In light of a recent study published in the Archives of Internal Medicine which found vitamin D inadequacy in 75 percent of Americans, University of Missouri College of Environmental Sciences assistant professor Catherine A. Peterson announced the finding of research conducted at the University's Department of Nutritional Sciences which correlated low vitamin D levels with an increased marker of inflammation. The study was described in the July, 2008 issue of the Journal of Inflammation.
The study included 69 healthy women, aged 25 to 82, classified as being high or low in vitamin D based on ultraviolet-B exposure. Blood samples were analyzed for serum 25-hydroxyvitamin D, hormone levels, and inflammation markers.
Not surprisingly, mean serum 25-hydroxyvitamin D levels were significantly greater in those with increased sun exposure compared with those in the low D group. Dr Peterson, along with colleague Mary E Hefferman, found that the inflammatory marker tumor necrosis factor-alpha (TNF-alpha) averaged 0.79 picograms per milliliter (pg/mL) in the high vitamin D group and 1.22 pg/mL among those categorized as low in the vitamin. Higher serum 25-hydroxyvitamin D levels were also correlated with lower TNF-alpha levels. The relationship remained after adjusting the analysis for other factors. In their discussion of the findings, the authors write that although it is difficult to discern vitamin D's mechanism, a previous study found that vitamin D down-regulated TNF-alpha-associated genes.
The study is the first to determine an inverse association between TNF-alpha and vitamin D levels in a healthy population. The finding could help explain the protective association found for vitamin D against inflammatory diseases such as heart disease and rheumatoid arthritis.
"The findings reveal that low vitamin D levels negatively impact inflammation and immune response, even in healthy women," Dr Peterson commented. "Increased inflammation normally is found in people with obesity or chronic diseases; a small decrease in vitamin D levels may aggravate symptoms in people who are sick."
"To improve vitamin D status and achieve its related health benefits, most people should get at least 1000 IU of vitamin D per day," she noted. "Only a few foods contain vitamin D naturally, such as fatty fish; other sources are dietary supplements and vitamin-D-fortified foods, including milk and orange juice."
"More studies are needed to fully characterize the relationship between vitamin D and TNF-alpha; but if proven effective, vitamin D therapy may show promise as adjunct to anti-TNF therapy in inflammatory disease states," the authors concluded.
The following acronyms represent the most dangerous pro-inflammatory cytokines. Health-conscious persons should become familiar with these terms because excess levels of these cytokines cause or contribute to many diseases states:
TNF-a tumor necrosis factor-alpha
IL-1(b) interleukin-1 beta
Scientists have identified dietary supplements and prescription drugs that can reduce levels of the pro-inflammatory cytokines. The docosahexaenoic acid (DHA) fraction of fish oil is the best documented supplement to suppress TNF-a, IL-6, IL-1(b), and IL-8 (Jeyarajah et al. 1999; James et al. 2000; Watanabe et al. 2000; Yano et al. 2000). A study on healthy humans and those with rheumatoid disease shows that fish oil suppresses these dangerous cytokines by up to 90% (James et al. 2000).
Other cytokine-lowering supplements are DHEA (Casson et al. 1993), vitamin K (Reddi et al. 1995; Weber 1997), GLA (gamma linolenic acid) (Purasiri et al. 1994), and nettle leaf extract (Teucher et al. 1996). Antioxidants, such as vitamin E (Devaraj et al. 2000) and N-acetyl-cysteine (Gosset et al. 1999), may also lower pro - inflammatory cytokines and protect against their toxic effects.
Prescription drugs like Enbrel ($10,000 a year) directly bind to TNF-a and block its interaction with TNF cell surface receptors. Enbrel has demonstrated significant clinical improvement in rheumatoid arthritis patients, as have high-dose fish oil supplements (Kremer 2000). High levels of TNF-a may persist even in people receiving Enbrel drug therapy. Even if Enbrel brings TNF-a down to a safe range, other inflammatory cytokines such as IL-6 and IL-1(b) may continue to wreak havoc throughout the body. High levels of tumor necrosis factor (TNF-a) are destructive to many vital tissues such as joint cartilage (e.g., rheumatoid arthritis) and heart muscle (e.g., congestive heart failure).
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The term “vitamin E” refers to a family of eight related, lipid-soluble, antioxidant compounds widely found in plants. The tocopherol and tocotrienol subfamilies are each composed of alpha, beta, gamma, and delta fractions having unique biological effects.
One or more members of the vitamin E family may:
Maintain cell membrane integrity and reduce cellular aging
Biotin is an unnumbered member of the B-complex family, normally only required in minute amounts. Biotin, a water-soluble vitamin, is used as a co-factor of enzymes involved in fatty acid metabolism, gluconeogenesis, and amino acid catabolism, making biotin essential in maintaining metabolic homeostasis. Biotin plays an important role in metabolic functioning as a coenzyme carrier of activated carbon dioxide in the TCA cycle (also known as the Krebs cycle). In its coenzyme form, biotin synthesizes glucose from noncarbohydrate sources, and synthesizes and breaks down certain fatty acids and amino acids.