Carnosine And Anti-Ageing
Quick Read Carnosine is a small molecule your muscles naturally produce that declines with age. Research suggests it fights three
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What if one of the most overlooked nutrients in the fertility conversation wasn’t a hormone, wasn’t a vitamin, and wasn’t something most people have ever thought to check? What if a trace mineral — one your body needs in amounts measured in micrograms — was quietly influencing sperm quality, egg development, pregnancy outcomes, and even your thyroid’s role in reproduction? That’s the case being built, study by study, for selenium. And while it’s not a fertility cure-all, the evidence gathering around it is genuinely worth understanding.
Vitacuity’s research database returned 15 papers on selenium and fertility. Here’s what they tell us — and just as importantly, what they don’t.
Selenium is what’s known as a trace element — your body needs only tiny amounts of it, but those amounts are non-negotiable. It works primarily by being incorporated into a family of proteins called selenoproteins — over 25 of them in the human body — which carry out a remarkable range of jobs [4]. The most relevant for fertility are the glutathione peroxidases (GPx), a group of antioxidant enzymes that neutralise damaging molecules called reactive oxygen species (ROS).
Here’s why that matters for reproduction: the process of making sperm, maturing eggs, and sustaining a pregnancy all involve intense biological activity — and intense biological activity generates oxidative stress, a kind of cellular “rust.” Selenium-dependent enzymes are a primary defence against that rust [5][6].
In the testes, selenium is found in unusually high concentrations. Some GPx proteins (specifically mGPx4 and snGPx4) don’t just act as antioxidants — they become structural components of the mature sperm tail itself, physically holding the sperm together [5]. In the ovaries, selenium similarly supports follicular health and the antioxidant environment that surrounds developing eggs [1].
There’s a second, less obvious pathway too: the thyroid connection. Selenium is essential for thyroid hormone metabolism, and the thyroid plays a central role in regulating reproductive hormones in both men and women [4][7]. Autoimmune thyroid conditions — where the immune system attacks the thyroid — are increasingly linked to fertility problems, and selenium appears to reduce the inflammatory activity driving those attacks [3][14].
The most striking evidence for selenium’s fertility role comes from animal research. In a 2008 study published in a peer-reviewed journal, male mice fed a selenium-deficient diet for four months showed a 67% reduction in their ability to fertilise eggs in vitro compared to mice on a selenium-sufficient diet [10]. Selenium-deficient sperm showed significantly increased lipid peroxidation (a marker of oxidative damage) in both the sperm cells and the testes, and electron microscopy revealed abnormal chromatin condensation — essentially, the DNA packaging inside the sperm was disrupted [10].
Evidence grade: Early stage — this is animal data. The magnitude of the effect is striking, but mice are not men, and we can’t simply extrapolate a 67% fertility drop to humans. What it does tell us is that the *mechanism* is real and biologically plausible.
Moving to human evidence, two studies stand out.
The first, a 2023 prospective clinical study published in *Biological Trace Element Research*, examined 65 infertile men with idiopathic oligoasthenoteratospermia (OAT) — a condition where sperm count, motility, and morphology are all below normal with no identified cause [15]. Participants received 200 µg/day of selenium orally for six months. The results were notable:
– Sperm concentration increased significantly (P < 0.001) - Progressive motility increased significantly (P < 0.001) - Total motility increased (P < 0.01) - Seminal antioxidant capacity (TAC and catalase) increased (P < 0.01) - Sperm DNA fragmentation decreased significantly (P < 0.001) [15]
DNA fragmentation matters because damaged sperm DNA is associated with failed fertilisation, poor embryo development, and miscarriage. The fact that selenium reduced it is clinically meaningful — if the finding holds up in larger trials.
The second human study examined a more specific population: 20 men with autoimmune thyroiditis (AT) but normal thyroid function [3]. After supplementation with 83 µg/day of selenium, participants showed higher sperm concentration, better progressive motility, improved morphology, lower semen leukocyte (white blood cell) concentration, and reduced DNA fragmentation compared to pre-treatment values [3].
