Falling Testosterone: The Evidence Is Clear. The Cause Is Not.

There is a criticism made of private men's health clinics, and it deserves to be stated properly rather than brushed past.

The criticism is that private clinics put men on testosterone who do not need it. That a man arrives tired, has a blood test, produces a result inside the reference range, and is treated anyway.

Where that happens, the criticism is correct. Treating a number because a man is tired, without establishing why he is tired, is poor medicine. It should be called out, and we would call it out.

But underneath the criticism sits a harder question, and it is asked far less often.

Normal compared with whom?

What the measurements actually show

Across several countries, using different datasets and different methods, researchers have found that men's testosterone concentrations have fallen over recent decades.

The clearest single finding comes from Finland. A study published in 2013 compared 3,271 men aged 25 to 74 across three national health surveys carried out in 1972, 1977 and 2002. Among men aged 60 to 69, mean total testosterone was approximately 21.9 nmol/L in those born between 1913 and 1922, and approximately 13.8 nmol/L in those born between 1942 and 1951. The difference persisted after adjustment for body mass index. The authors were direct about what they could and could not account for, writing that the study offered no explanation for the change they had measured. ^[1]

A much larger Israeli analysis reached a similar conclusion by a different route. Using routine laboratory data from roughly 102,334 men tested between 2006 and 2019, it reported a significant decline that was independent of age. Among men aged 21, mean testosterone fell from approximately 19.68 nmol/L in 2006 to 2009, to approximately 17.76 nmol/L in 2016 to 2019. The authors concluded that rising obesity was unlikely to account for the trend on its own. ^[2]

In the United States, the Massachusetts Male Aging Study followed men across three waves of data collection ending in 2004. It found a substantial decline that was independent of age, and the authors reported that it did not appear attributable to observed changes in explanatory factors, including health and lifestyle characteristics such as smoking and obesity. ^[3]

The pattern is not confined to older men. An analysis of 4,045 adolescent and young adult American males, drawn from the national NHANES survey between 1999 and 2016, found total testosterone significantly lower in the later survey cycles than in 1999 to 2000. Raised body mass index was associated with lower testosterone, as would be expected. The decline nevertheless remained significant among men whose body mass index was normal. ^[4]

Taken together, those four studies cover men born from 1913 through to the late 1990s, with blood drawn between 1972 and 2019. That matters, because it means this is not one generational step that happened somewhere in the middle of the last century and then settled. In every one of those studies, the men measured later come in lower than the men measured earlier, and the most recent of them was still finding it in samples taken in 2019.

Four populations, four study designs, one direction of travel. That is the sort of consistency that makes a finding difficult to dismiss, even where each individual study has limitations. All of these analyses compare measurements taken decades apart, and laboratory methods for measuring testosterone changed over that period. The authors themselves raise this, and it is a real constraint on how confidently any of it can be read.

Where "normal" comes from

A reference range is not a diagnosis. It is a description of how a measurement was distributed within a defined reference population, chosen according to stated criteria.

The most widely used modern range for total testosterone was published in 2017. It gives approximately 264 to 916 ng/dL, which converts to approximately 9.2 to 31.8 nmol/L. It is a more carefully constructed range than most, because it was not simply taken from whoever happened to walk into a laboratory. It was derived from 1,185 men aged 19 to 39 who were not obese and were free of major illness. ^[5]

That construction matters, and it cuts against a claim often made about reference ranges. People sometimes argue that the normal range is merely an average of an unwell population and can therefore be disregarded. The 2017 range was built specifically to avoid that problem. Anyone who dismisses it on those grounds is arguing against an older generation of laboratory ranges, not against this one.

There is a further practical point that is easy to miss. The 2017 range was intended for assays calibrated to a reference method. A number produced by an uncalibrated commercial assay is not automatically comparable to it. This is one of several reasons why a single result, arriving without context, tells a man less than he thinks it does.

What the 2017 range can tell us is where testosterone concentrations fell within a carefully selected healthy population at the time it was measured. What it cannot tell us is where an equivalent healthy population would have sat in 1950, because comparable measurements from that era do not exist.

We are not going to claim that they do, and we are not going to argue from the secular decline that today's reference range must therefore be set too low. That is an interesting hypothesis. It is not an established fact, and we would rather say so.

