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Biomedical subjects

W R Hazzard

Publications and source records attributed to W R Hazzard.

At least 37 records · Page 2Linked to original sources
PubMed1997

Ways to make "usual" and "successful" aging synonymous. Preventive gerontology.

Preventive gerontology is the study and practice of those elements of lifestyle, environment, and health care management that will provide the maximal longevity of highest quality for individuals and the population. As such, it focuses on a personalized hygiene agenda that varies in its emphasis according to a person's age, sex, and risk factor profile. It includes a matrix of strategies relating to diet, exercise, and the avoidance of substance abuse and adverse environmental exposure. Preventive gerontology carries differential emphases according to the life stage of a person, featuring long-term, low-cost, and low-risk lifestyle strategies in youth and middle age (generally to age 75) and more short-term, low-risk interventions in old age (> 75), especially secondary prevention, according to individualized estimates of risk, cost, and benefit. The aggregate effect of widespread application of this approach--especially insofar as it is coupled with a rising level of education and continued psychosocial development--will be progressive congruency between usual and successful aging. A by-product will also be an ever-advancing median age of the population and, inevitably, a growth in long-term health and social service needs. Responsible planning for this consequence of success in the 21st century will require a rededication of North Americans to care for those in need regardless of age.

Aged↗
PubMed1995

Elder abuse: definitions and implications for medical education.

Elder abuse is a growing problem as the number of dependent older persons increases and the proportions of middle-aged and younger children--who themselves are struggling with problems of their own families and finances--decline. As this occurs, older women increasingly will dominate the ranks of the elderly. These realities make it imperative for medical students to become familiar with the care of older persons, including abused older persons, who, at present, constitute at least 2% of the population over 65. The author outlines the causes of elder abuse (e.g., previous abusive relationships in a family increase the likelihood of elder abuse); lists important barriers to diagnosis and management of the abused (e.g., the physician's uncomfortable position between protecting confidentiality, serving as an advocate for the patient, and needing to collaborate with the family--and often the abuser); and outlines the various forms of intervention that are available (e.g., assistance of adult protection services). Education in elder abuse should be distributed across the entire medical student curriculum (many examples are given) and should be dominated by case-based learning at a variety of sites, such as hospitals, clinics, and subacute care units. The author closes by reiterating the urgent need to prepare physicians now to deal with a problem of increasing magnitude, severity, and ugliness.

Adult↗
PubMed1994

Geriatric medicine.

To decrease the level of disability in elderly persons, physicians must focus attention on lifestyle choices made by younger adults. Health practices can be influenced by educational programs in the general population and by counseling on an individual level. The optimal duration of estrogen therapy after menopause remains conjectural.

Geriatrics↗
PubMed1992

Metabolism of apolipoprotein B in members of a family with accelerated atherosclerosis: influence of apolipoprotein E-3/E-2 pattern.

Familial combined hyperlipidemia (FCHL) appears to be the most common, simply inherited hyperlipidemia strongly associated with coronary heart disease. In the family examined in this study, two of the siblings who met diagnostic criteria for FCHL had extensive clinical atherosclerosis before age 30, unusually premature for this form of hyperlipidemia. Lipoproteins and low-density lipoprotein (LDL) apolipoprotein (apo) B metabolism were characterized in these siblings in an attempt to gain insight into the cause of the rapid atherosclerosis in the two siblings so affected. LDL apo B production rates were very high in all three siblings (25 to 30 mg/kg/d), consistent with FCHL. beta-Very-low-density lipoprotein-beta (beta-VLDL) was present in the plasma of both siblings with accelerated atherosclerosis. The isoapolipoprotein E pattern in both of these siblings was E-3/E-2. In the third sibling, who was free of premature clinical atherosclerosis and lacked plasma beta-VLDL, the pattern was E-3/E-3. Thus, the heterozygote apo E-3/E-2 pattern may be related to the accumulation of beta-VLDL in persons with a very high apo B production rate. The abnormal accumulation of beta-VLDL may be one of the possible explanations for the rapid, premature atherosclerosis in the two siblings with FCHL in this kindred. Both male members in this kindred also had low levels of high-density lipoproteins, and thus may have had an additional risk of developing atherosclerosis due to this lipoprotein abnormality as well.

Adult↗
PubMed1992

Dyslipoproteinemia in the elderly. Should it be treated?

No clear consensus has emerged as to whether or not aggressive screening, surveillance, and management of lipid disorders in the elderly is indicated. Informal polling would suggest a highly conservative approach beyond age 70 but near universal support for such therapy below age 60, with gradations of enthusiasm in between. Studies to identify the cardiovascular risk factors in older persons have been initiated, as has been an intervention trial to lower elevated LDL cholesterol levels in older subjects with an HMG CoA reductase inhibitor. By the year 2000, the present, highly individualized and subjective treatment of lipid disorders in elderly patients may be replaced by more objective, uniform guidelines for such management. In the meantime the question remains, "Should dyslipoproteinemia be treated in the elderly?" And the answer remains, "Perhaps."

Aged↗
PubMed1991

A dose-response relationship between sex hormone-induced change in hepatic triglyceride lipase and high-density lipoprotein cholesterol in postmenopausal women.

In previous studies, we have demonstrated a temporal relationship between the postheparin hepatic triglyceride lipase (HTGL) response to sex steroids and the high-density lipoprotein (HDL) cholesterol response. To determine if this relationship is dose-dependent, we compared the effect of three graduated doses of orally administered estradiol and norgestrel in two groups of six postmenopausal women. With estradiol administration, postheparin HTGL activity decreased from 91 +/- 46 to 50 +/- 29 nmol/min/mL, baseline to high dose (P less than .05); HDL cholesterol increased from 54 +/- 6 to 64 +/- 10 mg/dL (P less than .05); HDL2 cholesterol increased from 16 +/- 4 to 23 +/- 7 mg/dL (P less than .05); and HDL3 cholesterol concentration did not change. With norgestrel administration, HTGL activity increased from 79 +/- 19 to 109 +/- 24 nmol/min/mL (P less than .05); HDL cholesterol decreased from 64 +/- 17 to 43 +/- 7 mg/dL (P less than .05); HDL2 cholesterol decreased from 21 +/- 17 to 6 +/- 5 mg/dL (P less than .05); and HDL3 cholesterol concentration decreased from 43 +/- 8 to 38 +/- 8 mg/dL (P less than .05). The HTGL activity response was inversely correlated with estrogen dose (rs = -.733, P = .0001) and directly correlated with progestin dose (rs = .895, P = .0001). The HDL cholesterol response was directly correlated with estrogen dose (HDL: rs = .741, P = .001; HDL2: rs = .586, P = 0.003) and inversely correlated with progestin dose (HDL: rs = -.933, P = .0001; HDL2: rs = -.866, P = .0001; HDL3: rs = -.576, P = .003).(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol, HDL↗