In accordance with US dietary guidance, incorporating variety into the diet can align with energy balance, though greater food variety in some categories may make energy balance more challenging. Thus, experimental and epidemiologic evidence is summarized on the relationship between food variety, food and energy intake, and energy balance. Lab-based, experimental research consistently demonstrates that greater variety within foods or sensory characteristics of food increases food and energy intake within an eating occasion. Epidemiologic evidence is less consistent, potentially driven by differing methodologies, particularly in defining and measuring food variety. Moreover, the effect of variety on energy balance appears to be moderated by food energy density. Integrating insights from experimental and epidemiologic research are essential for strengthening food variety guidance including developing evidence-based definitions of food variety, understanding moderators of the relationship, and developing practical guidance interpretable to consumers.

Purpose of reviewThe present review organises the recent literature on the role of memory in eating behaviours and provides an overview of the current evidence relating to the associations between memory and weight gain.Recent findingsResearch over the last few years has highlighted working memory as an important cognitive process that underpins many aspects of appetite control. Recent work on episodic memory and appetite has replicated work showing that manipulating memory for recent eating affects later consumption and extended this work to examine associations between individual differences in memory and eating behaviours. Poorer episodic memory ability is related to a reduced sensitivity to internal states of hunger and satiety and a tendency towards uncontrolled eating. There is also recent evidence to suggest that working memory and episodic memory impairments are related to weight gain and high BMI.SummaryWorking memory and episodic memory are core cognitive processes that are critical for food-related decision-making, and disruption to these processes contributes to problems with appetite control and weight gain, which suggests that weight loss programmes might be improved by the addition of cognitive training.

Given the high rates of pediatric and adult obesity, it is imperative to identify early risk factors that might contribute to excess weight gain. This review aims to investigate the relationship between childhood behavioral problems with the development and persistence of obesity. Specifically, this review highlights the association of obesity with (1) neurocognitive constructs, such as executive functioning and inhibition/impulsivity, and (2) disorders commonly diagnosed in childhood, including attention deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Consistent evidence supports a relationship between childhood behavioral problems, executive functioning, inhibition/impulsivity, ADHD, and ASD with obesity across the lifespan. Longitudinal studies suggest behavior problems, neurocognitive functioning deficits, and ADHD symptoms in childhood predict weight gain over time. Identifying risk factors in childhood that promote obesity may help develop targeted intervention and prevention programs. Additional research should elucidate mechanisms that account for these relationships.

Functional magnetic resonance imaging (fMRI) using visual food cues provides insight into brain regulation of appetite in humans. This review sought evidence for genetic determinants of these responses. Echoing behavioral studies of food cue responsiveness, twin study approaches detect significant inherited influences on brain response to food cues. Both polygenic (whole genome) factors and polymorphisms in single genes appear to impact appetite regulation, particularly in brain regions related to satiety perception. Furthermore, genetic confounding might underlie findings linking obesity to stereotypical response patterns on fMRI, i.e., associations with obesity may actually reflect underlying inherited susceptibilities rather than acquired levels of adiposity. Insights from twin studies show that genes powerfully influence brain regulation of appetite, emphasizing the role of inherited susceptibility factors in obesity risk. Future research to delineate mechanisms of inherited obesity risk could lead to novel or more targeted interventional approaches.

The primary objective of this review is to identify dietary patterns with beneficial effects on cardiovascular health of adults with type 2 diabetes. The prevalence of diabetes is increasing globally. People with diabetes have a greater risk for cardiovascular disease. Mediterranean diet, dietary approaches to stop hypertension diet, vegetarian diet, traditional Korean diet, Japanese diet, and low-glycemic-index diet can reduce cardiovascular disease risk in people with diabetes. Dietary intake is a key modifiable factor in the management of diabetes and plays a significant role in limiting the incidence of cardiovascular diseases.

