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J Sorkin

Publications and source records attributed to J Sorkin.

8 recordsLinked to original sources

Body fat distribution and flow-mediated endothelium-dependent vasodilation in older men.

OBJECTIVE: Recent studies indicate that abdominal fat accumulation, in particular intra-abdominal fat, is related to impaired endothelial function in young healthy volunteers. The aim of this study was to examine whether the distribution of body fat depots is related to impaired endothelial function in older men. METHODS: Cross-sectional sample of 38 older (68+/-1 y) sedentary (VO(2max)=2.4+/-0.1 l/min) men. Flow-mediated endothelial dependent vasodilation (EDD) was assessed in the brachial artery in response to reactive hyperemia using high-resolution ultrasound. Abdominal subcutaneous and visceral fat depots were assessed by computed tomography scan (CT-scan) at the L(4)-L(5) region in the supine position. Percentage body fat was assessed via dual-energy X-ray absorptiometry (DEXA). RESULTS: Flow-mediated percentage change in brachial artery was 7.6+/-0.7%, suggesting an impaired flow-mediated EDD. Using simple linear regression analysis, there were no statistically significant relationship observed between flow-mediated EDD and the indices of total and abdominal adiposity (percentage body fat=29.3+/-0.9%, r=-0.11; total abdominal fat area=465+/-23 cm(2), r=-0.1; intra-abdominal fat area=200+/-14 cm(2), r=-0.14; subcutaneous fat area=265+/-13 cm(2), r=-0.05; BMI=29.3+/-0.9 kg/m(2), r=-0.07; and waist to hip ratio=0.98+/-0.01, r=-0.20). CONCLUSION: These findings suggest that in older sedentary men there is no clear correlation between adiposity and body fat distribution and impairment of flow-mediated endothelium dependent vasodilation.

Absorptiometry, Photon↗

Heritability of life span in the Old Order Amish.

Although a familial contribution to human longevity is recognized, the nature of this contribution is largely unknown. We have examined the familial contribution to life span in the Old Order Amish (OOA) population of Lancaster County, Pennsylvania. Analyses were conducted on 1,655 individuals, representing all those born prior to 1890 and appearing in the most widely available genealogy, surviving until at least age 30 years, and with known date of death. Mean age at death (+/-SD) in this population was 70.7 +/- 15.6 years, and this did not change appreciably over time. Parental and offspring ages at death were significantly correlated, as were ages of death among siblings. Offspring longevity was correlated with longevity of both parents, and in more or less additive fashion. For example, mean offspring age at death was 69.4 +/- 15.3 years in individuals for whom both parents died before the age of 75 years (n = 280) and increased to 73.5 +/- 16.0 years in individuals for whom neither parent died before the age of 75 years (n = 311). These differences were highly significant (P = 0.006). We estimated heritability of life span to be 25% +/- 5%, suggesting that the additive effects of genes account for one quarter of the total variability in life span in the OOA. We conclude that longevity is moderately heritable in the OOA, that the genetic effects are additive, and that genetic influences on longevity are likely to be expressed across a broad range of ages. Published 2001 Wiley-Liss, Inc.

Adult↗

Effects of strength training on total and regional body composition in older men.

The effects of a 16-wk strength-training program on total and regional body composition were assessed by dual-energy X-ray absorptiometry (DEXA), magnetic resonance imaging (MRI), and hydrodensitometry in 13 untrained healthy men [60 +/- 4 (SD) yr]. Nine additional men (62 +/- 6 yr) served as inactive controls. The strength-training program resulted in substantial increases in both upper (39 +/- 8%; P < 0.001) and lower (42 +/- 14%; P < 0.001) body strength. Total fat-free mass (FFM) increased by 2 kg (62.0 +/- 7.1 to 64.0 +/- 7.2 kg; P < 0.001), and total fat mass decreased by the same amount (23.8 +/- 6.7 to 21.8 +/- 6.0 kg; P < 0.001) when measured by DEXA. When measured by hydrodensitometry, similar increases in FFM (61.3 +/- 7.8 to 63.0 +/- 7.6 kg; P < 0.01) and decreases in fat mass (23.8 +/- 7.9 to 22.1 +/- 7.7 kg; P < 0.001) were observed. When measured by DEXA, FFM was increased in the arms (6.045 +/- 0.860 to 6.418 +/- 0.803 kg; P < 0.01), legs (19.416 +/- 2.228 to 20.131 +/- 2.303 kg; P < 0.001), and trunk (29.229 +/- 4.108 to 30.134 +/- 4.184 kg; P < 0.01), whereas fat mass was reduced in the arms (2.383 +/- 0.830 to 2.128 +/- 0.714 kg; P < 0.01), legs (7.583 +/- 1.675 to 6.945 +/- 1.551 kg; P < 0.001), and trunk (12.216 +/- 4.143 to 11.281 +/- 3.653 kg; P < 0.01) as a result of training.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗

Salivary gland function and glucose metabolic status.

To study the relationship between glucose metabolic status and salivary gland function in different-aged persons, subjects with diabetes mellitus (DM = 11), impaired glucose tolerance (IGT = 26), and controls (n = 26), aged 24 to 93, were examined in the oral physiology component of the Baltimore Longitudinal Study of Aging. All were generally healthy (except DM) and nonmedicated. The controls and subjects with IGT were classified using World Health Organization criteria, and diabetic status was assessed using Hb1Ac levels. Unstimulated and 2% citrate-stimulated parotid and submandibular salivary flow rates were collected, and subjective responses to questions about salivary hypofunction were evaluated. No statistically significant differences were observed between the three groups, nor between young and old subjects with altered glucose metabolism. These findings suggest that among well-controlled individuals with altered glucose metabolism, salivary gland function is not significantly impaired.

