Diabetes is a leading cause of cardiovascular disease. Persons with diabetes are at greater risk for early cardiac mortality, and for repeat events if they survive their first cardiac event. Recently, low serum concentrations of vitamin D have been associated with increased risk for cardiac events. Evidence indicates that persons with diabetes have lower serum concentrations of vitamin D. In addition, persons at risk for diabetes or metabolic syndrome have inadequate serum concentrations of vitamin D. This review will assess the evidence relative to the impact of vitamin D in the development of diabetes, metabolic syndrome, and diabetes complications. Studies that address vitamin D and its impact on metabolic outcomes as well as possible mechanisms of action are provided. Finally, the assessment and suggested treatment for vitamin D deficiency is addressed. Effective detection and treatment of inadequate vitamin D concentrations in persons with diabetes or those at risk for diabetes may be an easy and cost-effective therapy which could improve their long-term health outcomes as well as their quality of life.
I got to this article via this ScienceDaily piece, Vitamin D Is The 'It' Nutrient Of The Moment. I've wondered about this before, my RSS is pretty much peppered constantly by Vitamin D related literature right now. I got into this because of its possible role in the evolution of human skin color, but I'm not surprised about the diabetes connection. South Asians have really high rates of diabetes, so I've read a fair amount on how to prevent diabetes, and Vitamin D supplementation is in there. As it happens, South Asians at high latitudes might suffer chronic Vitamin D deficiencies due to lower radiation levels...though honestly it looks like many South Asians are fat,* so I think that's probably a bigger population level factor right now.
* There are interpopulational differences in obesity in the United States. Some of it breaks down by race; black people are fatter than white people. Some of it by region; Southerners are fatter than Coloradans. Some by socioeconomics; poor people are fatter than rich people. As far as "Asian Americans" goes, I'm willing to bet that the majority of obese Asian Americans in the United States are South Asian. I'm not sure if we're fatter on average than whites (I wouldn't be surprised if we are, especially if you control for SES), but we sure are fatter than East Asians.
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I wonder why east asians are so skinny, compared to browns. I mean both populations have a similar carbohydrate-based diet, and have been part of areas that had rice paddy agriculture for similar amounts of time, relative to the western europeans. If anything, the more pedomorphic east asians should be chubbier, after living in not only colder places but the fact that children are chubbier than adults.
I live in a part of the US with fairly large #s of South Asians and East Asians. At least where I am the South Asians are pretty chubby. Even the immigrants. The East Asians are much skinnier, and the East Asian immigrant parents especially so.
The South Asians aren't as fat as the blacks, but seem just as fat as the chubby whites. Black women seem to have locked down the #1 spot on the obesity meter, I don't think any other ethnic group can challenge them.
My last two doctors have been pleasantly plump Indians. Nice guys, both immigrants.
Chubbiness is yet another reason why it makes little sense to group South Asians and East Asians together as some pan-asian ethnic group. Most South Asians I know look like dark-skinned white guys.
And hairiness. I've dated some Indian girls. They tend to be rather ... hirsute. Italian girls have the same problem. That's one big plus for East Asian girls and blondes. The no body hair thing is very nice.
I think this problem of hirsute women requires global genetic engineering. Maybe we can put something in the water supply. Women should not be hairier than men. I can only hope Obama (who seems pretty hairless and therefore understands where I'm coming from) will address this crisis in his first 100 days!
Adiposity in Relation to Vitamin D Status
Precisely measured total body fat is inversely associated with 25-OH-D levels and is positively associated with PTH levels. The associations were weaker if anthropometric measures were used, indicating a specific role of adipose tissue. Regardless of the possible underlying mechanisms, it may be relevant to take adiposity into account when assessing vitamin D requirements. ...In a more recent study by Wortsman et al. (11), the capacity of the skin to produce vitamin D was not altered in obesity. However, the increase in serum vitamin D3 after sun exposure was 57% less in obese compared with nonobese subjects. The increase in serum vitamin D3 after oral supplementation was similar in obese and nonobese subjects. This supports the hypothesis of a decreased release of endogenously produced vitamin D into the circulation due to more storage in sc fat in obese subjects (11). The fact that in our study leg fat was more strongly related to 25-OH-D levels compared with trunk fat supports the idea that endogenously produced vitamin D is particularly stored in the sc fat depot
who seems pretty hairless and therefore understands where I'm coming from
africans have less body hair than "caucasoids." but, that is because southern caucasoids are classified with northern ones. nordics and africans probably have about the same amount of body hair. east asians and native americans the least. instead of the 20-40 window they should call the threading window ;-)
p.s. the non-trivial proportion of southeast asian ancestry among bengalis makes them a bit different i assume. i'm less hairy than most white dudes, as assman intuited from a photo of my forearm in a katpik.
