Weight loss and subsequent body weight maintenance are difficult for obese individuals despite the wide variety of dietary regimens and approaches. A substantial body of scientific evidence has shown that by simply varying the macronutrient distribution and composition of dietary factors, weight losses of varying amounts, longer-term body weight maintenance periods, better appetite regulation, and changes in features of the metabolic syndrome can be achieved. At present, renewed efforts are underway to increase the protein content of weight-loss diets, simultaneously restrict fat consumption to no more than 30%, favor polyunsaturated fat, have carbohydrates account for between 40 and 50% of total energy intake, and promote the consumption of low-glycemic foods. The present article reviews the scientific evidence for the effects of several dietary manipulations and sustainable strategies for weight loss and body weight stability as well as for treating specific features of the metabolic syndrome.

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Epigenetics could contribute to explain individual differences in weight loss after an energy restriction intervention. Here, we identify novel potential epigenetic biomarkers of weight-loss comparing DNA methylation patterns of high and low responders to a 2 hypocaloric diet. Twenty-five overweight/obese men followed an 8-week caloric restriction intervention. DNA was isolated from peripheral blood mononuclear cells and treated with bisulfite. The basal and endpoint epigenetic differences between high and low responders were analysed by methylation microarray, which was also useful to compare the epigenetic changes due to the nutrition intervention. Subsequently, Sequenom EpiTYPER technology was used to validate several relevant CpGs and the surrounding regions.DNA methylation levels in several CpGs located in ATP10A and CD44 genes showed statistical baseline differences depending on the weight-loss outcome. At the treatment endpoint, DNA methylation levels of several CpGs on WT1 promoter were statistically more methylated in the high than in the low responders. Finally, different CpG sites from WT1 and ATP10A were significantly modified as a result of the intervention.In summary, hypocaloric diet-induced weight loss in humans could alter DNA methylation status of specific genes. Moreover, baseline DNA methylation patterns may be used as epigenetic markers that could help to predict weight loss.

Malnutrition is very prevalent in geriatric patients with hip fracture. Nevertheless, its importance is not fully recognized. The objective of this paper is to review the impact of malnutrition and of nutritional treatment upon outcomes and mortality in older people with hip fracture. We searched the PubMed database for studies evaluating nutritional aspects in people aged 70 years and over with hip fracture. The total number of studies included in the review was 44, which analyzed 26,281 subjects (73.5% women, 83.6 ± 7.2 years old). Older people with hip fracture presented an inadequate nutrient intake for their requirements, which caused deterioration in their already compromised nutritional status. The prevalence of malnutrition was approximately 18.7% using the Mini-Nutritional Assessment (MNA) (large or short form) as a diagnostic tool, but the prevalence was greater (45.7%) if different criteria were used (such as Body Mass Index (BMI), weight loss, or albumin concentration). Low scores in anthropometric indices were associated with a higher prevalence of complications during hospitalization and with a worse functional recovery. Despite improvements in the treatment of geriatric patients with hip fracture, mortality was still unacceptably high (30% within 1 year and up to 40% within 3 years). Malnutrition was associated with an increase in mortality. Nutritional intervention was cost effective and was associated with an improvement in nutritional status and a greater functional recovery. To conclude, in older people, the prevention of malnutrition and an early nutritional intervention can improve recovery following a hip fracture.

The consumption of legumes (4 servings/week) within a hypocaloric diet resulted in a specific reduction in proinflammatory markers, such as CRP and C3 and a clinically significant improvement of some metabolic features (lipid profile and BP) in overweight/ obese subjects, which were in some cases independent from weight loss.

Objective: The recently discovered peptide irisin has been hypothesized to be a regulator of body metabolism. The objective of this work was to evaluate whether circulating human irisin levels are modulated by body size and changes in adiposity during an energy restriction treatment and the subsequent weight regain.Methods: A group of 94 obese patients (50 men, 44 women; 49.4 6 9.4 years; BMI 35.6 6 4.5 kg/m 2 ) participated in a weight loss program following an 8-week hypocaloric diet (230% energy expenditure) with a weight maintenance follow-up. The patients were evaluated at 0, 8, and 24 weeks after starting treatment. In addition, 48 normal-weight subjects (16 men, 32 women; 35.71 6 8.8 years; BMI 22.9 6 2.2 kg/m 2 ) participated as controls. Plasma irisin, body weight, body composition, and hormones controlling energy homeostasis were measured.Results: Irisin levels were higher in obese subjects (353.1 6 18.6 ng/mL) than in those of normal-weight (198.4 6 7.8 ng/mL; P 0.001) and were also higher in men (340.9 6 20 ng/mL) than in women (267.6 6 12 ng/mL; P < 0.05). Moreover, irisin plasma levels were significantly correlated with high levels of direct and indirect adiposity markers, such as weight, BMI, waist circumference, and fat mass, as measured by bioimpedance, but not with height or leptin levels. Interestingly, irisin levels paralleled body weight reduction after the dietary treatment (week 8) and again returned to the baseline levels at 24 weeks in those patients regaining the lost weight.Conclusions: Irisin strongly reflects body fat mass, suggesting that the irisin circulating levels are conditioned by adiposity level. Am. J. Hum. Biol. 26:198-207, 2014.

