Vitamins D and the Immune System

[johnnysausages]

ncbi.nlm.nih.gov/pmc/articles/PMC3166406/

As the vitamin D receptor is expressed on immune cells (B cells, T cells and antigen presenting cells) and these immunologic cells are all are capable of synthesizing the active vitamin D metabolite, vitamin D has the capability of acting in an autocrine manner in a local immunologic milieu. Vitamin D can modulate the innate and adaptive immune responses. Deficiency in vitamin D is associated with increased autoimmunity as well as an increased susceptibility to infection.

When considered alongside the low vitamin D concentrations posted by many members, does this information not add weight to the theory of an autoimmune response to the return of DHT to the body?

ncbi.nlm.nih.gov/pmc/articles/PMC2906676/

This paper discusses the possibility of supplementing with a vitamin D metabolite (1,25(OH)2VD3) to modulate immune response. It also talks about Vitamin A metabolites but I’m currently at work so I haven’t the time to digest that information at the moment.

Given that 1,25(OH)2VD3 has a physiological protective role in dampening or limiting potentially pathogenic immune responses at the cellular level, one might predict that interfering with its effects could predispose to hypersensitivity or autoimmunity7. Consistent with this idea, levels of serum 1,25(OH)2VD3 are often decreased in patients with type I diabetes123 and SLE8,124, and 1,25(OH)2VD3 levels are inversely correlated with disease activity in patients with rheumatoid arthritis125. Moreover, VD3 deficiency accelerates intestinal inflammation in IL-10-deficient mice, which develop inflammatory bowel disease126. VD3 deficiency might also predispose to type I diabetes7,127. However, although children with rickets (typically caused by insufficient dietary supply of vitamin D) have a higher incidence of diabetes than VD3-sufficient children7, they are also more susceptible to infection7,128, which suggests that VD3 might also be important for protective immune responses. This effect could be partially mediated by the capacity of 1,25(OH)2VD3 to increase the bactericidal capacity of macrophages5,23.

It has been proposed that 1,25(OH)2VD3 could also be used as an adjuvant in immunomodulatory therapy in transplantation. 1,25(OH)2VD3 and a 1,25(OH)2VD3 analogue prolonged the survival of mouse cardiac allografts138,139, and decreased the rates of allograft rejection and increased survival in a rat model of liver transplantation140 and in fully mismatched mouse pancreatic islet transplants141. In addition, a 1,25(OH)2VD3 analogue provided significant protection from graft-versus-host disease (GVHD) in rats142. Moreover, 1,25(OH)2VD3 and a 1,25(OH)2VD3 analogue significantly prevented chronic allograft rejection in a rat model of renal transplantation143 and delayed chronic allograft rejection in a mouse model of aortic transplantation139.

There are obvious risks to decreasing levels of vitamin D (bone reabsorption) but for anyone who might be targeting a recovery strategy based on suppressing the immune system, might it be beneficial to cease vitamin D supplementation as part of that?

[johnnysausages]

Further to this, I Googled, 1,25(OH)2VD3 and found out that it is also known as calcitriol. It is available in the UK under the brand names Rocaltrol and Silkis. Some information is provided via the link below.

drugs.webmd.boots.com/drugs/drug … triol.aspx

EDIT: I realise now that my idea in the original post of allowing vitamin D to drop was entirely the wrong conclusion to draw. Please ignore that conclusion and forgive me my skim reading.