Evidence grade: Promising — these are small studies (65 and 20 participants respectively), and neither includes a long-term follow-up on pregnancy rates. But both used objective, standardised semen parameters, and the direction of effect is consistent.
On the female side, a 2022 systematic review in a peer-reviewed journal searched eight major databases and identified seven eligible studies on selenium and female fertility [1]. The review found positive correlations between serum selenium levels and:
– Antioxidant concentration in follicular fluid — the fluid surrounding developing eggs – Reduction in anti-thyroid antibodies — relevant because thyroid autoimmunity can disrupt ovulation and implantation – Oocyte production — the number of eggs available – Follicle number [1]
The authors concluded that selenium supplementation shows promise in women with this micronutrient deficiency for improving reproductive efficiency and protecting pregnancy outcomes — while noting that further studies are still required [1].
Evidence grade: Promising — the systematic review methodology is solid, but only seven studies met the eligibility criteria, which tells you the human evidence base here is still relatively thin.
A 2020 randomised double-blind, placebo-controlled trial — one of the more rigorous study designs available — examined 36 infertile women with polycystic ovary syndrome (PCOS) who were candidates for IVF [13]. Participants received either 200 µg/day of selenium or a placebo for eight weeks.
RT-PCR analysis (a technique for measuring gene activity) showed that selenium:
– Downregulated IL-1 (an inflammatory marker) — P < 0.004 - Downregulated TNF-α (another inflammatory marker) — P = 0.02 – Upregulated VEGF (vascular endothelial growth factor, involved in blood vessel formation in the uterus) — P = 0.001 [13]
Notably, selenium had no significant effect on clinical symptoms, or on two other inflammatory markers (IL-8 and TGF-β) [13]. This is an honest finding — not everything improved — but the anti-inflammatory effect on two key markers in a PCOS population is biologically interesting.
Evidence grade: Promising — n=18 per group, eight-week duration, no pregnancy outcome data. The gene expression findings are intriguing but this needs replication in larger trials.
A 2020 review published in *Thyroid Research* laid out the pregnancy evidence [7]. Key points:
– Selenium concentrations in UK women of reproductive age were reported to be low, declining further during pregnancy – Low serum selenium has been found in women with pre-eclampsia (dangerous high blood pressure in pregnancy) – Low maternal selenium may be a marker for risk of preterm birth – Low selenium in pregnant women was linked to impaired fetal growth and increased risk of delivering a small-for-gestational-age infant, via reduced placental antioxidant defence – Selenium administration during pregnancy was found to reduce markers of thyroid autoimmunity and lower the incidence of maternal hypothyroidism in the postpartum period [7]
A broader 2022 review in *Frontiers in Nutrition* reinforced this picture, noting that selenium deficiency during pregnancy is associated with miscarriage, pre-eclampsia, gestational diabetes, fetal growth restriction and preterm birth — though importantly, selenium excess carries similar risks, which is a critical nuance [2].
Evidence grade: Promising to conflicted — observational associations are consistent, but large randomised controlled trials in pregnancy are lacking. The direction of evidence is clear; the causality is less certain.
Several papers in our database highlight a crucial but often overlooked connection: selenium, the thyroid, and fertility are deeply intertwined [3][4][7][14]. The thyroid is one of the most selenium-rich organs in the body, and selenoproteins are essential for converting inactive thyroid hormone (T4) into its active form (T3) [4].
Autoimmune thyroid conditions like Hashimoto’s disease are associated with both low selenium and fertility problems. A 2013 review in *Hormones* confirmed that selenium supplementation — primarily as selenomethionine at around 200 µg/day — consistently reduces anti-thyroid antibody levels in clinical trials [14]. The male-fertility study mentioned earlier [3] similarly found that selenium improved not just sperm parameters but also thyroid hormone profiles in men with autoimmune thyroiditis.
A 2025 mouse study took this further, exploring what researchers called the “gut-thyroid-fertility axis” — the idea that selenium affects fertility partly by altering gut microbiome composition, which in turn influences thyroid function and reproductive hormones [9]. Selenium-supplemented mice showed increased plasma testosterone and testicular glutathione peroxidase activity, alongside meaningful changes in gut microbiome diversity. This is intriguing emerging science — but firmly early stage evidence from animal models.