The aim of this review is to describe and discuss weight loss-induced variations in appetite in women and factors responsible for these changes. Studies have shown postweight loss increases in fasting and postprandial appetite in individuals engaged in weight loss trials, especially in women. Similarly, appetite-related peptides associated to the homeostatic control of feeding, such as leptin, ghrelin and peptide YY, were also found to be altered in way that promotes increased appetite after weight loss interventions. Sustained caloric deficits also drive increases in the frequency and strength of food cravings, food reward and seem to enhance oro-sensory sensations in women who lost weight. The menstrual cycle has also been to shown to influence caloric intake in women, more specifically food cravings. On the other hand, caloric restriction seems to increase cognitive restraint, decrease habitual disinhibition and susceptibility to hunger among women engaged in weight loss trials. Neural analysis corroborates these results, showing increased activation in brain areas involved in food reward and self-control processing. In conclusion, evidence supports that weight loss increases appetite sensations, and promotes changes in homeostatic and non-homeostatic control of feeding, which collectively seem to upregulate appetite in women.

Preoperative weight loss regimens prior to bariatric surgery have been a routine and common practice for many centers, in the US and around the world. The mandated participation in such programs has largely been influenced by loco-regional payer requirements. The relationship between adherence to a mandatory weight loss regimen and achieved preoperative weight loss as well as the clinical impact of preoperative weight loss on bariatric outcomes remains uncertain. This review examines the available current literature, in the context of previous findings, regarding the impact of mandated preoperative weight loss regimens and mandatory weight loss on bariatric outcomes. The reviewed studies do not provide sufficient evidence that mandatory participation in a preoperative weight loss regimen prior to bariatric surgery is associated with achieved weight loss or durable bariatric outcome benefit. Preoperative weight loss, when achieved, may confer a positive benefit on postoperative complications; however, this is not a consistent finding in the literature and requires further validation. The practice of mandating participation in a preoperative weight loss regimen or requiring mandatory weight loss prior to bariatric surgery is not supported by current literature and may serve as an obstacle to medically necessary and potentially life-saving treatment.

The continued success of bariatric surgery to treat obesity and obesity-associated metabolic conditions creates a need for a strong understanding of clinical nutrition both before and after these procedures. Surgically induced alteration of gastrointestinal physiology can affect the nutrition of individuals, especially among those who have undergone malabsorptive procedures. While uncommon, a subset of patients may develop protein-calorie malnutrition. In these cases, nutrition support should be tailored to the severity of malnutrition. Among all patients who undergo bariatric surgery, high rates of micronutrient deficiencies have been observed. To mitigate these deficiencies, empiric supplementation with multivitamins, calcium citrate, and vitamin D is generally recommended. Periodic surveillance should be performed for commonly deficient micronutrients, including thiamin (B1), folate (B9), cobalamin (B12), iron, and vitamin D. Following Roux-en-Y gastric bypass, serum levels of copper and zinc should also be monitored. In addition, lipid-soluble vitamins should be monitored following biliopancreatic diversion with/without duodenal switch.

The purpose of this review is to provide an introduction to quality of life (QOL) outcomes after bariatric surgery and a summary of the current evidence. QOL has been emphasized in bariatric surgery since the NIH Consensus Conference statement in 1991. Initial studies were limited to 1- and 2-year follow-up. More recent findings have expanded the follow-up period up to 12years, providing a better description of the impact on long-term QOL. Overall, there is little to no consensus regarding the definition of QOL or the ideal survey. Bariatric surgery has the greatest impact on physical QOL, and the impact on mental health remains unclear. There are some specific and less frequently reported threats to quality of life after bariatric surgery that are also discussed. Obesity has a definite impact on quality of life, even without other comorbidities, and surgery for obesity results in significant and lasting improvements in patient-reported quality of life outcomes. This conclusion is limited by a wide variety of survey instruments and absence of consensus on the definition of QOL after bariatric surgery.

Obesity is a common comorbidity in individuals with spina bifida. Carrying excess weight exacerbates the inherent health challenges associated with spina bifida, impedes the individual's ability to self-manage their condition, and creates further challenges for family members and caregivers. This manuscript provides a narrative review of key issues for understanding and prevention of obesity in persons with spina bifida within the context of the social ecological model. Specific variables related to obesity and spina bifida include individual factors (i.e., body composition and measurement issues, energy needs, eating patterns, physical activity, and sedentary activity) family factors (i.e., parenting/family, peers), community factors (i.e., culture, built environment, healthcare and healthcare providers, and school), and societal factors (i.e., policy issues). Due to the complex etiology of obesity and its increased prevalence in individuals with spina bifida, it is critical to initiate prevention efforts early with a multifactorial approach for this at-risk population. Increased research is warranted to support these efforts.