone step by step. If the raw material stays short, the workshop is held back. The reverse does not hold — once there is enough raw material, adding more does not make extra testosterone, just as a bakery with plenty of flour does not bake more bread because another truckload arrives.
Alcohol presses from both ends: at one end it interferes with the production steps in the testes; at the other it pushes more testosterone down the path that turns it into estrogen. So lowering testosterone and raising estrogen are not two separate effects; they are two sides of the same one.
Myth · Why testosterone boosters mostly fail
No use, or oversold by marketingAshwagandha: a small effect on chronic stress; for testosterone there are only scattered, weak signals — not enough to use it as a testosterone boosterMaca: libido may improve subjectively, but testosterone does not change noticeablyTribulus: several randomized trials were negativeZMA (a combination of zinc, magnesium and vitamin B6): pointless for healthy people who are not short of these nutrientsAssorted "testosterone booster" blends: the evidence for them is scarce and of low qualityDehydroepiandrosterone (DHEA): not recommended as a testosterone booster (it has side effects, and how much of it turns into testosterone in the body is unpredictable)
The pitch for these products shares one flaw: it skips the question of which link it acts on. The testosterone chain has only a few places that can be moved — how often the hypothalamus pulses, the production steps in the testes, the share held by in the blood, and the receptor inside the cell. Anything that genuinely raises testosterone has to say which link it moves, and why that link happens to be the one stuck in you. If it cannot say which link, that is usually because it moves none of them.
There is a deeper layer: testosterone is governed by negative feedback. Even if something did push blood testosterone up a little, the upstream would read the rise and cut its commands to pull it back. The loop itself limits how far "adding a little from outside" can go — unless you add at drug-dose levels, and that is , not a supplement. The road that actually works is moving whatever is pressing the brake (losing weight, treating , lowering cortisol, giving sleep back) and letting the body reset its own output. The first fights a negative-feedback loop; the second works with it.
For men aged 40–60 whose complaint is simply "low energy and trouble losing weight", 6 solid months of lifestyle change often means they never need to get as far as adding testosterone.
In practice · A 6-month lifestyle plan
Here the lifestyle factors that affect testosterone are arranged into a 6-month plan you can follow. Many of the problems described as "low-T symptoms" improve clearly once this is done well, and never get as far as .Priorities, by return on effort:
First: lose belly fat. If your waist is over the cut-off, this is the highest-return step. Losing 5–10% of body weight brings testosterone back up somewhat, through less aromatase in visceral fat and better insulin sensitivity. Watching your waist tells you more than watching your weightSecond: sleep well, and check for sleep apnea. In a small experiment, a week of only 5 hours a night lowered testosterone by 10–15%. If you snore and are sleepy by day, screen yourself with the STOP-BANG questionnaire first and get a sleep study if needed; once is confirmed, a breathing machine () is the single most effective treatment for it. Getting back to 7–9 hours a night is the baselineThird: strength training plus enough protein. 2–3 sessions a week of big compound lifts with gradually heavier loads, together with 1.2–1.6 g/kg of protein a day, keep muscle and improve insulin sensitivity. There is no need to follow "special testosterone-boosting workout" marketing; standard strength training is enoughFourth: lower cortisol. Chronically high cortisol holds down the HPG axis. Mindfulness, belly breathing, regular exercise and counseling () all help; as mood improves, testosterone often rises indirectlyBaseline habits: drink less, don't smoke. Long-term heavy drinking (more than 21 units of alcohol a week) lowers testosterone and raises estrogen
Don't be led astray on nutrition: there is no "miracle food for testosterone". Making sure you are not short of zinc (supplement only if deficient), that vitamin D is adequate ( at least 20 ng/mL, i.e. 50 nmol/L) and that you eat some healthy fat (a very low-fat diet actually lowers testosterone) is enough. For ashwagandha, maca, tribulus, ZMA and assorted "testosterone booster" blends, the evidence in healthy men is weak or absent — don't spend your money there.
