Iris Shai

Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet

BACKGROUND Trials comparing the effectiveness and safety of weight-loss diets are frequently limited by short follow-up times and high dropout rates. METHODS In this 2-year trial, we randomly assigned 322 moderately obese subjects (mean age, 52 years; mean body-mass index [the weight in kilograms divided by the square of the height in meters], 31; male sex, 86%) to one of three diets: low-fat, restricted-calorie; Mediterranean, restricted-calorie; or low-carbohydrate, non-restricted-calorie. RESULTS The rate of adherence to a study diet was 95.4% at 1 year and 84.6% at 2 years. The Mediterranean-diet group consumed the largest amounts of dietary fiber and had the highest ratio of monounsaturated to saturated fat (P<0.05 for all comparisons among treatment groups). The low-carbohydrate group consumed the smallest amount of carbohydrates and the largest amounts of fat, protein, and cholesterol and had the highest percentage of participants with detectable urinary ketones (P<0.05 for all comparisons among treatment groups). The mean weight loss was 2.9 kg for the low-fat group, 4.4 kg for the Mediterranean-diet group, and 4.7 kg for the low-carbohydrate group (P<0.001 for the interaction between diet group and time); among the 272 participants who completed the intervention, the mean weight losses were 3.3 kg, 4.6 kg, and 5.5 kg, respectively. The relative reduction in the ratio of total cholesterol to high-density lipoprotein cholesterol was 20% in the low-carbohydrate group and 12% in the low-fat group (P=0.01). Among the 36 subjects with diabetes, changes in fasting plasma glucose and insulin levels were more favorable among those assigned to the Mediterranean diet than among those assigned to the low-fat diet (P<0.001 for the interaction among diabetes and Mediterranean diet and time with respect to fasting glucose levels). CONCLUSIONS Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets. The more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet) suggest that personal preferences and metabolic considerations might inform individualized tailoring of dietary interventions. (ClinicalTrials.gov number, NCT00160108.)

Adolescent BMI trajectory and risk of diabetes versus coronary disease.

BACKGROUND The association of body-mass index (BMI) from adolescence to adulthood with obesity-related diseases in young adults has not been completely delineated. METHODS We conducted a prospective study in which we followed 37,674 apparently healthy young men for incident angiography-proven coronary heart disease and diabetes through the Staff Periodic Examination Center of the Israeli Army Medical Corps. The height and weight of participants were measured at regular intervals, with the first measurements taken when they were 17 years of age. RESULTS During approximately 650,000 person-years of follow-up (mean follow-up, 17.4 years), we documented 1173 incident cases of type 2 diabetes and 327 of coronary heart disease. In multivariate models adjusted for age, family history, blood pressure, lifestyle factors, and biomarkers in blood, elevated adolescent BMI (the weight in kilograms divided by the square of the height in meters; mean range for the first through last deciles, 17.3 to 27.6) was a significant predictor of both diabetes (hazard ratio for the highest vs. the lowest decile, 2.76; 95% confidence interval [CI], 2.11 to 3.58) and angiography-proven coronary heart disease (hazard ratio, 5.43; 95% CI, 2.77 to 10.62). Further adjustment for BMI at adulthood completely ablated the association of adolescent BMI with diabetes (hazard ratio, 1.01; 95% CI, 0.75 to 1.37) but not the association with coronary heart disease (hazard ratio, 6.85; 95% CI, 3.30 to 14.21). After adjustment of the BMI values as continuous variables in multivariate models, only elevated BMI in adulthood was significantly associated with diabetes (β=1.115, P=0.003; P=0.89 for interaction). In contrast, elevated BMI in both adolescence (β=1.355, P=0.004) and adulthood (β=1.207, P=0.03) were independently associated with angiography-proven coronary heart disease (P=0.048 for interaction). CONCLUSIONS An elevated BMI in adolescence--one that is well within the range currently considered to be normal--constitutes a substantial risk factor for obesity-related disorders in midlife. Although the risk of diabetes is mainly associated with increased BMI close to the time of diagnosis, the risk of coronary heart disease is associated with an elevated BMI both in adolescence and in adulthood, supporting the hypothesis that the processes causing incident coronary heart disease, particularly atherosclerosis, are more gradual than those resulting in incident diabetes. (Funded by the Chaim Sheba Medical Center and the Israel Defense Forces Medical Corps.).

