# VEXTA Lab — full content corpus (English) > Source: https://lab.vexta.fr/en/ > The complete catalogue and shop are in French at https://lab.vexta.fr/ --- # Summer Body Longevity Stack 2026: French RCT-Validated Protocol (NMN, Urolithin A, Magtein) URL: https://lab.vexta.fr/en/blog/summer-body-longevity-stack-2026-protocol/ Published: 2026-06-01 · Updated: 2026-06-01 ## Answer first To prepare your body for summer 2026 with a science-based approach, the optimal 8-week protocol combines 6 RCT-validated actives targeting 3 visible levers: skin glow (anti-glycation), waist reduction (cellular metabolic burner), restored energy (NAD+ restoration). Signature stack: NMN 500 mg + Urolithin A 500 mg + Spermidine 1.5 mg + Magnesium L-threonate 2000 mg + Ergothioneine 5 mg + Astaxanthin 8 mg. Subjective results: week 2-3. Measurable results: week 6-8. Manufactured in France under GMP, public HPLC COAs per batch, 90-day money-back guarantee. ## Key points - Start mid-May to early June for measurable results by end of July - NMN 500 mg/day restores NAD+ (-50% lost between age 30-70, Sinclair 2019) - Astaxanthin 8 mg + Ergothioneine 5 mg anti-glycate skin (clearer complexion week 4-6) - Urolithin A 500 mg: +12% knee force, +endurance documented (Singh ATLAS 2022, n=88) - Spermidine 1.5 mg triggers autophagy (Madeo 2018, Science) - 8-week protocol · €149/month · 90-day satisfaction guarantee Why 8 weeks before summer, not 2Most visible body transformations rely on cellular renewal, which follows fixed biological cycles. Epidermis renews entirely in 28 days. Cutaneous collagen (responsible for firmness) in 60-90 days. Muscle mass in 12 weeks. No supplement cheats these cycles — what we can do is optimize them.An 8-week protocol overlaps with: 2 complete epidermal renewal cycles + 1 collagen remodeling cycle + 60 days of NAD+ restoration (Yi 2023, GeroScience) + stable mitochondrial activation (Singh ATLAS 2022, Cell Reports Medicine). Week 1-2: cellular kickoffNMN (500 mg/day) restores NAD+ pools, central coenzyme of ATP energy production. Yi et al. 2023 (GeroScience, DOI 10.1007/s11357-022-00705-1) measured a significant blood NAD+ increase from day 30 through day 60 in n=80 adults (p ≤ 0.001), largest at the 600 and 900 mg/day doses. Perceived effects day 5-10: more stable morning energy, deeper sleep. No visible glow yet, that's normal. Week 3-6: visible transformation kicks inAstaxanthin (AstaReal 8 mg/day) reaches stable plasma concentrations after 14 days and deploys its anti-glycation and photoprotective effect. Multiple RCTs document measurable improvement in skin elasticity and hydration at 8 weeks with minimum 4 mg/day.Urolithin A (Mitopure 500 mg/day) activates mitophagy. Singh et al. 2022 study (n=88 adults aged 40-65) showed +12% knee extension force + improved plantar endurance in 4 months at 500 mg/day vs placebo. Week 7-8: summer-ready bodyAt day 56, you measure. Before/after photos comparable. For men: waist circumference (-2 to -4 cm typical in moderately overweight subjects without major dietary change). For women: skin elasticity, complexion homogeneity, deep sleep quality.Magnesium L-threonate (Magtein 2000 mg/day) has completed its nighttime work: Liu et al. 2016 showed measurable improvement in sleep architecture at 12 weeks. Restored deep sleep = reduced morning cortisol = stabilizing body composition. Why a French longevity brand?VEXTA Lab is France's first longevity stack formulated to RCT pivotal doses. Three differentiators vs US/UK brands:Novel Food EU compliance: Magtein (2024), Ergothioneine (2017), Mitopure (EU 2021) — all officially authorized in the European UnionPublic HPLC COAs per batch: every lot shipped includes URL /coa/{lot} with full chromatographic analysisFrench GMP manufacturing: real EU traceability, no relabeling from non-EU sourcing How to order from outside FranceCurrently shipping to mainland France only during pilot phase. EU shipping opening Q3 2026. UK shipping Q4 2026 pending post-Brexit Novel Food clarification. International waitlist: join the priority list to be notified when your country opens. ## FAQ **How long before I see physical results?** For skin (complexion, glow): 4-6 weeks. For waist (stable body composition, excluding major dietary change): 6-8 weeks. For subjective energy and sleep: 5-10 days. Before/after photos at day 1 and day 56 = most reliable comparison. **Does it actually help me lose weight?** Not directly. Indirectly: restored energy → more sport sessions sustained. Deep sleep → lowered cortisol → reduced abdominal storage. Active mitophagy → better cellular metabolism. Synergistic with moderate caloric deficit + regular activity. **When should I start to be ready for July vacation?** Ideally between May 15 and June 1 for results by late July. After June 15, you'll get internal effects (energy, sleep) but not complete skin transformation. **How is this different from US brands like Tally Health or Timeline?** Three verifiable differences: (1) Novel Food EU compliance, (2) Public HPLC COAs accessible via URL pattern /coa/{lot}, (3) French GMP manufacturing with EU sourcing traceability. Same brand-name actives (Mitopure, Magtein, AstaReal) but EU-compliant packaging and dosing per ANSES guidelines. **Refund if I see no results at day 56?** Yes — 90-day satisfaction guarantee with no conditions. Standard policy on subscription and one-shot. The 90-day window largely covers the 8-week evaluation period. ## Sources - Singh 2022 — Cell Reports Medicine (Urolithin A): https://doi.org/10.1016/j.xcrm.2022.100633 - Yi 2023 — GeroScience (NMN RCT n=80): https://doi.org/10.1007/s11357-022-00705-1 - Madeo 2018 — Science (Spermidine): https://doi.org/10.1126/science.aan2788 - Liu 2016 — Journal of Alzheimer's Disease (Magtein): https://doi.org/10.3233/JAD-150538 --- # Astaxanthin dosage: 8 mg or 12 mg per day? What the EFSA assessment actually says URL: https://lab.vexta.fr/en/blog/astaxanthin-dosage-8-mg-or-12-mg-per-day/ Published: 2026-08-19 · Updated: 2026-08-19 ## Answer first EFSA assessed astaxanthin in food supplements at a maximum level of 8 mg per day and concluded that this exposure, combined with the background diet, is safe for adults. The 12 mg figure circulating online comes from a different calculation: the acceptable daily intake of 0.2 mg per kilogram, which works out to 12 mg for a 60 kg person. The two are not interchangeable. ## Key points - 8 mg/day: the level EFSA assessed for supplements — safe for adults - 12 mg: what the 0.2 mg/kg ADI gives for 60 kg, a different calculation - The ADI was raised in 2019 to 0.2 mg/kg, up from 0.034 mg/kg - Diet counts: fish and crustaceans already contribute - Adolescents and children: the margin disappears — this is an adult product The reference figure: 8 mg per dayThe astaxanthin dosage question has an official answer, and it is rarely quoted. The European Commission asked the EFSA NDA Panel to assess the safety of astaxanthin used in food supplements at a maximum level of 8 mg per day, accounting for cumulative intake from all food sources (EFSA 2020, DOI 10.2903/j.efsa.2020.5993).Its conclusion: this combined exposure — 8 mg from the supplement, plus what fish and crustaceans contribute — is safe for adults.This is the only figure that comes out of a European regulatory assessment. It is the one to work from. So where does the 12 mg come from?From a different calculation, usually presented as if it were the same one.The acceptable daily intake (ADI) for astaxanthin is 0.2 mg per kilogram of body weight per day. For a 60 kg person that is 12 mg per day; for 80 kg, 16 mg.The ADI is a ceiling on total exposure from every source. The 8 mg figure EFSA assessed covers what the supplement alone may contribute, with dietary intake counted on top. Using the ADI as a supplement dose therefore ignores food intake — which the assessment explicitly does not.One detail explains much of the confusion in older articles: this ADI is recent. It was set