How to judge it: follow the full plan for 6 months, then decide whether to test testosterone or see a doctor. Dealing with the reversible causes first is the evidence-based path; the reverse, "test testosterone and then start TRT", is how testosterone clinics sell, not medicine.
Chapter 4
When to use testosterone, and risks
Testosterone replacement therapy () does work when there is a genuine indication, but few people actually meet one, and its costs are often played down.
The heaviest cost: your own production line stops. Testosterone's negative-feedback loop turns against you here — testosterone added from outside pushes the blood level up, the upstream reads "enough", and it stops sending commands. Once the commands stop, the local testosterone concentration inside the testes, far higher than in the blood, collapses — and sperm can only develop in that high concentration. So sperm production falls sharply and the testes become softer and smaller. The number in the blood looks fine, while inside the testes the lights are off.
That is why men who want children should not go straight onto TRT, and should first consider treatments that push from upstream (such as clomiphene or hCG): they raise testosterone while protecting sperm production.
It is also why, once TRT starts, many men stay on it long term: stopping the outside supply is easy, but getting an upstream that has been idle for a long time to run on its own again takes months or longer, and a return to the old level is not guaranteed.
The heaviest cost: your own production line stops. Testosterone's negative-feedback loop turns against you here — testosterone added from outside pushes the blood level up, the upstream reads "enough", and it stops sending commands. Once the commands stop, the local testosterone concentration inside the testes, far higher than in the blood, collapses — and sperm can only develop in that high concentration. So sperm production falls sharply and the testes become softer and smaller. The number in the blood looks fine, while inside the testes the lights are off.
That is why men who want children should not go straight onto TRT, and should first consider treatments that push from upstream (such as clomiphene or hCG): they raise testosterone while protecting sperm production.
It is also why, once TRT starts, many men stay on it long term: stopping the outside supply is easy, but getting an upstream that has been idle for a long time to run on its own again takes months or longer, and a return to the old level is not guaranteed.
Mechanism · Why added testosterone halts sperm production
Put the three approaches on the same chain and the difference is plain.Adding testosterone from outside ()
The drug goes into the blood. Once blood testosterone is high, the signal the hypothalamus and pituitary read is "enough", so GnRH pulses thin out and and fall. The problem: sperm development does not need the blood concentration. It needs a much higher local concentration, supplied on the spot by the Leydig cells inside the testes — and that local concentration depends entirely on the orders LH sends. With no orders, the local concentration collapses, and sperm development on the Sertoli-cell side breaks off halfway. That is why a blood test can show plenty of testosterone while a semen analysis finds almost no sperm — the two numbers are not measuring the same place at all.
Human chorionic gonadotropin (hCG)
Its shape is close to LH, like a key that fits the same lock. It settles directly on the Leydig cells and fills in the order, bypassing the suppressed upstream. The testes keep producing, the high local concentration holds, and sperm production continues. So it can raise blood testosterone without shutting the workshop.
Clomiphene
Takes a third road: it blocks 's receptors in the hypothalamus and pituitary. Estradiol is the most sensitive brake in negative feedback — plug the brake's connector and the upstream wrongly reads the hormone as short, so it turns up GnRH pulses and LH together. The whole axis, top to bottom, is still the body's own, so sperm production is usually preserved.
The same logic explains why recovery after stopping is slow
A pathway left unused for a long time — from the hypothalamus's pulse rhythm to how the testicular cells respond to LH — needs time to recalibrate, and is not guaranteed to return to where it was. So starting without a clear indication is a decision that is hard to undo, not the kind you reverse the day after stopping the drug.
Red blood cells sit on the same map
Testosterone already pushes up the signal that makes red blood cells. Testosterone from outside lifts the blood level beyond what the body normally reaches, the signal is pushed up with it, the hematocrit (the share of the blood made up of red cells) rises, the blood thickens, and the risk of clots may rise too. So monitoring red cells is not paperwork; it tracks a consequence with a clear mechanism. And taking blood off when needed is not a wellness gesture; it thins the thickened blood back down.
