For years, researchers have observed a troubling trend: testosterone levels in men seem to be declining across generations. This hormone, crucial for male health, has been linked to energy, mood, muscle mass, and even heart health. But a recent analysis is challenging what was long assumed — suggesting the supposed decline may be based on a surprising technical detail in how testosterone is measured.
This article examines the evidence, explores global trends, and unpacks what might really be going on with men's testosterone levels — along with practical, evidence-backed strategies for supporting healthy levels naturally.
Table of Contents
- Testosterone Is Declining — Or Is It?
- Global Evidence of Falling T
- The Obesity Explanation
- The New Study That Changes Everything
- How to Support Testosterone Naturally
- Summary: Four Evidence-Based Strategies
- References
Testosterone Is Declining — Or Is It?
2007 was a turbulent year.
On one hand, it was the year the iPhone launched — putting the addictive power of social media into the palms of billions and reshaping daily life in ways that are still being studied.
On the other hand, that year brought striking data from a study published in one of the most respected hormone-focused journals in medicine.
Researchers had gathered blood samples from about 1,500 men at three different time points between 1987 and 2004. The purpose was straightforward: to see what was happening to testosterone levels over time [1].
Data obtained from 1,374, 906, and 489 men at T1, T2, and T3 respectively — totaling 2,769 observations taken on 1,532 men.
Testosterone naturally declines with age. In men, after age 30, levels decrease by approximately 1–2% per year on average [2]. This pattern is well established and not inherently pathological — it is a normal part of male physiology.
But that 2007 study uncovered something more troubling. Not only were testosterone levels declining with age within individuals, but it appeared they might be declining with each new generation as well [1].
The implication was alarming: something in the modern environment might be systematically suppressing testosterone across the male population.
And this goes well beyond reproductive concerns. Low testosterone weakens bones, decreases energy, and negatively affects mood [3]. It is also associated with elevated all-cause and cardiovascular mortality [4].
Researchers were compelled to determine whether this generational decline was real — and if so, what was driving it.
Global Evidence of Falling T
The search for answers extended beyond the United States.
A large population study in Denmark also uncovered falling testosterone levels over time [5]. A study in Finland reported the same pattern [6]. A more recent investigation, again in the U.S., found that the trend continued into the 2010s [7].
"TT levels were lower in the later (2011–2016) than in the earlier (1999–2000) cycles (all p < 0.001)."
Across multiple countries and multiple study designs, the data appeared consistent: testosterone levels in men were declining. Researchers described it as a worldwide phenomenon — not limited to any single population or region.
The Obesity Explanation
Why might this be happening? The question prompted significant scientific debate.
Various explanations have been proposed. Some researchers pointed to pesticide exposure as a potential hormonal disruptor in modern diets [8].
Others cited microplastics, which have been shown to reduce testosterone levels in mouse studies [9].
Aluminum has also been investigated as a potential contributor [10].
But most of these proposals struggle to fully account for the observed pattern. One factor, however, has emerged as particularly significant: obesity. Even so, obesity alone does not explain the complete picture.
Excess body fat reduces testosterone through mechanisms involving insulin resistance, elevated aromatase activity (which converts testosterone to estrogen), and other metabolic pathways. The relationship is bidirectional: low testosterone by itself also contributes to weight gain, creating a negative feedback loop [11].
"Low testosterone by itself leads to increasing adiposity, creating a self-perpetuating cycle of metabolic complications."
Globally, obesity rates have surged. In adults, prevalence has more than doubled since 1990. Among adolescents, it has quadrupled [12]. Given the established link between excess body fat and reduced testosterone, rising obesity rates would logically contribute to a population-level decline.
In the Danish study, the testosterone decline disappeared statistically when researchers adjusted for increasing BMI [5] — suggesting obesity might be a key mediating variable.
But the mystery was not fully solved. Rising obesity rates appeared to explain some, but not all, of the observed decline.
A pivotal study from Israel examined testosterone levels drawn from tests conducted on over 100,000 men between 2006 and 2019 [13]. Consistent with prior findings, the researchers observed a population-wide fall in testosterone over the study period [13].
Yet when they examined BMI trends, they found no increase in average BMI across the same timeframe. This meant the drop in testosterone levels could not be explained solely by rising obesity [13].
Researchers in the most recent U.S. study reached a similar conclusion: testosterone was declining even among men with normal BMI [7].
Something else had to be driving the trend — or so it seemed.
The New Study That Changes Everything
A recent analysis offers an entirely unexpected explanation — one that challenges the foundational assumption underlying the entire testosterone-decline narrative.