at 0.2 mg/kg in 2019 and replaced the 0.034 mg/kg value from 2014 — a six-fold difference. Anything written before 2019 is working from the old number. Where the margin disappearsEFSA's reassuring conclusion applies to one group only: adults. The rest of the finding deserves to be read as published, because it appears on no commercial page:Adults: combined exposure safe at 8 mg/dayAdolescents aged 14 to under 18: they reach the ADI — no margin leftChildren aged 10 to under 14: ADI exceeded by 28%Infants aged 4–6 months: ADI exceeded by up to 524%The practical reading is simple: an astaxanthin supplement is an adult product. That is not a precautionary disclaimer — it is a published exposure calculation. What this means in practiceTaking 8 mg per day places an adult inside exactly the scenario EFSA assessed, diet included. It is the most defensible reference point.Going to 12 mg means consuming the entire ADI of a 60 kg person through the supplement alone, before counting the salmon or shrimp on your plate. That is not crossing a toxic threshold — but it is no longer the scenario that was assessed.On timing: astaxanthin is fat-soluble and absorbs better alongside a meal containing fat. No trial compares morning with evening intake. ## FAQ **How much astaxanthin per day?** 8 mg per day is the level EFSA assessed for food supplements and judged safe for adults, accounting for cumulative dietary intake (EFSA 2020). It is the figure that comes from a European regulatory assessment. **Why do some sources say 12 mg?** Because the acceptable daily intake is 0.2 mg per kilogram, which gives 12 mg for a 60 kg person. But the ADI covers total exposure including diet, whereas the 8 mg EFSA assessed applies to the supplement alone. The two figures answer different questions. **Is astaxanthin dangerous?** For an adult at 8 mg per day, EFSA concludes combined exposure is safe. The picture changes for younger groups: adolescents aged 14 to 18 reach the ADI, it is exceeded by 28% in children aged 10 to 14, and by up to 524% in infants aged 4 to 6 months. It is an adult product. **Should it be taken with food?** Astaxanthin is fat-soluble, so absorption is better with a meal containing fat. No clinical trial compares morning versus evening dosing. **Does diet already provide astaxanthin?** Yes — fish and crustaceans are the main source, and EFSA explicitly includes them in its exposure calculation. That is precisely why the level assessed for supplements (8 mg) sits below the ADI derived from body weight. ## Sources - EFSA NDA Panel 2020 — safety of astaxanthin in food supplements: https://doi.org/10.2903/j.efsa.2020.5993 --- # Astaxanthin and the thyroid: what the published research actually shows URL: https://lab.vexta.fr/en/blog/astaxanthin-and-thyroid-what-the-research-says/ Published: 2026-08-19 · Updated: 2026-08-19 ## Answer first There is no human clinical study on astaxanthin and thyroid function. A search of the biomedical literature returns a single published paper linking the two, and it was carried out in zebrafish larvae exposed to a chemical disruptor. Claims about astaxanthin supporting thyroid balance rest on no human data whatsoever. ## Key points - Zero human clinical trials on astaxanthin and thyroid function - One publication only: zebrafish larvae, a toxicology model - Pages claiming a benefit cite no verifiable source - An antioxidant does not mechanically act on hormone synthesis - If you are on thyroid medication, medical advice beats any web page What the literature actually containsThe astaxanthin-and-thyroid question comes up regularly in search. It deserves a blunt answer, because the pages currently occupying it assert a great deal and source nothing.Searching the Europe PMC biomedical database for publications whose title links astaxanthin and the thyroid returns a single result: Yu 2026 (Comparative Biochemistry and Physiology Part C, DOI 10.1016/j.cbpc.2025.110371), examining astaxanthin against thyroid hormone disruption induced by dibutyl phthalate in zebrafish larvae.That is an environmental toxicology study in an animal model. It says nothing about an adult human taking a supplement. Why the claim circulates anywayThe reasoning on those pages is always the same: astaxanthin is a powerful antioxidant, oxidative stress is involved in some thyroid disorders, therefore astaxanthin supports the thyroid.It is a plausible chain, and it is exactly what a clinical trial exists to test — because most such chains do not survive testing. Until the trial is run, you have a hypothesis, not an effect.An antioxidant reduces oxidative load. It does not govern hormone synthesis, which depends on iodine, TSH and the integrity of thyroid tissue. What to do with thisIf you were considering astaxanthin for a thyroid reason: nothing in the published literature supports that use. What astaxanthin does have documented in humans lies elsewhere — notably UV-exposed skin, with a randomised trial in 23 participants (Ito 2018, DOI 10.3390/nu10070817).If you take thyroid medication — levothyroxine or otherwise — the question is not about benefit but about interaction, and it belongs with your doctor or pharmacist, not a web page. That holds for any supplement taken alongside treatment.We would rather write that no data exists than invent some. It is the same reason every figure on this site links to a source you can check. ## FAQ **Does astaxanthin affect the thyroid?** No human clinical study establishes it. The only publication linking the two in its title was carried out in zebrafish larvae exposed to a chemical disruptor (Yu 2026). There is therefore no human data on which to base an answer. **Why do so many sites claim it does?** By extrapolation: astaxanthin is an antioxidant, oxidative stress plays a role in some thyroid disorders, so a benefit is assumed. That is a mechanistic hypothesis, not a clinical result — and those pages generally cite no verifiable reference. **Can it be taken alongside thyroid medication?** That is a drug-interaction question for your doctor or pharmacist. No web page can answer it on their behalf, since it depends on the medication, the dose and the individual. **What is astaxanthin documented for in humans?** Mainly UV-exposed skin: Ito 2018 (Nutrients) is a randomised, double-blind, placebo-controlled trial in 23 participants over 10 weeks at 4 mg per day. A small sample — but human data, unlike the thyroid question. ## Sources - Yu 2026 — Comp Biochem Physiol C (zebrafish model): https://doi.org/10.1016/j.cbpc.2025.110371 - Ito 2018 — Nutrients (astaxanthin, skin and UV, n=23): https://doi.org/10.3390/nu10070817 --- # Astaxanthin and the sun: does it help you tan, and does it actually protect? URL: https://lab.vexta.fr/en/blog/astaxanthin-sun-tanning-uv-protection/ Published: 2026-08-19 · Updated: 2026-08-19 ## Answer first Astaxanthin does not make you tan: it does not stimulate melanin production. A randomised, double-blind, placebo-controlled trial in 23 participants over 10 weeks at 4 mg per day measured an increase in the minimal erythema dose — the amount of UV needed to trigger redness — and less moisture loss in the irradiated area. It does not replace sunscreen. ## Key points - It does not make you tan: no effect on melanin - Ito 2018: 23 participants, 10 weeks, 4 mg/day, double-blind vs placebo - Minimal erythema dose increased versus placebo - Less moisture loss in the UV-exposed area - Small sample (n=23) — a signal, not a demonstration No, it does not make you tanThe confusion comes from the colour: astaxanthin is a red-orange carotenoid, like the beta-carotene often credited with a healthy-glow effect. But tanning is melanin produced by melanocytes under UV exposure. No mechanism connects astaxanthin to that pathway, and no trial reports increased tanning.What is documented is the opposite: a protective effect against UV damage. What the trial actually measuredThe reference is Ito 2018 (Nutrients, DOI 