Clinical · Indications, risks and formulations
The indications are actually narrow (Endocrine Society 2018 guideline). The clearest is classical hypogonadism: a congenital or acquired structural problem in the hypothalamus-pituitary unit or the testes, such as Klinefelter syndrome, undescended testes, damage after chemotherapy, or a pituitary tumor. The late-onset hypogonadism (LOH) that gets discussed so often also has a high bar. Total testosterone has to be low on at least 2 morning blood draws (a common cut-off is < 300 ng/dL; the Endocrine Society 2018 guideline uses the lower end of the 264–916 ng/dL range); there must be matching symptoms, of which the three sexual symptoms (low libido, lost morning erections, weaker erectile function) carry the most weight; and the five reversible causes (obesity, sleep apnea, opioids, depression, chronic disease) must already have been checked — only then can be considered. Short of that, the evidence-based answer is to complete 6 months of lifestyle change first, not a shot. In one-year trials in men over 65 with low testosterone, the benefits of TRT that the evidence actually supports fall mainly on sexual function and ; mood improved only a little, and energy and memory were not supported by the trials — all far smaller than the marketing suggests.Notice that the two kinds of indication are different at the level of mechanism. In classical hypogonadism a link in the chain is truly broken and cannot be repaired (testes removed or damaged by chemotherapy, or a growth in the pituitary), and the testosterone put in replaces a link that is genuinely missing. In LOH the whole chain is still there, only running slower or held down by something else — topping it up goes around whatever is holding it down instead of solving it. That difference is why the same drug is replacement therapy in the first group and closer to an enhancer in the second.
The impact on fertility is the point most often left unsaid. Testosterone from outside shuts down and through negative feedback, and sperm production in the testes stalls with them: in most users, sperm counts fall sharply within 4–6 months (often by more than 90%), recovery after stopping takes months or longer, and some men do not recover fully. So men who want children should not start TRT directly; they should first consider clomiphene or hCG, which can raise testosterone while keeping sperm production going. For someone already on TRT who now wants children, the usual approach is to stop, add hCG under medical supervision, and wait 6–12 months — and full recovery is not guaranteed.
Other risks to monitor: a rise in red blood cells may raise the risk of clots, so blood counts need regular checks, with blood taken off if needed; men with known prostate cancer should not use it, and should be checked regularly during treatment; existing sleep apnea may get worse; and there are side effects such as breast tenderness, acne and hair loss. On the heart: in the TRAVERSE trial (Lincoff 2023, n=5,246, men with low testosterone and raised cardiovascular risk), TRT did not increase major cardiovascular events (, HR, 0.96 — practically no difference from placebo), but atrial fibrillation, acute kidney injury and pulmonary embolism were slightly more common. It is often described as a 4-year trial; in fact mean follow-up was 33 months and mean time actually on treatment was 21.7 months — a real difference, because it decides whether the trial can speak to longer-term risk. Formulations include gel, intramuscular injections every 1–2 weeks, small frequent injections under the skin, and pellets implanted under the skin every few months; each trades fluctuation against convenience, and the doctor chooses according to the case.
The difference between formulations comes down to the shape of the blood-level curve. The longer the gap between injections, the bigger the swing between peak and trough: some men feel wired on the peak days and back where they started on the trough days, and the higher the peak, the more testosterone aromatase converts into — breast tenderness usually shows up during the peak. Frequent small doses and gel flatten the curve; the cost is doing it more often, and gel can rub off onto other people (contact transfer). This is not about which one is better; it is trading steadiness for convenience.