Why the honest answer is more useful than a confident one

There is no shortage of plausible explanations. Obesity, physical inactivity, disturbed sleep, metabolic disease, several classes of medication and possible environmental exposures can all influence testosterone concentrations, and some of them are well established at the level of the individual patient.

The difficulty is that the studies above looked for those explanations and did not find enough of them. The Finnish decline survived adjustment for body mass index. The American decline persisted among men whose weight was normal. The Israeli authors judged obesity unlikely to account for the trend by itself.

The careful way to put this is that the observed decline is not fully explained by the factors measured in these studies. That is a statement about the limits of the available evidence. It is not a claim that some unidentified cause has been found, and it should not be read as one. Association is not causation, and an unexplained residual is not the same as an answer.

A similar caution applies to the parallel argument about falling sperm counts, which is often quoted alongside this one. That literature is genuinely contested. A 2023 systematic review and meta-regression covering samples collected in the United States and Western Europe between 1993 and 2018 found no significant trend in sperm concentration. ^[6] Where serious researchers disagree, we would rather tell you that than select the more alarming number.

What this does, and does not, justify

It does not justify prescribing testosterone to men who do not need it.

Testosterone therapy has real effects that have to be weighed. It can raise haematocrit and cause erythrocytosis, which requires monitoring. It suppresses sperm production, and it is generally not appropriate for a man who is actively planning a family. Prescribed to the right patient and monitored properly, it is an established treatment. Prescribed casually, it is not a small decision, and for most men who start it, it is not a short course.

What the evidence does justify is taking the symptoms seriously enough to measure properly.

In the United Kingdom, the British Society for Sexual Medicine guideline sets out how that measurement should be done. Testosterone should be measured between approximately 7am and 11am, confirmed with at least two measurements, preferably around four weeks apart, and interpreted alongside symptoms and clinical context rather than in isolation. For a symptomatic man, a total testosterone below 12 nmol/L, confirmed on appropriate testing, usually warrants consideration of treatment. The guideline also describes a range between approximately 8 and 14 nmol/L in which a therapeutic trial may be considered depending on symptoms and clinical circumstances, and it is worth noting that the recommendations in that middle range rest on a lower level of evidence than the stronger ones. ^[7]

It is also worth being open about the fact that expert bodies do not agree on everything here.

Where low testosterone appears to be a consequence of obesity, the European Association of Urology, the European Society of Endocrinology and the Endocrine Society all place weight loss and lifestyle intervention first. ^[8][9][10] The British Society for Sexual Medicine takes a more permissive view on treating appropriately selected symptomatic men, particularly where management of lifestyle and comorbidity has already been attempted without success, or is unlikely to succeed. ^[7]

The difference is one of emphasis and threshold rather than a straight disagreement, and treating reversible causes remains part of good practice under every one of those guidelines. But a clinic that presents this area as settled is not describing it accurately.

Where this sits in Britain

Every study above was done somewhere else. Finland, Israel, the United States. As far as we can establish, no equivalent study has ever been published in a British population. Nobody has looked properly at whether British men's testosterone has fallen across generations, which means we cannot tell you that it has, and we are not going to imply it.

What Britain does have is evidence about how testosterone gets measured and treated here. For a man sitting in Plymouth, that is arguably the more useful half.

Start with the number itself. In 2023 the Society for Endocrinology and the Association for Clinical Biochemistry and Laboratory Medicine published a joint position statement on how testosterone deficiency should be confirmed. It reported that the lower limit of normal used by UK laboratories ranges from 4.9 to 11 nmol/L. ^[11]

Read that again. More than a two-fold difference. The same blood, sent to two different NHS laboratories, can be reported as normal by one and low by the other. When we said earlier that a reference range is not a diagnosis, this is what that means in practice in this country.

Then there is what has been done with those numbers. Researchers in Newcastle examined national prescription data and found that testosterone dispensed in UK community pharmacies rose from 157,602 items in 2001 to 298,134 in 2010, with the cost to the NHS rising by 267 per cent. In their own region, requests from GPs for testosterone testing rose by 137 per cent over the same period. The proportion of those men found to have unequivocally low testosterone went from 5.2 per cent to 6.3 per cent. ^[12]

Prescribing nearly doubled. The number of men who clearly needed it barely moved.

