A closer look at weight, drug use and steroid-related fertility risks, with EAU guidance on recovery, hormone testing and testosterone treatment.
In a report last updated December 12, 2023, The Economic Times carried PTI coverage of how weight, recreational drugs and anabolic steroids relate to male fertility.
This article is for informational purposes only and is not medical advice. Personal decisions about testing, fertility or hormone treatment belong with a qualified clinician.
The PTI report discusses several reproductive outcomes that are easy to blur together: sexual desire, sexual function, testosterone production and sperm measures. Its coverage matters because a concern about fertility is not answered by discussing testosterone alone.
According to the report, obesity-related hormonal changes can adversely affect several aspects of semen quality:
The same report says excess weight's fertility effects can be reversible. It presents regular exercise and a healthy diet as ways to support weight reduction and sperm quality.
The focus here is reproductive health, not appearance. In a fertility assessment, weight changes are part of the history a clinician may need to understand.
The report associates cocaine, benzodiazepines and heroin with adverse reproductive effects. It also names methamphetamine, oxycodone and ecstasy. The effects it discusses involve sexual desire, testosterone production, sperm production and sperm quality.
A useful clinical history therefore needs more than a general statement about drug use. The European Association of Urology (EAU) includes lifestyle and behavioural risk factors in its assessment, providing a way to discuss relevant exposures with a clinician.
The report describes anabolic steroids used to change appearance or improve physical performance. It says they can reduce testicular size, reduce or stop sperm production and contribute to impotence and infertility.
This is a reproductive warning, not just a discussion about muscle or a blood-test result. For a fuller account of the same topic, Testostra explains how steroid use relates to male hormone health.
The Economic Times report also cites an estimate that about one in 16 men globally use anabolic steroids at some point in life. That is a reported lifetime-use estimate, not a measure of how many men are currently using steroids.
The EAU guideline addresses steroid-related sperm suppression directly. It identifies stopping anabolic steroids as the initial management approach for men with this problem.
The EAU guideline recommends a broader evaluation for male infertility:
The guideline identifies total testosterone and gonadotropins as useful in classifying hypogonadism. These hormone results serve a different purpose from semen analysis. A testosterone result alone does not establish whether sperm production is normal.
That distinction is central to understanding why testosterone and fertility need separate assessment. It also explains why a fertility discussion should not end with a single hormone number.
The evaluation framework separates three questions that may otherwise become mixed together:
These questions do not call for the same test or automatically lead to the same treatment. They give the clinician a way to connect reproductive goals with the relevant results. For readers reviewing a lab report, the useful question is not simply whether testosterone is low. It is which concern the assessment is meant to address.
The EAU advises against using testosterone therapy to treat male infertility. It separately recommends testosterone therapy for symptomatic men with primary or secondary hypogonadism who are not considering parenthood.
These recommendations answer different clinical questions. One concerns infertility, while the other concerns treatment of symptomatic hypogonadism. The treatment goal matters as much as the name of the hormone being discussed.
Physique-focused anabolic steroid use should not be presented as interchangeable with medically supervised treatment for confirmed hypogonadism. Yet medical supervision does not turn testosterone into a fertility treatment. For someone who wants children, the EAU guideline's distinction makes parenthood plans an essential part of the treatment discussion.
The PTI report should be read as a news summary of evidence, not as a new clinical guideline. Its claims need to be separated from the strength and scope of the supporting guidance.
The report's account of obesity does not predict how a particular man's semen measures would change with weight loss. Its discussion of recreational drugs also groups substances with different uses and risk profiles. Those associations should not be read as equal effects from every dose or pattern of use.
Marijuana needs a separate qualification. The report describes research on marijuana and sperm quality as inconclusive, despite mentioning evidence that frequent use may reduce sperm quality. A settled causal claim would go beyond that account.
The EAU says sperm numbers and quality usually improve over six to 12 months after anabolic steroid cessation. It grades the recommendation to withdraw steroids before considering further treatment as weak. The guideline describes management as based on case reports and clinical experience, with no common indication for treating this steroid-related disorder.
The PTI report says most men begin producing sperm again within a year. It also describes a study in which more than half of previously infertile men still had no sperm or very few sperm after a six-month hormone-treatment course. The report does not provide the study's authors, sample size or organisation.
These descriptions address different things: the return of sperm production, changes in sperm measures and findings after treatment. They cannot be combined into a personal recovery timetable. Neither permanent infertility nor rapid recovery should be assumed from a history of steroid use alone.
This report does not create a reason to change medical practice immediately. Its value is in reinforcing established distinctions: fertility assessment is broader than a testosterone test, and treating low testosterone is not the same as treating infertility.
For clinical conversations, the relevant topics include:
Separating sexual symptoms from fertility concerns can help clarify what the assessment is trying to answer.
In its 2026 statement, the Endocrine Society said evidence was insufficient to support population-level testosterone screening in asymptomatic men. That is a separate policy point from the 2023 fertility report.
This does not mean testosterone testing has no role in male infertility. The EAU specifically includes hormonal evaluation in its infertility assessment and identifies hormone measurements as useful for classifying hypogonadism. The sources address different situations: evaluation for a clinical concern and screening people without symptoms. Neither turns a risk factor mentioned in a newspaper report into a diagnosis.
Bottom line: the evidence supports a more complete conversation with a qualified clinician, not a self-directed change to hormones or medication. Decisions about fertility evaluation and treatment should remain individual clinical decisions.
Fertility planning can complicate the meaning of a low testosterone result and the purpose of treatment. Testostra explains total testosterone, free testosterone and SHBG within broader male hormone education to reduce confusion about biomarkers while keeping clinical decisions with qualified professionals.
Testostra follows testosterone research, clinical guidance and emerging evidence without turning general information into personal treatment advice.
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