The analysis focused on a methodological issue that had lingered quietly in the background: how testosterone levels are measured.
This concern had been flagged as early as 2020. Researchers reporting on the U.S. testosterone decline included an important qualification alongside their findings: the dataset they relied upon incorporated different measurement methods across different time periods [7].
Why does this matter? Because different measurement technologies can produce systematically different results — even when measuring the same underlying biological reality.
Consider an analogy: a traveller weighs a carry-on bag at home and finds it just under the airline's 10 kg limit. At the airport, the airline's scale reads 11 kg. The bag did not gain weight on the way there. The difference reflects the measurement tool, not any real change in the bag. Concluding the bag "got heavier" would be a measurement artefact — not a physical fact.
Measurement method matters. When different tools are used at different time points, observed differences may reflect the technology rather than the underlying biology.
This is precisely what the new analysis investigated. The researchers examined U.S. health data across five distinct time periods using the same national dataset that had previously been cited to demonstrate testosterone decline [7, 14].
Here is the critical detail: the first two time periods used one measurement method, while the latter three used an entirely different method [14].
The earliest two cycles used the Roche Elecsys immunoassay, whereas cycles from 2011 onward used the LC-MS/MS assay.
The newer LC-MS/MS method tends to produce lower readings than immunoassay methods for the same testosterone concentration.
When the five time periods are plotted on a graph — with bars representing the proportion of men with low testosterone and colours indicating which measurement method was used — a striking pattern emerges: there is a large jump in apparent low testosterone that coincides precisely with the switch in measurement method [14].
"The marked increase in the fraction of healthy males with TT < 300 ng/dL from 2004 (12%) to 2011 (22%) coincides with the migration from immunoassay to LC-MS/MS."
The implication is significant. The apparent trend of falling testosterone in U.S. population data may be, at least in part, a measurement artefact — not a true biological decline.
The study authors argue that a revised diagnostic threshold is needed to account for the systematic differences between methods. When that adjustment is applied, the proportion of men with low testosterone stays flat — or even declines [14].
"This suggests that the Endocrine Society's proposed low cutoff of 264 ng/dL may be a more accurate threshold going forward, than the historically used 300 ng/dL."
This completely reframes the narrative. Over the three most recent measurement periods — all using the same LC-MS/MS methodology — the percentage of men with low testosterone is actually decreasing.
The answer to why testosterone levels appear to be falling may be straightforward: they are not.
However, the Israeli study remains a complicating factor. The U.S. measurement-switch explanation does not apply there, because the Israeli researchers explicitly stated that the same testing methodology was used consistently throughout their data collection period [13].
"All the samples were measured using the same lab methods... at a single central lab."
Yet that study has its own significant methodological limitation: the men tested were not a random sample of the population. They were tested because a physician had referred them — meaning their doctor already suspected a testosterone problem [13].
Selecting participants on the basis of clinical suspicion of low testosterone introduces substantial selection bias. The sample would naturally skew toward men with lower levels, and any change in referral patterns over time could produce apparent trends that do not reflect changes in the broader population.
So while the Israeli study cannot be explained away by the measurement-method argument, it carries its own question marks about representativeness.
The most defensible conclusion from the totality of this evidence is that the thesis of a generational testosterone decline is at least in serious doubt. The most prominent U.S. data supporting it appears to reflect a methodological switch rather than a biological reality. The Israeli data, while concerning, is subject to selection bias that limits its generalisability.
As with many areas of medicine, the narrative that captured headlines may have outrun the strength of the underlying evidence.
How to Support Testosterone Naturally
Whatever the generational picture turns out to be, the evidence is clear on one point: testosterone declines with age in individual men. After age 30, average levels fall by roughly 1–2% per year [2]. Even in the absence of clinical deficiency, supporting healthy testosterone production makes physiological sense.
Research points to four well-supported strategies.
1. Reduce Excess Body Fat
For men who are overweight, reducing body fat is the most impactful intervention available. Obesity is strongly and consistently associated with lower testosterone levels [15]. A comprehensive review of the literature identified weight loss as the primary first-line intervention for improving testosterone in men with obesity [15].
The mechanisms are well understood: adipose tissue expresses aromatase, an enzyme that converts testosterone to oestrogen. Greater fat mass means greater aromatase activity, which reduces circulating testosterone while simultaneously increasing oestrogen. Weight loss reverses this process.
Sustainable weight loss is best achieved through dietary change and increased physical activity. For some individuals, medications such as GLP-1 receptor agonists (including semaglutide or tirzepatide) can support meaningful, clinically significant weight reduction.