That paper is called "A UK epidemic of testosterone prescribing". It was written by British endocrinologists, and it is the sharpest version of the criticism this article opened with. We would rather put it in front of you ourselves than wait for somebody else to.

Two further British facts are worth having. There is no NICE clinical guideline on male testosterone deficiency, so practice here runs on specialist society guidance instead, which is part of why laboratories differ from one another. And when the European Male Ageing Study applied strict criteria to men aged 40 to 79 across eight centres including Manchester, requiring symptoms alongside both a low total and a low free testosterone, 2.1 per cent of men met the definition. ^[13] That is two men in a hundred, which is a long way from the figures that appear in advertising.

None of this means testosterone deficiency is rare, or that it does not matter. It means the honest number depends entirely on where the line is drawn, and that a man is owed a clear account of where his clinic drew it, and why.

What we do

Our approach is to assess, investigate, identify causes where they exist, diagnose, and treat only where treatment is clinically indicated.

In practice that means testing in the morning, between 7am and 11am, because that is when concentrations are highest and it is the only timing against which the guideline thresholds mean anything. It means repeating the test, because testosterone fluctuates and a single reading is not a diagnosis. It means measuring the markers that change how a result should be read, including SHBG, LH and FSH, so that a low number can be placed in context rather than simply acted upon. And it means taking a proper history, because the number is one input among several.

None of that is unusual. It is simply what the guideline asks for, done properly, by a doctor who holds a postgraduate diploma in endocrinology.

It also means looking for the causes that are worth correcting in their own right. Weight, sleep, alcohol, other medication and undiagnosed metabolic disease all belong in that conversation, and addressing them is not a delaying tactic. It is treatment.

Some men will go through that process and turn out not to need testosterone treatment at all.

That is not a failed appointment. It is a successful clinical outcome, and it is one we are comfortable reaching.

The part nobody can answer yet

So here is where it sits.

It is not one generation. That is the part to hold on to.

Finnish men born in the 1940s had less testosterone in their sixties than Finnish men born in the 1910s, and on its own that would be a curiosity about men who are now very old or dead. But the Israeli data runs to 2019, and the youngest men in it were born in the 1990s. The American survey data covers men who were between fifteen and thirty-nine at some point between 1999 and 2016. The line shows up there too.

So it is not a step that happened once, somewhere in the middle of the last century, and then stopped. It moved in Finland. It moved in Israel. It moved in Massachusetts. It moved in the American national survey data, in different decades, measured by different people on different machines, in studies that were never designed to agree with each other and did anyway. And it was still there in blood taken in 2019.

Ageing does not explain it. Obesity does not explain it. The men who were not carrying any extra weight went down as well.

You can read the papers yourself. They are listed at the bottom of this page and most of them are a harder read than they need to be. But when you get to the end of them you will find the authors doing roughly what we are doing now, which is standing in front of a large, well-documented and entirely unexplained hole in the middle of male physiology, and saying so out loud, because the alternative is to make something up.

We are not going to make something up. And you should be careful of anyone who does, particularly if they are selling.

Here is the part that matters, though. Not knowing why is not the same as not knowing what to do.

A man of forty-five who is tired in a way that sleep does not fix, who has stopped doing the things he used to do and has not told anybody, does not need the whole mystery solved before someone takes a proper look at him. He needs a blood test taken at the right hour of the morning, and then taken again. He needs someone who understands what SHBG does to the answer. He needs a conversation about his weight, his sleep, his drinking, his other medication, and what is actually going on in his life. Sometimes that conversation ends in treatment. Often it does not, and he leaves knowing something useful either way.

None of that requires anyone to know why the graphs are pointing downwards. It has been possible for years, and it is possible in Plymouth on a Tuesday afternoon.

The cause is still out there somewhere, and better people than us will find it eventually.

We are considerably easier to find in the meantime.

If you have symptoms and you want them assessed properly, book a men's health assessment at Eden Clinic, 23 Mayflower Street, Plymouth, PL1 1QJ. Call 0333 335 6414. We will come back to you within one working day.

Eden Clinic is registered with the Care Quality Commission. Our clinical lead is Dr Angela Servis, BMBS, MRCGP, PgDip Aes, PgDip Endo, who has practised medicine for eighteen years, seventeen of them as a medical officer in the British Army. She is a member of the British Society for Sexual Medicine, the European Society for Sexual Medicine, the International Society for Sexual Medicine and the Androgen Society.

