Mycotoxins and Male Fertility: What the Aflatoxin Research Actually Shows

A man can have an abnormal semen analysis and be told very little about why it is abnormal. Or his result can sit just inside the reference range while fertilisation, embryo development or pregnancy still does not proceed as expected.

At that point, the investigation needs to move beyond counting sperm. It needs to ask what has been affecting the system that produces them.

A 2024 scientific review examined one possible part of that picture: exposure to aflatoxins, a group of mycotoxins produced by certain Aspergillus moulds. The paper brings together research on reproductive hormones, testicular tissue, sperm quality and the biological pathways through which aflatoxin B1 may cause damage.

It is interesting research. It is also research that can easily be overstated.

First, what is aflatoxin exposure?

Aflatoxins are not simply another name for any mould found in a damp building. They are a specific group of toxins produced by particular mould species, and the best-established route of human exposure is through contaminated food. Grains, maize, nuts, seeds, spices and animal feed can be affected, particularly where crops have been grown or stored in warm, humid conditions.

That distinction matters. A history of living in a mould-affected home may still be clinically relevant, but this paper is primarily about aflatoxin exposure, much of which is dietary. We should not take research on one mycotoxin and use it as proof for every possible mould exposure.

What did the review find?

The review describes several ways in which aflatoxin B1 could interfere with male reproductive health. In animal and cell studies, exposure has been associated with:

• lower luteinising hormone, follicle-stimulating hormone and testosterone;
• disruption of the hypothalamic–pituitary–testicular signalling axis;
• damage to Leydig and Sertoli cells, which are central to hormone production and sperm development;
• disruption of the blood–testis barrier;
• reduced sperm count, motility and viability, with more abnormal sperm;
• oxidative stress, inflammation, mitochondrial dysfunction and activation of cell-death pathways.

This gives us a biologically coherent explanation for how a toxic exposure might influence sperm production and quality. But a plausible mechanism is not the same as proof that it is causing a particular couple's fertility problem.

What do we know in humans?

This is where the evidence becomes much thinner.

The review cites an older epidemiological study from Nigeria in which aflatoxin concentrations were higher in infertile men than in fertile controls. That is a signal worth taking seriously, but it is not enough to establish causation. It cannot tell us whether aflatoxin was the main driver of infertility, one contributor among several, or a marker of other environmental and nutritional differences between the groups.

The authors themselves are clear that human clinical research is still needed. Most of the detailed evidence in the paper comes from rodents, farm animals and cultured cells. Those studies help us understand possible mechanisms; they do not give us a validated clinical protocol for men trying to conceive.

Why oxidative stress keeps appearing

Oxidative stress is one of the most consistent themes in the paper. It occurs when the production of reactive molecules exceeds the body's ability to neutralise and repair their effects. Sperm are particularly vulnerable because their membranes contain large amounts of polyunsaturated fatty acids and they carry tightly packed DNA with limited capacity for repair.

This is relevant beyond mycotoxins. Smoking, heat, infection, inflammation, metabolic dysfunction, poor sleep and other environmental exposures can all increase oxidative pressure. Aflatoxin may be one more contributor—but it should not automatically become the only explanation.

That is why I would not look at a high DNA fragmentation result and jump immediately to mould. I would look at the entire pattern: symptoms, home and occupational history, food exposure, travel, infection history, medications, hormones, metabolic markers, heat, smoking, alcohol and the timing of changes in semen quality.

What this research does not justify

The review discusses compounds and interventions that appeared protective in experimental models, including selenium, caffeic acid, silymarin, probiotics and several plant extracts. This is the part of a paper that is most likely to be taken out of context.

These were predominantly animal or cell experiments, often using doses and exposure conditions that cannot be translated directly into routine human care. The paper explicitly says that clinical trials are required.

So this research does not mean that every man with a fertility problem should take a long list of antioxidants, probiotics or binders. More is not necessarily better. High-dose supplementation can be unhelpful or harmful, and an indiscriminate protocol can obscure the clinical question instead of answering it.

When exposure history deserves attention

I would be more interested in this line of investigation when there is a combination of clues, for example:

• an unexplained deterioration in semen parameters;
• high sperm DNA fragmentation or evidence of oxidative stress;
• recurrent poor fertilisation, embryo arrest or early pregnancy loss;
• occupational or agricultural exposure;
• regular consumption of poorly stored grains, nuts, spices or imported foods from high-risk environments;
• a clear change in health after a move, workplace change or major environmental exposure;
• symptoms affecting more than one system, rather than an isolated fertility result.

None of these proves mycotoxin toxicity. They tell us that the question may deserve a place in the timeline.

What a sensible male fertility investigation looks like

Both partners should participate in a comprehensive fertility investigation. On the male side, that may include more than a standard semen analysis:

• review of the full reproductive and health history;
• repeat semen testing when appropriate, because results fluctuate;
• sperm DNA fragmentation or oxidative-stress assessment where clinically relevant;
• reproductive hormones and metabolic markers;
• investigation of infection, inflammation and the seminal microbiome when indicated;
• review of medication, heat, smoking, alcohol, sleep, nutrition and occupational exposures;
• targeted environmental investigation only when the history creates a reasonable clinical question.

The point is not to order every available test. It is to choose tests that answer the unanswered questions in that person's history.

My clinical reading of this paper

The paper does not give us permission to diagnose male infertility from a mould story alone. What it does is reinforce something I see repeatedly: environmental exposure is not separate from reproductive health simply because it is absent from the standard fertility form.

Sperm develop over roughly three months. The sample tested today reflects the biological conditions of the preceding weeks and months. If semen quality changes, the timeline matters.

Aflatoxin research gives us a credible reason to ask better questions about food, work and environment. It also gives us a reason to remain disciplined about evidence. The correct response is neither to dismiss the exposure nor to make it responsible for everything.

If your male fertility investigation stopped at count, motility and morphology, or if semen quality changed without a clear explanation, the most practical next step is a structured review of the whole timeline. Before booking, you may want to read how I investigate complex fertility cases. You can then book an Introductory Fertility Review, where we can identify the clinical questions that are still unanswered and select tests accordingly.

Research source

Ye D, Hao Z, Tang S, Velkov T, Dai C. Aflatoxin Exposure-Caused Male Reproductive Toxicity: Molecular Mechanisms, Detoxification, and Future Directions. Biomolecules. 2024;14(11):1460. Read the paper.

This article is educational and does not replace individual medical advice, diagnosis or treatment. Diagnosis and any prescribed treatment should be provided by a qualified medical professional.