How do sock ply changes affect residual-limb fluid volume in people with transtibial amputation?

The purpose of this research was to investigate the influence of sock addition and removal on residual-limb fluid volume in people using prosthetic limbs. We used bioimpedance analysis to measure residual-limb extracellular fluid volume on 28 transtibial amputee subjects during 30 min test sessions. Upon addition of a one-ply polyester sock, residual-limb fluid volume changes ranged from -4.0% to 0.8% (mean -0.9 +/- 1.3%) of the initial limb fluid volume. Changes for sock removal ranged from -1.2% to 2.8% (mean 0.5 +/- 0.8%). Subjects who reduced in fluid volume with both addition and removal of a sock and subjects with high positive ratios between the fluid-volume loss upon sock addition and gain upon sock removal (high add/remove [AR] ratios) tended to have arterial disease, were obese, and were smokers. Subjects with low positive AR ratios, subjects who increased in fluid volume both with sock addition and removal, and a single subject who increased in fluid volume with sock addition and decreased with sock removal tended to be nonsmokers and either individuals in good health without complications or individuals without arterial problems. Results are relevant for the anticipation of limb volume changes during prosthetic fitting and toward the design of adjustable-socket technologies.

Preliminary investigation of residual-limb fluid volume changes within one day.

The purpose of this research was to investigate rates of residual-limb fluid volume change within one day for people with transtibial limb loss. Rates of fluid volume change during 30 min test sessions of sitting, standing, and walking activities were measured twice a day, once in the morning and once in the afternoon, on 12 regular prosthesis users with the use of bioimpedance analysis. Between test sessions, all subjects consumed food and drink, and subject activity ranged from low to high. The rate of fluid volume change within sessions ranged from -8.5 to 5.9 %/h (median: -2.2%/h). The rate of fluid volume change between sessions ranged from -2.7 to 0.9 %/h (median: -1.0%/h). The between-session rate of fluid volume change correlated highly with afternoon within-session rates of change (r = 0.9) but was not well correlated with morning within-session rates of change (r = 0.8). Subjects with peripheral arterial complications showed greater fluid volume loss rates during test sessions than between sessions. Rate of fluid volume change may be affected by sitting, standing, and walking activities; presence of peripheral arterial complications; being female; time since amputation; and wearing the socket without doffing for extended periods.

The association between birth weight and visceral fat in middle-age adults.

OBJECTIVE: Low birth weight, a proxy for fetal underdevelopment, is associated with increased risk of developing type 2 diabetes during adulthood. Low birth weight is also associated with central obesity, but little is known about the association between birth weight and visceral adiposity. The purpose of this study is to test the hypothesis that lower birth weight is associated with increased amounts of visceral fat in middle-age adults. RESEARCH METHODS AND PROCEDURES: This is an observational study of 91 adults (58 men and 33 women) 40+/-6 years of age (mean+/-standard deviation). Ethnicity was either Japanese American (79%) or non-Hispanic white (21%). Birth weight was obtained from State Departments of Health. Measurements included smoking status, BMI, and visceral (intra-abdominal) fat measured by computed tomography. RESULTS: Visceral fat was not associated with birth weight after adjustment for age, sex, ethnicity, BMI, or smoking status (p=0.76). There was no evidence that the association between birth weight and visceral fat varied by age, sex, or ethnicity. DISCUSSION: We found no evidence that low birth weight is associated with increased visceral fat in middle-age adults.

Equivalent insulin resistance in latent autoimmune diabetes in adults (LADA) and type 2 diabetic patients.

Insulin resistance is a primary component in the pathophysiology of type 2 diabetes. In latent autoimmune diabetes in adults (LADA), insulin resistance has been reported to be significantly lower than in autoantibody-negative type 2 diabetes (T2DM), but whether this might be related to differences in body mass index (BMI) has not been excluded. Furthermore, previous studies have used limiting inclusive criteria for LADA, requiring only the presence of GADA or IA-2A. To apply more inclusive criteria for LADA, consistent with recent recommendations, we defined LADA by clinical manifestations characteristic of T2DM, but with the presence of any combination of GADA, IA-2A, ICA, or IAA. We recruited 43 LADA patients, 70 T2DM patients, and 150 non-diabetic controls. Insulin resistance was assessed by both the homeostasis model assessment and the quantitative insulin sensitivity check index, and BMI was calculated. We found that insulin resistance in LADA is equivalent to that of T2DM. When insulin resistance is assessed as a function of BMI, both diabetic populations demonstrated an insulin resistance equally greater than normal controls. The interaction between insulin resistance and BMI in the two diabetic groups was significantly different from that demonstrated in non-diabetic controls. In summary, LADA demonstrates insulin resistance of similar magnitude to T2DM, but with the concurrent component of an immune attack against the pancreatic beta-cells. LADA patients may be at significant risk for metabolic consequences of insulin resistance other than glucose metabolism, such as those described in the metabolic syndrome. As complications and treatment regimens specific to LADA are realized, improved means of identification of LADA will become increasingly important.

Is central obesity associated with cirrhosis-related death or hospitalization? A population-based, cohort study.

