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\"The Adrenal Reset Diet is the first scientifically sound, patient-tested weight-loss plan developed by a natural endocrinologist, Dr. Alan Christianson. He heals readers in any of the three stages of adrenal impairment--Stressed, Wired and Tired, or Crashed. Readers learn their stage and receive distinct strategies for diet, activity, and lifestyle change to bring them to Thriving. Recent study participants halved their cortisol levels in just 30 days--and lost an average of 9 pounds!\"-- Provided by publisher.

The potential endocrine-disrupting effects of perfluoroalkyl substances (PFASs) have been demonstrated in animal studies, but whether PFASs may interfere with body weight regulation in humans is largely unknown. This study aimed to examine the associations of PFAS exposure with changes in body weight and resting metabolic rate (RMR) in a diet-induced weight-loss setting. In the 2-year POUNDS Lost randomized clinical trial based in Boston, Massachusetts, and Baton Rouge, Louisiana, that examined the effects of energy-restricted diets on weight changes, baseline plasma concentrations of major PFASs were measured among 621 overweight and obese participants aged 30-70 years. Body weight was measured at baseline and 6, 12, 18, and 24 months. RMR and other metabolic parameters, including glucose, lipids, thyroid hormones, and leptin, were measured at baseline and 6 and 24 months. Participants lost an average of 6.4 kg of body weight during the first 6 months (weight-loss period) and subsequently regained an average of 2.7 kg of body weight during the period of 6-24 months (weight regain period). After multivariate adjustment, baseline PFAS concentrations were not significantly associated with concurrent body weight or weight loss during the first 6 months. In contrast, higher baseline levels of PFASs were significantly associated with a greater weight regain, primarily in women. In women, comparing the highest to the lowest tertiles of PFAS concentrations, the multivariate-adjusted mean weight regain (SE) was 4.0 (0.8) versus 2.1 (0.9) kg for perfluorooctanesulfonic acid (PFOS) (Ptrend = 0.01); 4.3 (0.9) versus 2.2 (0.8) kg for perfluorooctanoic acid (PFOA) (Ptrend = 0.007); 4.7 (0.9) versus 2.5 (0.9) kg for perfluorononanoic acid (PFNA) (Ptrend = 0.006); 4.9 (0.9) versus 2.7 (0.8) kg for perfluorohexanesulfonic acid (PFHxS) (Ptrend = 0.009); and 4.2 (0.8) versus 2.5 (0.9) kg for perfluorodecanoic acid (PFDA) (Ptrend = 0.03). When further adjusted for changes in body weight or thyroid hormones during the first 6 months, results remained similar. Moreover, higher baseline plasma PFAS concentrations, especially for PFOS and PFNA, were significantly associated with greater decline in RMR during the weight-loss period and less increase in RMR during the weight regain period in both men and women. Limitations of the study include the possibility of unmeasured or residual confounding by socioeconomic and psychosocial factors, as well as possible relapse to the usual diet prior to randomization, which could have been rich in foods contaminated by PFASs through food packaging and also dense in energy. In this diet-induced weight-loss trial, higher baseline plasma PFAS concentrations were associated with a greater weight regain, especially in women, possibly explained by a slower regression of RMR levels. These data illustrate a potential novel pathway through which PFASs interfere with human body weight regulation and metabolism. The possible impact of environmental chemicals on the obesity epidemic therefore deserves attention. ClinicalTrials.gov NCT00072995.

\"Nutrition powerhouse and #1 New York Times bestselling author of The Fast Metabolism Diet, Haylie Pomroy, creates a food-based, supercharged weight-loss plan for those who have hit a plateau and need to microrepair metabolic function. Readers choose which of the 3 plans and goals that suit them best--and lose up to 3 pounds in 3 days, 5 in 5, or 10 in 10.\"-- Provided by publisher.