References

1. Perheentupa A, Mäkinen J, Laatikainen T, Vierula M, Skakkebaek NE, Andersson A-M, Toppari J. A cohort effect on serum testosterone levels in Finnish men. European Journal of Endocrinology 2013;168(2):227–233. PMID 23161753. DOI 10.1530/EJE-12-0288.
2. Chodick G, Epstein S, Shalev V. Secular trends in testosterone: findings from a large state-mandate care provider. Reproductive Biology and Endocrinology 2020;18:19. PMID 32151259. DOI 10.1186/s12958-020-00575-2.
3. Travison TG, Araujo AB, O'Donnell AB, Kupelian V, McKinlay JB. A population-level decline in serum testosterone levels in American men. Journal of Clinical Endocrinology and Metabolism 2007;92(1):196–202. PMID 17062768. DOI 10.1210/jc.2006-1375.
4. Lokeshwar SD, Patel P, Fantus RJ, Halpern J, Chang C, Kargi AY, Ramasamy R. Decline in serum testosterone levels among adolescent and young adult men in the USA. European Urology Focus 2021;7(4):886–889. PMID 32081788. DOI 10.1016/j.euf.2020.02.006.
5. Travison TG, Vesper HW, Orwoll E, Wu F, Kaufman JM, Wang Y, Lapauw B, Fiers T, Matsumoto AM, Bhasin S. Harmonized reference ranges for circulating testosterone levels in men of four cohort studies in the United States and Europe. Journal of Clinical Endocrinology and Metabolism 2017;102(4):1161–1173. PMID 28324103. DOI 10.1210/jc.2016-2935.
6. Cipriani S, Ricci E, Chiaffarino F, Esposito G, Dalmartello M, La Vecchia C, Negri E, Parazzini F. Trend of change of sperm count and concentration over the last two decades: a systematic review and meta-regression analysis. Andrology 2023;11(6):997–1008. PMID 36709405. DOI 10.1111/andr.13396.
7. Hackett G, Kirby M, Rees RW, Jones TH, Muneer A, Livingston M, Ossei-Gerning N, David J, Foster J, Kalra PA, Ramachandran S. The British Society for Sexual Medicine guidelines on male adult testosterone deficiency, with statements for practice. World Journal of Men's Health 2023;41(3):508–537. PMID 36876744. DOI 10.5534/wjmh.221027.
8. European Association of Urology. Guidelines on Sexual and Reproductive Health, Male Hypogonadism chapter, 2025 edition.
9. Pasquali R, Casanueva F, Haluzik M, van Hulsteijn L, Ledoux S, Monteiro MP, Salvador J, Santini F, Toplak H, Dekkers OM. European Society of Endocrinology clinical practice guideline: endocrine work-up in obesity. European Journal of Endocrinology 2020;182(1):G1–G32. DOI 10.1530/EJE-19-0893.
10. Endocrine Society. Statement on testosterone replacement therapy. 16 July 2026.
11. Jayasena CN, de Silva NL, O'Reilly MW, MacKenzie F, Marrington R, Jones TH, Livingston M, Downie P, Hackett G, David J, Boot C, Patel M, Tarling J, Wu F, Quinton R. Standardising the biochemical confirmation of adult male hypogonadism: a joint position statement by the Society for Endocrinology and Association of Clinical Biochemistry and Laboratory Medicine. Annals of Clinical Biochemistry 2023;60(4):223–227. DOI 10.1177/00045632231179022.
12. Gan EH, Pattman S, Pearce SHS, Quinton R. A UK epidemic of testosterone prescribing, 2001–2010. Clinical Endocrinology 2013;79(4):564–570. PMID 23480258. DOI 10.1111/cen.12178.
13. Wu FCW, Tajar A, Beynon JM, Pye SR, Silman AJ, Finn JD, O'Neill TW, Bartfai G, Casanueva FF, Forti G, Giwercman A, Han TS, Kula K, Lean MEJ, Pendleton N, Punab M, Boonen S, Vanderschueren D, Labrie F, Huhtaniemi IT. Identification of late-onset hypogonadism in middle-aged and elderly men. New England Journal of Medicine 2010;363(2):123–135. PMID 20554979. DOI 10.1056/NEJMoa0911101.