BACKGROUND & AIMS: We aimed to determine the interaction between body fat distribution (central versus peripheral) and increased body mass index (BMI) with regards to the risk of cirrhosis-related death or hospitalization. METHODS: Participants included 11,434 persons aged 25-74 years without evidence of cirrhosis at entry into the study or during the first 5 years of follow-up who were subsequently followed for a mean of 12.9 years as part of the first National Health and Nutrition Examination Survey. Participants were categorized into "normal-weight" (BMI < 25 kg/m 2 , N = 5750), "overweight" (BMI 25 to < 30 kg/m 2 , N = 3770), and "obese" (BMI > or = 30 kg/m 2 , N = 1914). The subscapular to triceps skinfold thickness ratio (SFR) was used to categorize body fat distribution into central (SFR > 1, N = 5211) and peripheral (SFR < or = 1, N = 6223). RESULTS: Cirrhosis resulted in death or hospitalization of 88 participants during 149,888 person-years of follow-up (59/100,000 person-years). Among persons with a central body fat distribution, cirrhosis-related deaths or hospitalizations were more common in obese persons (115/100,000 person-years, adjusted hazard ratio 2.2, 95% confidence interval [CI] 1.1-4.6) and in overweight persons (94/100,000 person-years, adjusted hazard ratio 1.5, 95% CI 0.8-3.0) compared to normal-weight persons (59/100,000 person-years). However, among persons with a peripheral fat distribution, there was no association between obesity (adjusted hazard ratio 0.7, 95% CI 0.3-1.6) or overweight (adjusted hazard ratio 0.8, 95% CI 0.2-2.8) and cirrhosis-related death or hospitalization. CONCLUSIONS: The risk of cirrhosis-related death or hospitalization appears to be increased in the presence of cirrhosis, but only among persons with a central fat distribution. The excess risk associated with central obesity might be related to insulin resistance and hepatic steatosis.

Potential of essential fatty acid deficiency with extremely low fat diet in lipoprotein lipase deficiency during pregnancy: A case report.

BACKGROUND: Pregnancy in patients with lipoprotein lipase deficiency is associated with high risk of maternal pancreatitis and fetal death. A very low fat diet (< 10% of calories) is the primary treatment modality for the prevention of acute pancreatitis, a rare but potentially serious complication of severe hypertriglyceridemia. Since pregnancy can exacerbate hypertriglyceridemia in the genetic absence of lipoprotein lipase, a further reduction of dietary fat intake to < 1-2% of total caloric intake may be required during the pregnancy, along with the administration of a fibrate. It is uncertain if essential fatty acid deficiency will develop in the mother and fetus with this extremely low fat diet, or whether fibrates will cross the placenta and concentrate in the fetus. CASE PRESENTATION: A 23 year-old gravida 1 woman with primary lipoprotein lipase deficiency was seen at 7 weeks of gestation in the Lipid Clinic for management of severe hypertriglyceridemia that had worsened with pregnancy. While on her habitual fat intake of 10% of total calories, her pregnancy resulted in an exacerbation of the hypertriglyceridemia, which prompted further restriction of fat intake to < 2% of total calories, as well as administration of gemfibrozil at a lower than average dose. The level of gemfibrozil, as the active metabolite, in the venous and arterial fetal cord blood was within the expected therapeutic range for adults. The clinical signs and a biomarker of essential fatty acid deficiency, namely the ratio of 20:3 [n-9] to 20:4 [n-6] fatty acids, were closely monitored throughout her pregnancy. Despite her extremely low fat diet, the levels of essential fatty acids measured in the mother and in the fetal blood immediately postpartum were normal. Normal essential fatty acid levels may have been achieved by the topical application of sunflower oil. CONCLUSIONS: An extremely low fat diet in combination with topical sunflower oil and gemfibrozil administration was safely implemented in pregnancy associated with the severe hypertriglyceridemia of lipoprotein lipase deficiency.

Association of bioavailable, free, and total testosterone with insulin resistance: influence of sex hormone-binding globulin and body fat.

OBJECTIVE: Previous reports of an association between low testosterone levels and diabetes risk were often confounded by covariation of sex hormone-binding globulin (SHBG) and testosterone measurements. Measurements of bioavailable and free testosterone, more reliable indexes of biologically active testosterone, were examined for their associations with markers of insulin resistance and body fat measures in 221 middle-aged nondiabetic men. RESEARCH DESIGN AND METHODS: Bioavailable and free testosterone were calculated from the concentrations of total testosterone, SHBG, and albumin, and they were not significantly correlated with SHBG (r = 0.07-0.1). In contrast, total testosterone correlated significantly with SHBG (r = 0.63). We evaluated the relationship between these measures of circulating testosterone and markers for insulin resistance (i.e., fasting insulin, C-peptide, and homeostasis model assessment for insulin resistance [HOMA-IR]) as well as total body fat (assessed by dual-energy X-ray absorptiometry [DEXA]) and abdominal fat distribution (assessed by single-slice computed tomography [CT]). RESULTS: Bioavailable, free, and total testosterone and SHBG all correlated significantly with fasting insulin (age-adjusted r = -0.15 [P = 0.03], -0.14 [P = 0.03], -0.32 [P < 0.0001], and -0.38 [P < 0.0001], respectively), fasting C-peptide (r = -0.18 [P = 0.009] to -0.41 [P < 0.0001]), HOMA-IR (r = -0.15 [P = 0.03] to - 0.39 [P < 0.0001]), and body fat measures (r = -0.17 [P = 0.008] to -0.44 [P < 0.0001]). Only SHBG and total testosterone were significantly associated with fasting glucose (r = -0.20 [P = 0.003] to -0.21 [P = 0.002]). In multivariate analysis, bioavailable or free testosterone was significantly and inversely associated with insulin, C-peptide, and HOMA-IR, but this was not independent of total body or abdominal fat. SHBG was a significant determinant of insulin, C-peptide, and HOMA-IR, independent of body fat. The associations between total testosterone and insulin resistance were confounded by SHBG. CONCLUSIONS: The inverse association between testosterone and insulin resistance, independent of SHBG, was mediated through body fat.