2. Engage in Resistance and Aerobic Exercise
Physical training — particularly resistance exercise — has a documented acute and chronic effect on testosterone levels.
Research shows that resistance training elevates testosterone, with the most pronounced responses associated with multi-joint compound movements (such as squats and deadlifts), high training volume, moderate-to-high intensity, and shorter rest intervals between sets [16]. These parameters appear to produce the optimal acute increase in serum testosterone.
Aerobic training also plays a role. A systematic review found that aerobic exercise moderately increases testosterone levels in men with obesity or type 2 diabetes [17] — populations where testosterone suppression is particularly common.
The combination of resistance and aerobic training appears to be more effective than either modality alone for supporting testosterone over the long term.
3. Prioritise Sleep
Testosterone secretion is closely coupled to sleep architecture. Levels peak during sleep, particularly during slow-wave and REM phases. Disrupting or shortening sleep reduces the opportunity for this nocturnal testosterone surge [18].
A controlled study restricted healthy young men to five hours of sleep per night for eight consecutive nights [19]. Testosterone levels were significantly lower across the restriction period compared to baseline — a striking demonstration of how rapidly sleep deprivation can suppress circulating testosterone in otherwise healthy men.
A subsequent meta-analysis confirmed that sleep duration plays a pivotal role in maintaining healthy testosterone levels [18]. For men concerned about testosterone, sleep quantity and quality represent a modifiable factor that is frequently overlooked.
4. Consider TMG (Betaine) Supplementation
Trimethylglycine — commonly known as TMG or betaine — is a methyl donor derived from beetroot and other foods. It participates in one-carbon metabolism and has been studied for its effects on muscle performance, body composition, and hormonal markers.
Two human studies are particularly relevant here. In the first, soccer players who supplemented with TMG showed increases in testosterone over the course of a competitive season compared to controls [20].
In a second study, participants followed a structured exercise programme while supplementing with TMG. Resting testosterone levels were significantly higher in the TMG group compared to the placebo group at the end of the intervention [21].
While the evidence base for TMG on testosterone is still emerging and not definitive, it represents one of the more plausible supplement candidates — particularly for individuals engaged in regular exercise, the context in which the research was conducted.
From the MicroVitamin range
MicroVitamin includes TMG (trimethylglycine / betaine), the same compound studied in the exercise and testosterone research above. MicroVitamin.
Summary: Four Evidence-Based Strategies
To support healthy testosterone levels, the research points to four practical interventions:
- Reduce excess body fat — weight loss is the most impactful intervention for men with obesity
- Exercise regularly — prioritise resistance training with multi-joint movements and adequate volume; complement with aerobic exercise
- Protect sleep quantity and quality — testosterone peaks during sleep; chronic restriction measurably suppresses levels
- Consider TMG supplementation — emerging evidence suggests benefit, particularly when combined with exercise
It is also worth keeping the broader evidence in perspective. The generational testosterone decline that has attracted significant media and clinical attention may, in substantial part, reflect a change in measurement methodology rather than a true biological trend. Individual testosterone trajectories — shaped by age, lifestyle, body composition, and sleep — remain the more clinically actionable focus.
References
1. https://pubmed.ncbi.nlm.nih.gov/17062768/
2. https://pmc.ncbi.nlm.nih.gov/articles/PMC6966696/
3. https://pmc.ncbi.nlm.nih.gov/articles/PMC10338218/
4. https://pubmed.ncbi.nlm.nih.gov/25269643/
5. https://pubmed.ncbi.nlm.nih.gov/17895324/
6. https://pubmed.ncbi.nlm.nih.gov/23161753/
7. https://pubmed.ncbi.nlm.nih.gov/32081788/
8. https://www.scientificamerican.com/article/pesticides-may-block-male-hormones/
9. https://www.mdpi.com/2305-6304/12/8/561
10. https://www.sciencedirect.com/science/article/abs/pii/S002432052400050X
11. https://pmc.ncbi.nlm.nih.gov/articles/PMC3955331/
12. https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
13. https://rbej.biomedcentral.com/articles/10.1186/s12958-020-00575-2
14. https://academic.oup.com/clinchem/article-abstract/71/5/609/8114673
15. https://pmc.ncbi.nlm.nih.gov/articles/PMC11745839/
16. https://pmc.ncbi.nlm.nih.gov/articles/PMC7739287/
17. https://pmc.ncbi.nlm.nih.gov/articles/PMC11519272/
18. https://www.sciencedirect.com/science/article/abs/pii/S138994572100544X
19. https://pmc.ncbi.nlm.nih.gov/articles/PMC4445839/
