Vitamin D Supplementation, Glycemic Control, and Insulin Resistance in Prediabetics: A Meta-Analysis.
J Endocr Soc. 2018 May 25;2(7):687-709. doi: 10.1210/js.2017-00472. eCollection 2018 Jul 1.
Mirhosseini N1, Vatanparast H2, Mazidi M3,4, Kimball SM1,5.
- Prediabetes both prevented and treated by monthly Vitamin D, etc.
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- Search VitaminDWiki for prediabetes OR prediabetic 473 items as of June 2018
Vitamin D reverses prediabetes
Vitamin D might also prevent becoming prediabetic
- Fewer mice became prediabetic when given Vitamin D, even when on high fat, high sugar diet – March 2017
More than Vitamin D can reduce prediabetes
- Zinc cut in half the rate of prediabetes progressing to diabetes (20 mg) – RCT Oct 2017
- Prediabetes reduced in half by those getting Magnesium Chloride – RCT April 2015
- Magnesium is associated with prevention and treatment of Diabetes – Meta-analysis Aug 2016
Vitamin D treats Diabetes
- Diabetics helped by vitamin D in 5 ways – meta-analysis June 2018
- Diabetes treated and prevented by more than 2,000 IU of vitamin D (need more and gut-friendly) - meta-analyses 2018
- Vitamin D treatment of diabetes (50,000 IU every 2 weeks) augmented by probiotic – RCT June 2018
- Standard vitamin D (not gut-friendly) is not as bioavailable for many Diabetics
- Reasons to suspect Diabetes is related to low vitamin D – Jan 2018
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Diabetes prevention is a public health priority. Vitamin D supplementation may help prevent the development of diabetes in persons at increased risk. We performed a meta-analysis of controlled clinical trials that assessed glycemic outcome measures among adults at risk for type 2 diabetes, including prediabetes, overweight, or obesity. We searched PUBMED/ MEDLINE, CINAHL, and Google Scholar databases for trials published prior to April 2017. Placebo-controlled clinical trials with random allocation to vitamin D with or without calcium supplementation were selected. Data collection included country, study design, inclusion criteria, sample size, form, and dose of vitamin D, supplementation interval, control group, duration, participant characteristics, comorbidities, baseline and follow-up serum 25-hydroxyvitamin D [25(OH)D] concentration, and available outcome measures [glycosylated hemoglobin (HbA1c), fasting plasma glucose, plasma glucose after 2-hour oral glucose tolerance test, and homeostatic model assessment of insulin resistance (HOMA-IR)]. Data synthesis was conducted using random-effect models (PROSPERO registration no. CRD42017055326). Twenty-eight trials, representing 3848 participants, met the eligibility criteria. Compared with the control group, vitamin D supplementation significantly reduced HbA1c level by -0.48% (95% CI, -0.79 to -0.18), fasting plasma glucose level by -0.46 mmol/L (95% CI, -0.74 to -0.19), and HOMA-IR level by -0.39 (95% CI, -0.68 to -0.11). Subgroup analysis revealed that the effects of vitamin D supplementation on different glycemic measures were influenced by age, calcium coadministration, vitamin D deficiency, serum 25(OH)D level after supplementation, and duration of supplementation. Vitamin D supplementation and improved vitamin D status improved glycemic measures and insulin sensitivity and may be useful as part of a preventive strategy for type 2 diabetes.
Interest in the protective effects of vitamin D supplementation against the progression of diabetes has heightened in recent years, and the current analysis underscores some of these benefits. We evaluated 28 studies combined, including 11 centered on prediabetics and 16 on populations at high risk, and found significant effects of vitamin D supplementation on insulin resistance and hyperglycemia. Vitamin D supplementation and increased serum 25(OH)D concentrations improved insulin sensitivity (decreased HOMA-IR), glucose metabolism, and glycemic control (reduced HbA1c and FPG). Our findings suggest that a serum 25(OH)D concentration above 86 nmol/L can improve measures of glucose metabolism and response to insulin in prediabetics. Serum 25(OH)D concentrations above 86 nmol/L were achieved with an average vitamin D supplementation of 88 mg/d (3500 IU/d) or more, taking body weight into account; Ekwaru et al.  previously showed that obese individuals often require two to three times the dose of vitamin D that an individual with a normal BMI requires to achieve the same 25(OH)D response. The greatest benefits were found in populations most at risk for early disease. We also found improvements in those considered vitamin D sufficient when they started vitamin D supplementation.
Subgroup analyses further demonstrated that both FPG and 2-hour postprandial plasma glucose reductions were enhanced with vitamin D taken in combination with calcium supplements, as were insulin resistance and fasting HOMA-IR. Longer duration of supplementation seemed to be more effective at reducing HOMA-IR than those shorter than 6 months. We used fasting HOMA-IR, which detects liver insulin resistance and shows
Vitamin D deficiency and type 2 diabetes are escalating health problems worldwide. The results presented here provide promising evidence that vitamin D supplementation improves glycemic control and attenuates insulin resistance in prediabetics or individuals at high risk of developing diabetes. The amount of vitamin D most likely to produce a response is ≥88 µg/d (3500 IU/d), a level that is close to the current upper level of intake recommended by Health Canada, the US Institute of Medicine, and the European Food Safety Authority. Even though the effect size for vitamin D is not comparable to the effect of metformin or other glycemic control medications, over a long period of time and when administered at the population level, vitamin D supplementation may offer an affordable, safe, and accessible preventive measure.Prediabetes treated by Vitamin D (34 ng, 3500 IU per day) – meta-analysis May 2018
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