Introduction: Mechanisms for liraglutide-induced weight loss are poorly understood. Objective: We investigated the effects of liraglutide on gastric emptying, glycemic parameters, appetite and energy metabolism in obese non-diabetic individuals. Design: Participants ( N =49, 18–75 years, body mass index: 30–40 kg m −2 ) were randomized to two of three treatments: liraglutide 1.8 mg, 3.0 mg, or placebo in a double-blind, incomplete crossover trial. After 5 weeks, 24-h energy expenditure (EE) and substrate oxidation were measured in a respiratory chamber. Gastric emptying (acetaminophen absorption method), glycemic parameters and appetite were assessed during a 5-h meal test. Ad libitum energy intake during a subsequent lunch was also assessed. Results: Five-hour gastric emptying (AUC 0–300 min ) was found to be equivalent for liraglutide 1.8 versus 3.0 mg (primary end point), and for both liraglutide doses versus placebo, as 90% confidence intervals for the estimated treatment ratios were contained within the prespecified interval (0.80–1.25). However, 1-h gastric emptying was 23% lower than placebo with liraglutide 3.0 mg ( P =0.007), and a nonsignificant 13% lower than placebo with liraglutide 1.8 mg ( P =0.14). Both liraglutide doses similarly reduced fasting glucose (0.5–0.6 mmol l −1 versus placebo, P <0.0001), glucose C max and 1-h AUC versus placebo; only liraglutide 3.0 mg reduced iAUC 0–300 min (by ∼26% versus placebo, P =0.02). Glucagon iAUC 0–300 min decreased by ∼30%, and iAUC 0–60 min for insulin and C-peptide was ∼20% lower with both liraglutide doses versus placebo. Liraglutide doses similarly increased mean postprandial satiety and fullness ratings, reduced hunger and prospective food consumption and decreased ad libitum energy intake by ∼16%. Liraglutide-associated reductions in EE were partly explained by a decrease in body weight. A relative shift toward increased fat and reduced carbohydrate oxidation was observed with liraglutide. Clinicaltrials.gov ID:NCT00978393. Funding: Novo Nordisk. Conclusion: Gastric emptying AUC 0–300 min was equivalent for liraglutide 1.8 and 3.0 mg, and for liraglutide versus placebo, whereas reductions in 1-h gastric emptying of 23% with liraglutide 3.0 mg and 13% with 1.8 mg versus placebo were observed. Liraglutide 3.0 mg improved postprandial glycemia to a greater extent than liraglutide 1.8 mg. Liraglutide-induced weight loss appears to be mediated by reduced appetite and energy intake rather than increased EE.

\"Turn your kitchen into a secret weapon for losing up to 20 pounds in 28 days through the fat-burning power of food! Use food as medicine to cook your way healthy in this must have companion to the bestselling diet sensation, The Fast Metabolism Diet. You will find over 200 simple, effective, mouthwatering, family-pleasing recipes designed to evoke change in your body with a plan that celebrates food, thrives on variety, and has you eating five to six times a day according to a three-phase plan strategically designed to keep your metabolism burning at lightening speeds. On phase 1 you will cook to unwind stress and support your adrenals with nourishing breakfasts like Strawberry Pancakes and French Toast with Peaches, as well as delicious entrees like the Mediterranean Turkey with Wild Rice, Halibut Stir Fry, and Brown Pasta with Meat Sauce. On Phase 2, you'll be cooking to unlock stored fat and feed the liver with protein-rich salads like the Grilled Turkey Bacon and Asparagus Salad, the Chicken Fajita Salad, and luxurious dinners like Lamb with Green Beans , Filet Mignon and Cabbage, and Rosemary Pork Tenderloin with Mustard Greens. Then on Phase 3, it is time to use your kitchen to unleash the burn and ignite the Fast Metabolism hormones with high healthy fat meals like the Sprouted Grain Breakfast Burrito, Steak Fajita Avocado Wraps, and Fried egg with Olive Oil Spinach. You'll prepare dairy free creamy soups and stews like Leek and Cauliflower Soup and Veggie Chili, and serve crowd-pleasing dinners like Turkey and Bell Pepper Casserole, and Cornish Game Hens with Mushroom Quinoa Stuffing As you cycle through all three phases each week you'll add kindling to your metabolic fire with amazing snacks like sweet potato fries, crispy kale chips, and fresh fruit salad, or mounds of veggies served with dips and dressings like the Black Bean Cilantro Dip, Mango Salsa, or creamy White Bean and Dill Hummus. And to top it all off, for each phase you'll be whipping up rich desserts and smoothies, like Baked Apple Crisp, Chocolate cherries, Coconut Almond Pudding, Melon-Mint Smoothie, and Blackberry Sorbet. Plus plenty of vegetarian, vegan, and gluten-free options, such as a hearty lentil chili, savory Artichoke-Avocado Salad, silky Butternut Squash Soup, and Garden Egg White Souffle. Full of helpful and affordable hints for cooking on each of the three phases, a wealth of freezer-friendly recipes to cook in bulk, and dozens of slow cooker options that can be prepared in under 5 minutes, this is the ideal tool for the busy mom, the on-the-go professional, or anyone who wants to make delicious, nutritious, home-cooked food part of his or her Fast Metabolism lifestyle\"-- Provided by publisher.

Overweight or obese patients with diabetes were assigned to lifestyle intervention with a weight-loss goal of 7% or to a control program of support and education. The intervention group had sustained weight loss but no significant reduction in cardiovascular events at 10 years. Weight loss is recommended for overweight or obese patients with type 2 diabetes. 1 This recommendation is based on short-term studies showing numerous benefits of weight loss, including improvements in glycemic control, risk factors for cardiovascular disease, quality of life, and other obesity-related coexisting illnesses. 2 However, it is unknown whether weight loss reduces the risk of cardiovascular morbidity and mortality in patients with type 2 diabetes. Epidemiologic studies involving patients with diabetes have had conflicting results, perhaps because of confounding from unintentional weight loss. 3 A meta-analysis 4 of cohort studies concluded that moderate intentional weight loss was associated with reduced mortality among . . .

