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Biomedical subjects

Stanley J Birge

Publications and source records attributed to Stanley J Birge.

7 recordsLinked to original sources

Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults.

BACKGROUND: Vitamin D deficiency is common in older adults and has been implicated in psychiatric and neurologic disorders. This study examined the relationship among vitamin D status, cognitive performance, mood, and physical performance in older adults. METHODS: A cross-sectional group of 80 participants, 40 with mild Alzheimer disease (AD) and 40 nondemented persons, were selected from a longitudinal study of memory and aging. Cognitive function was assessed using the Short Blessed Test (SBT), Mini-Mental State Exam (MMSE), Clinical Dementia Rating (CDR; a higher Sum of Boxes score indicates greater dementia severity), and a factor score from a neuropsychometric battery; mood was assessed using clinician's diagnosis and the depression symptoms inventory. The Physical Performance Test (PPT) was used to measure functional status. Serum 25-hydroxyvitamin D levels were measured for all participants. RESULTS: The mean vitamin D level in the total sample was 18.58 ng/mL (standard deviation: 7.59); 58% of the participants had abnormally low vitamin D levels defined as less than 20 ng/mL. After adjusting for age, race, gender, and season of vitamin D determination, vitamin D deficiency was associated with presence of an active mood disorder (odds ratio: 11.69, 95% confidence interval: 2.04-66.86; Wald chi(2) = 7.66, df = 2, p = 0.022). Using the same covariates in a linear regression model, vitamin D deficiency was associated with worse performance on the SBT (F = 5.22, df = [2, 77], p = 0.044) and higher CDR Sum of Box scores (F = 3.20, df = [2, 77], p = 0.047) in the vitamin D-deficient group. There was no difference in performance on the MMSE, PPT, or factor scores between the vitamin D groups. CONCLUSIONS: In a cross-section of older adults, vitamin D deficiency was associated with low mood and with impairment on two of four measures of cognitive performance.

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Prevention of osteoporotic fractures in the elderly.

Osteoporosis is a common and preventable disorder of the older adult skeleton that predisposes an individual to an increased risk of fracture, a major cause of disability in older adults. Most patients with osteoporosis have an identifiable cause of bone loss. Factors contributing to osteoporotic fractures are more often associated with disordered neuromuscular function affecting postural stability than disordered skeletal integrity. Effective pharmacologic agents are available for the prevention and treatment of osteoporosis. Prevention of osteoporotic fractures in the elderly, particularly nonvertebral fractures, presents unique challenges. Fracture prevention requires identification and management of disorders that contribute to falls, the prevention of falls, and reduction of the impact force of falls. Thus, both pharmacological and nonpharmacological strategies need to be employed. The presence of multiple co-morbidities further complicates management of osteoporosis in the elderly population.

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The use of estrogen in older women.

The menopause is associated with a relatively abrupt decline in the ovarian production of estrogen that results in a state of estrogen deficiency. This estrogen deficiency state is associated with an accelerated expression of cardiovascular disease, osteoporosis, urogenital atrophy, dermal aging, an increased expression of colorectal cancer, an alteration in the expression of breast cancer that results in more malignant forms of the disease, and the loss of neurons from the brain that is associated with a more rapid decline in cognitive function, balance, and an earlier expression of Alzheimer's disease. Macular degeneration and cataract formation may be additional consequences of the estrogen deficiency state. Thus the estrogen deficiency state may be characterized as a state of accelerated aging. The abrupt transition from the reproductive state of multiple estrogen-dependent neural systems within the brain may affect their function as manifested by the typical menopausal symptoms of hot flashes, mood changes, sleep disturbance, and cognitive impairment. This transition may trigger a cascade of events that contributes to the acceleration of brain aging and the expression of neurodegenerative processes as Alzheimer's disease. This article discusses the use of estrogen to prevent these age-related changes.

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Prevention of brain aging and dementia.

The brain is subjected to multiple factors that result in damage to its cellular constituents, the neuron and supporting cells, and the neural networks that form the bases of cognitive ability. Like other systems, the brain has remarkable capacity to repair that damage and to adapt or compensate for the loss of neurons and the disruption of the neural architecture. Brain aging and dementia can be conceptualized as a balance between neuronal injury and repair. This balance can be affected not only by genetic and age-related factors but also by multiple environmental factors. The latter includes many factors, including education, nutrition, exercise, socialization, and stress. As individuals, we have the potential to modify these factors through lifestyle choices. Advances in neuroscience have led to the development of pharmacologic agents that can ameliorate the effects of even genetic (e.g., statins and antihypertensive agents) and age-related (e.g., antioxidants and estrogen replacement) factors. By altering the balance between neuronal injury and repair, we can delay the expression and progression of the neurodegenerative processes of brain aging, AD, and related dementias.

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