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Vitamin D: Part II

Quick Hit Summary

Vitamin D appears protective against both type I and type II diabetes. One study indicated that infants supplemented with vitamin D were 1/3 less likely to develop Type I diabetes vs. those who failed to supplement. With respect to type II diabetes, epidemiology studies have also suggested that taking a vitamin D and calcium supplement (>1,200 mg calcium and >800 IU vitamin D) may be a proactive approach towards staving off the disease. Epidemiology studies also indicate that Vitamin D may be protective against heart disease. These protective effects of vitamin D appear to be through its ability to modulate the inflammatory response and influence various hormone secretions.

Vitamin D

Figure 1 The molecular Structure of Vitamin D312

In part I of this series, we reviewed sources of vitamin D and saw how prevalent insufficiency was in the US population. Additionally, we discussed its relationship with breast, prostrate and colon cancer. In the second part of this series, we will examine the relationship between Vitamin D, diabetes and cardiovascular health.

Vitamin D & Diabetes

Although further investigation is still needed, emerging evidence indicates that vitamin D influences both type 1 and type 2 diabetes.

Type 1 diabetes often begins during the juvenile years of ones life and is characterized by a lack of natural insulin production. In healthy individuals, the islet cells of the pancreas are responsible for manufacturing this vital hormone. However, in type 1 diabetes this process goes awry as the body launches an abnormal immune response, destroying the islet cells. Thus, one is unable to synthesize insulin. Numerous observational studies have looked at the association between type 1 diabetes and vitamin D intake during early childhood. One particularly large study, conducted in 7 European countries (>3100 participants), looked at the development of type 1 diabetes with respect to vitamin D supplementation during infancy. Researchers observed that infants who received a vitamin D supplement were a 1/3 less likely to develop type 1 diabetes vs. those who did not receive any supplement1. The authors hypothesized that vitamin D’s ability to modulate inflammation prevented the islet cells of the pancreas from being destroyed via an abnormal auto-immune response

Type II diabetes is characterized by reduced glucose uptake by one’s cells in response to insulin(referred to as decreased insulin sensitivity) and/or decreased insulin secretion by the pancreatic islet cells. Numerous animal studies have demonstrated improved insulin secretion in vitamin D deficient rats upon administering vitamin D23. One pilot study also suggests that vitamin D improves glucose uptake in women who suffer from insulin insensitivity4.

Multiple studies have examined the co-administration of calcium and vitamin D on type 2 diabetes. Analyzing data obtained from the Nurses Health Study, researchers looked at the influence of vitamin D and calcium on the onset of type 2 diabetes5. This study involved >80,000 women over the course of 20 years. At the completion of the study, it was found that those with high dietary intakes of calcium and vitamin D (>1,200 mg calcium and >800 IU vitamin D) were 33% less likely to develop type 2 diabetes vs. those with low intakes (< 600 mg calcium and 400 IU vitamin D). In a more recent study, 92 individuals with impaired fasting glucose levels were divided into 2 groups6. For three years, each group took a daily pill consisting of either calcium and vitamin D (500 mg calcium citrate and 700 IU vitamin) or a placebo substance. Both insulin sensitivity and fasting blood glucose were measured at the start and end of the trial. Compared to baseline values, it was found that those receiving calcium and vitamin D had significantly better outcomes vs. those receiving a daily placebo.

Although promising, the presence of calcium along with the vitamin D somewhat clouds the results of these trials. It’s possible that calcium, rather than vitamin D, may directly be responsible for the improvement in diabetic symptoms. However, research has clearly established that vitamin D is required for adequate calcium absorption. Thus, vitamin D may indirectly improve insulin secretion and sensitivity by improving ones serum calcium levels. Personally, I feel that vitamin D exerts its effects through direct interaction with pancreatic and other cells of interest as well as indirectly by increasing dietary calcium absorption.

Cardiovascular Disease

The possible link between cardiovascular disease (CVD) and serum vitamin D levels was first observed in the early 1990’s when researchers noticed that heart disease was more prevalent in those who received less sunlight exposure7. Thus, they hypothesized that decreased vitamin D stores, resulting from lack of UV-B exposure, may be partially responsible to the development of CVD.

Numerous epidemiological studies have supported this hypothesis. A couple particularly interesting studies were carried out by Giovannucci et al.8 and Wang et al9. Giovannucci et al looked at 1,354 men between the ages of 40-75 who had no previous family history of CVD8. Additionally, none of the study’s participants had CVD at the onset of the study. Blood samples and diet questionnaires were completed at the start of the trial and every 2 years thereafter for the next 10 years. At the conclusion of the ten years, the study’s researchers compared serum vitamin D levels and the onset of heart disease (both fatal and nonfatal myocardial infarction) amongst participants. Results indicated that those with deficient levels of vitamin D in there blood, were 2x as likely to develop CVD vs. individuals classified as having sufficient circulating amounts (deficient and sufficient defined as [ 25OH-D ] <.15ng/ml and > 30ng/ml). In a similarly designed study, Wang et al. looked at 688 individuals with hypertension, and discovered that those with low serum vitamin D were 2x as likely to develop CVD vs. those with greater vitamin D present9. Wang et al. also examined the relationship between vitamin D and CVD in 1,081 individuals without hypertension. In contrast to Giovannucci et al , Wang et al. found no relationship linking these variables together. This may have been the result of using lower cutoff markers defining vitamin D deficiency and sufficiency (deficient: < 15ng/ml; sufficient > 15 ng/ml).

