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Approximately 2 billion people suffer from Tuberculosis each year. Tuberculosis or simply TB is an infectious and highly contagious disease of the body especially lungs. It spreads mainly via Mycobacterium tuberculosis which is a tough and highly resistant microbe.

Tuberculosis is a serious, infectious and often fatal disease of the lungs. It can also affect other parts of the body. But the most common type of Tuberculosis is pulmonary Tuberculosis. It is more common in women than in men. The causative agent is a Gram-positive bacterium (Mycobacterium tuberculosis).

Tuberculosis or simply TB is a spreadable disease caused by Mycobacterium tuberculosis. This organism has a hard, waxy cell wall that makes it highly resistant to unfavorable environments and drugs. It evades the mucus lining of the windpipe and enters the lungs.

The goal of treating Tuberculosis is to protect the patient from possible disability and death. Another objective is to reduce the spread of Tuberculosis infection to others. TB may be a stubborn infection but with the right measures at the right time, it can be cured.

Cutting edge: vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin.\nLiu PT, Stenger S, Tang DH, Modlin RL.\nJ Immunol. 2007 Aug 15;179(4):2060-3.\nPMID: 1767546

Liu PT, Stenger S, Tang DH, Modlin RL. Cutting Edge: Vitamin D-Mediated Human Antimicrobial Activity against Mycobacterium tuberculosis Is Dependent on the Induction of Cathelicidin. J Immunol. 2007 Aug 15;179(4):2060-3. PMID: 17675463 [PubMed - in pr

Martineau AR, Honecker FU, Wilkinson RJ, Griffiths CJ. Vitamin D in the treatment of pulmonary tuberculosis. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):793-8. Epub 2007 Jan 12. Review. PMID: 17223549 [PubMed - indexed for MEDLINE]

In healthy people who have been exposed to tuberculosis, a single oral dose of vitamin D enhances their immunity against this bacterial infection.

Vitamin D in preventive medicine: are we ignoring the evidence? Zittermann A. Br J Nutr. 2003 May;89(5):552-72. Review. PMID: 12720576 Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.

"Hypervitaminosis D is a state of vitamin D toxicity. The recommended daily allowance is 400 IU per day. Overdose has been observed at 1925 µg/d (77,000 IU per day). Acute overdose requires between 15,000 µg/d (600,000 IU per day) and 42,000 µg/d (1,680,000 IU per day) over a period of several days to months, with a safe intake level being 250 µg/d (10,000 IU per day).[1] Foods contain low levels, and have not been known to cause overdose. Overdose has occurred due to industrial accidents, for example when incorrectly formulated pills were sold or missing industrial concentrate cans misused as cans of milk. Vitamin D toxicity is unlikely except when certain medical conditions are present, such as primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma."

The BCG vaccine (which stands for Bacillus Calmette-Guérin vaccine) protects against Tuberculosis, commonly known as TB. TB is a serious infection which affects the lungs, but it can affect other parts of the body such as the bones, joints and kidneys. It can also cause meningitis.

Vitamin D in defense of the human immune response.\nAdams JS, Liu PT, Chun R, Modlin RL, Hewison M.\nAnn N Y Acad Sci. 2007 Nov;1117:94-105. Epub 2007 Jul 26. Review.\nPMID: 17656563\nDOI: 10.1196/annals.1402.03

Martineau AR, Wilkinson RJ, Wilkinson KA, Newton SM, Kampmann B, Hall BM, Packe GE, Davidson RN, Eldridge SM, Maunsell ZJ, Rainbow SJ, Berry JL, Griffiths CJ. A single dose of vitamin D enhances immunity to mycobacteria. Am J Respir Crit Care Med. 2007

Bikle DD. What is new in vitamin D: 2006-2007. Curr Opin Rheumatol. 2007 Jul;19(4):383-8. PMID: 17551371 [PubMed - in process]

This critical nutrient builds bones, helps fight infection and may protect against some cancers. Do we get enough?

Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence? Br J Nutr. 2003 May;89(5):552-72. Review. PMID: 12720576 [PubMed - indexed for MEDLINE]

The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Gombart AF. Future Microbiol. 2009 Nov;4:1151-65. PMID: 19895218 Vitamin D deficiency has been correlated with increased rates of infection. Since the early 19th century, both environmental (i.e., sunlight) and dietary sources (cod liver) of vitamin D have been identified as treatments for TB. The recent discovery that vitamin D induces antimicrobial peptide gene expression explains, in part, the 'antibiotic' effect of vitamin D and has greatly renewed interest in the ability of vitamin D to improve immune function. Subsequent work indicates that this regulation is biologically important for the response of the innate immune system to wounds and infection and that deficiency may lead to suboptimal responses toward bacterial and viral infections. The regulation of the cathelicidin antimicrobial peptide gene is a human/primate-specific adaptation and is not conserved in other mammals. The capacity of the vitamin D receptor to act as a high-affinity receptor for vitamin D and a low-affinity receptor for secondary bile acids and potentially other novel nutritional compounds suggests that the evolutionary selection to place the cathelicidin gene under control of the vitamin D receptor allows for its regulation under both endocrine and xenobiotic response systems. Future studies in both humans and humanized mouse models will elucidate the importance of this regulation and lead to the development of potential therapeutic applications