Ethnicity, obesity, and risk of type 2 diabetes in women : A 20-year follow-up study

OBJECTIVE—To examine ethnic differences in risk of type 2 diabetes, taking dietary and lifestyle risk factors into account. RESEARCH DESIGN AND METHODS—A prospective (1980–2000) cohort (from The Nurses’ Health Study) including 78,419 apparently healthy women (75,584 whites, 801 Asians, 613 Hispanics, and 1,421 blacks) was studied. Detailed dietary and lifestyle information for each participant was repeatedly collected every 4 years. RESULTS—During 1,294,799 person-years of follow-up, we documented 3,844 incident cases of diabetes. Compared with whites, the age-adjusted relative risks (RRs) were 1.43 (95% CI 1.08–1.90) for Asians, 1.76 (1.32–2.34) for Hispanics, and 2.18 (1.82–2.61) for blacks. After adjustment for BMI, the RRs changed to 2.26 (1.70–2.99) for Asians, 1.86 (1.40–2.47) for Hispanics, and 1.34 (1.12–1.61) for blacks. For each 5-unit increment in BMI, the multivariate RR of diabetes was 2.36 (1.83–3.04) for Asians, 2.21 (1.75–2.79) for Hispanics, 1.96 (1.93–2.00) for whites, and 1.55 (1.36–1.77) for blacks (P for interaction <0.001). For each 5-kg weight gain between age 18 and the year 1980, the risk of diabetes was increased by 84% (95% CI 58–114) for Asians, 44% (26–63) for Hispanics, 38% (28–49) for blacks, and 37% (35–38%) for whites. A healthy diet high in cereal fiber and polyunsaturated fat and low in trans fat and glycemic load was more strongly associated with a lower risk of diabetes among minorities (RR 0.54 [95% CI 0.39–0.73]) than among whites (0.77 [0.72–0.84]). CONCLUSIONS—The risk of diabetes is significantly higher among Asians, Hispanics, and blacks than among whites before and after taking into account differences in BMI. Weight gain is particularly detrimental for Asians. Our data suggest that the inverse association of a healthy diet with diabetes is stronger for minorities than for whites.

Multivariate Assessment of Lipid Parameters as Predictors of Coronary Heart Disease Among Postmenopausal Women Potential Implications for Clinical Guidelines

Background—Over the past decade, lipid measurements have been significantly improved and standardized. We evaluated the usefulness of multiple plasma lipid parameters in predicting coronary heart diseases (CHD) among women. Methods and Results—Among 32 826 women from the Nurses’ Health Study who provided blood samples at baseline, 234 CHD events were documented during 8 years of follow-up. In a nested study, these cases were matched to controls (1:2) for age, smoking, fasting status, and month of blood draw. We estimated the relative risk (RR) for each lipid parameter, adjusted for C-reactive protein, homocysteine, body mass index, family history, hypertension, diabetes, postmenopausal hormone use, physical activity, alcohol intake, and blood draw parameters. The RRs associated with an increase of ≈1 SD (mg/dL) were as follows: HDL cholesterol (HDL-C) (RR=0.6 [0.5 to 0.8], SD=17), apolipoprotein B100 (apoB100) (RR=1.7 [1.4 to 2.1], SD=32), LDL cholesterol (LDL-C) (RR=1.4 [1.1 to 1.7], SD=36), total cholesterol (TC) (RR=1.4 [1.1 to 1.6], SD=40), and triglycerides (RR=1.3 [1.0 to 1.5], SD=80). Among the lipid indexes, the RRs were: apoB100/HDL-C (RR=1.7 [1.4 to 2.1], SD=1.0), TC/HDL-C (RR=1.6 [1.3 to 1.9], SD=1.3), LDL-C/HDL-C (RR=1.5 [1.3 to 1.9], SD=1.0), and non–HDL-C (RR=1.6 [1.3 to 1.9], SD=42 mg/dL). After simultaneous control for several lipid biomarkers, HDL-C was the primary contributor of the variation in multivariate models (P=0.01), followed by LDL-C (P=0.01), whereas triglycerides and apoB100 did not contribute further information. HDL-C–related ratios were the strongest contributors to predicting CHD (P<0.0001). Conclusions—Lower levels of HDL-C may be a key discriminator of higher CHD events among postmenopausal women. HDL-C–related ratios (such as TC/HDL-C) provide a powerful predictive tool independently of other known CHD risk factors.

