Micronutrient status

Micronutrient status — whether the vitamins and minerals the body runs on are present in sufficient amounts

Absorption increases it.

Micronutrient-bioavailability review 2025, Front Nutr — the bioavailable (absorbable) fraction of a nutrient determines micronutrient status; low bioavailability drives inadequacy/deficiency despite intake. PMC12673670

Digestion increases it.

10.1177/03946320241313426 — https://www.merckmanuals.com/professional/gastrointestinal-disorders/malabsorption-syndromes/overview-of-malabsorption — Digestive function determines absorption, and micronutrient is a node touching multiple outcomes here. A supplement that is not absorbed is not a dose. doi 10.1177/03946320241313426

Gut barrier increases it.

10.3389/fnut.2019.00048 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3389/fnut.2019.00048

Liver increases it.

10.3390/biomedicines11041094 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3390/biomedicines11041094

Calms body-wide inflammation reduces it.

10.1186/s12967-023-04138-y — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.1186/s12967-023-04138-y

Oxidative stress reduces it.

10.1186/s12879-025-12377-1 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. Verbatim: “COVID-19 patients are prone to depleted levels of antioxidant substances due to their increase utilization in counterbalancing the negative effect of free radicals”. doi 10.1186/s12879-025-12377-1 · PMID 33614035 · PMC7871282

Master antioxidant increases it.

Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. Sources: PMC13074595; doi 10.3390/ijms26146740; doi 10.1139/H07-174. doi 10.3390/ijms26146740 · PMC13074595

Antioxidant defense increases it.

10.3389/fcell.2021.728172 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3389/fcell.2021.728172

Insulin sensitivity increases it.

10.3389/fnut.2024.1458700 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3389/fnut.2024.1458700

Thyroid increases it.

10.3389/fendo.2023.1089315 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3389/fendo.2023.1089315

Cellular fuel increases it.

Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. Sources: PMC13074595; doi 10.3390/ijms26146740; doi 10.1139/H07-174. doi 10.3390/ijms26146740 · PMC13074595

Cellular aging reduces it.

https://www.merckmanuals.com/professional/nutritional-disorders/undernutrition/overview-of-undernutrition — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. Sources: PMC13074595; doi 10.3390/ijms26146740; doi 10.1139/H07-174. doi 10.3390/ijms26146740 · PMC13074595

Alcohol metabolism reduces it.

37049411 — https://www.merckmanuals.com/professional/nutritional-disorders/vitamin-deficiency-dependency-and-toxicity/thiamin-deficiency — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. Sources: PMC13074595; doi 10.3390/ijms26146740; doi 10.1139/H07-174. doi 10.3390/ijms26146740 · PMC13074595

Kidney increases it.

10.3390/biomedicines12040911 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3390/biomedicines12040911

It increases Thyroid hormone conversion.

Deiodinase previously had NO upstream edge at all, leaving the thyroid arm unrooted. Verified at source (Redox Biol 2022, doi 10.1016/j.freeradbiomed.2022.09.024 / S0891584922006062): the iodothyronine deiodinases DIO1, DIO2 and DIO3 are a family of selenoproteins — selenocysteine is structural, encoded by in-frame TGA codons, so selenium is not a modulator but a requirement of the enzyme. DIO1 and DIO2 activate T4 to T3; DIO3 inactivates both. Selenium deficiency decreased DIO1 activity in rat liver and kidney, and selenium depletion reduced basal DIO2 expression and activity in a human cell line, reversible by selenium supplementation in a dose- and time-dependent manner. The caveat the review states itself, and it matters for any selenium claim: selenium status has a modest impact on DIO expression and translation. The most thoroughly investigated regulator of DIO1 is T3 itself — the Dio1 gene shows roughly 175-fold induction across the hypo- to hyperthyroid transition. Thyroid hormone status, growth factors and cytokines are named as the main regulators; selenium is a permissive requirement, not the lever. Iodine status has no direct effect on DIO expression, and whether iron status directly affects DIOs remains controversial. doi 10.1016/j.freeradbiomed.2022.09.024

It reduces Hair pigment loss.

Clinical case reports document premature graying caused by B12 deficiency that fully reversed after supplementation, with hair pigment returning to normal. An intervention with an endpoint clears a bar that a correlation does not. The association evidence is small and the authors say so. The largest series is a 71-case retrospective analysis from a single urban clinic, whose own conclusion is larger case-control studies ARE mandated for discerning the correlation. The supporting case-control studies enrolled 25 and 60 patients. All are retrospective, all single-center, and all concentrated in one region — which is a real limitation on generalising, not a slight on the work. And the limit that matters most: gray hair caused by genetics OR normal aging cannot be reversed through nutrition. The reversible fraction is the deficiency fraction. Anything sold on B12 reversing age-related graying is selling the wrong arm of this edge. The link rests on the peer-reviewed retrospective series and the review that cites the reversal reports. doi 10.1016/j.ad.2025.08.012 · PMID 28584374

It increases Muscle.

