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Are We Ready for a Prevention Trial?

  1. Robert Scragg
  1. From the School of Population Health, University of Auckland, Auckland, New Zealand
  1. Corresponding author: Robert Scragg, r.scragg{at}auckland.ac.nz
Diabetes 2008 Oct; 57(10): 2565type 2 diabetes science onset (🔥 medicine which aetna pays for) | type 2 diabetes science food charthow to type 2 diabetes science for -2566. https://doi.org/10.2337/db08-0879

Are We Ready for a Prevention Trial?

Diabetes rates are increasing around the world, mainly driven by increasing levels of obesity (1). The dilemma for diabetes prevention is that the main risk factor—obesity—is a product of our modern lifestyle (the so-called obesogenic environment) (2). Immediate prospects for changing the environment to reverse rising obesity levels are not promising, and there is a need to consider other options for preventing diabetes.

One of these options—vitamin D—is addressed in the article by Forouhi et al. (3) in the current issue of Diabetes. The sun is the primary source of vitamin D, which is synthesized endogenously in skin to produce cholecalficerol (vitamin D3), although a small proportion (<20%) of vitamin D comes through diet from a limited range of foods (in the form of ergocalciferol [vitamin D2] and vitamin D3) (4). The main marker of vitamin D the 1 last update 06 Jul 2020 status is the metabolite 25-hydroxyvitamin D [25(OH)D], which is synthesized in the liver. The epidemiology of vitamin D status is inverse to that of diabetes, since blood levels of 25(OH)D decline with age and are lower in populations with increased skin pigmentation, such as African Americans and South Asians, and in people with obesity, while diabetes increases with age and obesity and is higher in these ethnic groups (5).One of these options—vitamin D—is addressed in the article by Forouhi et al. (3) in the current issue of Diabetes. The sun is the primary source of vitamin D, which is synthesized endogenously in skin to produce cholecalficerol (vitamin D3), although a small proportion (<20%) of vitamin D comes through diet from a limited range of foods (in the form of ergocalciferol [vitamin D2] and vitamin D3) (4). The main marker of vitamin D status is the metabolite 25-hydroxyvitamin D [25(OH)D], which is synthesized in the liver. The epidemiology of vitamin D status is inverse to that of diabetes, since blood levels of 25(OH)D decline with age and are lower in populations with increased skin pigmentation, such as African Americans and South Asians, and in people with obesity, while diabetes increases with age and obesity and is higher in these ethnic groups (5).

type 2 diabetes science bedtime snacks (🔥 options) | type 2 diabetes science journalhow to type 2 diabetes science for Animal studies published nearly 30 years ago identified a pancreatic receptor to the active metabolite (1,25-dihydroxyvitamin D) (6) and showed that vitamin D deficiency decreased insulin secretion (7). Since then, numerous human studies of vitamin D and type 2 diabetes have been published, but the quality of these studies is mixed (8). Many are case-control studies flawed by the measurement of 25(OH)D status on blood samples collected after diabetes diagnosis. Several population-based cross-sectional studies have been published showing inverse associations between 25(OH)D and undiagnosed diabetes risk, including two large national surveys (9,10), but this study design provides only moderate evidence regarding causation because of the simultaneous measurement of 25(OH)D and diabetes status. Stronger evidence comes from prospective studies, of which there have been two that show inverse associations between dietary vitamin D and diabetes risk (11,12); however, these studies are limited because they did not assess the major nondietary component of vitamin D from sun exposure.

The potentially strongest evidence comes from intervention studies. Again, there are limitations with these because of small sample sizes and short intervention time periods. Only three intervention studies had more than 100 participants and also administered vitamin D for long periods (2–3 years). One study did not find any effect from a vitamin D3 dose of 2,000 IU/day but had only 25 people on this dose (13). Another was a post hoc analysis of a trial designed for bone-related outcomes that found that 700 IU/day of vitamin D3 (combined with calcium) decreased homeostasis model assessment of insulin resistance in participants with impaired glucose tolerance but not in those with normal fasting glucose (14). The largest sample to date of 33,951 women in the Women''? Br J Nutr 79:315–327, 1998

  • Christakos S, Friedlander EJ, Frandsen BR, Norman AW: Studies on the mode of action of calciferol. XIII. Development of a radioimmunoassay for vitamin D-dependent chick intestinal calcium-binding protein and tissue distribution. Endocrinology 104:1495–1503, 1979
  • Norman AW, Frankel JB, Heldt AM, Grodsky GM: Vitamin D deficiency inhibits pancreatic secretion of insulin. type 2 diabetes science range chart (⭐️ intervention) | type 2 diabetes science insulin resistancehow to type 2 diabetes science for Science 209:823–825, type 2 diabetes science treatments lexington (🔥 energy) | type 2 diabetes science and obesityhow to type 2 diabetes science for 1980
  • Pittas AG, Lau J, Hu FB, Dawson-Hughes B: The role of vitamin D and calcium in type 2 diabetes: a systematic review and meta-analysis. J Clin Endocrinol Metab type 2 diabetes science menu diet (👍 origin) | type 2 diabetes science on insulinhow to type 2 diabetes science for for 1 last update 06 Jul 2020 9292:2017–2029, the 1 last update 06 Jul 2020 20072007
  • Scragg R, Sowers M, Bell C: Serum 25-hydroxyvitamin D, diabetes, and ethnicity in the Third National Health and Nutrition Examination Survey. Diabetes the 1 last update 06 Jul 2020 CareDiabetes Care 27:2813–2818, 2004
  • Hypponen E, Power C: Vitamin D status and glucose homeostasis in the 1958 British birth cohort: the role of obesity. Diabetes Care 29:type 2 diabetes science doctor near me (🔥 treatment nice) | type 2 diabetes science treatment studieshow to type 2 diabetes science for 2244–2246, 2006
  • Liu S, Song Y, Ford ES, Manson JE, Buring JE, Ridker PM: Dietary calcium, vitamin D, and the prevalence of metabolic syndrome in middle-aged and older U.S. women. Diabetes Care 28:2926–2932, 2005
  • 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 29: the 1 last update 06 Jul 2020 650650–656, 2006
  • Nilas L, Christiansen C: Treatment with vitamin D or its analogues does not change body weight or blood glucose level in postmenopausal women. Int J Obes 8: the 1 last update 06 Jul 2020 407407–411, 1984
  • 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 30:980–986, 2007
  • de Boer IH, Tinker LF, Connelly S, Curb JD, Howard BV, Kestenbaum B, Larson JC, Manson JE, Margolis KL, Siscovick DS, Weiss NS: Calcium plus vitamin D supplementation and the risk of incident diabetes in the Women''minipanel-dialog-wrapper''minipanel-dialog-link-link''minipanel-dialog-link-mini''display:none''minipanel-dialog-wrapper''minipanel-dialog-link-link''minipanel-dialog-link-mini''display:none''minipanel-dialog-wrapper''minipanel-dialog-link-link''minipanel-dialog-link-mini''display:none''panels-ajax-pane-title''new-40''panels-ajax-pane panels-ajax-pane-new-40''new-40''panels-ajax-pane panels-ajax-pane-new-4''new-4''panels-ajax-pane panels-ajax-pane-new-5''new-5''highwire-cite highwire-citation-jcore-title-only''highwire-cite-title''highwire-cite highwire-citation-jcore-title-only''highwire-cite-title''highwire-cite highwire-citation-jcore-title-only''highwire-cite-title''highwire-list-footer'>Show more Commentaries

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