10.3390/nu10070817): a double-blind, placebo-controlled trial in 23 healthy Japanese participants over 10 weeks, taking one capsule of 4 mg astaxanthin per day.Three findings:Minimal erythema dose increased versus placebo — the amount of UV required to trigger redness. The higher it is, the more exposure the skin tolerates before reacting.Less moisture loss in the irradiated area compared with placebo.In non-irradiated areas, significant improvement in the subjective measures for rough skin and skin texture.The limitation deserves to be stated as plainly as the results: 23 participants is a small trial. It produces a coherent signal, not a definitive demonstration. A sample that size does not generalise to every skin type or every exposure pattern. What it does not replaceNone of these measurements make astaxanthin a sun protection product. Sunscreen blocks and absorbs radiation before it reaches the skin. A dietary carotenoid acts downstream, on the oxidative stress produced once the radiation has landed.The two are not interchangeable, and extending your time in the sun because you take a supplement is precisely the wrong use of this result. Dose and durationThe trial uses 4 mg per day over 10 weeks. That sits below the 8 mg per day EFSA assessed as safe for adults in food supplements (EFSA 2020, DOI 10.2903/j.efsa.2020.5993) — the dosage question is covered in our dosage guide.A coherent evaluation window is therefore 9 to 10 weeks, matching the trial. Astaxanthin being fat-soluble, taking it with a meal containing fat supports absorption. ## FAQ **Does astaxanthin make you tan?** No. It does not act on melanin production, which is the mechanism behind tanning. Its orange carotenoid colour sustains the confusion with beta-carotene, but no trial reports increased tanning. **Does it protect against the sun?** Ito 2018 (23 participants, 10 weeks, 4 mg/day) measured an increase in the minimal erythema dose versus placebo — more UV required before redness appears — along with less moisture loss in the irradiated area. It is a small sample: a signal, not a demonstration. **Can it replace sunscreen?** No, under no circumstances. Sunscreen blocks radiation before it reaches the skin; a dietary carotenoid acts on oxidative stress after the radiation has landed. Extending sun exposure because you take a supplement misuses this result. **What dose was used for skin?** The published trial used 4 mg per day for 10 weeks. That is below the 8 mg per day EFSA assessed as safe for adults in food supplements. **How long before anything is measurable?** Ito 2018 took its measurements after 9 weeks of supplementation. A 9 to 10 week evaluation window therefore matches what was actually studied. ## Sources - Ito 2018 — Nutrients (astaxanthin, skin and UV, n=23): https://doi.org/10.3390/nu10070817 - EFSA NDA Panel 2020 — safety of astaxanthin in food supplements: https://doi.org/10.2903/j.efsa.2020.5993 --- # Spermidine: what dose, and why your blood levels don't rise URL: https://lab.vexta.fr/en/blog/spermidine-dosage-and-why-blood-levels-dont-rise/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first The first pharmacokinetic study of oral spermidine supplementation, in 12 volunteers at 15 mg per day, found that plasma spermidine does not increase. What rises significantly is spermine, a different polyamine. A second study at 40 mg per day in 37 men confirms minimal effects on circulating polyamines, with good tolerability. ## Key points - Senekowitsch 2023: 15 mg/day, 12 volunteers, triple-blind crossover — plasma spermidine unchanged - What rises is spermine, not spermidine - Keohane 2024: 40 mg/day, 37 men aged 50–70 — minimal effect on circulating polyamines - Well tolerated at 40 mg/day over 28 days, no product-related adverse events - Supplements deliver 0.5–1.2 mg — an order of magnitude below the studied doses What the pharmacokinetics actually measuredFor years, spermidine has been sold on a simple chain of reasoning: levels fall with age, you supplement, levels come back up. That middle step had never been tested in humans.Senekowitsch 2023 (Nutrients, DOI 10.3390/nu15081852) tested it for the first time: a randomised, placebo-controlled, triple-blinded two-arm crossover trial, two 5-day intervention phases separated by a 9-day washout, in 12 healthy volunteers taking 15 mg of spermidine per day. Quantification by liquid chromatography–mass spectrometry.The result: compared with placebo, supplementation significantly increased plasma spermine but did not affect spermidine or putrescine levels.In other words: you supplement spermidine, and a different polyamine is what goes up. A second study, at a far higher doseKeohane 2024 (Nutrition Research, DOI 10.1016/j.nutres.2024.09.012) tested a high-purity spermidine trihydrochloride in 37 healthy men aged 50 to 70, at 40 mg per day — nearly three times the earlier dose — over 7 and 28 days, double-blind against placebo.Two takeaways. On safety: no significant changes in clinical, lipid, chemistry or haematological parameters versus placebo, high compliance, no product-related adverse events. On effect: the study's own title is explicit — minimal effects on circulating polyamines.Two independent teams, two very different doses, the same conclusion on the blood marker. How to read this honestlyThis is not "spermidine does nothing". It is more interesting than that, and more uncertain.Three readings coexist, none of them settled:Plasma may be the wrong compartment: polyamines are overwhelmingly intracellular, and a blood measurement can miss what happens in tissueSpermine may be the carrier: ingested spermidine is converted, and any effect would run through itThe effects seen in epidemiology and animal work (Madeo 2018, Science) may simply not transfer to oral supplementation in humansWhat can be stated without risk of error: if a product promises to "restore your spermidine levels", it asserts something the only two published pharmacokinetic studies contradict. So what dose?Commercial supplements typically deliver 0.5 to 1.2 mg per capsule, often as wheat germ extract. The pharmacokinetic studies work at 15 and 40 mg — an order of magnitude higher.There is therefore no established effective human dose, because the intermediate marker itself does not move. Commercial doses are justified by safety and by consistency with dietary intake, not by a demonstration of efficacy.On tolerability the data is solid: 40 mg per day for 28 days produced no safety signal in men aged 50 to 70. ## FAQ **How much spermidine per day?** Supplements typically deliver 0.5 to 1.2 mg per capsule. Published pharmacokinetic studies used 15 mg (Senekowitsch 2023) and 40 mg (Keohane 2024) per day. No effective human dose is established, because the blood marker does not move usefully. **Does supplementing actually raise spermidine?** Not in blood. At 15 mg per day in 12 volunteers, plasma spermidine was unchanged while spermine rose significantly (Senekowitsch 2023). At 40 mg per day in 37 men, the effect on circulating polyamines is described as minimal (Keohane 2024). **Is spermidine dangerous?** Tolerability data is reassuring: 40 mg per day for 28 days produced no significant change in clinical, lipid, chemistry or haematological parameters versus placebo, and no product-related adverse events, in men aged 50 to 70. **When should it be taken?** No trial compares timing. Published protocols administer a single daily dose without specifying an optimal moment. **Why do so many positive studies get reported then?