Meta-Analysis Comparing Mediterranean to Low-Fat Diets for Modification of Cardiovascular Risk Factors

BACKGROUND Evidence from individual trials comparing Mediterranean to low-fat diets to modify cardiovascular risk factors remains preliminary. METHODS We systematically searched MEDLINE, EMBASE, Biosis, Web of Science, and the Cochrane Central Register of Controlled Trials from their inception until January 2011, as well as contacted experts in the field, to identify randomized controlled trials comparing Mediterranean to low-fat diets in overweight/obese individuals, with a minimum follow-up of 6 months, reporting intention-to-treat data on cardiovascular risk factors. Two authors independently assessed trial eligibility and quality. RESULTS We identified 6 trials, including 2650 individuals (50% women) fulfilling our inclusion criteria. Mean age of enrolled patients ranged from 35 to 68 years, mean body mass index from 29 to 35 kg/m(2). After 2 years of follow-up, individuals assigned to a Mediterranean diet had more favorable changes in weighted mean differences of body weight (-2.2 kg; 95% confidence interval [CI], -3.9 to -0.6), body mass index (-0.6 kg/m(2); 95% CI, -1 to -0.1), systolic blood pressure (-1.7 mm Hg; 95% CI, -3.3 to -0.05), diastolic blood pressure (-1.5 mm Hg; 95% CI, -2.1 to -0.8), fasting plasma glucose (-3.8 mg/dL, 95% CI, -7 to -0.6), total cholesterol (-7.4 mg/dL; 95% CI, -10.3 to -4.4), and high-sensitivity C-reactive protein (-1.0 mg/L; 95% CI, -1.5 to -0.5). The observed heterogeneity across individual trials could, by and large, be eliminated by restricting analyses to trials with balanced co-interventions or trials with restriction of daily calorie intake in both diet groups. CONCLUSION Mediterranean diets appear to be more effective than low-fat diets in inducing clinically relevant long-term changes in cardiovascular risk factors and inflammatory markers.

Altered autophagy in human adipose tissues in obesity.

CONTEXT Autophagy is a housekeeping mechanism, involved in metabolic regulation and stress response, shown recently to regulate lipid droplets biogenesis/breakdown and adipose tissue phenotype. OBJECTIVE We hypothesized that in human obesity autophagy may be altered in adipose tissue in a fat depot and distribution-dependent manner. SETTING AND PATIENTS Paired omental (Om) and subcutaneous (Sc) adipose tissue samples were used from obese and nonobese (n = 65, cohort 1); lean, Sc-obese and intraabdominally obese (n = 196, cohort 2); severely obese persons without diabetes or obesity-associated morbidity, matched for being insulin sensitive or resistant (n = 60, cohort 3). RESULTS Protein and mRNA levels of the autophagy genes Atg5, LC3A, and LC3B were increased in Om compared with Sc, more pronounced among obese persons, particularly with intraabdominal fat accumulation. Both adipocytes and stromal-vascular cells contribute to the expression of autophagy genes. An increased number of autophagosomes and elevated autophagic flux assessed in fat explants incubated with lysosomal inhibitors were observed in obesity, particularly in Om. The degree of visceral adiposity and adipocyte hypertrophy accounted for approximately 50% of the variance in omental Atg5 mRNA levels by multivariate regression analysis, whereas age, sex, measures of insulin sensitivity, inflammation, and adipose tissue stress were excluded from the model. Moreover, in cohort 3, the autophagy marker genes were increased in those who were insulin resistant compared with insulin sensitive, particularly in Om. CONCLUSIONS Autophagy is up-regulated in adipose tissue of obese persons, especially in Om, correlating with the degree of obesity, visceral fat distribution, and adipocyte hypertrophy. This may co-occur with insulin resistance but precede the occurrence of obesity-associated morbidity.

