Sunweavers: Supporting Native American Women's Vitamin D Research

This study is currently recruiting participants. (see Contacts and Locations)
Verified March 2014 by University of Wisconsin, Madison
Sponsor:
Information provided by (Responsible Party):
University of Wisconsin, Madison
ClinicalTrials.gov Identifier:
NCT01490333
First received: November 29, 2011
Last updated: March 26, 2014
Last verified: March 2014
  Purpose

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.


Condition Intervention Phase
Vitamin D Deficiency
Cardiovascular Diseases
Dietary Supplement: Vitamin D3
Phase 2

Study Type: Interventional
Study Design: Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Investigator)
Primary Purpose: Prevention
Official Title: Sunweavers: Supporting Native American Women's Vitamin D Research

Resource links provided by NLM:


Further study details as provided by University of Wisconsin, Madison:

Primary Outcome Measures:
  • Change in markers of endothelial function [ Time Frame: Baseline visit, 3 month visit and 6 month visit. ] [ Designated as safety issue: No ]
    This will be determined by evaluating CRP and lipid panel

  • Change in arterial stiffness with vitamin D3 supplementation [ Time Frame: one year ] [ Designated as safety issue: No ]
    Change in arterial stiffness will be evaluated with radial tonometry.


Secondary Outcome Measures:
  • Plasma concentration of pro-inflammatory cytokines [ Time Frame: Baseline visit, 3 month visit, and 6 month visit. ] [ Designated as safety issue: No ]
    This will be evaluated by assessing TNF alpha, IL6, VCAM and ICAM


Estimated Enrollment: 100
Study Start Date: July 2011
Estimated Study Completion Date: April 2014
Estimated Primary Completion Date: April 2014 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Experimental: 2500 IU Vitamin D3 Dietary Supplement: Vitamin D3
The vitamin D3 will be taken daily.
Active Comparator: 400 IU Vitamin D3 Dietary Supplement: Vitamin D3
The vitamin D3 will be taken daily.

Detailed Description:

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.

  Eligibility

Ages Eligible for Study:   55 Years to 75 Years
Genders Eligible for Study:   Female
Accepts Healthy Volunteers:   Yes
Criteria

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.
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01490333

Contacts
Contact: Diane Krueger, B.S. 608-265-6410 dckruege@wisc.edu
Contact: Ellen Fidler, B.S. 608-265-6410 efidler@wisc.edu

Locations
United States, Wisconsin
Stockbridge-Munsee Nation Recruiting
Bowler, Wisconsin, United States, 54416
Contact: Nancy Miller-Korth    715-793-4144    nancy.miller-roth@mohican-nsn.gov   
Principal Investigator: Neil Binkley, M.D.         
Bad River Nation Recruiting
Lac du Flambeau, Wisconsin, United States, 54538
Contact: Irina Haller, Ph.D    218-786-8185    IHaller@smdc.org   
Principal Investigator: Neil Binkley, M.D.         
University of Wisconsin Osteoporosis Clinical Research Program Recruiting
Madison, Wisconsin, United States, 53705
Contact: Diane Krueger, B.S.    608-265-6410    dckruege@wisc.edu   
Principal Investigator: Neil Binkley, M.D.         
Sponsors and Collaborators
University of Wisconsin, Madison
Investigators
Principal Investigator: Neil Binkley, M.D. University of Wisconsin, Madison
  More Information

No publications provided

Responsible Party: University of Wisconsin, Madison
ClinicalTrials.gov Identifier: NCT01490333     History of Changes
Other Study ID Numbers: H-2010-0118
Study First Received: November 29, 2011
Last Updated: March 26, 2014
Health Authority: United States: Institutional Review Board

Additional relevant MeSH terms:
Cardiovascular Diseases
Vitamin D Deficiency
Avitaminosis
Deficiency Diseases
Malnutrition
Nutrition Disorders
Vitamins
Vitamin D
Ergocalciferols
Cholecalciferol
Micronutrients
Growth Substances
Physiological Effects of Drugs
Pharmacologic Actions
Bone Density Conservation Agents

ClinicalTrials.gov processed this record on September 22, 2014