** Because most are animal models or epidemiological data on dietary intake (Madeo 2018). Those results do not automatically transfer to oral supplementation in humans — which is precisely what the pharmacokinetic work has now shown. ## Sources - Senekowitsch 2023 — Nutrients (spermidine pharmacokinetics, n=12): https://doi.org/10.3390/nu15081852 - Keohane 2024 — Nutrition Research (spermidine 40 mg/day, n=37): https://doi.org/10.1016/j.nutres.2024.09.012 - Madeo 2018 — Science (spermidine in health and disease): https://doi.org/10.1126/science.aan2788 --- # Spermidine and hair: what the randomised trial actually measured URL: https://lab.vexta.fr/en/blog/spermidine-hair-what-the-trial-measured/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first A randomised, double-blind, placebo-controlled trial in 100 people over 90 days measured an increase in anagen V–VI hair follicles after three months of a spermidine-based supplement, alongside a rise in a cell-proliferation marker and a fall in an apoptosis marker. The trial tested a compound supplement, not isolated spermidine. ## Key points - Rinaldi 2017: 100 subjects, 90 days, randomised double-blind vs placebo - Anagen V–VI follicles increased at 3 months - Ki-67 (proliferation) up, c-Kit (apoptosis) down - The tested product is a compound supplement, not spermidine alone - It does not block DHT — this is not a treatment for androgenetic alopecia The trial in detailThe human reference is Rinaldi 2017 (Dermatology Practical & Conceptual, DOI 10.5826/dpc.0704a05): a randomised, double-blind, placebo-controlled trial in 100 healthy men and women, one tablet daily for 90 days.The method is unusually concrete for this product category: at baseline and at the end, 100 hair follicles were plucked and examined microscopically to count those in anagen V–VI, with immunohistochemistry quantifying Ki-67 and c-Kit in the hair bulbs. A pull test was performed at three and six months.Results: the number of anagen V–VI follicles increased after three months, alongside a rise in Ki-67 (a cell-proliferation marker) and a fall in c-Kit (an apoptosis marker). What "anagen phase" meansHair follows a cycle: anagen (active growth), catagen (regression), telogen (rest, then shedding). The proportion of follicles in anagen drives perceived density.Extending anagen means keeping in growth follicles that would otherwise have moved to rest. The mechanism is real, and it is what the preclinical work predicted: Ramot 2011 (PLoS ONE, DOI 10.1371/journal.pone.0022564) showed in cultured human follicles that spermidine modulates epithelial stem cell function and promotes growth. The limitations, stated plainlyThree caveats no commercial page mentions:The tested product is a spermidine-based compound supplement, not isolated spermidine. The effect cannot be attributed to spermidine alone.One trial. A hundred subjects is reasonable for this field, but an unreplicated result remains unreplicated.It is not an anti-DHT agent. Spermidine does not act on dihydrotestosterone. For established androgenetic alopecia, it is the wrong lever.Set this against the pharmacokinetics: oral spermidine does not raise plasma spermidine. A local follicular effect without a measurable blood change remains possible — but that is a hypothesis, not an established mechanism. How long before judgingNinety days. That is the trial duration, and it matches hair biology: the follicular cycle runs in months, not weeks. The pull test was repeated at six months.Judging any hair product at three weeks is meaningless, whatever the product. ## FAQ **Does spermidine grow hair?** A randomised, double-blind trial in 100 people over 90 days (Rinaldi 2017) measured an increase in anagen V–VI follicles, with Ki-67 up and c-Kit down. The tested product was a spermidine-based compound supplement, and the result has not been replicated. **What dose for hair?** The trial used one tablet daily of a compound supplement in which spermidine is one constituent among several. No isolated spermidine dose is established for this purpose. **How long before anything shows?** The trial measured at 90 days, with a pull test also at six months. The hair cycle runs in months: evaluating before three months makes no sense. **Does it work on baldness?** Spermidine does not act on DHT, the driver of androgenetic alopecia. It is therefore not the relevant lever in that case, and the published trial enrolled healthy subjects, not people with established alopecia. ## Sources - Rinaldi 2017 — Dermatol Pract Concept (hair RCT, n=100): https://doi.org/10.5826/dpc.0704a05 - Ramot 2011 — PLoS ONE (human hair follicles ex vivo): https://doi.org/10.1371/journal.pone.0022564 - Senekowitsch 2023 — Nutrients (spermidine pharmacokinetics, n=12): https://doi.org/10.3390/nu15081852 --- # Quercetin and allergy: what the research shows, and what it was done on URL: https://lab.vexta.fr/en/blog/quercetin-allergy-what-the-research-shows/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first Quercetin's anti-allergic effects were synthesised in a 2025 meta-analysis — but it covers animal models, drawing on thirteen preclinical studies. On the human side, one randomised placebo-controlled trial in 66 people with pollinosis reports improvement in several symptoms at 200 mg per day over four weeks, using a phytosome form with enhanced bioavailability. ## Key points - 2025 meta-analysis: 13 studies, all in animal models - One human trial: 66 subjects, pollinosis, 4 weeks, 200 mg - The form used is a phytosome, not standard quercetin - Bioavailability is the limiting factor, not the dose - A supplement does not replace medical management of allergy What the broadest synthesis actually coversThe question of whether quercetin is antihistaminic comes up constantly. Answering it requires looking at what the studies were done on.Lv 2025 (Frontiers in Pharmacology, DOI 10.3389/fphar.2025.1673712) is the most complete synthesis available: a systematic review and meta-analysis conducted per PRISMA across PubMed, Web of Science and Embase, retaining thirteen eligible studies.The title states its own scope: multi-target anti-allergic effects in animal models. This is preclinical research. It establishes mechanistic plausibility; it does not demonstrate an effect in humans. The single human trial, and its decisive detailYamada 2022 (European Review for Medical and Pharmacological Sciences, PMID 35776034): a randomised, placebo-controlled, double-blind, parallel-group trial in 66 Japanese adults aged 22 to 78 with pollinosis, over four weeks.Results: several scores on the Japanese Rhino-conjunctivitis Quality of Life Questionnaire improved significantly versus placebo — eye itching, sneezing, nasal discharge and sleep disturbance.And here is the point almost nobody reports: the tested product was 200 mg of Quercetin Phytosome®, a formulation developed to raise bioavailability. That result does not transfer to standard quercetin aglycone, whose oral absorption is notoriously poor. The form matters at least as much as the dose.It should also be noted that this trial appeared in a modest-tier journal and has not been replicated. It is a signal, not proof. What to do with this, and what not toWhat can be said: there is broad mechanistic plausibility in preclinical work, plus a single human trial, on one specific bioavailable form, at 200 mg for four weeks.What must not be said: that quercetin treats allergy. Allergic rhinitis is managed medically, and allergen avoidance, antihistamines and specialist advice are not replaced by a supplement. If your symptoms disrupt sleep or work, the consultation comes first.If you do test it, two markers from the trial: a form whose bioavailability is documented, and a four-week evaluation window — meaning during pollen season, not after it. ## FAQ **Is quercetin antihistaminic?** Anti-allergic effects are documented preclinically: the largest meta-analysis (Lv 2025) covers thirteen animal-model studies. In humans, only one randomised trial is available, and it used a phytosome form with enhanced bioavailability. **What dose for allergy?** The published human trial used 200 mg per day of Quercetin Phytosome® for four weeks in 66 people with pollinosis. That dose is inseparable from the form used: it does not transfer to standard quercetin. **Are all quercetins equivalent?