Changes in Triglyceride Levels and Risk for Coronary Heart Disease in Young Men

Context Whether the serum triglyceride level is an independent risk factor for coronary heart disease (CHD) is not clear. Contribution The authors measured triglyceride levels and performed stress electrocardiographies 5 years apart on 13593 young Israeli male career soldiers and did coronary angiography if the stress test was abnormal. Triglycerides and change in triglyceride levels strongly predicted incident CHD after adjustment for known CHD risk factors and lifestyle. Decreases in triglyceride levels were associated with adoption of a healthier lifestyle and lower CHD risk. The lowest CHD risk occurred when triglyceride levels remained low. Caution The participants were healthy male soldiers. Implication In healthy young men, triglycerides and changes in triglyceride levels are an independent CHD risk factor. The Editors A recent meta-analysis (1) and most published papers suggest a moderate association between fasting triglyceride levels and coronary heart disease (CHD) (211). Of the lipid fractions, the triglyceride-rich very-low-density lipoprotein particle is probably the most sensitive to lifestyle modification (8). For example, estimates from meta-analyses suggest that for every 4.5 kg (approximately 10 lb) of stable weight reduction, triglyceride levels decrease by at least 0.068 mmol/L (6 mg/dL) (12). Accordingly, a considerable increase in the proportion of hypertriglyceridemic patients accompanies the obesity epidemic (6, 9). In addition, aerobic exercise, independent of weight loss, has been shown to modestly reduce triglyceride levels in a dose-dependent fashion (13). Hence, when assessing the risk associated with triglyceride levels, triglyceride measurement at a single time point (typically at enrollment) may not be a reliable indicator of a persons long-term triglyceridemia during follow-up. Whether changes in triglyceride levels over time can improve cardiovascular risk assessment is largely unknown, particularly in young adults, in whom information on the association between triglycerides and CHD is not available (1). For 13953 apparently healthy young adult men (mean age, 32 years; range, 26 to 45 years) from the MELANY (Metabolic, Lifestyle, and Nutrition Assessment in Young Adults) study (14), we obtained 2 measurements of fasting serum triglycerides and lifestyle variables 5 years apart and followed for incident cases of angiography-proven CHD. Here, we estimate the effect of baseline triglyceride levels (time 1) and changes (between time 1 and time 2) in triglyceride levels on CHD risk. Methods The MELANY Study The MELANY study, which was designed to investigate risk factors for common diseases in young adults, is being conducted at the Israel Defense Forces Staff Periodic Examination Center (SPEC), Zrifin, Israel. All career service personnel are evaluated every 5 years between 25 and 35 years of age and every 3 years thereafter until they are discharged from service. A computerized database established in 1992 is the source of data for the MELANY study. At each SPEC visit, participants complete a detailed questionnaire that assesses demographic, nutritional, lifestyle, and medical factors. Thereafter, blood samples are drawn after a 14-hour fast and analyzed. A trained medical technician measures height, weight, and blood pressure (by mercury sphygmomanometers), and a physician at the center performs a complete physical examination. Inclusion and Exclusion Criteria We included apparently healthy men 26 to 45 years of age who had fasting triglyceride levels less than 3.39 mmol/L (<300 mg/dL) at their initial SPEC visit. We used the cutoff value of 3.39 mmol/L (300 mg/dL) because SPEC persons with greater triglyceride values are subjected to additional interventionsnutritional, pharmacologic, or both. Of 15155 men age 26 to 45 years, 1202 were excluded because they had diabetes (type 1 or 2) (n= 227) or CHD (n= 17) at baseline; had fasting triglyceride levels of 3.39 mmol/L or greater (300 mg/dL) (n= 676); or were receiving long-term medications (n= 282), including lipid-lowering medications. Therefore, for analysis of the association between baseline triglyceride levels and incident CHD, we included 13953 men. In studying the effect of changes in triglyceride levels on CHD, we excluded an additional 413 men who did not have a triglyceride measurement from the second SPEC visit (n= 363) or had received a diagnosis of diabetes (n= 38) or CHD (n= 12) between the first and second SPEC visit or during the second visit. Women were not included because the number of new cases of CHD in women was too small to facilitate meaningful analysis. Outcome Definition The outcome definition of the study was clinically significant CHD (angiography-proven stenosis >50% in at least 1 coronary artery) or fatal or nonfatal myocardial infarction (MI). At each sequential SPEC visit, all Israel Defense Forces military personnel older than 35 years of age who were