In practice: avoid testosterone clinics and online TRT services — many of them look only at the lab value and do not check the five reversible causes. If you do use TRT, see an endocrinologist or urologist for a full evaluation and long-term monitoring. If you want children, consider clomiphene or hCG first. Remember that TRT is often a long-term treatment: once it starts, your own HPG axis does not easily recover by itself.
Myth · Will TRT make me 25 again?
The picture testosterone clinics and anti-aging marketing love to sell: one testosterone shot, and energy, muscle, libido, brainpower and mood all come back. Set that against the actual trial data item by item and the picture turns out to be heavily airbrushed.What is genuinely shown to do comes from the TTrials, a set of (790 men over 65 with low testosterone, treated for one year):
Sexual function: libido, erections and satisfaction improved significantly in the statistical sense — TRT's most certain benefit (Snyder 2016, the main paper): improved, but this result comes from a different TTrials paper (Snyder 2017, *JAMA Intern Med*, n=211: volumetric bone density of the spine's trabecular bone rose 7.5%, versus 0.8% on placebo), not the main oneMemory and cognition: no improvement after a year of treatment — again from a different paper (Resnick 2017, *JAMA*, n=493). This is the paper that punctures the claim that "TRT fixes brain fog"Energy and vitality: no significant benefit on the fatigue scale in the main paperWalking distance: no significant difference within the physical function trial itself; significant only when all three trials were pooledMood and depressive symptoms: slightly better than placebo — mind the direction. The main paper reports a "small improvement", not "no effect". Calling it no effect is the most common misquotation of this trial, and it backfires on anyone debunking the marketing: the other side only has to pull up the paper and the whole argument loses credibility. The honest version is that the effect is real but small, and the men enrolled had not been diagnosed with depression — it cannot support "a shot that cures low mood"
Costs the marketing plays down:
Fertility: testosterone from outside shuts down and through negative feedback; in most users sperm counts fall sharply within 4–6 months (often by more than 90%), and some men do not fully recover after stopping. People who want children should not start TRT directly, and should consider clomiphene or hCG first — testosterone clinics often leave this outExcess red blood cells: a rising hematocrit may raise the risk of clots, so it needs monitoring, with blood taken off if neededProstate: men with known prostate cancer should not use it; should be checked regularly during treatmentLong-term dependence: once started, the HPG axis does not easily recover by itself, so treatment often continues long term
So the accurate picture is this: with a genuine indication (classical hypogonadism; or total testosterone below 300 ng/dL on at least 2 morning draws, plus matching sexual symptoms, with the five reversible causes checked), TRT does work, and the main payoff is in sexual function and bone. But for someone who "just wants more energy, or to feel young again", and does not meet guideline criteria, the evidence-based answer is to complete the 6-month lifestyle plan first, not to get a shot at a testosterone clinic. Treat TRT as a prescription drug for a specific deficit, not an anti-aging supplement.
Chapter 5
Whether to test, when to see a doctor
The whole thing comes down to one line: deal with the reversible causes first, then touch the hormone.
Before deciding whether to test testosterone, there are two gates you can pass on your own. The first is symptoms: the ones truly tied to testosterone are the sexual ones — libido, morning erections, erectile function — because the brain areas that run these have the densest androgen receptors. If your list is only tiredness and low drive, don't test yet. The second is the reversible causes: waist size, snoring, long-term opioid use, mood, chronic disease. If one of them applies, deal with it first; testosterone often comes back on its own.
See a doctor promptly if you have
Breast pain plus a lump (to rule out breast cancer and male breast enlargement, gynecomastia)Narrowing of your field of vision plus headache (to rule out a pituitary tumor)An unexplained rise in (for a prostate evaluation)Sudden severe fatigue plus marked weight loss (to screen for chronic disease)Infertility plus low testosterone (see a reproductive urology specialist)
Before deciding whether to test testosterone, there are two gates you can pass on your own. The first is symptoms: the ones truly tied to testosterone are the sexual ones — libido, morning erections, erectile function — because the brain areas that run these have the densest androgen receptors. If your list is only tiredness and low drive, don't test yet. The second is the reversible causes: waist size, snoring, long-term opioid use, mood, chronic disease. If one of them applies, deal with it first; testosterone often comes back on its own.