Evidence grade: Promising (thyroid-selenium link in humans); Early stage (gut-thyroid-fertility axis)
The selenium-fertility story is biologically compelling, but there are significant gaps that any honest account must acknowledge.
The dose question is genuinely tricky. Unlike many nutrients, selenium has a narrow window between beneficial and harmful. Both deficiency *and* excess are associated with reproductive problems [2][4][5]. The studies reviewed here used doses ranging from 83 µg/day [3] to 200 µg/day [13][15] — all within what is generally considered safe, but the optimal dose for fertility specifically has not been established in well-powered human trials.
Most of the mechanistic evidence is still animal-based. The striking 67% reduction in fertilisation capacity from selenium deficiency came from mice [10]. The 2025 gut-thyroid-fertility axis work is also mouse data [9]. These findings are biologically plausible and consistent with human data, but we cannot assume direct equivalence.
Human trials are mostly small and short. The largest human trial here had 65 participants [15]; the IVF/PCOS trial had just 36 [13]. None of the studies we reviewed tracked live birth rates as a primary outcome, which is ultimately the most relevant measure for anyone trying to conceive. We have improvements in surrogate markers — sperm parameters, antibody levels, gene expression — but the leap to “more babies born” hasn’t been proven in an RCT.
The female fertility evidence is particularly thin. The systematic review covering female fertility identified only seven eligible studies across eight major databases [1]. This is a meaningful gap given that female factor infertility is as common as male factor.
Geographic variation matters. Selenium content in food depends heavily on soil selenium levels, which vary enormously by region. The UK, much of Europe, and parts of Australasia have notably selenium-depleted soils compared to the US or parts of Asia [7][8]. Studies from high-selenium regions may not translate to populations in low-selenium areas — and UK adults are particularly likely to be in the lower range.
The form of selenium may matter. Organic selenium (selenomethionine, found in food and many supplements) is absorbed and retained differently from inorganic forms (like sodium selenite) [4][8]. The 2025 mouse study found different effects from different selenium compounds [9]. Human studies comparing forms head-to-head are still limited.
Here’s how a sensible, well-informed person should think about this.
Selenium is a trace mineral where both deficiency and excess cause harm — but in the UK and much of Europe, deficiency is the far more common problem. Soil depletion means that even a balanced diet may not reliably deliver adequate selenium, particularly in people not eating Brazil nuts or much seafood [7][4]. For anyone in their reproductive years, or thinking seriously about fertility, this matters.
If you’re a man concerned about sperm quality, the human evidence — while not definitive — consistently points in one direction: selenium at 200 µg/day for several months improves sperm concentration, motility, and reduces DNA fragmentation in men with identified sperm abnormalities [15][3]. This is promising, not proven. But it’s also a safe, low-cost intervention with a reasonable biological rationale.
If you have autoimmune thyroid disease (Hashimoto’s or postpartum thyroiditis), selenium supplementation has among the strongest evidence in this entire field — consistently reducing thyroid antibody levels across multiple clinical trials [14][7]. Given that thyroid dysfunction is a significant driver of both male and female fertility problems, this connection deserves more attention than it typically receives.
For women, the evidence is earlier stage but directionally consistent: low selenium is associated with poorer follicular antioxidant environment, higher thyroid antibody levels, and worse pregnancy outcomes. The IVF/PCOS trial showing reduced inflammation markers at 200 µg/day is encouraging [13].
On the dose: 200 µg/day is the most commonly used dose in the fertility trials reviewed here, and it’s within safe limits for adults — the tolerable upper intake level in Europe is 300 µg/day. However, given that selenium accumulates (it’s not simply excreted like water-soluble vitamins), the sensible approach is not to exceed 200 µg/day from supplements, especially if your diet already includes selenium-rich foods. This is one case where “more is not more.” A standard supplement dose of 100–200 µg/day is appropriate; exceeding that without good reason is not.
