ZINC

Tldr; Zinc is an essential mineral found in high levels in animal tissues and eggs, legumes, and fish. It is exceptionally high in shellfish such as oyster.

Zinc is most commonly touted to be important as it is a cofacter in over 300 enzymes involved in gene expression, cell proliferation and signal transduction and deficiencies of zinc may reduce the activity of these enzymes.

One of its main functions is acting as a prosthetic group for various enzymes called metalloproteins and is also involved in regulating the immune system.

Studies have shown that ZnC has the potential to increase the migration and proliferation of colonic epithelial cells in vitro. This indicates that the compound could aid in promoting gastric healing by interacting with the epithelial cells found in the gastrointestinal (GI) tract. ZnC has demonstrated significant protective effects in animal models of NSAID- induced GI injury. ZnC has also been shown to prevent increased intestinal permeability from NSAID-induced injury in humans. Evidence for this effect is strong, having been demonstrated in a randomized, double blinded and placebo controlled trial with a crossover design. The effective dose of ZnC in this study (37.5 mg twice/day) is easily achievable with over the counter supplements.

Zinc is naturally occurring in the brain and acts as a neuromodulator. It is particularly concentrated in the hippocampus and pineal gland and is released during neuronal activity.

Zinc has been implicated in the regulation of serotonin uptake in specific areas of the brain. Research suggests that high concentrations of zinc are required for this effect, which may be physiologically relevant. Some antidepressant medications may reduce serotonin uptake in these brain regions if zinc levels are low.

Zinc has been noted to increase serum BDNF levels, with the magnitude of increase correlating highly with increases in serum zinc.

It should be noted that high levels of zinc, usually not achieved through supplementation unless taken in abnormally high doses, can potentially play a role in cell death during hypoxia or ischemia.

The addition of zinc (220mg twice daily) to fluoxetine therapy (20mg) for obsessive compulsive disorder (OCD) is able to reduce symptoms.

Zinc deficiencies are known to reduce appetite, and this is usually the first symptom of a zinc deficiency.

While zinc at 30mg elemental zinc appears to be slightly effective as an addition to D-amphetamine therapy, it does not appear to inherently have a significant therapeutic benefit.

Serum zinc concentrations and zinc status are negatively correlated with the risk of developing depression, and in persons who are depressed zinc status is further negatively correlated with the severity of depression. Supplementation of zinc at 25mg (elemental) or higher has preliminary evidence for working in humans either as adjuvant therapy with SSRIs or inherently.

Zinc deficiency is associated with impaired memory formation and impaired signalling of the BDNF growth factor, and improving zinc status is associated with betterment on both accounts.
An abnormally high zinc intake is also associated with memory impairment, and oddly it is associated with a reduction rather than surplus of zinc in the brain.

There is mixed evidence for whether zinc higher than the standard dietary intake is beneficial or negative for spatial memory formation, although at least one study noted that low dose copper exerted a protective effect against zinc (in a study where zinc had a negative effect).

In persons who suffered from stroke and have inadequate dietary intake, cognitive improvements following stroke appear to be accelerated relative to placebo.

Normalizing a zinc deficiency appears to be assosiated with a reduced risk for arterial plaque buildup (atherosclerosis).

Due to inhibiting GSK-3β, zinc can increase the activity of glycogen synthesis.

Zinc may positively influence insulin signalling via preventing a negative regulator (GSK3β) from suppressing insulin signalling. It can also augment uptake of glucose into cells that express insulin-sensitive GLUT4, but not other GLUT transporters.

While plasma measurements of zinc may not be completely reliable, studies suggest that individuals with both type I and type II diabetes are more likely to experience zinc deficiency which can be remedied fairly rapidly with zinc supplementation.

While plasma measurements of zinc may not be completely reliable, studies suggest that individuals with both type I and type II diabetes are more likely to experience zinc deficiency which can be remedied fairly rapidly with zinc supplementation. Adequate zinc levels are important for glucose metabolism in individuals with diabetes or insulin resistance. Zinc supplementation can improve glucose levels, insulin levels, and insulin sensitivity in those who are deficient in zinc. However, in individuals who are already sufficient in zinc, further supplementation may not provide any additional benefits.

Zinc deficiency is known to lead to a reduced count of T-cells and subsequently depressed humoral and cell-mediated immunity. Extremely high doses of supplemental zinc lead to impaired lymphocyte stimulation by T-cells in response to phytohemagglutinin, as well as reduced chemotaxis and phagocytosis from polymorphonuclear leukocytes. These effects suggest a greater susceptibility to infection.

Administering high doses of zinc at the onset of the common cold (rather than as a preventive measure) has shown to be effective in reducing the severity and duration of the illness. Supplementation of zinc daily as a preventative appears to reduce the rate of getting colds.

When used alone (monotherapy) to treat pneumonia, zinc typically does not seem to be more effective than a placebo. When zinc is used as an adjuvant with another drug for pneumonia treatment, it is generally found to be ineffective compared to the placebo group receiving the drug alone. In children, using 10-20mg of elemental zinc daily as a preventative for two weeks was unable to influence the occurrence of pneumonia.

Insufficient zinc levels can result in lower expression of androgen receptors and decreased testosterone synthesis in cells, leading to a reduction in the overall impact of testosterone.

In human instances of zinc deficiency, relatively modest supplemental dosages appear to be able to increase circulating testosterone concentrations.

Men with adequate zinc levels may experience preservation of zinc concentrations when engaging in strenuous exercise, but there is no evidence that zinc has any effect on testosterone levels in the absence of exercise.

In men with infertility, a rise in DHT levels is observed, indicating that the decreased zinc concentration (which enhances the activity of the 5α-reductase enzyme) is more significant.

Insufficient levels of zinc can lead to extensive damage to testicular function, which includes reduced production and release of testosterone, lowered fertility, decreased quality of sperm, and a higher likelihood of cell death.

A person with celiac disease who consumes gluten may experience intestinal distress and malabsorption due to their gluten intolerance, which can hinder the absorption of zinc and lead to a deficiency. This complication can be prevented by avoiding gluten and the need for zinc supplementation may be eliminated.

Pruritus (itch) during hemodialysis is alleviated with 440mg zinc sulfate daily over the period of one month to a degree larger than placebo.

Doses of elemental zinc between 30-160mg are associated with a higher incidence of altered taste perception and nausea.