Diversity in the genetic profile between individuals and specific ethnic groups affects nutrient requirements, metabolism and response to nutritional and dietary interventions. Indeed, individuals respond differently to lifestyle interventions (diet, physical activity, smoking, etc.). The sequencing of the human genome and subsequent increased knowledge regarding human genetic variation is contributing to the emergence of personalized nutrition. These advances in genetic science are raising numerous questions regarding the mode that precision nutrition can contribute solutions to emerging problems in public health, by reducing the risk and prevalence of nutrition-related diseases. Current views on personalized nutrition encompass omics technologies (nutrigenomics, transcriptomics, epigenomics, foodomics, metabolomics, metagenomics, etc.), functional food development and challenges related to legal and ethical aspects, application in clinical practice, and population scope, in terms of guidelines and epidemiological factors. In this context, precision nutrition can be considered as occurring at three levels: (1) conventional nutrition based on general guidelines for population groups by age, gender and social determinants; (2) individualized nutrition that adds phenotypic information about the person's current nutritional status (e.g. anthropometry, biochemical and metabolic analysis, physical activity, among others), and (3) genotype-directed nutrition based on rare or common gene variation. Research and appropriate translation into medical practice and dietary recommendations must be based on a solid foundation of knowledge derived from studies on nutrigenetics and nutrigenomics. A scientific society, such as the International Society of Nutrigenetics/Nutrigenomics (ISNN), internationally devoted to the study of nutrigenetics/nutrigenomics, can indeed serve the commendable roles of (1) promoting science and favoring scientific communication and (2) permanently working as a ‘clearing house' to prevent disqualifying logical jumps, correct or stop unwarranted claims, and prevent the creation of unwarranted expectations in patients and in the general public. In this statement, we are focusing on the scientific aspects of disciplines covering nutrigenetics and nutrigenomics issues. Genetic screening and the ethical, legal, social and economic aspects will be dealt with in subsequent statements of the Society.

BackgroundDietary total antioxidant capacity (TAC) has been assumed as a useful tool to assess the relationship between the cumulative antioxidant food capacity and several chronic disorders. The aim of this cross-sectional study was to investigate the potential relationships of dietary TAC with adiposity, metabolic and oxidative stress markers in healthy young adults.MethodsThis study enrolled 266 healthy subjects (105 men/ 161 women; 22 ± 3 years-old; 22.0 ± 2.7 kg/m2). Dietary intake, anthropometry, blood pressure, lifestyle features, and biochemical data were assessed with validated procedures.ResultsIn linear regression analyses, dietary TAC values were inversely associated with glycemia, total cholesterol:HDL-c ratio, triglycerides and oxidized-LDL concentrations, and positively associated with HDL-c concentrations, independently of gender, age, smoking status, physical activity, vitamin use supplement, waist circumference, energy intake, fatty acid intake. In addition, plasma TAC was negatively correlated with ox-LDL concentrations (r= -0.20, P = 0.003), independently of the assessed confounding variables. Finally, dietary TAC values were inversely related to waist circumference values (r= -0.17, P = 0.005) as well as to lower mild central obesity occurrence (waist circumference ≥ 80/ 94 cm for women/ men, respectively).ConclusionDietary TAC values are inversely associated with glucose and lipid biomarkers as well as with central adiposity measurements in healthy young adults, indicating dietary TAC as a useful tool to assess the health benefits of cumulative antioxidant capacity from food intake. In addition, the independent and inverse relationships of ox-LDL concentrations with dietary and plasma TAC respectively suggest a putative role of antioxidant rich-diet in the link between redox state and atherogenesis at early stage.