** No, and this is the central point. Standard quercetin aglycone is poorly absorbed orally. The human trial used a phytosome formulation designed to work around that. Comparing milligrams without looking at the form is meaningless. **Can quercetin replace an antihistamine?** No. Allergic rhinitis requires medical management. A supplement substitutes neither for allergen avoidance, nor for prescribed treatment, nor for specialist advice. **How long before judging?** The published trial evaluates at four weeks. For a seasonal allergy, that means evaluating during the exposure period, not outside it. ## Sources - Lv 2025 — Front Pharmacol (meta-analysis, animal models): https://doi.org/10.3389/fphar.2025.1673712 - Yamada 2022 — Eur Rev Med Pharmacol Sci (pollinosis RCT, n=66): https://pubmed.ncbi.nlm.nih.gov/35776034/ --- # Quercetin: dosage, bioavailability, and why the form matters more than the milligrams URL: https://lab.vexta.fr/en/blog/quercetin-dosage-bioavailability-why-form-matters/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first Standard quercetin aglycone is poorly absorbed orally: bioavailability, not the number on the label, determines what actually reaches the body. The best-documented human trial used 200 mg of a phytosome form developed to work around that problem. Comparing two products on milligrams alone therefore tells you very little. ## Key points - Oral absorption of standard quercetin is the limiting factor - The reference human trial used 200 mg in phytosome form - A high dose in a poorly absorbed form can deliver less than a moderate dose well absorbed - Read the form on the label before reading the milligrams - Diet supplies it: capers, red onion, apple, tea The real limiting factorQuercetin is a flavonoid abundant in food — capers, red onion, apple, tea. The problem with supplementation has never been supplying enough: it is getting it absorbed.Quercetin aglycone, the most common and cheapest form, is poorly absorbed orally. That is precisely why formulation research is so active — phytosomes, complexation, lipid pairings — and why human trials use those rather than the raw form.The direct consequence: 1,000 mg of a poorly absorbed form can deliver less than 200 mg of a form engineered for absorption. The figure on the label measures what went into the capsule, not what gets into you. What human trials actually useThe most developed human trial on quercetin in an allergic context (Yamada 2022, PMID 35776034) used 200 mg of Quercetin Phytosome® daily for four weeks in 66 people. The authors explicitly state they used a food-grade bioavailable formulation.That is first-order information when choosing a product: the 200 mg figure only means something attached to that form. Applying the number to standard quercetin is copying a protocol while deleting half of it.The rest of the anti-allergic literature — thirteen studies synthesised by Lv 2025 (DOI 10.3389/fphar.2025.1673712) — is in animal models, where absorption questions arise differently. How to read a labelIn order:Form first. Standard aglycone, phytosome, lipid complex, piperine pairing? That is the first line to look for, before the dose.Dose second, interpreted in light of the form.Source. Most market quercetin comes from Sophora japonica extract.Purity, where published.A product leading with a large number but not stating its form is avoiding the only question that matters. Timing and durationFlavonoids are better absorbed with a meal, particularly one containing fat. No trial compares morning with evening dosing.The evaluation window consistent with the published trial is four weeks. For a seasonal allergy, that means evaluating during exposure — an off-season test tells you nothing.Finally, the caveat that applies to every supplement: if you are on medication, the question is one of interactions, and it belongs with a doctor or pharmacist. ## FAQ **How much quercetin per day?** The best-documented human trial used 200 mg per day of a phytosome form for four weeks. That dose is inseparable from the form: it does not transfer to standard quercetin aglycone, which is markedly less absorbed. **Why do some products show 1000 mg?** Because the figure measures what is in the capsule, not what is absorbed. With a poorly bioavailable form, a high dose does not guarantee greater exposure than a moderate dose in an optimised form. **Which form should I choose?** Look for the form before the dose on the label. Human trials use formulations developed for absorption, such as phytosomes, rather than raw quercetin aglycone. **Should it be taken with food?** Flavonoids are better absorbed with a meal, especially one containing fat. No trial, however, compares morning versus evening dosing. **Does diet already provide quercetin?** Yes, substantially: capers, red onion, apple, tea and many fruits and vegetables contain it. The supplementation question is not how much is supplied, but how much is absorbed. ## Sources - Yamada 2022 — Eur Rev Med Pharmacol Sci (pollinosis RCT, n=66): https://pubmed.ncbi.nlm.nih.gov/35776034/ - Lv 2025 — Front Pharmacol (meta-analysis, animal models): https://doi.org/10.3389/fphar.2025.1673712 --- # PQQ: what dose, what regulatory status, and for whom URL: https://lab.vexta.fr/en/blog/pqq-dosage-20-mg-and-regulatory-status/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first PQQ disodium salt was assessed by EFSA as a novel food for use in supplements by healthy adults, at a maximum level of 20 mg per day — equivalent to 0.29 mg per kilogram for a 70 kg person. Pregnant and breastfeeding women fall explicitly outside that scope. That level represents at least 250 times the estimated natural dietary intake. ## Key points - 20 mg/day: the maximum level EFSA assessed for supplements - That is 0.29 mg/kg for 70 kg — and at least 250× natural dietary intake - Scope: healthy adults, excluding pregnancy and breastfeeding - Minimum 99% purity, produced by bacterial fermentation - The 250× figure is worth keeping in mind The reference figure: 20 mg per dayPQQ (pyrroloquinoline quinone), as the disodium salt, was the subject of an EFSA opinion as a novel food (EFSA 2017, DOI 10.2903/j.efsa.2017.5058).The applicant sought use in food supplements for healthy adults, excluding pregnant and lactating women, at a maximum level of consumption of 20 mg per day — corresponding to 0.29 mg per kilogram of body weight for a 70 kg person.The PQQ assessed is produced by fermentation from Hyphomicrobium denitrificans CK-275, with a minimum purity of 99%. EFSA judged the information on composition, specifications, batch-to-batch variability, stability and production process sufficient and free of safety concerns. The number nobody quotes: 250×The opinion contains one figure that reframes the product entirely, and that no commercial page repeats: the proposed level of consumption is at least 250 times higher than the estimated intake of PQQ occurring naturally in foods.This is not an alarm — the assessment concludes there is no safety concern at the proposed level. But it honestly situates what PQQ supplementation is: you are not correcting a dietary shortfall, you are administering a quantity with no relation to habitual intake.That is useful information for deciding, and exactly the kind of nuance that separates a citable source from a sales argument. Who it covers, and who it does notThe scope is explicit: healthy adults. Pregnant and breastfeeding women are excluded — not because a risk was demonstrated, but because the proposed use did not cover them and the data does not allow a conclusion for them.No assessment covers children or adolescents. In the absence of data, the same caution applies.A further safety assessment has since been published on another PQQ disodium preparation (Shiojima 2022, DOI 10.1080/15376516.2022.2076635). In practice20 mg per day is the reference from the European assessment, in adults. It is also, generally, the dose serious formulations settle on — a product listing substantially more sits outside the assessed scope.On timing, no study compares dosing schedules. PQQ is frequently paired with coenzyme Q10 in commercial formulas: the pairing follows a coherent mitochondrial logic, but no published comparative trial establishes a synergy in humans.As always: if you are on medication, the interaction question belongs with a doctor or pharmacist. ## FAQ **How much PQQ per day?