participating in the current analysis had a treadmill exercise test (Bruce protocol [15]) in the presence of a board-certified cardiologist. End points for the exercise test were clinically significant ST-segment depression (>2 mm in 2 contiguous leads, measured 80 ms after the J point), intolerable symptoms of angina and exhaustion, or achievement of the target heart rate. All cases with a pathologic stress test were referred for coronary angiography. In participants with a borderline stress test, or when participants reported angina symptoms without diagnostic electrocardiographic changes, stress perfusion imaging with thallium-201 was performed. Those with a pathologic thallium-201 cardiac scan underwent coronary angiography. All Israel Defense Forces personnel obtain primary care between scheduled SPEC visits at designated military clinics, and all medical records are stored in the same central database, thereby facilitating ongoing, tight, and uniform follow-up. Individuals presenting with symptoms of angina, MI, or both between SPEC visits were also referred for coronary angiography after consultation with a board-certified cardiologist. Laboratory Methods Investigators performed biochemical analyses of fresh blood samples in an adjacent core laboratory facility that handles 1.2 million samples per year. The laboratory is authorized to perform tests according to the International Organization for Standardization standard 9002. The United Kingdom National External Quality Assessment Service, Sheffield, United Kingdom, performed periodic assessment of quality control on a regular basis. All lipid levels were directly measured, except for low-density lipoprotein (LDL) levels, which were calculated. Investigators measured all biochemical markers by using a BM/Hitachi 917 automated analyzer (Boehringer, Mannheim, Germany). Statistical Analysis For the primary analysis, we included 13953 untreated, apparently healthy young men with triglyceride levels lower than 3.39 mmol/L (<300 mg/dL). We used a general linear model to assess the age-adjusted means and proportions of the populations characteristics across quintiles of triglycerides and to fit the median of the quintiles as a continuous variable to estimate the trend of variables across quintiles (Table 1). We conducted Cox proportional hazards analysis during the 10.5-year follow-up to estimate the hazard ratios and 95% CIs for the development of CHD (the dependent variable) according to triglyceride levels at time 1 (first measurement). In stepwise models (Table 2), we added the values for body mass index (BMI), high-density lipoprotein (HDL) cholesterol, and family history of CHD separately to the age-adjusted model to evaluate their potential role as confounders. In the final multivariate model, we controlled for age, BMI, HDL cholesterol, family history of CHD, fasting plasma glucose, mean arterial blood pressure, physical activity, and smoking status. Because the total cholesterolHDL cholesterol ratio is a predictor of CHD (8), we performed a secondary analysis that included this ratio instead of HDL cholesterol in the multivariate model. Table 1. Baseline (Time 1) Characteristics, by Quintile of Triglyceride Level Table 2. Hazard Ratios for Coronary Heart Disease, by Quintile of Time-1 Triglyceride Level To assess the risk associated with changes in triglyceride levels, we analyzed data from 13540 men who had 2 triglyceride measurements (obtained at time 1 and time 2, 5 years apart) that were available before the end of follow-up or before being censored after a diagnosis of CHD or diabetes. In the model, time 2 was considered the baseline of 5.2 years of subsequent follow-up, whereas time 1 was considered prebaseline. We cross-classified triglyceride levels at each time point by tertiles: median levels of 0.68, 1.18, and 2.08 mmol/L (60, 104, and 184 mg/dL) at time 1 and 0.79, 1.33, and 2.49 mmol/L (70, 118, and 220 mg/dL) at time 2. In parallel, we determined changes in BMI, smoking status, physical activity, and habit of eating breakfast between time 2 and time 1 (Figure 1). Next, we evaluated the joint risk attributed to triglyceride levels at time 1 and time 2, categorized according to low (bottom), intermediate, and high (top) tertiles, and we used men with triglyceride levels in the low tertile at both time 1 and time 2 as a reference group (low/low group; hazard ratio, 1.0). To evaluate the direct association of changes in triglyceride levels (Figure 2), we used a multivariate model to further adjust for the interval between the 2 measurements and for the changes between time 2 and time 1 in BMI and lifestyle variables (physical activity, smoking, and habit of eating breakfast). We included these variables by calculating differences () in BMI and creating 3 groups of each categorical variable (smoking, physical activity, and habit of eating breakfast) based on their status at time 1 and time 2 (yes/yes, yes/no, no/yes, or no/no). Figure 1. Changes in selected lifestyle variables