See a doctor promptly if you have
Breast pain plus a lump (to rule out breast cancer and male breast enlargement, gynecomastia)Narrowing of your field of vision plus headache (to rule out a pituitary tumor)An unexplained rise in (for a prostate evaluation)Sudden severe fatigue plus marked weight loss (to screen for chronic disease)Infertility plus low testosterone (see a reproductive urology specialist)
In practice · Whether to test, in five steps
Is my testosterone low? A five-step self-checkStep 1 · Checklist
Tick the items below; at least 3 are needed before testosterone is worth testing:
Clearly reduced libido lasting at least 6 monthsMorning erections clearly reduced or goneWeaker erectile functionUnexplained loss of muscle strength (training and diet unchanged)Chronic fatigue (after sleep problems, depression and chronic illness have been ruled out)Unexplained weight gain (especially around the belly)
Fewer than 3 ticked: no need to test testosterone; put your effort into lifestyle, sleep and mood. Even with 3 ticked, if they are all among the last three (strength, fatigue, weight), go back to Step 2 first: those three more often have other causes.
Step 2 · Check the five reversible causes
A body mass index () of 28 or more, or a waist of 90 cm or more in men (China's adult cut-offs; internationally, BMI 30 and a waist of 102 cm are common): lose 5–10% of your weight firstSnoring plus daytime sleepiness: assess for sleep apnea with the STOP-BANG questionnaireLong-term opioids or sedatives: discuss with the doctor who prescribes themChronic stress plus mood problems: counseling, such as cognitive behavioral therapy ()Type 2 diabetes or another chronic disease: control the underlying disease
It is advisable to deal with these for 6–12 months first, then evaluate testosterone.
Step 3 · Blood tests (if you do want to test)
7–10 amAvoid a period of acute illness, the 2 weeks after surgery, and a day of extremely hard trainingMeasure total testosterone, free testosterone (calculated with the Vermeulen formula), , , , and Method: liquid chromatography–tandem mass spectrometry (LC-MS/MS)Repeat the test 1 time, 4–6 weeks later
Step 4 · Reading the results
Total testosterone above 400 ng/dL: normal; look for other causesTotal testosterone 300–400 with normal free testosterone: most likely a borderline SHBG issue; no neededTotal testosterone below 300 on at least 2 occasions, 3 or more sexual symptoms, and reversible causes dealt with: see an endocrinologist or urologistTotal testosterone below 200: abnormal whether or not reversible causes are present; it should be evaluated
Step 5 · Treatment paths
Classical hypogonadism: TRTLOH and wanting children: clomiphene or hCG (not TRT)LOH and no plans for children: discuss TRT formulation and monitoring with your doctor"Just want more energy", but not meeting guideline criteria: lifestyle first, no TRT
The order of this table is not arbitrary. It asks about symptoms first, then reversible causes, and draws blood last, because each earlier step is cheaper and explains more people. A test-first process sends a large number of men who are only sleeping badly or over a waist cut-off down an expensive road that does not solve their problem; pass the first two gates, and the men who still need to go further are already few — which fits with true LOH affecting only about 2% of men.
Red flag · What each see-a-doctor sign points to
The five see-a-doctor signs listed at the start of the chapter Whether to test, when to see a doctor are not a random pick of "more serious symptoms". Each one points to a specific place, and none of them is explained by "low testosterone" — which is exactly why they are listed on their own.Narrowing field of vision plus headache → the pituitary
The pituitary sits in a small bony pocket at the base of the brain, and the optic nerves from the two eyes cross just above it (the optic chiasm). When something grows on the pituitary, this crossing is often the first thing pushed on; what shows up is the outer field of vision narrowing first on both sides, like wearing blinkers that keep getting deeper. At the same time it can scramble the whole hormone axis from the top, so low testosterone and a vision problem can arrive together. What makes this sign so valuable is that it is one of the few clues linking low testosterone directly to a lesion that can be located.
