Sunweavers: Supporting Native American Women's Vitamin D Research
| Status: | Completed |
|---|---|
| Conditions: | Other Indications, Peripheral Vascular Disease, Gastrointestinal |
| Therapuetic Areas: | Cardiology / Vascular Diseases, Gastroenterology, Other |
| Healthy: | No |
| Age Range: | 55 - 75 |
| Updated: | 2/7/2015 |
| Start Date: | July 2011 |
| End Date: | April 2014 |
| Contact: | Diane Krueger, B.S. |
| Email: | dckruege@wisc.edu |
| Phone: | 608-265-6410 |
Cardiovascular disease (CVD) and diabetes occur commonly among Native Americans (NA), and
are leading causes of death among northern US NAs. Moreover, low vitamin D status occurs
commonly in this same population. An increasing amount of evidence indicates a correlation
between low vitamin D status and CVD and diabetes by contributing to a heightened
pro-inflammatory environment within the endothelial lining of blood vessels leading to
atherosclerotic disease, and an impaired sensitivity to insulin leading to diabetes. Our
fundamental hypothesis is that low vitamin D status is a risk factor for CVD by causing a
proinflammatory milieu, thereby leading to endothelial dysfunction. Additionally, the
investigators hypothesize that vitamin D supplementation will reduce inflammation, thereby
restoring endothelial function and ultimately reducing CVD risk.
are leading causes of death among northern US NAs. Moreover, low vitamin D status occurs
commonly in this same population. An increasing amount of evidence indicates a correlation
between low vitamin D status and CVD and diabetes by contributing to a heightened
pro-inflammatory environment within the endothelial lining of blood vessels leading to
atherosclerotic disease, and an impaired sensitivity to insulin leading to diabetes. Our
fundamental hypothesis is that low vitamin D status is a risk factor for CVD by causing a
proinflammatory milieu, thereby leading to endothelial dysfunction. Additionally, the
investigators hypothesize that vitamin D supplementation will reduce inflammation, thereby
restoring endothelial function and ultimately reducing CVD risk.
Low vitamin D status is endemic due to 21st century lifestyle, which limits sun exposure,
and inadequate dietary intake. An increasing body of data relates low vitamin D status to
increased risk for non-musculoskeletal morbidities including, most notably, cardiovascular
disease (CVD) and type II diabetes mellitus (T2DM). CVD, for which T2DM is a major risk
factor, causes over one-third of all deaths in the US. Moreover, American Indians (AI) and
Alaskan Natives (AN) are 20% more likely to develop CVD and 2.2 times more likely to develop
DM than non-Hispanic whites. In fact, AI of the Great Lakes Region (Bemidji Area) have the
third highest DM rate in the nation, an age-adjusted DM mortality rate almost three-fold
higher than the all-race mortality, and the highest rates of CVD among AI nationally. In
this population, where CVD and DM are two of the top four causes of death, our preliminary
work finds low vitamin D status commonplace.
As low vitamin D status, CVD and T2DM are epidemic among AI, the investigators hypothesize
that low vitamin D is causally related to CVD and T2DM by establishing a pro-inflammatory
milieu, which in turn predisposes to CVD and T2DM. As such, vitamin D supplementation
should reduce markers of inflammation and thereby ultimately reduce risk for CVD and T2DM.
This work will explore this possibility by evaluating the effect of vitamin D status on
endothelial function (measured by arterial reactivity), plasma biomarkers of inflammation
and glucose homeostasis in 100 postmenopausal AI women. Subjects will receive vitamin D3,
either 400 or 2,500 IU, daily for six months. The investigators will define the effects of
vitamin D status, and subsequent response to supplementation, on endothelial function,
arterial stiffness (flow-mediated vasodilation (FMD) of the brachial artery, and carotid to
femoral pulse wave velocity (PWV)), plasma markers of inflammation and glucose homeostasis.
All study participants will have fasting laboratory and noninvasive vascular ultrasound
studies performed at baseline and following three and six months of study. Plasma
concentration of pro-inflammatory cytokines will be measured as secondary outcome variables.
Fasting blood glucose, insulin and the adipocytokines leptin and adiponectin, will be
measured as exploratory outcomes for potential future studies.
and inadequate dietary intake. An increasing body of data relates low vitamin D status to
increased risk for non-musculoskeletal morbidities including, most notably, cardiovascular
disease (CVD) and type II diabetes mellitus (T2DM). CVD, for which T2DM is a major risk
factor, causes over one-third of all deaths in the US. Moreover, American Indians (AI) and
Alaskan Natives (AN) are 20% more likely to develop CVD and 2.2 times more likely to develop
DM than non-Hispanic whites. In fact, AI of the Great Lakes Region (Bemidji Area) have the
third highest DM rate in the nation, an age-adjusted DM mortality rate almost three-fold
higher than the all-race mortality, and the highest rates of CVD among AI nationally. In
this population, where CVD and DM are two of the top four causes of death, our preliminary
work finds low vitamin D status commonplace.
As low vitamin D status, CVD and T2DM are epidemic among AI, the investigators hypothesize
that low vitamin D is causally related to CVD and T2DM by establishing a pro-inflammatory
milieu, which in turn predisposes to CVD and T2DM. As such, vitamin D supplementation
should reduce markers of inflammation and thereby ultimately reduce risk for CVD and T2DM.
This work will explore this possibility by evaluating the effect of vitamin D status on
endothelial function (measured by arterial reactivity), plasma biomarkers of inflammation
and glucose homeostasis in 100 postmenopausal AI women. Subjects will receive vitamin D3,
either 400 or 2,500 IU, daily for six months. The investigators will define the effects of
vitamin D status, and subsequent response to supplementation, on endothelial function,
arterial stiffness (flow-mediated vasodilation (FMD) of the brachial artery, and carotid to
femoral pulse wave velocity (PWV)), plasma markers of inflammation and glucose homeostasis.
All study participants will have fasting laboratory and noninvasive vascular ultrasound
studies performed at baseline and following three and six months of study. Plasma
concentration of pro-inflammatory cytokines will be measured as secondary outcome variables.
Fasting blood glucose, insulin and the adipocytokines leptin and adiponectin, will be
measured as exploratory outcomes for potential future studies.
Inclusion Criteria:
- Ambulatory, community dwelling AI woman
- Postmenopausal up to age 75 years; for women below age 55, postmenopausal status must
be confirmed by documentation of serum FSH>30 IU/L and estradiol < 20 pg/ml unless a
bilateral oophorectomy is documented.
Exclusion Criteria:
- Serum 25(OH)D < 10 or > 60 ng/ml.
- Known CVD (history of MI, coronary artery bypass graft surgery, percutaneous coronary
intervention, stroke, transient ischemic attack, peripheral arterial disease with
claudication).
- Uncontrolled thyroid disease (thyroid stimulating hormone level outside of normal
range).
- Change in dose of lipid lowering medications within the preceding six weeks.
- Mastectomy of the right breast
- Non-English speaking, illiterate, impaired decision making.
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