Rising rates of gestational diabetes mellitus (GDM) and related complications have prompted calls to identify potentially modifiable risk factors that are associated with gestational diabetes mellitus (GDM). We systematically reviewed the scientific literature for observational studies examining specific dietary and/or physical activity (PA) factors and risk of GDM. Our search included PubMed, Medline, CINAHL/EBSCO, Science Direct and EMBASE, and identified 1167 articles, of which 40 met our inclusion criteria (e.g., singleton pregnancy, reported diet or PA data during pre-pregnancy/early pregnancy and GDM as an outcome measure). Studies were assessed for quality using a modified Quality Criteria Checklist from American Dietetic Association. Of the final 40 studies, 72% obtained a positive quality rating and 28% were rated neutral. The final analysis incorporated data on 30,871 pregnant women. Dietary studies were categorised into either caffeine, carbohydrate, fat, protein, calcium, fast food and recognized dietary patterns. Diets such as Mediterranean Diet (MedDiet), Dietary Approaches to Stop Hypertension (DASH) diet and Alternate Healthy Eating Index diet (AHEI) were associated with 15–38% reduced relative risk of GDM. In contrast, frequent consumption of potato, meat/processed meats, and protein (% energy) derived from animal sources was associated with an increased risk of GDM. Compared to no PA, any pre-pregnancy or early pregnancy PA was associated with 30% and 21% reduced odds of GDM, respectively. Engaging in >90 min/week of leisure time PA before pregnancy was associated with 46% decreased odds of GDM. We conclude that diets resembling MedDiet/DASH diet as well as higher PA levels before or in early pregnancy were associated with lower risks or odds of GDM respectively. The systematic review was registered at PROSPERO () as CRD42016027795.

SummaryVery-low-energy diets (VLEDs) and ketogenic low-carbohydrate diets (KLCDs) are two dietary strategies that have been associated with a suppression of appetite. However, the results of clinical trials investigating the effect of ketogenic diets on appetite are inconsistent. To evaluate quantitatively the effect of ketogenic diets on subjective appetite ratings, we conducted a systematic literature search and metaanalysis of studies that assessed appetite with visual analogue scales before (in energy balance) and during (while in ketosis) adherence to VLED or KLCD. Individuals were less hungry and exhibited greater fullness/satiety while adhering to VLED, and individuals adhering to KLCD were less hungry and had a reduced desire to eat. Although these absolute changes in appetite were small, they occurred within the context of energy restriction, which is known to increase appetite in obese people. Thus, the clinical benefit of a ketogenic diet is in preventing an increase in appetite, despite weight loss, although individuals may indeed feel slightly less hungry (or more full or satisfied). Ketosis appears to provide a plausible explanation for this suppression of appetite. Future studies should investigate the minimum level of ketosis required to achieve appetite suppression during ketogenic weight loss diets, as this could enable inclusion of a greater variety of healthy carbohydrate-containing foods into the diet.

OBJECTIVEThe prevalence of gestational diabetes mellitus (GDM) is rising. There is little evidence to demonstrate the effectiveness of one dietary therapy over another. We aimed to investigate the effect of a low–glycemic index (LGI) versus a conventional high-fiber diet on pregnancy outcomes, neonatal anthropometry, and maternal metabolic profile in GDM.RESEARCH DESIGN AND METHODSNinety-nine women (age 26–42 years; mean ± SD prepregnancy BMI 24 ± 5 kg/m2) diagnosed with GDM at 20–32 weeks’ gestation were randomized to follow either an LGI (n = 50; target glycemic index [GI] ~50) or a high-fiber moderate-GI diet (HF) (n = 49; target GI ~60). Dietary intake was assessed by 3-day food records. Pregnancy outcomes were collected from medical records.RESULTSThe LGI group achieved a modestly lower GI than the HF group (mean ± SEM 47 ± 1 vs. 53 ± 1; P < 0.001). At birth, there was no significant difference in birth weight (LGI 3.3 ± 0.1 kg vs. HF 3.3 ± 0.1 kg; P = 0.619), birth weight centile (LGI 52.5 ± 4.3 vs. HF 52.2 ± 4.0; P = 0.969), prevalence of macrosomia (LGI 2.1% vs. HF 6.7%; P = 0.157), insulin treatment (LGI 53% vs. HF 65%; P = 0.251), or adverse pregnancy outcomes.CONCLUSIONSIn intensively monitored women with GDM, an LGI diet and a conventional HF diet produce similar pregnancy outcomes.