Breast pain plus a lump → the balance of androgens and estrogens
Men have breast tissue; androgens normally keep it from developing. When testosterone falls, or the share converted to by aromatase rises (obesity, liver disease and some medicines all do this), the balance tips and the gland starts to grow — you can feel it, and pressing it hurts. What matters: a lump on one side that is hard, off-center from the nipple or comes with skin changes is not the same thing as this symmetric growth on both sides, and a doctor has to tell them apart.
An unexplained rise in → the prostate
Prostate growth is driven by androgens throughout life (more precisely, by testosterone after it has been converted to dihydrotestosterone, DHT), so any evaluation that involves testosterone looks at the prostate too. This does not mean testosterone caused something; it means that before you change a hormone, you need to know the current state of that gland.
Sudden severe fatigue plus marked weight loss → look for another disease
This combination points the opposite way from typical testosterone decline: men whose testosterone falls slowly usually end up, slowly, with weight going up (especially around the belly), not dropping weight in a short time. So when this cluster appears, the first job is to rule out another whole-body problem, not to fit it onto low testosterone. Symptoms that point the opposite way are a strong clue; don't treat them as a variant of the same thing.
Infertility plus low testosterone → first separate the upstream from the testes
This is also why the blood tests include and . If testosterone is low and LH and FSH are high, the upstream has been pushing harder and the orders keep going out — the problem is the testicular workshop itself. If testosterone is low and LH and FSH are not high, or even low, the orders were never sent, and the problem lies in the hypothalamus or pituitary. The same low testosterone has, in these two cases, entirely different causes, next tests and treatments: long-term opioid use, obesity and pituitary disease belong to the second group; damage after chemotherapy, undescended testes and Klinefelter syndrome belong to the first. So LH is not a filler item on the lab slip; it is the fork that separates two completely different roads.
Background · Where the testosterone chain leads next
The testosterone chain connects to several body systems, and a few stories on the site pick it up from different directions:The chapter Muscle protein synthesis in the Protein & Amino Acids story: the building line testosterone switches on in muscle, and how leucine starts itThe chapter Hormones that shape bone in the Bone System story: the step where aromatase in bone converts testosterone into , which then holds back the osteoclastsThe chapter Metabolic syndrome: five signs in the Endocrine System story: the loop formed by fat, aromatase and negative feedback, and how insulin resistance and weight loss move testosteroneThe chapter Plaque cascade in the Cardiovascular System story: the background for any discussion of whether testosterone treatment is safe for the heartThe chapter What insomnia is and why it happens in the Insomnia story: testosterone output depends on night-time sleep, and poor sleep pulls it down
Follow any one of them and you run into the same hypothalamic-pituitary-gonadal axis (HPG axis) again.
Back to the question this story started with: the name andropause describes something real (testosterone falling slowly with age), but it is not a male version of menopause. By the EMAS definition, true LOH affects only about 2% of men; more of the symptoms filed under "low testosterone" improve clearly with serious lifestyle change. The testosterone-clinic industry has systematically widened the indications; the evidence-based approach runs the other way: treat testosterone as a prescription drug for a specific deficit, with a full evaluation and long-term monitoring when there is a genuine indication.
