Thesis--University of Wisconsin--Madison. / Typescript. Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1984. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographies.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1984. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographies.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1960. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Vitamin D is an important secosteroid hormone that is responsible for calcium and phosphorus homeostasis. Vitamin D deficiency and insufficiency are an ever increasing global problem. Very few foods naturally contain vitamin D; such as salmon, and sundried or ultraviolet irradiated mushrooms. Few foods are fortified with vitamin D such as milk, orange juice, cereal and bread. Little is known about the vitamin D levels in certain fish such as sardines. The purpose of this study was to find out whether sardines and mackerel are a good source of vitamin D such as wild salmon. It was hypothesized that both sardines and mackerel are a good source of vitamin D. Based on the results, sardines are a good source of vitamin D. One serving size (3.5 ounces, about 5 fish) of sardines has about 330.8 IU's of vitamin D3. This is equal to 66.2 IU's of vitamin D3 per fish. Mackerel on the other hand does not have as much vitamin D3 as sardines. A standard serving of mackerel (3.5 ounces, about 3 fish) has 81.6 IU's of vitamin D3. This is approximately 27.2 IU's of vitamin D3 per fish. Both mackerel and sardines are good sources of vitamin D3.

No description available.

No description available.

Objectives: Vitamin D deficiency is highly prevalent and has been linked to increased morbidity and mortality. There has been an increase in testing for vitamin D with a concomitant increase in costs. While individual factors are significantly linked to vitamin D status, prior studies have not yielded a model predictive of vitamin D status or 25(OH)D levels. The purpose of this investigation was to determine if a prediction model of vitamin D could be developed using extensive demographic data and laboratory parameters. Methods: Patient data from 6 Veterans Administration Medical Centers were extracted from medical charts. Results: For the 14,920 available patients, several factors including triglyceride level, race, total cholesterol, body mass index, calcium level, and number of missed appointments were significantly linked to vitamin D status. However, these variables accounted for less than 15% of the variance in vitamin D levels. While the variables correctly classified vitamin D deficiency status for 71% of patients, only 33% of those who were actually deficient were correctly identified as deficient. Conclusion: Given the failure to find a sufficiently predictive model for vitamin D deficiency, we propose that there is no substitute for laboratory testing of 25(OH)D levels. A baseline vitamin D 3 daily replacement of 1000-2000 IU initially with further modification based on biannual testing appears to factor in the wide variation in dose response observed with vitamin D replacement and is especially important in high-risk groups such as ethnic minorities.

Using data from the Health, Aging, and Body Composition study, we examined whether low 25-hydroxyvitamin D (25[OH]D) concentrations were associated with prevalent or incident cognitive impairment. Serum 25(OH)D concentrations were measured in 2,786 older adults and categorized as <20 ng/mL, 20 to <30 ng/mL, or ≥30 ng/mL. Cognitive impairment was defined as a score >1.5 standard deviations below race and education specific means on either digit symbol substitution test or modified mini-mental state test. Logistic regression determined the odds of cognitive impairment at baseline and year 5 by 25(OH)D category. 25(OH)D concentrations were <30 ng/mL in 57.3% of whites and 84.6% of blacks. After excluding participants with baseline cognitive impairment (n = 340), 13% of whites and 13% of blacks developed cognitive impairment by year 5. In whites, 25(OH)D concentrations <30 ng/mL were not associated with prevalent or incident cognitive impairment. Black participants with 25(OH)D concentrations <20 ng/mL had a higher odds of prevalent, but not incident cognitive impairment (OR (95% CI): 2.05 (1.08–3.91), p = 0.03) compared to participants with 25(OH)D concentrations ≥30 ng/mL. Low 25(OH)D concentrations were associated with twofold higher odds of prevalent cognitive impairment in blacks.

Medial calcification refers to mineral deposition in the middle layer of arteries. This mineralization is common in chronic kidney disease patients and causes an increased chance of cardiovascular complications. Calcitriol, the active form of vitamin D, is often administered to these patients to treat an associated condition, secondary hyperparathyroidism. Unfortunately, calcitriol treatment may promote vascular calcification due to increasing serum calcium and phosphate. We examined the effects of calcitriol supplementation on vascular smooth muscle cell (VSMC) calcification, through atomic absorption, scanning electron microscopy, and western blot analysis. Additionally, we examined the effects of the combinations of calcitriol, fibroblast growth factor 23 (FGF-23), and klotho. We determined that calcitriol supplementation alone increased calcification but was not associated with a transition towards an osteoblast-like phenotype. On the other hand, the combination of calcitriol and FGF-23 caused a decrease in calcification, but this decrease was attenuated with the further addition of klotho.