Practically speaking: If you’re in the UK, eating an average British diet, and concerned about fertility or pregnancy, the risk of being selenium-insufficient is real and the cost of a selenium supplement is minimal. For most people, supplementing at 100–200 µg/day is a sensible, low-risk choice — particularly for anyone with thyroid autoimmunity, or men with sperm quality concerns. Brazil nuts are the food shortcut: one or two a day typically provides around 100 µg, though the content varies enormously by origin.
The big picture on selenium and fertility? It’s not magic. But it’s a mineral your reproductive system genuinely depends on, the research is pointing consistently in one direction, and most people in the UK are not getting enough. That’s a combination worth taking seriously.
[1] Selenium and female fertility — systematic review (2022). DOI: 10.1055/s-0042-1744288 | https://pubmed.ncbi.nlm.nih.gov/35668679/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9948146/
[2] Selenium in reproduction and pregnancy — review (2022). DOI: 10.3389/fnut.2022.1011850 | https://pubmed.ncbi.nlm.nih.gov/36386927/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9659920/
[3] Selenium supplementation in men with autoimmune thyroiditis and male infertility — clinical study (year not listed in record). DOI: 10.3390/jcm10163755 | https://pubmed.ncbi.nlm.nih.gov/34442049/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8397047/
[4] Selenium, selenoproteins, thyroid homeostasis and reproductive health — review (year not listed in record). DOI: 10.3390/nu13093256 | https://pubmed.ncbi.nlm.nih.gov/34579133/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8469766/
[5] Role of selenium in male reproduction — a review (2014). https://pubmed.ncbi.nlm.nih.gov/24613013/
[6] Selenium, selenoproteins and spermatogenesis — review (2024). DOI: 10.1016/j.heliyon.2024.e34975 | https://pubmed.ncbi.nlm.nih.gov/39144956/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11320318/
[7] Selenium in pregnancy — review (2020). DOI: 10.1186/s13044-020-00090-x | https://pubmed.ncbi.nlm.nih.gov/33014140/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7528225/
[8] Profiling of selenium absorption and accumulation after L-selenomethionine supplementation (2017). https://pubmed.ncbi.nlm.nih.gov/28393316/
[9] Dietary selenium and the gut-thyroid-fertility axis in male mice (2025). DOI: 10.1080/13510002.2025.2495367 | https://pubmed.ncbi.nlm.nih.gov/40277453/ | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035940/
[10] Effect of dietary selenium deficiency on in vitro fertilising ability of mice spermatozoa (2008). https://pubmed.ncbi.nlm.nih.gov/17973196/
[11] The effect of micronutrient supplements on female fertility — review (2013). https://pubmed.ncbi.nlm.nih.gov/23571830/
[12] Selenium transport, homeostasis and male reproduction — review (2025). DOI: 10.1016/j.bbrc.2025.151879 | https://pubmed.ncbi.nlm.nih.gov/40279800/
[13] The effects of selenium supplementation on clinical symptoms and gene expression related to inflammation and VEGF in infertile women candidate for IVF (2020). DOI: 10.1007/s12011-019-01715-5 | https://pubmed.ncbi.nlm.nih.gov/30963410/
[14] Selenium supplementation and autoimmune thyroid diseases — review (2013). https://pubmed.ncbi.nlm.nih.gov/24021243/
[15] The effect of selenium therapy on semen parameters, antioxidant capacity, and sperm DNA fragmentation in men with idiopathic oligoasthenoteratospermia (2023). DOI: 10.1007/s12011-023-03638-8 | https://pubmed.ncbi.nlm.nih.gov/36959435/
This article is for informational purposes only and does not constitute medical advice. Food supplements should not be used as a substitute for a varied and balanced diet and healthy lifestyle. If you are pregnant, breastfeeding, taking medication or have a medical condition, consult your doctor before taking any supplement. These statements have not been evaluated by the Food and Drug Administration (FDA) or the Medicines and Healthcare products Regulatory Agency (MHRA). This product is not intended to diagnose, treat, cure, or prevent any disease.
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