There have been a few randomized clinical controlled trials. The most notable one to date is the Women’s Health Initiative (WHI) which involved >36,000 postmenopausal women10. Over the course of 7 years, participants were randomized into either a treatment group receiving 400 IU/d of vitamin D & 1000 mg/d of calcium or a control group that received a placebo. With respect to cardiovascular incidences and death, no significant differences were found between groups at the study’s conclusion. Various discrepancies may explain the differences in results reported between various epidemiology studies and the WHI11. Many researchers believe that 400 IU of vitamin D/day is too small of an amount to really improve ones vitamin D status enough to achieve the cardiovascular benefits. Furthermore, for ethical health reasons (ie-osteoporosis), individuals of the control group were allowed to take vitamin D/calcium supplements on their own. As a result, the mean daily intake between the two groups was relatively the same (365 IU vs. 368 IU).

Their have been a few proposed mechanism to explain the relationship between vitamin D and CVD. Notable ones include Vitamin D lowering blood pressure (via the renin-angiotensin system), affecting parathyroid hormones and decreasing circulating inflammatory factors7.

In the conclusion of this series, we’ll examine the association between vitamin D, bone metabolism & pain relief and advice on dietary vitamin D consumption.

References

1 The EURODIAB Substudy 2 Study Group. Vitamin D supplementin early childhood and risk for type I (insulin-dependent) diabetes mellitus. Diabetologia 1999;42:51– 4.

2 Chertov BS, Sivitz WI, Baranetsky NG et al. Cellular mechanisms of insulin release: the effects of vitamin D deficiency and repletion on rat insulin secretion.Endocrinology 1983; 113: 1511–1518.

3 Palomer X, González-Clemente JM, Blanco-Vaca F, Mauricio D. Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. Diabetes Obes Metab. 2008 Mar;10(3):185-97.

4 von Hurst PR, Stonehouse W, Coad J. Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient – a randomised, placebo-controlled trial. Br J Nutr. 2009 Sep 28:1-7.

5 Pittas AG, Dawson-Hughes B, Li T, Van Dam RM, Willett WC, Manson JE, Hu FB. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care. 2006 Mar;29(3):650-6.

6 Pittas AG, Harris SS, Stark PC, Dawson-Hughes B. The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults. Diabetes Care. 2007 Apr;30(4):980-6. Epub 2007 Feb 2.

7 Judd SE, Tangpricha V. Vitamin D deficiency and risk for cardiovascular disease. Am J Med Sci. 2009 Jul;338(1):40-4.

8 Giovannucci E, Liu Y, Hollis BW, Rimm EB. 25-Hydroxyvitamin D and risk of myocardial infarction in men: a prospective study. Arch Intern Med 2008;168:1174–80.

9 Wang TJ, Pencina MJ, Booth SL, et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 2008;117:503–11.

10 Hsia J, Heiss G, Ren H, et al. Calcium/vitamin D supplementation and cardiovascular events: Women’s Health Initiative. Circulation. 2007;115(7):846-854.

11 Nemerovski CW, Dorsch MP, Simpson RU, Bone HG, Aaronson KD, Bleske BE. Vitamin D and Cardiovascular Disease. Pharmacotherapy 2009;29(6):691–708).

12 Accessed May 31, 2010 from: http://en.wikipedia.org/wiki/File:Cholecalciferol-3d.png

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Written on September 30, 2009 by Sean Casey
Last Updated: June 19, 2010

This information is not intended to take the place of medical advice.Please check with your health care providers prior to starting any new dietary or exercise program. CasePerformance is not responsible for the outcome of any decision made based off the information presented in this article.

About the Author: Sean Casey is a graduate of the University of Wisconsin-Madison with degrees in both Nutritional Science-Dietetics and Kinesiology-Exercise Physiology. Sean graduated academically as one of the top students in both the Nutritional Science and Kinesiology departments.
Field Experience: During college, Sean was active with the UW-Badgers Strength and Conditioning Department. He has also spent time as an intern physical preparation coach at the International Performance Institute in Bradenton, FL. He also spent time as an intern and later worked at Athletes Performance in Tempe, AZ. While at these locations he had the opportunity to train football, soccer, baseball, golf and tennis athletes. Sean is also active in the field of sports nutrition where he has consulted with a wide variety of organizations including both elite (NFL’s Jacksonville Jaguars) and amateur athletic teams. His nutrition consultation services are avalable by clicking on the Nutrition Consultation tab.

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