References · 9
- Wu, F. C. W., Tajar, A., Beynon, J. M., Pye, S. R., Silman, A. J., Finn, J. D., et al. (2010). Identification of late-onset hypogonadism in middle-aged and elderly men. The New England Journal of Medicine, 363(2), 123-135. 10.1056/NEJMoa0911101
- Bhasin, S., Brito, J. P., Cunningham, G. R., Hayes, F. J., Hodis, H. N., Matsumoto, A. M., Snyder, P. J., Swerdloff, R. S., Wu, F. C., & Yialamas, M. A. (2018). Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 103(5), 1715-1744. 10.1210/jc.2018-00229
- Camacho, E. M., Huhtaniemi, I. T., O'Neill, T. W., Finn, J. D., Pye, S. R., Lee, D. M., et al. (2013). Age-associated changes in hypothalamic-pituitary-testicular function in middle-aged and older men are modified by weight change and lifestyle factors: longitudinal results from the European Male Ageing Study. European Journal of Endocrinology, 168(3), 445-455. 10.1530/EJE-12-0890
- Benjafield, A. V., Ayas, N. T., Eastwood, P. R., Heinzer, R., Ip, M. S. M., Morrell, M. J., et al. (2019). Estimation of the global prevalence and burden of obstructive sleep apnoea: a literature-based analysis. The Lancet Respiratory Medicine, 7(8), 687-698. 10.1016/S2213-2600(19)30198-5
- Snyder, P. J., Bhasin, S., Cunningham, G. R., Matsumoto, A. M., Stephens-Shields, A. J., Cauley, J. A., et al. (2016). Effects of testosterone treatment in older men. The New England Journal of Medicine, 374(7), 611-624. Main TTrials paper: sexual function improved; mood and depressive symptoms slightly better than placebo; no significant benefit for vitality. Bone density and cognition are reported in separate TTrials papers, not this one. 10.1056/NEJMoa1506119
- Snyder, P. J., Kopperdahl, D. L., Stephens-Shields, A. J., Ellenberg, S. S., Cauley, J. A., Ensrud, K. E., et al. (2017). Effect of testosterone treatment on volumetric bone density and strength in older men with low testosterone: A controlled clinical trial. JAMA Internal Medicine, 177(4), 471-479. N=211; 1 year of treatment raised spine trabecular volumetric BMD 7.5% vs 0.8% on placebo. 10.1001/jamainternmed.2016.9539
- Resnick, S. M., Matsumoto, A. M., Stephens-Shields, A. J., Ellenberg, S. S., Gill, T. M., Shumaker, S. A., et al. (2017). Testosterone treatment and cognitive function in older men with low testosterone and age-associated memory impairment. JAMA, 317(7), 717-727. N=493; 1 year of testosterone was not associated with improved delayed paragraph recall, visual memory, executive function, or spatial ability. 10.1001/jama.2016.21044
- Lincoff, A. M., Bhasin, S., Flevaris, P., Mitchell, L. M., Basaria, S., Boden, W. E., et al. (2023). Cardiovascular safety of testosterone-replacement therapy (TRAVERSE). The New England Journal of Medicine, 389(2), 107-117. In 5,246 men 45-80 with low T and CV risk, TRT was non-inferior for MACE but showed more atrial fibrillation, pulmonary embolism, and acute kidney injury. 10.1056/NEJMoa2215025
- National Health and Family Planning Commission of the People's Republic of China. (2013). Criteria of weight for adults (WS/T 428-2013). Health industry standard, issued 2013-04-18, effective 2013-10-01. Table 1, weight classes by BMI in kg/m2: obesity is BMI at or above 28.0; overweight 24.0 up to 28.0; normal weight 18.5 up to 24.0; underweight below 18.5. Table 2, central obesity by waist circumference in cm: pre-central-obesity is 85 up to 90 in men and 80 up to 85 in women; central obesity is 90 or more in men and 85 or more in women. Clause 3.4 puts the waist tape at the midpoint between the lower costal margin and the iliac crest, on the mid-axillary line. Clause 1 limits the standard to adults 18 and over, for epidemiological screening and preliminary clinical diagnosis, and states that it does not apply to some groups, such as athletes and pregnant or postpartum women. www.nhc.gov.cn/ewebeditor/uploadfile/2013/08/20130808135715967.pdf