維生素D與HDL低和LDL高相關。很可能背後的原因是相同的：在太陽底下跑得少了？

來源: 於 2018-11-28 09:52:43 [博客] [舊帖] [給我悄悄話] 本文已被閱讀：次
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https://www.lipidjournal.com/article/S1933-2874(15)00384-0/fulltext

The pathophysiology for deficient 25(OH)D causing an atherogenic lipid profile is unclear. Inadequate dietary intake of vitamin D may reduce calcium absorption in the gastrointestinal system. Prior studies have shown that deficient dietary intake of calcium is associated with higher body weight and a more atherogenic lipid metabolism,53, 54 potentially due to increased lipid metabolism in the body or reduced intake of cholesterol in the gut. However, the observed association between 25(OH)D and dyslipidemia may be confounded by shared metabolic risk factors rather than a causal mechanism. Serum 25(OH)D has been shown to be decreased in obese patients, in whom sequestration of 25(OH)D in body fat reduces detectable 25(OH)D in the serum.55 This phenomenon results in an inverse association between BMI and 25(OH)D. Given that BMI is also associated with dyslipidemia, the presence of obesity may explain the observed association of 25(OH)D with dyslipidemia. Unfortunately, we did not have BMI available in our data set to adjust for this potentially confounding variable. There also appears to be an association between lipid-lowering medication usage and increases in 25(OH)D,56, 57 suggesting that the observed association between low 25(OH)D levels and dyslipidemia may be due to patients with lipid derangements not being on statin therapy.

Although vitamin D supplementation is inexpensive, widely available, and effective in raising serum 25(OH)D, clinical trials have yet to find any link between vitamin D supplementation and changes in lipid profile or reduced CVD mortality.15, 18, 58, 59, 60, 61 Mendelian randomization studies have used single nucleotide polymorphisms leading to variations in 25(OH)D to examine vitamin D's role in the development of an atherogenic lipid profile and CVD.49, 62, 63 These studies have shown evidence that single nucleotide polymorphisms causing a genetically increased RLP-C49 and BMI62 are associated with reduced 25(OH)D. This supports the notion that 25(OH)D may be a marker for overall health rather than an independent risk factor for CVD. As there is not currently any definitive evidence that vitamin D has a causal role in atherosclerotic CVD,21 the associations seen in observational studies may be due to confounding factors that impact both serum 25(OH)D and serum lipids