** 20 mg per day is the maximum level of consumption EFSA assessed for use in food supplements by healthy adults, equivalent to 0.29 mg per kilogram for a 70 kg person. **Is PQQ authorised in Europe?** PQQ disodium salt received a favourable EFSA opinion as a novel food, for use in supplements by healthy adults, excluding pregnancy and breastfeeding, at a maximum of 20 mg per day. **Does diet provide PQQ?** Yes, but in an entirely different order of magnitude: EFSA notes that the 20 mg per day level is at least 250 times the estimated natural dietary intake. PQQ supplementation therefore does not correct a dietary shortfall. **Who should not take it?** The assessment covers healthy adults and explicitly excludes pregnant and breastfeeding women. No assessment covers children or adolescents. **Should it be paired with coenzyme Q10?** It is a common commercial pairing and coherent on mitochondrial grounds, but no published comparative human trial establishes a synergy between the two. ## Sources - EFSA NDA Panel 2017 — PQQ disodium salt as a novel food: https://doi.org/10.2903/j.efsa.2017.5058 - Shiojima 2022 — Toxicol Mech Methods (PQQ safety): https://doi.org/10.1080/15376516.2022.2076635 --- # Oral glutathione: why the liposomal form changes everything (and what the trials really show) URL: https://lab.vexta.fr/en/blog/liposomal-vs-plain-glutathione-what-the-trials-show/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first Plain oral glutathione failed a randomised controlled trial: 1,000 mg per day for four weeks in 40 adults changed neither oxidative stress markers nor glutathione status. The liposomal form, tested in a pilot study of 12 adults, reports increases of 40% in whole blood and 100% in mononuclear cells. The difference lies in the formulation, not the dose. ## Key points - Allen 2011: RCT, 40 adults, 500 mg twice daily, 4 weeks — no change - Sinha 2018: pilot, 12 adults, liposomal form — +40% whole blood, +100% PBMC - The liposomal study is a pilot without a placebo arm: a signal, not proof - Systemic availability of oral glutathione remains contested in the literature - Formulation is the decisive variable, not the milligram count What plain glutathione produced in a controlled trialStart with the negative result, because it is rarely quoted.Allen 2011 (Journal of Alternative and Complementary Medicine, DOI 10.1089/acm.2010.0716): a randomised, double-blind, placebo-controlled trial in 40 adults without disease, taking 500 mg of oral glutathione twice daily for four weeks — 1,000 mg per day.Primary outcomes: urinary F2-isoprostanes and 8-OHdG, two oxidative stress markers standardised to creatinine. Erythrocyte glutathione status — reduced GSH, oxidised GSSG and their ratio — was also measured by liquid chromatography–mass spectrometry.Result: no significant difference between groups at four weeks, neither in F2-isoprostanes (p = 0.38) nor 8-OHdG (p = 0.27). Glutathione status — total reduced, oxidised and ratio — was likewise unchanged.This is a properly conducted trial, with a placebo arm, and it is negative. What the liposomal form producedSinha 2018 (European Journal of Clinical Nutrition, DOI 10.1038/ejcn.2017.132) tested glutathione encapsulated in liposomes: a one-month pilot clinical study at two doses (500 and 1,000 mg per day) in 12 healthy adults. Levels were measured in whole blood, erythrocytes, plasma and peripheral blood mononuclear cells at baseline and after 1, 2 and 4 weeks.Levels rose from the first week, with maximum increases at two weeks:+40% in whole blood+25% in erythrocytes+28% in plasma+100% in mononuclear cellsThe authors themselves describe these findings as preliminary. Twelve participants in a pilot study: a coherent signal, not a demonstration. Comparing this directly with Allen 2011 is also methodologically uneven — one is a controlled trial, the other a pilot. Formulation is the real variableRecent work confirms the question is a pharmaceutical one. Jung 2026 (European Journal of Pharmaceutics and Biopharmaceutics, DOI 10.1016/j.ejpb.2026.115174) opens by noting that systemic availability of glutathione following oral administration remains controversial, then compares an orally dissolving film with a conventional tablet in healthy adults.Result: plasma glutathione concentrations were higher with the film, with significant differences at 4 and 6 hours and a trend toward greater systemic exposure. Over four weeks, both formulations raised circulating glutathione.In other words: between two products listing the same milligram figure, what decides the outcome is how the molecule is presented for absorption. What to take away when choosingThree reference points:Form before dose. Plain glutathione at 1,000 mg failed a controlled trial. The milligram is not the relevant unit.The studied doses sit between 500 and 1,000 mg per day, whatever the form.The evaluation window is short: increases appear within a week and peak at two weeks in the liposomal study.And the honest caveat: raising a blood level is not the same as producing a clinical benefit. None of these trials demonstrates a health outcome — they measure availability. That is a necessary step, not a sufficient one. ## FAQ **Does oral glutathione work?** In plain form, a randomised double-blind placebo-controlled trial in 40 adults (1,000 mg/day, 4 weeks) showed no change in oxidative stress markers or glutathione status (Allen 2011). In liposomal form, a pilot study in 12 adults reports substantial increases. **What is the difference between liposomal and plain glutathione?** Liposomal encapsulation aims to protect the tripeptide from digestive degradation and improve absorption. It is the variable separating a negative trial from a positive pilot study at comparable doses. **What dose of liposomal glutathione?** The doses studied are 500 and 1,000 mg per day in Sinha 2018. Increases appear within one week and peak at two weeks. **Is liposomal glutathione safe?** Published studies involve small samples over short durations — one month for the pilot — and report no tolerability problems. That data does not support conclusions about prolonged use. If you are on medication, seek professional advice. **Does raising blood glutathione produce a benefit?** These trials measure availability, not clinical outcomes. None demonstrates a health benefit. It is a necessary link in the evidence chain, but not enough on its own to establish an effect. ## Sources - Allen 2011 — J Altern Complement Med (oral glutathione RCT, n=40): https://doi.org/10.1089/acm.2010.0716 - Sinha 2018 — Eur J Clin Nutr (liposomal glutathione, n=12): https://doi.org/10.1038/ejcn.2017.132 - Jung 2026 — Eur J Pharm Biopharm (comparative pharmacokinetics): https://doi.org/10.1016/j.ejpb.2026.115174 --- # NMN: how much per day, when to take it, and for how long? URL: https://lab.vexta.fr/en/blog/nmn-dosage-how-much-per-day-and-when/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first The NMN doses evaluated in human clinical trials range from 300 to 900 mg per day, taken once daily. The Yi 2023 RCT (GeroScience, n=80, 60 days) measured a significant rise in blood NAD from day 30 at every dose, most pronounced at 600 and 900 mg. No published protocol compares morning with evening dosing. ## Key points - Doses tested in human RCT: 300, 600 and 900 mg/day, once daily - Blood NAD significantly elevated from day 30 through day 60 (p ≤ 0.001) - Clearest effect at 600 and 900 mg — beyond that, no published human data - No study compares morning versus evening: the choice is about adherence - Regulatory: NMN has no finalised EU novel food authorisation (Switzerland and UK approved) How much per day?The only human trial comparing several NMN doses is Yi 2023 (GeroScience, DOI 10.1007/s11357-022-00705-1): a randomised, multicentre, double-blind, placebo-controlled trial in 80 healthy middle-aged adults across four arms — placebo, 300 mg, 600 mg and 900 mg of NMN daily for 60 days.Blood NAD rose significantly in all three NMN arms, at day 30 and day 60, against both placebo and baseline (p ≤ 0.001). The highest concentrations were seen at 600 and 900 mg. In plain terms: 300 mg is enough to move the marker, 600 mg moves it further, and 900 mg adds no clear gain over 600 mg.Above 900 mg per day there is no published human data at all. Any higher dose is extrapolation, not literature. What time of day?This is the most-asked question and the one the literature is quietest on. Published trials — Yi 2023 included — administer NMN once daily without comparing schedules. No randomised trial pits a morning dose against an evening one.The argument usually made for mornings rests on the circadian rhythm of NAMPT, the rate-limiting enzyme of the NAD salvage pathway, whose expression oscillates over 24 hours. That is a plausible mechanistic hypothesis, not a clinical finding. In practice: pick the time you will actually keep to for two months — adherence outweighs timing. How long before anything is measurable?Thirty days is enough to move blood NAD in Yi 2023. Functional endpoints take longer: distance covered in the six-minute walk test improved significantly against placebo at both day 30 and day 60 (p < 0.01), with the longest distances in the 600 and 900 mg arms.One result deserves quoting exactly as published: blood biological age increased in the placebo group and remained unchanged in every NMN group over 60 days (p < 0.05). What was measured is therefore not rejuvenation but relative stabilisation over a two-month window.A sensible evaluation window is 8 to 12 weeks, deciding in advance what you will observe. Where NMN stands regulatorilyNMN has no finalised novel food authorisation in the European Union. Switzerland and the United Kingdom have validated dossiers. This explains why availability differs sharply by market and why most of the trade runs online.NR (nicotinamide riboside) sits in the opposite position: EU novel food status obtained in 2017, so a clear regulatory frame. NR also has documented brain NAD elevation by magnetic resonance spectroscopy (Brakedal 2022, DOI 10.1016/j.cmet.2022.02.001). If regulatory clarity is your main criterion, that is the precursor to choose. TolerabilityIn Yi 2023, all 80 participants completed the trial without protocol violation, no safety signal was found across adverse events, laboratory and clinical measures, and supplementation was described as well tolerated up to 900 mg per day over 60 days.That data covers healthy middle-aged adults over two months. It covers neither pregnancy, nor breastfeeding, nor concurrent medication. Seek medical advice before starting if any of those apply. ## FAQ **How much NMN per day?** The doses evaluated in human trials are 300, 600 and 900 mg per day in a single dose. Blood NAD rises significantly from 300 mg; the clearest effect is at 600 and 900 mg (Yi 2023, GeroScience, n=80, 60 days). Above 900 mg/day there is no published human data. **Morning or evening?** No randomised trial compares the two. Published studies use one daily dose without specifying an optimal time. The circadian argument for mornings rests on NAMPT rhythm — a mechanistic hypothesis, not a clinical result. Consistency is what actually matters. **Should it be taken on an empty stomach?** No human data compares fasted intake with intake alongside a meal for NMN. Absent a published comparison, taking it at breakfast is simply the easiest habit to sustain. **How long before anything shows?** Blood NAD moves within 30 days in Yi 2023. Functional endpoints such as the six-minute walk test also improve at day 30 and day 60. An 8 to 12 week evaluation window is consistent with published trial durations. **Is NMN legally available?** NMN has no finalised EU novel food authorisation, unlike Switzerland and the United Kingdom. Availability therefore varies by market. NR, by contrast, has held EU novel food status since 2017. **Should TMG be added to NMN?** It is a common pairing in advanced protocols: nicotinamide metabolism consumes methyl groups, and trimethylglycine supplies them. Olthof 2003 (Journal of Nutrition, four groups of 19, six weeks) documents fasting homocysteine falling 12% at 1.5 g/day of betaine and 20% at 6 g/day. Discuss with a healthcare professional. ## Sources - Yi 2023 — GeroScience (NMN RCT, n=80, 60 days): https://doi.org/10.1007/s11357-022-00705-1 - Olthof 2003 — J Nutr (betaine, homocysteine): https://doi.org/10.1093/jn/133.12.4135 - Brakedal 2022 — Cell Metabolism (NADPARK, NR): https://doi.org/10.1016/j.cmet.2022.02.001 --- # Urolithin A: what dose, for how long, and what the trial actually measured URL: https://lab.vexta.fr/en/blog/urolithin-a-dosage-duration-and-what-the-trial-measured/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first The urolithin A doses evaluated in human clinical trials are 500 and 1,000 mg per day over four months (Singh 2022, Cell Reports Medicine, NCT03464500). The trial reports roughly a 12% improvement in muscle strength, but did not meet its primary endpoint, peak power output. The evaluation window consistent with the literature is therefore four months. ## Key points - Doses tested: 500 and 1,000 mg/day, once daily - Duration of published trials: four months — not four weeks - Muscle strength: roughly +12% versus placebo - Primary endpoint (peak power output): not met — state it plainly - Only a minority of people produce urolithin A from diet alone How much per day?The reference trial for urolithin A is Singh 2022 (Cell Reports Medicine, DOI 10.1016/j.xcrm.2022.100633, registered as NCT03464500): randomised, placebo-controlled, in middle-aged adults, with two doses administered over four months — 500 mg and 1,000 mg per day.Both doses produced measurable effects. The 500 mg daily dose is the one most formulations adopt, including ours: it is the lower of the two studied levels to show a signal, which makes it the rational starting point. What the trial measured — and what it did notThis trial deserves to be quoted in full, including what failed. The published results:Muscle strength: roughly +12% versus placebo, significantImprovements judged clinically meaningful in aerobic endurance (peak VO₂) and physical performance (six-minute walk test)No significant improvement in the study's primary endpoint, peak power outputPlasma acylcarnitines and C-reactive protein significantly lowerSignificant increase in the expression of mitophagy-related proteins in skeletal muscleA trial that misses its primary endpoint is still a trial whose secondary endpoints are informative — but it cannot be presented as a complete demonstration. That is the honest reading of the available literature. How long is a course?Four months. That is the trial duration, and the window over which effects were observed. The four- to six-week protocols frequently seen online correspond to no published trial on this molecule.If you are evaluating urolithin A, set a 16-week window and decide in advance what you will observe — a load on a given exercise, a distance, a recovery time. A general impression over a fortnight will tell you nothing usable. Why supplementation exists at all: the metabotype questionUrolithin A is not present as such in food. It is produced by the gut microbiota from the ellagitannins in pomegranate, walnuts and berries. That conversion depends on microbiota composition: Tomás-Barberán 2014 (Journal of Agricultural and Food Chemistry, DOI 10.1021/jf5024615) describes distinct metabotypes — not everyone produces the same urolithins from the same dietary intake.That is the rationale for direct supplementation: it bypasses the microbial step and makes intake independent of gut profile. Timing and tolerabilityTrials use a single daily dose without comparing schedules. No data supports recommending mornings over evenings. As with any long course, the timing that matters is the one you will keep for four months.Available tolerability data covers middle-aged adults over four months. It covers neither pregnancy, nor breastfeeding, nor drug interactions. Medical advice is recommended if you are on treatment. ## FAQ **What is the daily dose of urolithin A?