Immunity Boosting Vitamins

It is essential to follow a healthy diet to ensure good immune function.‏  Studies show that while certain dietary patterns may lead to impaired immune function, other dietary patterns promote optimal immune function.

Dietary patterns and inpidual foods have associations with increased disease risk, greater risk of allergy, and impaired immune response.‏ Western-type diets‏ tend to contain high levels of saturated fat, ultra-processed foods, added sugar and salt, and overall calories. This diet is often low in foods associated with better health, such as vegetables, fruits, and fatty fish, and has strong links to an increased risk of chronic disease.‏

Western-type diets induce inflammation and alter immune system function, promoting disease development.‏ In contrast, diets rich in whole foods, such as vegetables, fruits, nuts, legumes, and seafood, and low in ultra-processed foods can reduce disease risk and ‏promote healthy immune function‏.

Additionally, a deficiency or insufficiency of ‏nutrients‏ essential to immune function, including vitamin D, zinc, and vitamin C, can also affect immune response. Nutrient ‏deficiencies‏ may be more common in those consuming ultra-processed diets low in whole, nutrient-dense foods.‏

Nutrition, Immunity and Infection

The immune system is functioning at all times, but cells become activated by the presence of pathogens. This activation results in a significant increase in the demand of the immune system for energy yielding substrates (glucose, amino acids and fatty acids). Activation of the immune response induces the production of lipid-derived mediators such as prostaglandins and leukotrienes and of many different types of protein including immunoglobulins, chemokines, cytokines, cytokine receptors, adhesion molecules and acute-phase proteins. This requires availability of the substrate fatty acids and amino acids, respectively. The immune response involves significant cellular proliferation, so increasing the number of immune cells available for defence: this requires DNA, RNA, protein and complex lipid synthesis and the ready availability of substrates to support this. The metabolic machinery involved in energy generation and biosynthesis requires many different vitamins and minerals as cofactors. Amino acids (e.g., arginine) are precursors for the synthesis of polyamines, which have roles in the regulation of DNA replication and cell pision.

Various micronutrients (e.g., iron, folate, zinc, magnesium) are also involved in nucleotide and nucleic acid synthesis. Some nutrients, such as vitamins A and D, and their metabolites are direct regulators of gene expression in immune cells and play a key role in the maturation, differentiation and responsiveness of immune cells. Creation of a pro-oxidant environment through generation of damaging reactive oxygen species is one element of innate immunity; the host needs protection against these through classic antioxidant vitamins (vitamins C and E) and the antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase); the latter require manganese, copper, zinc, iron and selenium.

In essence, good nutrition creates an environment in which the immune system is able to respond appropriately to challenge, irrespective of the nature of the challenge. Conversely poor nutrition creates an environment in which the immune system cannot respond well.

Vitamin A, Immunity and Infection

Vitamin A is important for normal differentiation of epithelial tissue and for immune cell maturation and function. Thus, vitamin A deficiency is associated with impaired barrier function, altered immune responses and increased susceptibility to a range of infections.

Vitamin A-deficient mice show breakdown of the gut barrier and impaired mucus secretion (due to loss of mucus-producing goblet cells), both of which would facilitate entry of pathogens. Many aspects of innate immunity, in addition to barrier function, are modulated by vitamin A and its metabolites.

Vitamin A controls neutrophil maturation and in vitamin A deficiency blood neutrophil numbers are increased, but they have impaired phagocytic function. Therefore, the ability of neutrophils to ingest and kill bacteria is impaired. Vitamin A also supports phagocytic activity and oxidative burst of macrophages, so promoting bacterial killing. Natural killer cell activity is diminished by vitamin A deficiency, which would impair antiviral defences.

Vitamin A controls dendritic cell and CD4+ T lymphocyte maturation and its deficiency alters the balance between T helper 1 and T helper 2 lymphocytes. Studies in experimental model systems indicate that the vitamin A metabolite 9-cis retinoic acid enhances T helper 1 responses. Retinoic acid promotes movement (homing) of T lymphocytes to the gut-associated lymphoid tissue. Interestingly, some gut-associated immune cells are able to synthesise retinoic acid. Retinoic acid is required for CD8+ T lymphocyte survival and proliferation and for normal functioning of B lymphocytes including antibody generation. Thus, vitamin A deficiency can impair the response to vaccination, as discussed elsewhere.

