IntroductionVitamin D is well known for its effects on calcium and bone metabolism. Vitamin D deficiency results in rickets in infants and small children and in osteomalacia and osteoporosis in adults. However, recent advances in the understanding of vitamin D have revolutionized our view of this old nutritional factor and suggested that it has much wider effects on the body than ever believed before. Major reasons for this situation are insufficient skin exposure to solar ultraviolet B radiation together with inadequate oral vitamin D intake.There is accumulating evidence that vitamin D deficiency/ insufficiency might contribute to the etiology of various chronic diseases such as cardiovascular disease, specific types of cancer, multiple sclerosis, and type 1 diabetes.3,4 Recent studies demonstrated that poor vitamin D status is independently associated with excess cancer mortality 7 and poor outcome in congestive heart failure individuals. 8 In addition, poor vitamin D status is associated with excess all-cause mortality in individuals with end-stage renal disease. 9 In 2007, Autier and Gandini 10 published a meta-analysis of randomized controlled trials on vitamin D and total mortality that were not primarily designed to assess mortality. The authors concluded that vitamin D supplementation is linked to lower all-cause mortality in middle-aged and elderly individuals with low serum concentrations of 25(OH)D than in unsupplemented subjects. Risk reduction was 7% during a mean follow-up of 5.7 years.Background: Inadequate vitamin D status is a worldwide problem. Evidence is accumulating that individuals with low vitamin D status have excess mortality rates. We calculated to which extent annual mortality rates can be reduced in the German population by optimizing vitamin D status.Results: Mean serum concentrations of 25-hydroxyvitamin D in the DEVID study cohort were 41 nmol/l (SD: 22 nmol/l). More than 90% of individuals had 25-hydroxyvitamin D concentrations below the threshold that was associated with lowest mortality risk in the two aforementioned trials (75 nmol/l). According to conservative estimations, at least 2.2% of all deaths or 18,300 lives annually can be saved by achieving 25(oH)D concentrations of at least 75 nmol/l in the entire adult German population. Available data provide evidence for an exponential increase in total mortality with deficient 25-hydroxyvitamin D concentrations.Methods: our calculations are based on (1) an annual mortality rate of 1.34% in the adult German population as provided by the Statistical Yearbook, (2) the actual vitamin D status in German adults with a high mortality risk as assessed in 1,343 individuals from 264 general practitioners in different German regions (DEVID study), and (3) data from two very large prospective cohorts (Dobnig et al. 2008;Melamed et al. 2008) about the excess mortality in individuals with inadequate vitamin D status.Conclusion: Improving vitamin D status in a population with inadequate vitamin D status might be an effective strategy to reduc...

ZusammenfassungDie Ursache der Sarkoidose ist bislang unbekannt. Vitamin D ist zur Behandlung der Erkrankung kontraindiziert. Wir fragen daher, was Sarkoidose verursacht und warum Vitamin D für die Betroffenen gefährlich sein kann und schlagen eine gegenteilige Hypothese vor: Sarkoidose ist ein physiologischer Prozess der Krebsabwehr, der Vitamin D als Substrat benötigt. Zur Prüfung der Hypothese haben wir anhand einer Literaturrecherche zahlreiche Fallberichte über Sarkoidose und Krebs gefunden sowie Fälle von Krebsmimikry durch Sarkoidose. Mehrere Berichte beschreiben Spontanheilungen der Krebserkrankung bei gleichzeitigem Auftreten einer Sarkoidose. Im Zusammenhang mit den Granulomen der Sarkoidose bilden Monozyten den Ort der Vitamin-D-Freisetzung. Darüber hinaus kann aktives Vitamin D Krebszellen mithilfe der Vitamin-D-Rezeptoren des Zellkerns kontrollieren. Dass Granulome „nicht verkäsend“ sind, wird als Resorption von humanen Molekülen der Krebszellen erklärt. Der Umstand, dass in den Granulomen der Sarkoidose meist Krebszellen fehlen, wird als Ergebnis einer gut funktionierenden Sarkoidose interpretiert. Wir betrachten die typische Synthese von aktivem Vitamin D in den Sarkoidose-Monozyten als Krebsabwehr. Die Hypothese muss durch weitere Untersuchungen untermauert werden.

Abstract:The cause of sarcoidosis is unknown, and vitamin D is contraindicated to treat the condition. We therefore ask what causes sarcoidosis and why vitamin D can be dangerous for those so afflicted. We propose a contrary hypothesis: sarcoidosis is a physiological process of defense against cancer that requires the substrate vitamin D. We tested this hypothesis, finding many case reports involving sarcoidosis and cancer-further cases of cancer mimicry by sarcoidosis. Several reports describe spontaneous healing of cancer in the presence of sarcoidosis. In the context of the granulomas of sarcoidosis, monocytes are the site of vitamin D release. Furthermore, active vitamin D can control cancer cells by using the vitamin D receptors of the nucleus. That granulomas consistently do not caseate is explained as a confrontation with human molecules and the cancer cells' complete absorption. The striking fact that granulomas of sarcoidosis mostly lack cancerous cells is interpreted as a result of a well-functioning sarcoidosis process. We view the typical sarcoidosis monocytic synthesis of active vitamin D as a successful defense against cancer: a theory we call the "endogenous program organizing cancer apoptosis" (EPOCA).