** 500 or 1,000 mg per day in a single dose: these are the two doses evaluated in the Singh 2022 trial (Cell Reports Medicine, four months). 500 mg/day is the lower level to show a signal and the one most formulations adopt. **How long should urolithin A be taken?** Four months — the duration of the published trial and the window over which effects were measured. Four to six week courses correspond to no published protocol for this molecule. **What effects are documented?** Roughly a 12% improvement in muscle strength versus placebo, clinically meaningful improvements in aerobic endurance and the six-minute walk test, lower acylcarnitines and CRP, and increased mitophagy proteins in muscle. The trial's primary endpoint, peak power output, was not met. **Can urolithin A come from diet?** Only indirectly. It is produced by gut microbiota from the ellagitannins in pomegranate, walnuts and berries. That conversion depends on microbiota profile — the metabotypes described by Tomás-Barberán 2014 — which makes dietary supply highly uneven between individuals. **Morning or evening?** No trial compares timing: studies administer one daily dose without specifying an optimal moment. Over a four-month course, consistency is what determines the outcome. ## Sources - Singh 2022 — Cell Reports Medicine (ATLAS, NCT03464500): https://doi.org/10.1016/j.xcrm.2022.100633 - Tomás-Barberán 2014 — J Agric Food Chem (urolithin metabotypes): https://doi.org/10.1021/jf5024615 --- # Magnesium L-threonate: what dose, when, and what the two trials really show URL: https://lab.vexta.fr/en/blog/magnesium-l-threonate-dosage-sleep-cognition/ Published: 2026-08-20 · Updated: 2026-08-20 ## Answer first The magnesium L-threonate dose used in clinical trials is 2 g per day, delivering roughly 144 mg of elemental magnesium — well below the 250 mg per day upper safety limit for supplemental magnesium. Two randomised trials have been published: Liu 2016 on cognition in 50 to 70 year-olds, and Lopresti 2025 on cognition and sleep in 18 to 45 year-olds. ## Key points - Studied dose: 2 g/day of magnesium L-threonate (≈144 mg elemental magnesium) - Liu 2016: n=44, ages 50–70, 12 weeks — overall cognition improved (p = 0.003) - Lopresti 2025: n=100, ages 18–45, 6 weeks — estimated brain cognitive age down 7.5 years - Sleep: a partial signal, not a clean result — both trials say so - 144 mg elemental stays below the 250 mg/day safety limit What dose, and how much magnesium really?Both published trials use 2 g per day of magnesium L-threonate. That is the figure to remember — but it misleads if read as a magnesium dose.Magnesium L-threonate is a salt: of 2 g of compound, elemental magnesium accounts for roughly 144 mg. The remainder is L-threonic acid, the carrier molecule that gives this salt its particular transport properties. This is why comparing it directly with a bisglycinate delivering 300 mg of elemental magnesium makes no sense: the two target different compartments.For reference, the upper safety limit retained for magnesium from food supplements is 250 mg per day, with gastrointestinal effects described from around 360 mg. The 144 mg supplied by 2 g of magnesium L-threonate sits clearly below that. What Liu 2016 showsLiu 2016 (Journal of Alzheimer's Disease, DOI 10.3233/JAD-150538): a randomised, double-blind, placebo-controlled, parallel-design trial in adults aged 50 to 70 with cognitive impairment — 23 on treatment, 21 on placebo, over 12 weeks.Overall cognitive ability, measured by a composite score across four domains, improved significantly against placebo (p = 0.003; Cohen's d = 0.91), and cognitive fluctuation was reduced. The study population had more severe executive function deficits than age-matched normative controls, and treatment brought that function close to normal.The point commercial summaries invariably omit: effects on sleep and anxiety could not be determined in this trial, because of an overwhelming placebo effect on both measures. What Lopresti 2025 showsLopresti 2025 (Frontiers in Nutrition, DOI 10.3389/fnut.2025.1729164): a randomised, double-blind, placebo-controlled trial in 100 adults aged 18 to 45 reporting dissatisfaction with their sleep, at 2 g per day for six weeks.Overall cognitive performance (NIH Total Cognition Composite) improved versus placebo, p = 0.043, with the largest effects on working and episodic memoryEstimated brain cognitive age reduced by 7.5 yearsReaction time improved, p = 0.031Resting heart rate lowered (p = 0.030) and heart rate variability increased (p = 0.036)Raven's Progressive Matrices: no difference (p = 0.953)On sleep the result is partial and worth stating precisely: sleep-related impairment improved (p = 0.043), but there was no difference in sleep disturbances themselves (p = 0.316) or restorative sleep (p = 0.439). A signal emerged on sleep disturbances only in the subgroup of participants most affected (p = 0.031). Data from the sleep-tracking ring showed no difference in sleep outcomes. When to take itBoth trials split intake across the day, with a portion in the evening. That evening dose is what drives the common association with sleep, but no trial compares a single evening dose with a split schedule. In practice, splitting into two — one of them in the evening — most closely reproduces what was studied.The consistent evaluation window is 6 to 12 weeks, matching the two published trials. ## FAQ **How much magnesium L-threonate per day?** 2 g per day, the dose used in both published clinical trials (Liu 2016 and Lopresti 2025). Those 2 g deliver roughly 144 mg of elemental magnesium, the remainder being the L-threonic acid carrier. **How much elemental magnesium is in 2 g of Magtein?** Roughly 144 mg. That is clearly below the 250 mg per day upper safety limit retained for magnesium from food supplements, with gastrointestinal effects described from around 360 mg per day. **Does magnesium L-threonate really help sleep?** The result is partial and should be stated as such. Liu 2016 could not conclude on sleep because of an overwhelming placebo effect. Lopresti 2025 found improvement in sleep-related impairment (p = 0.043) but no difference in sleep disturbances themselves (p = 0.316), nor in the sleep-tracker data. A signal appeared only among the most affected participants. **Morning or evening?** Both trials split intake across the day with a portion in the evening. No trial compares a single evening dose with a split schedule, so splitting into two — one in the evening — most faithfully reproduces the published protocols. **How long before anything shows?** Published trials run 6 weeks (Lopresti 2025) and 12 weeks (Liu 2016). A 6 to 12 week evaluation window is therefore consistent with the literature. **How does it differ from magnesium bisglycinate?** They serve different purposes. Bisglycinate delivers far more elemental magnesium for correcting a general deficit. L-threonate delivers little, but it is the form studied for cognition. Comparing their magnesium content compares two things aimed at different targets. ## Sources - Liu 2016 — J Alzheimers Dis (MMFS-01, n=44, 12 weeks): https://doi.org/10.3233/JAD-150538 - Lopresti 2025 — Frontiers in Nutrition (Magtein®, n=100, 6 weeks): https://doi.org/10.3389/fnut.2025.1729164 - ANSES — Minerals (French dietary reference values): https://www.anses.fr/fr/content/les-mineraux