High-quality protein and leucine metabolites preserve lean mass. Same caveat as the Vitamin D → Skeletal Muscle Mass link: they fail to consistently restore function independently, and anabolic resistance means higher levels of dietary protein and amino acids ARE required to stimulate muscle protein synthesis effectively - the dose that worked at 30 does not work at 70. doi 10.3390/ijms26146740 · PMC13074595

It reduces Attention regulation.

Iron is the rate-limiting cofactor for tyrosine hydroxylase in catecholamine synthesis, and the reviews place ADHD’s causes squarely in brain catecholamines. The cofactor role is established biochemistry but NO retrieved source measures iron repletion improving attention as an endpoint - and this is the same bar that refused the Iron Status → Hair Greying link. Shown as weaker evidence: just as graying needed a repletion study with a pigment endpoint, this needs one with an attention endpoint. (PMC4033238; doi 10.1016/j.biopsych.2011.03.003; PMC2265273. doi 10.1016/j.biopsych.2011.03.003 · PMC4033238

It increases Sustained focus.

Iron is the rate-limiting cofactor for tyrosine hydroxylase in catecholamine synthesis, and the reviews place ADHD’s causes squarely in brain catecholamines. The cofactor role is established biochemistry but NO retrieved source measures iron repletion improving attention as an endpoint - and this is the same bar that refused the Iron Status → Hair Greying link. Shown as weaker evidence: just as graying needed a repletion study with a pigment endpoint, this needs one with an attention endpoint. (PMC4033238; doi 10.1016/j.biopsych.2011.03.003; PMC2265273. doi 10.1016/j.biopsych.2011.03.003 · PMC4033238

It increases Liver.

A diet rich in fermented milk, cereals, coffee and tea increases microbial richness and reduces hospitalisations in patients with cirrhosis. A human clinical endpoint - hospitalisations - from a dietary exposure, which is rarer in this literature than mechanism. doi 10.1038/s41522-022-00352-6 · PMC11265038

It increases Digestion.

Named across six gut-liver axis reviews. The main alteration is dysbiosis - A decrease in beneficial bacteria, an increase in potentially harmful microbes, and a loss of overall microbial diversity - with intestinal barrier integrity determining the levels of microbial metabolites, ENDOTOXINS and ammonia that reach the liver and systemic circulation. doi 10.1038/s41522-022-00352-6 · PMC11265038

It reduces Neurovascular calm.

Named across six migraine pathophysiology reviews. Migraine pathogenesis is widely accepted to be attributed to neuroinflammation and sensitization of the trigeminovascular system. PMID 36361791 · PMC10933035

It increases Physical performance.

Named across the retrieved reviews as a determinant of this outcome. doi 10.1139/H07-174 · PMC10102650

It reduces Urate clearance.

The architecture is unusually clean and worth stating: gout has two separable stages. Stage one is metabolic - urate underexcretion through renal and gut mechanisms is the major mechanism for hyperuricemia in most people, via URAT1, GLUT9 and ABCG2. Stage two is immunological - MSU crystals function as damage-associated molecular patterns which, upon phagocytosis by macrophages, activate the NLRP3 inflammasome through a two-step process: priming via NF-kB signaling and activation via lysosomal rupture, potassium efflux, and mitochondrial ROS. And the two stages come apart in people: not all individuals with hyperuricemia show deposition of MSU crystals OR develop gout. Local factors decide - reduced joint temperature, low pH, high sodium concentration, and preexisting joint damage. A urate number is not a diagnosis. The treatment target is explicit: long-term lowering of serum urate to less than 360 MICROMOL/L leads to crystal dissolution and ultimately to suppression of flares. PMID 39712248 · PMC8268734

It increases Recovery.

10.3390/nu15030521 — Recovery is assembled from the sarcopenia and VO2max literatures; none of the papers cited studied recovery itself. Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3390/nu15030521

It increases Vitamin D status.

https://www.degruyterbrill.com/document/doi/10.7556/jaoa.2018.037/html — Drawn from the reviews of this outcome. doi 10.7556/jaoa.2018.037/html

It increases Omega-3 status.

10.3389/fmolb.2025.1623547 — Drawn from the reviews of this outcome. doi 10.3389/fmolb.2025.1623547

It increases Resists infection.

The headline on this pathway is a disappointment and it must stay there: the lack of effect of prophylactic vitamin C supplementation on the incidence of common cold in normal populations throws doubt on the utility of this wide practice. Regular supplementation decreases cold duration by 8 percent (3-12) and severity by 15 percent (CI 9-21) - but does not reduce how often you get one. With one striking exception that defines WHO it works for: a subgroup of six studies of marathon runners, skiers, and soldiers exposed to significant cold AND/OR physical stress experienced, on average, 50 percent reduction in common cold incidence. Extreme physical stress is the condition under which it prevents. PMC10712193

Female Fertility (Oocyte Competence) →

Endurance Eternal (Pigment Preservation) →

Lung Power (Respiratory Capacity) →