SummaryVery-low-energy diets (VLEDs) and ketogenic low-carbohydrate diets (KLCDs) are two dietary strategies that have been associated with a suppression of appetite. However, the results of clinical trials investigating the effect of ketogenic diets on appetite are inconsistent. To evaluate quantitatively the effect of ketogenic diets on subjective appetite ratings, we conducted a systematic literature search and metaanalysis of studies that assessed appetite with visual analogue scales before (in energy balance) and during (while in ketosis) adherence to VLED or KLCD. Individuals were less hungry and exhibited greater fullness/satiety while adhering to VLED, and individuals adhering to KLCD were less hungry and had a reduced desire to eat. Although these absolute changes in appetite were small, they occurred within the context of energy restriction, which is known to increase appetite in obese people. Thus, the clinical benefit of a ketogenic diet is in preventing an increase in appetite, despite weight loss, although individuals may indeed feel slightly less hungry (or more full or satisfied). Ketosis appears to provide a plausible explanation for this suppression of appetite. Future studies should investigate the minimum level of ketosis required to achieve appetite suppression during ketogenic weight loss diets, as this could enable inclusion of a greater variety of healthy carbohydrate-containing foods into the diet.

Both energy restriction and weight loss have beneficial effects on insulin action and glycemic control in obesity and mild NIDDM. The effect of energy restriction is related to changes in individual macronutrients, whereas weight loss effects relate to changes in abdominal fat.

Key PointsQuestionWhat are the long-term effects of severe vs moderate energy restriction on lean mass and other aspects of body composition?FindingsThis randomized clinical trial included 101 postmenopausal women with obesity. At 12 months, participants who had undergone severe energy restriction experienced approximately 2-fold greater weight and fat loss, approximately 1.5 times as much loss of whole-body lean mass (proportional to total weight lost), and approximately 2.5 times as much loss of total hip bone mineral density compared with participants who had undergone moderate energy restriction.MeaningAlthough severe energy restriction is an effective obesity treatment, caution is necessary when implementing it in postmenopausal women, especially those with osteopenia or osteoporosis.

Leptin expression and secretion are strongly correlated with body fat mass in animals and humans in cross-sectional studies, and experimental alterations in body fat content are associated with parallel changes in leptin expression and secretion [1,2]. Leptin expression and secretion in animals is also acutely influenced by food restriction and refeeding [2,3]. In obese humans and animals undergoing energy restriction, amelioration of many of the metabolic abnormalities associated with obesity is apparent before any major effect on body fat content. In an investigation of the mechanisms responsible for these early effects we have studied metabolic responses after 4 and 28 days of energy restriction in a group of moderately obese human subjects with and without non-insulindependent diabetes mellitus (NIDDM). We report here the responses of circulating leptin concentrations under these conditions, and their relationships to changes in macronutrient intakes and body composition. Subjects and methodsSubjects: Nine (5 female, 4 male) obese subjects (BMI = 31.6 ± 0.8 (mean ± SEM) kg/m 2 ) with normal glucose tolerance and no family history of NIDDM, and 9 (4 female, 5 male) obese subjects (BMI = 32.3 ± 0.9) with mild NIDDM (fasting plasma glucose Summary The response of serum leptin to short (4 days) and prolonged (28 days) energy restriction (50 % reduction in energy intake) was determined in 18 (9 male, 9 female) moderately obese humans (body mass index 32.0 ± 0.6 kg/m 2 mean ± SEM), 9 of whom had mild non-insulin-dependent diabetes mellitus (NIDDM). Body composition was assessed before and at the end of the energy restriction using DEXA. The subjects lost a measured 2.6 ± 0.4 kg of body fat after 28 days and an estimated 0.3 kg at 4 days. Serum leptin fell to 64 ± 3 % of baseline levels at day 4 and further to 46 ± 4 % at day 28. In a multiple correlation analysis, the change in leptin concentration at day 4 was significantly related to the change in dietary carbohydrate intake (partial r = 0.68, p < 0.005) but not to changes in fat (r = 0.12) or protein (r = 0.02) intakes. There was a 1 : 1 relationship between the changes in leptin and dietary carbohydrate (regression slope = 1.0 ± 0.3). Gender, or the presence of NIDDM had no effects on these responses. This pronounced fall in serum leptin in association with reduced carbohydrate intake before substantial loss of body fat suggests a role for leptin in defending the body's carbohydrate stores and implicates leptin in the satiating effects of carbohydrate. Dietary or other interventions which maintain leptin levels during weight reduction may lead to improvements in weight loss. [Diabetologia (1997) 40: 348-351]

High egg consumption did not have an adverse effect on the lipid profile of people with T2D in the context of increased MUFA and PUFA consumption. This study suggests that a high-egg diet can be included safely as part of the dietary management of T2D, and it may provide greater satiety. This trial was registered at the Australia New Zealand Clinical Trials Registry (http://www.anzctr.org.au/) as ACTRN12612001266853.