The inability of current recommendations to control the epidemic of diabetes, the specific failure of the prevailing low-fat diets to improve obesity, cardiovascular risk, or general health and the persistent reports of some serious side effects of commonly prescribed diabetic medications, in combination with the continued success of low-carbohydrate diets in the treatment of diabetes and metabolic syndrome without significant side effects, point to the need for a reappraisal of dietary guidelines. The benefits of carbohydrate restriction in diabetes are immediate and well documented. Concerns about the efficacy and safety are long term and conjectural rather than data driven. Dietary carbohydrate restriction reliably reduces high blood glucose, does not require weight loss (although is still best for weight loss), and leads to the reduction or elimination of medication. It has never shown side effects comparable with those seen in many drugs. Here we present 12 points of evidence supporting the use of low-carbohydrate diets as the first approach to treating type 2 diabetes and as the most effective adjunct to pharmacology in type 1. They represent the best-documented, least controversial results. The insistence on long-term randomized controlled trials as the only kind of data that will be accepted is without precedent in science. The seriousness of diabetes requires that we evaluate all of the evidence that is available. The 12 points are sufficiently compelling that we feel that the burden of proof rests with those who are opposed.

Previous cross-sectional studies show that puberty is associated with a reduction in insulin sensitivity (S I ), but no longitudinal studies have examined this change in detail. This study is a longitudinal study in 60 children (33 male and 27 female subjects; 32 Caucasian and 28 African-American) examined at Tanner stage I (age 9.2 ؎ 1.4 years) and after 2.0 ؎ 0.6 years of follow-up, by which time 29 children remained at Tanner stage I and 31 had progressed to Tanner stage III or IV. Tanner stage was assessed by physical examination. S I , the acute insulin response (AIR), and the disposition index (DI) were determined by the tolbutamide-modified intravenous glucose tolerance test and minimal modeling, body fat mass was assessed by dual-energy X-ray absorptiometry, visceral fat was determined by computed tomography, and fasting blood was analyzed for hormone levels. In children progressing to Tanner stage III, S I fell significantly by 32% (4.4 ؎ 3.0 to 3.0 ؎ 1.7 ؋ 10 ؊4 min ؊1 /[IU/ml]), AIR increased by 30%, DI fell by 27%, and there was a significant increase in fasting glucose (93.5 ؎ 5.0 to 97.0 ؎ 4.1 mg/dl) and insulin (14.3 ؎ 8.1 to 18.6 ؎ 11.0 IU/ml). In children remaining at Tanner stage I, there was a slight increase in S I (6.4 ؎ 3.1 to 7.4 ؎ 3.5 ؋ 10 ؊4 min ؊1 /[IU/ml]) with no significant change in AIR or fasting glucose and insulin. The pubertal fall in S I was more consistent in AfricanAmericans; remained significant after controlling for age, sex, and change in fat mass, visceral fat, and fatfree mass; and was similar in children at low, medium, and high body fat. Change in S I was not significantly related to change in fasting hormone levels, but change in AIR was significantly related to change in androstendione (r ‫؍‬ 0.39; P ‫؍‬ 0.04). Pubertal transition from Tanner stage I to Tanner stage III was associated with a 32% reduction in S I, and increases in fasting glucose, insulin, and AIR. These changes were similar across sex, ethnicity, and obesity. The significant fall in DI suggests conservation in ␤-cell function or an inadequate ␤-cell response to the fall in S I . The fall in S I was not associated with changes in body fat, visceral fat, IGF-I, androgens, or estradiol. Diabetes 50:2444 -2450, 2001 P ubertal insulin resistance has been well documented in several cross-sectional studies (1-7). The fall in insulin sensitivity (S I ) during puberty is associated with a compensatory increase in insulin secretion (7). The regulatory purpose of these changes in insulin action and secretion is not clear but is thought to be selective for glucose but not protein metabolism (2) and to provide a mechanism for increasing the anabolic effects of insulin and growth hormone during a period of rapid somatic growth (1,8). The original observation of pubertal insulin resistance was reported in 1987 when Amiel et al. (5) showed that insulin-stimulated glucose metabolism was ϳ30% lower in a sample of children at Tanner stages II-IV compared with children at Tanner stage I or adults. Previous cross-section...

The major conclusions related to the overall benefits and risks of MHT expressed as the number of women per 1000 taking MHT for 5 yr who would experience benefit or harm. Primary areas of benefit included relief of hot flashes and symptoms of urogenital atrophy and prevention of fractures and diabetes. Risks included venothrombotic episodes, stroke, and cholecystitis. In the subgroup of women starting MHT between ages 50 and 59 or less than 10 yr after onset of menopause, congruent trends suggested additional benefit including reduction of overall mortality and coronary artery disease. In this subgroup, estrogen plus some progestogens increased the risk of breast cancer, whereas estrogen alone did not. Beneficial effects on colorectal and endometrial cancer and harmful effects on ovarian cancer occurred but affected only a small number of women. Data from the various Women's Health Initiative studies, which involved women of average age 63, cannot be appropriately applied to calculate risks and benefits of MHT in women starting shortly after menopause. At the present time, assessments of benefit and risk in these younger women are based on lower levels of evidence.