Tod's link has the right idea: the arrow most plausibly points from metabolic syndrome to D deficiency, not the other way around. In fact this is the case for most vitamin deficiencies -- C, D and B vitamins for sure, mineral retention as well. The problem with metabolic syndrome is that so many homeostatic mechanisms depend on insulin signaling as a master switch that we should expect to see all sorts of weird correlations.
High Vitamin D may cause obesity Lean phenotype and resistance to diet-induced obesity in VDR knockout mice correlates with induction of uncoupling protein-1 in white adipose tissue
The test that is diagnosing all this putative 'deficiency' is not of the activated form of vitamin D
"The 25-hydroxy vitamin D test is the most accurate measure of the amount of vitamin D in the body. In the kidney, 25-hydroxy vitamin D changes into an active form (called 25-hydroxy vitamin D. The active form helps control blood levels of calcium and phosphate. Moderately low
Vitamin D may protect against some autoimmune diseases.
http://www.springerlink.com/content/h1254n7r14087723/">Prevention of autoimmune diabetes in NOD mice by 1,25 dihydroxyvitamin D3
Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system
Vitamin D is an important immune system regulator. The active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown to inhibit the development of autoimmune diseases, including inflammatory bowel disease (IBD). Paradoxically, other immune system-mediated diseases (experimental asthma) and immunity to infectious organisms were unaffected by 1,25(OH)2D3 treatment
The latitude South Asians live at has nothing to do with them suffering Vitamin D deficiency or rickets, it's their traditional diet. An epidemiological model of privational rickets and osteomalacia The discovery of late rickets and osteomalacia in the Glasgow Muslim community in 1961 (Dunnigan et al. 1962) was followed by a study of 7 d weighed dietary intakes in rachitic and normal Muslim schoolchildren and in a control group of white schoolchildren (Dunnigan & Smith, 1965). Surprisingly, the dietary vitamin D intakes of rachitic Asian children, normal Asian children and Glasgow white children were similar. The higher fibre
and phytate intakes of the Asian children were not considered aetiologically significant.
Studies of daylight outdoor exposure showed no significant differences between the summer and non-summer exposures of rachitic and normal Muslim schoolchildren or between Muslim and white schoolchildren (Dunnigan, 1977). These patterns of daylight outdoor exposure did not conform to the Muslim âpurdahâ stereotype, although sunbathing was unknown in the Asian community. It was also evident that many Glasgow white schoolchildren went out relatively little, even in fine weather, in a form of âcultural purdahâ. Similar patterns of apparently adequate daylight outdoor exposure were noted in Asian women with privational osteomalacia wearing Western dress in London (Compston, 1979). These observations did not support the hypothesis that Asian rickets and osteomalacia resulted from deficient exposure to UVR or from deficient dietary vitamin D intake relative to white women and children in whom privational rickets and
osteomalacia were unknown outside infancy and old age.
The suggestion that Asian rickets in the UK might be related to the consumption of unleavened bread was supported by Mellanbyâs (1949) earlier identification of an anticalcifying factor in oatmeal, subsequently shown to be phytic acid, and by evidence of âsunshineâ rickets in Iranian village children consuming large quantities of unleavened bread (tanok) with abundant exposure to UVR (Rheinhold, 1972).
According to this the fad for Vitamin D pills is all wrong
Vitamin D discovery outpaces FDA decision making
(Biologists)... need to help them understand the steroidal nature of vitamin D. To help them understand that this substance is intimately involved in the transcription of hundreds, probably thousands, of genes that determine the course of immune disease and cancers. In particular, we must ensure that every researcher understands the importance of measuring the concentration of the actual transcriptional activator, 1,25-dihydroxyvitamin-D