Vitamin A-deficient children provided with vitamin A showed a higher antibody response to tetanus vaccination than seen in vitamin A-deficient children. Vitamin A deficiency predisposes to respiratory infections, diarrhoea and severe measles. Systematic reviews and meta-analyses of trials in children with vitamin A report reduced all-cause mortality, reduced incidence, morbidity and mortality from measles and from infant diarrhoea, and improved symptoms in acute pneumonia.

B-group Vitamins

B vitamins are involved in intestinal immune regulation, thus contributing to gut barrier function. Folic acid deficiency in animals causes thymus and spleen atrophy, and decreases circulating T lymphocyte numbers. Spleen lymphocyte proliferation is also reduced but the phagocytic and bactericidal capacity of neutrophils appears unchanged. In contrast, vitamin B12 deficiency decreases phagocytic and bacterial killing capacity of neutrophils, while vitamin B6 deficiency causes thymus and spleen atrophy, low blood T lymphocyte numbers and impaired lymphocyte proliferation and T lymphocyte-mediated immune responses. Vitamins B6 and B12 and folate all support the activity of natural killer cells and CD8+ cytotoxic T lymphocytes, effects which would be important in antiviral defence. Patients with vitamin B12 deficiency had low blood numbers of CD8+ T lymphocytes and low natural killer cell activity.

In a study in healthy older humans, a vitamin B6-deficient diet for 21 days resulted in a decreased percentage and total number of circulating lymphocytes, and a decrease in T and B lymphocyte proliferation and IL-2 production. Repletion over 21 days using vitamin B6 at levels below those recommended did not return immune function to starting values, while repletion at the recommended intake did.

Vitamin C

Vitamin C is required for collagen biosynthesis and is vital for maintaining epithelial integrity. It also has roles in several aspects of immunity, including leucocyte migration to sites of infection, phagocytosis and bacterial killing, natural killer cell activity, T lymphocyte function (especially of CD8+ cytotoxic T lymphocytes) and antibody production. A vitamin C-deficient diet in healthy young adult humans decreased mononuclear cell vitamin C content by 50% and decreased the T lymphocyte-mediated immune responses to recall antigens. Vitamin C deficiency in animal models increases susceptibility to a variety of infections.

People deficient in vitamin C are susceptible to severe respiratory infections such as pneumonia.Vitamin C supplementation has also been shown to decrease the duration and severity of upper respiratory tract infections, such as the common cold, especially in people under enhanced physical stress.

Vitamin D

Vitamin D receptors have been identified in most immune cells and some cells of the immune system can synthesise the active form of vitamin D from its precursor, suggesting that vitamin D is likely to have important immunoregulatory properties. Vitamin D enhances epithelial integrity and induces antimicrobial peptide (eg, cathelicidin) synthesis in epithelial cells and macrophages, directly enhancing host defence.

Vitamin D promotes differentiation of monocytes to macrophages and increases phagocytosis, superoxide production and bacterial killing by innate immune cells. It also promotes antigen processing by dendritic cells although antigen presentation may be impaired. Vitamin D is also reported to inhibit T-cell proliferation and production of cytokines by T helper 1 lymphocytes and of antibodies by B lymphocytes, highlighting the paradoxical nature of its effects. Effects on T helper 2 responses are not clear and vitamin D seems to increase number of regulatory T lymphocytes.

A systematic review and meta-analysis of the influence of vitamin D status on influenza vaccination (nine studies involving 2367 inpiduals) found lower seroprotection rates to influenza A virus subtype H3N2 and to influenza B virus in those who were vitamin D deficient. There is an inverse linear relationship between vitamin D levels and respiratory tract infections.

Supplementation of Japanese schoolchildren with vitamin D for 4 months during winter decreased the risk of influenza by about 40%. Vitamin D supplementation can reduce the risk of respiratory tract infections.