Among patients with type 2 diabetes and stage 4 chronic kidney disease, bardoxolone methyl, as compared with placebo, did not reduce the risk of end-stage renal disease or cardiovascular death. Cardiovascular events in the bardoxolone group prompted trial termination. Type 2 diabetes mellitus is the most important cause of progressive chronic kidney disease in the developed and developing worlds. Various therapeutic approaches to slow progression, including restriction of dietary protein, glycemic control, and control of hypertension, have yielded mixed results. 1 – 3 Several randomized clinical trials have shown that inhibitors of the renin–angiotensin–aldosterone system significantly reduce the risk of progression, 4 – 6 although the residual risk remains high. 7 None of the new agents tested during the past decade have proved effective in late-stage clinical trials. 8 – 12 Oxidative stress and impaired antioxidant capacity intensify with the progression of chronic kidney disease. 13 In . . .

OBJECTIVE: Metformin produced weight loss and delayed or prevented diabetes in the Diabetes Prevention Program (DPP). We examined its long-term safety and tolerability along with weight loss, and change in waist circumference during the DPP and its long-term follow-up. RESEARCH DESIGN AND METHODS: The randomized double-blind clinical trial of metformin or placebo followed by a 7–8-year open-label extension and analysis of adverse events, tolerability, and the effect of adherence on change in weight and waist circumference. RESULTS: No significant safety issues were identified. Gastrointestinal symptoms were more common in metformin than placebo participants and declined over time. During the DPP, average hemoglobin and hematocrit levels were slightly lower in the metformin group than in the placebo group. Decreases in hemoglobin and hematocrit in the metformin group occurred during the first year following randomization, with no further changes observed over time. During the DPP, metformin participants had reduced body weight and waist circumference compared with placebo (weight by 2.06 ± 5.65% vs. 0.02 ± 5.52%, P < 0.001, and waist circumference by 2.13 ± 7.06 cm vs. 0.79 ± 6.54 cm, P < 0.001 in metformin vs. placebo, respectively). The magnitude of weight loss during the 2-year double-blind period was directly related to adherence (P < 0.001). Throughout the unblinded follow-up, weight loss remained significantly greater in the metformin group than in the placebo group (2.0 vs. 0.2%, P < 0.001), and this was related to the degree of continuing metformin adherence (P < 0.001). CONCLUSIONS: Metformin used for diabetes prevention is safe and well tolerated. Weight loss is related to adherence to metformin and is durable for at least 10 years of treatment.

In the 2·8 years of the Diabetes Prevention Program (DPP) randomised clinical trial, diabetes incidence in high-risk adults was reduced by 58% with intensive lifestyle intervention and by 31% with metformin, compared with placebo. We investigated the persistence of these effects in the long term. All active DPP participants were eligible for continued follow-up. 2766 of 3150 (88%) enrolled for a median additional follow-up of 5·7 years (IQR 5·5–5·8). 910 participants were from the lifestyle, 924 from the metformin, and 932 were from the original placebo groups. On the basis of the benefits from the intensive lifestyle intervention in the DPP, all three groups were offered group-implemented lifestyle intervention. Metformin treatment was continued in the original metformin group (850 mg twice daily as tolerated), with participants unmasked to assignment, and the original lifestyle intervention group was offered additional lifestyle support. The primary outcome was development of diabetes according to American Diabetes Association criteria. Analysis was by intention-to-treat. This study is registered with ClinicalTrials.gov, number NCT00038727. During the 10·0-year (IQR 9·0–10·5) follow-up since randomisation to DPP, the original lifestyle group lost, then partly regained weight. The modest weight loss with metformin was maintained. Diabetes incidence rates during the DPP were 4·8 cases per 100 person-years (95% CI 4·1–5·7) in the intensive lifestyle intervention group, 7·8 (6·8–8·8) in the metformin group, and 11·0 (9·8–12·3) in the placebo group. Diabetes incidence rates in this follow-up study were similar between treatment groups: 5·9 per 100 person-years (5·1–6·8) for lifestyle, 4·9 (4·2–5·7) for metformin, and 5·6 (4·8–6·5) for placebo. Diabetes incidence in the 10 years since DPP randomisation was reduced by 34% (24–42) in the lifestyle group and 18% (7–28) in the metformin group compared with placebo. During follow-up after DPP, incidences in the former placebo and metformin groups fell to equal those in the former lifestyle group, but the cumulative incidence of diabetes remained lowest in the lifestyle group. Prevention or delay of diabetes with lifestyle intervention or metformin can persist for at least 10 years. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

In this study involving severely obese patients with type 2 diabetes, Roux-en-Y gastric bypass and biliopancreatic diversion achieved better glucose control than conventional medical therapy as assessed at 2 years. The prevalence of type 2 diabetes mellitus is rapidly increasing worldwide, in parallel with the current obesity epidemic. In 2010, the global prevalence of type 2 diabetes was estimated at 8.3% of the adult population, a proportion that is projected to increase to 9.9% by 2030. 1 As many as 23% of patients with morbid obesity have type 2 diabetes, 2 and the prevalence of screening-detected diabetes is 8%. 2 Global spending on diabetes was estimated to be at least $376 billion in 2010 and projected to be $490 billion in 2030. 3 Conventional medical treatment of type 2 diabetes only partially achieves adequate . . .