Dietary Intervention to Reverse Carotid Atherosclerosis

Background— It is currently unknown whether dietary weight loss interventions can induce regression of carotid atherosclerosis. Methods and Results— In a 2-year Dietary Intervention Randomized Controlled Trial–Carotid (DIRECT-Carotid) study, participants were randomized to low-fat, Mediterranean, or low-carbohydrate diets and were followed for changes in carotid artery intima-media thickness, measured with standard B-mode ultrasound, and carotid vessel wall volume (VWV), measured with carotid 3D ultrasound. Of 140 complete images of participants (aged 51 years; body mass index, 30 kg/m2; 88% men), higher baseline carotid VWV was associated with increased intima-media thickness, age, male sex, baseline weight, blood pressure, and insulin levels (P<0.05 for all). After 2 years of dietary intervention, we observed a significant 5% regression in mean carotid VWV (−58.1 mm3; 95% confidence interval, −81.0 to −35.1 mm3; P<0.001), with no differences in the low-fat, Mediterranean, or low-carbohydrate groups (−60.69 mm3, −37.69 mm3, −84.33 mm3, respectively; P=0.28). Mean change in intima-media thickness was −1.1% (P=0.18). A reduction in the ratio of apolipoprotein B100 to apolipoprotein A1 was observed in the low-carbohydrate compared with the low-fat group (P=0.001). Participants who exhibited carotid VWV regression (mean decrease, −128.0 mm3; 95% confidence interval, −148.1 to −107.9 mm3) compared with participants who exhibited progression (mean increase, +89.6 mm3; 95% confidence interval, +66.6 to +112.6 mm3) had achieved greater weight loss (−5.3 versus −3.2 kg; P=0.03), greater decreases in systolic blood pressure (−6.8 versus −1.1 mm Hg; P=0.009) and total homocysteine (−0.06 versus +1.44 &mgr;mol/L; P=0.04), and a higher increase of apolipoprotein A1 (+0.05 versus −0.00 g/L; P=0.06). In multivariate regression models, only the decrease in systolic blood pressure remained a significant independent modifiable predictor of subsequent greater regression in both carotid VWV (β=0.23; P=0.01) and intima-media thickness (β=0.28; P=0.008) levels. Conclusions— Two-year weight loss diets can induce a significant regression of measurable carotid VWV. The effect is similar in low-fat, Mediterranean, or low-carbohydrate strategies and appears to be mediated mainly by the weight loss–induced decline in blood pressure. Clinical Trial Registration— http://www.clinicaltrials.gov. Unique Identifier: NCT00160108.