Adult↗

Age as independent determinant of glucose tolerance.

It has been proposed that the decline in glucose tolerance with age is not a primary aging effect but is secondary to a combination of other age-associated characteristics, i.e., disease, medication, obesity, central and upper-body fat deposition, and inactivity. To test this hypothesis, we first eliminated from analysis the Baltimore Longitudinal Study of Aging participants with identifiable diseases or medications known to influence glucose tolerance. Seven hundred forty-three men and women, aged 17-92 yr, remained for analysis. As indices of fatness, body mass index and percent body fat were determined. As indices of body fat distribution, waist-hip ratio and subscapular triceps skin-fold ratio were calculated. As indices of fitness, physical activity level, determined by detailed questionnaire, and maximum 02 consumption were calculated. We tested whether the effect of age on glucose tolerance remains when data were adjusted for fatness, fitness, and fat distribution; 2-h glucose values were 6.61, 6.78, and 7.83 mM for young (17-39 yr), middle-aged (40-59 yr), and old (60-92 yr) men and 6.22, 6.22, and 7.28 mM for the three groups of women, respectively. The differences between the young and middle-aged groups were not significant, but the old groups had significantly higher values than young or middle-aged groups. Fatness, fitness, and fat distribution can account for the decline in glucose tolerance from the young adult to the middle-aged years. However, age remains a significant determinant of the further decline in glucose tolerance of healthy old subjects.

Adipose Tissue↗

The role of obesity and cardiovascular fitness in the impaired glucose tolerance of aging.

The prevalence of impaired glucose tolerance (IGT) increases with aging. Although some data suggest that age is independently associated with IGT, other studies suggest that age-associated changes in body composition and reduced cardiovascular fitness are responsible for the development of IGT. We, therefore, examined the relationship of age, total and regional adiposity, and level of fitness (VO2max) to the presence of IGT in 155 healthy, nondiabetic, nonsmoking, older community dwelling men. Sixty-two of 155 men (40%) had IGT, while 93 men (60%) had normal glucose tolerance (WHO criteria). The subjects with IGT were of similar age (61.0 +/- 1.0 vs. 59.0 +/- 0.7 years, p = 0.49) and had the same maximal aerobic capacity, (VO2max) (42.0 +/- 1.0 vs. 44.0 +/- 0.8 mL/kg ffm/min, p = 0.42), but had a higher waist to hip ratio (WHR) (0.98 +/- 0.01 vs. 0.96 +/- 0.01, p = 0.005) and percent body fat (30.0 +/- 0.4 vs. 26.0 +/- 0.6, p = 0.004) than the men with normal glucose tolerance. In univariate analysis, the 2-h glucose level correlated positively with percent body fat (r = 0.30, p = 0.0002), WHR (0.24, p = 0.002), and age (r = 0.17, p = 0.03) and negatively with VO2max (r = -0.23, p = 0.005). In both multiple logistic and linear regression analyses, percent body fat was the only independent predictor of IGT (p = 0.002). These results suggest that the age-associated increase in total adiposity is a major contributor to the development of IGT in middle-aged and older men. Thus, lifestyle modifications that reduce body fat should reduce the risk for IGT and the development of noninsulin-dependent diabetes mellitus in the elderly.

Aged↗

Comorbidities and the entry of patients with peripheral arterial disease into an exercise rehabilitation program.

BACKGROUND: Exercise rehabilitation is advocated to improve function in patients with peripheral arterial disease (PAD) who have intermittent claudication. Patients with PAD often have comorbid medical problems that may interfere with their ability to safely participate in exercise rehabilitation programs. There is a paucity of information regarding the medical comorbidities and the evaluation of PAD patients before their participation in exercise rehabilitation studies. The purpose of this study was to identify comorbidities that predicted exclusion of PAD patients from participation in an aerobic exercise rehabilitation clinical trial. METHODS: This was a prospective cohort study of 225 consecutive outpatient volunteers (mean age 68 +/- 8 years, SD) with a history of Fontaine Stage II PAD recruited for exercise rehabilitation. Patient eligibility was determined by a history and physical exam, blood chemistries, measurement of ankle to brachial index (ABI), and an exercise treadmill test. RESULTS: Seventy-nine volunteers (35%) were medically ineligible: 22 because of symptomatic coronary artery disease, 12 because of severe PAD, and the rest for a variety of medical problems. In stepwise logistic regression analyses, low ABI and use of insulin were predictors of exclusion, whereas peripheral revascularization was an indicator of inclusion. Age, a history of coronary artery disease, myocardial infarction, coronary bypass surgery, and hypertension were not independent determinants of eligibility. CONCLUSIONS: Insulin-requiring diabetes and a low ABI increase the likelihood that older patients with PAD will be ineligible to participate in a research exercise rehabilitation program, whereas peripheral revascularization was associated with inclusion. Whether intensive medical management and peripheral revascularization would enable the claudicants deemed ineligible for entry into the exercise rehabilitation program to safely exercise remains to be determined.

Aged↗