In adults, visceral fat accumulation is associated with insulin resistance and dyslipidemia. The cause-and-effect nature of these relationships is not clear. The objective of the present study was to determine if similar relationships exist in prepubertal children. Specifically, we determined whether visceral fat was associated with fasting insulin, insulin sensitivity (Si), serum triglyceride (TG) concentration, or serum HDL cholesterol (HDL-C) concentration; whether visceral fat or Si was independently related to lipids; and whether ethnicity influenced the relationship between visceral fat and risk factors. Subjects were 61 prepubertal African-American and Caucasian children. Total body fat was determined by dual-energy X-ray absorptiometry, visceral fat by computed tomography, and insulin sensitivity by the tolbutamide-modified, frequently sampled intravenous glucose tolerance test with minimal modeling. In multiple linear regression analysis (adjusting for total fat, sex, and ethnicity), visceral fat was independently related to TG (P < 0.05) and fasting insulin (P < 0.001), but not Si (P = 0.425). Total body fat was independently related to Si (P < 0.001). Si was independently related to fasting insulin (P < 0.001) but not to TG or HDL-C (P = 0.941 and 0.201, respectively). Si in African-Americans was 42% lower than in Caucasians (0.50 +/- 0.05 vs. 0.86 +/- 0.11 x 10(-5) min(-1) x pmol(-1) x l, mean +/- SE after adjusting for total fat, P < 0.001). Nonetheless, ethnicity was not independently related to either TG or HDL-C (P = 0.075 and 0.619, respectively, after adjusting for total and visceral fat and sex). The slopes of the relationships of total and visceral fat with risk factors did not differ with ethnicity. In conclusion, visceral fat appears metabolically unique in children, being independently associated with elevated TG and insulin but not Si. Obese children and African-American children were more insulin resistant, independent of visceral fat accumulation. Lower Si was associated with higher, faster insulin, but not dyslipidemia. Thus, obesity, visceral fat accumulation, and ethnicity in children may confer negative, but independent, health risks.

The mechanism(s) of load-induced muscle hypertrophy is as yet unclear, but increasing evidence suggests a role for locally expressed insulin-like growth factor I (IGF-I). We investigated the effects of concentric (CON) vs. eccentric (ECC) loading on muscle IGF-I mRNA concentration. We hypothesized a greater IGF-I response after ECC compared with CON. Ten healthy subjects (24.4 +/- 0.7 yr, 174.5 +/- 2.6 cm, 70.9 +/- 4.3 kg) completed eight sets of eight CON or ECC squats separated by 6-10 days. IGF-I, IGF binding protein-4 (IGFBP-4), and androgen receptor (AR) mRNA concentrations were determined in vastus lateralis muscle by RT-PCR before and 48 h after ECC and CON. Serum total testosterone (TT) and IGF-I were measured serially across 48 h, and serum creatine kinase activity (CK), isometric maximum voluntary contraction (MVC), and soreness were determined at 48 h. IGF-I mRNA concentration increased 62% and IGFBP-4 mRNA concentration decreased 57% after ECC (P < 0.05). Changes after CON were similar but not significant (P = 0.06-0.12). AR mRNA concentration increased (P < 0.05) after ECC (63%) and CON (102%). Serum TT and IGF-I showed little change. MVC fell 10% and CK rose 183% after ECC (P < 0.05). Perceived soreness was higher (P < 0.01) after ECC compared with CON. Results indicate that a single bout of mechanical loading in humans alters activity of the muscle IGF-I system, and the enhanced response to ECC suggests that IGF-I may somehow modulate tissue regeneration after mechanical damage.

This review examines whether the relations and metabolic parameters necessary for the development of syndrome X are present in children and whether the metabolic complications of obesity in children are explained by excess intraabdominal adipose tissue (IAAT), or visceral fat. Despite the limited use of imaging techniques in research studies, an increasing number of studies reported on IAAT and its relation to disease risk in children and adolescents. For this article we reviewed studies that documented the early accumulation of IAAT in children and adolescents and the factors that contribute to variation in the degree of IAAT accumulation. We also reviewed studies that showed the clinical relevance of IAAT in children and adolescents through significant relations with adverse health effects including dyslipidemia and glucose intolerance in obese and nonobese children and adolescents of different ethnic groups.

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The purpose of this study was to determine what effect aerobic and resistance exercise training has on gain of visceral fat during the year following weight loss. After being randomly assigned to aerobic training, resistance training, or no exercise training, 45 European‐American (EA) and 52 African‐American (AA) women lost 12.3 ± 2.5 kg on a 800 kcal/day diet. Computed tomography was used to measure abdominal subcutaneous and visceral adipose tissue, whereas total fat and regional fat (leg, arm, and trunk) were measured by dual energy X‐ray absorptiometry after weight loss and 1 year following the weight loss. Because not all the subjects adhered to the 2 time/week 40 min/day exercise training during the 1‐year follow‐up, subjects were divided into five groups for analysis: aerobic adherers, aerobic nonadherers, resistance adherers, resistance nonadherers, and no exercise. No significant differences were observed between the aerobic training and resistance training adherers for any variable. However, the aerobic (3.1 kg) and resistance (3.9 kg) exercise adherers gained less weight than any of the other three groups (all >6.2 kg). In addition, the two exercise adherence groups did not significantly increase visceral fat (<0.8%) as compared with the 38% increase for the two nonadhering exercise groups and the 25% for the nonexercise group. In conclusion, as little as 80 min/week aerobic or resistance training had modest positive effects on preventing weight regain following a diet‐induced weight loss. More importantly, both aerobic and resistance training prevented regain of potentially harmful visceral fat.