Changes in Triglyceride Levels Over Time and Risk of Type 2 Diabetes in Young Men

OBJECTIVE—The association between changes in triglyceride concentrations over time and diabetes is unknown. We assessed whether two triglyceride determinations obtained 5 years apart can predict incident type 2 diabetes. RESEARCH DESIGN AND METHODS—Triglyceride levels at baseline (time 1) and 5 years later (time 2), followed by subsequent follow-up of 5.5 years, were measured in 13,953 apparently healthy men (age 26–45 years) with triglycerides <300 mg/dl (<3.39 mmol/l). RESULTS—During 76,742 person-years, 322 cases of diabetes occurred. A multivariate model adjusted for age, BMI, total cholesterol–to–HDL cholesterol ratio, family history of diabetes, fasting glucose, blood pressure, physical activity, and smoking status revealed a continuous independent rise in incident diabetes with increasing time 1 triglyceride levels (Ptrend < 0.001). Men in the lowest tertile of time 1 triglyceride levels who progressed to the highest tertile over follow-up (low-high) exhibited a hazard ratio (HR) of 12.62 (95% CI 3.52–31.34) compared with those remaining in the lowest tertile at both time points (reference group: low-low). Whereas men who were at the top triglyceride level tertile throughout follow-up (high-high) had a HR for diabetes of 7.08 (2.52–14.45), those whose triglyceride level decreased to the lowest tertile (high-low) exhibited a HR of 1.97 (0.67–6.13). Alterations in triglyceride levels during follow-up were associated with changes in BMI, physical activity, and eating breakfast habit (P < 0.05), but remained an independent modifier of diabetes risk even after adjustment for such changes. CONCLUSIONS—Two measurements of fasting triglyceride levels obtained 5 years apart can assist in identifying apparently healthy young men at increased risk for diabetes, independent of traditional risk factors and of associated changes in BMI and lifestyle parameters.

Glycemic Effects of Moderate Alcohol Intake Among Patients With Type 2 Diabetes A multicenter, randomized, clinical intervention trial

OBJECTIVE—In a randomized controlled trial, we assessed the effect of daily moderate alcohol intake on glycemic control in the fasting and postprandial states in patients with type 2 diabetes who previously had abstained from alcohol. RESEARCH DESIGN AND METHODS—We randomly assigned 109 patients (41–74 years old) with established type 2 diabetes who abstained from alcohol to receive 150 ml wine (13 g alcohol) or nonalcoholic diet beer (control) each day during a 3-month multicenter trial. The beverages were consumed during dinner. Diet and alcohol consumption were monitored. RESULTS—During the intervention, 17% of participants (12% from the alcohol group) dropped out, leaving 91 who completed the trial. Within the alcohol group, fasting plasma glucose (FPG) decreased from 139.6 ± 41 to 118.0 ± 32.5 mg/dl after 3 months compared with 136.7 ± 15.4 to 138.6 ± 27.8 mg/dl in the control subjects (Pv = 0.015). However, alcohol consumption had no effect on 2-h postprandial glucose levels (difference of 18.5 mg/dl in the control group vs. 17.7 mg/dl in the alcohol group, Pv = 0.97). Patients in the alcohol group with higher baseline A1C levels had greater reductions in FPG (age-adjusted correlation −0.57, Pv < 0.001). No significant changes were observed in the levels of bilirubin, alkaline phosphatase, alanine aminotransferase, or aspartate aminotransferase, and no notable adverse effects were reported. Participants in the alcohol group reported an improvement in the ability to fall asleep (Pv < 0.001). CONCLUSIONS—Among patients with type 2 diabetes who had previously abstained from alcohol, initiation of moderate daily alcohol consumption reduced FPG but not postprandial glucose. Patients with higher A1C may benefit more from the favorable glycemic effect of alcohol. Further intervention studies are needed to confirm the long-term effect of moderate alcohol intake.