Subsequent Obesity Research Articles

Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity.

Sweet taste receptors (STRs) on the tongue mediate gustatory sweet sensing, but their expression in the gut, pancreas, and adipose tissue suggests a physiological contribution to whole body nutrient sensing and metabolism. However, little is known about the function and contribution of these sugar sensors during metabolic stress induced by overnutrition and subsequent obesity. Here, we investigated the effects of high-fat/low-carbohydrate (HF/LC) diet on glucose homeostasis and energy balance in mice with global disruption of the sweet taste receptor protein T1R2. We assessed body composition, energy balance, glucose homeostasis, and tissue-specific nutrient metabolism in T1R2 knockout (T1R2-KO) mice fed a HF/LC diet for 12 wk. HF/LC diet-fed T1R2-KO mice gained a similar amount of body mass as did WT mice, but had reduced fat mass and increased lean mass relative to WT mice. T1R2-KO mice were also hyperphagic and hyperactive. Ablation of the T1R2 sugar sensor protected mice from HF/LC diet-induced hyperinsulinemia and altered substrate utilization, including increased rates of glucose oxidation and decreased liver triglyceride (TG) accumulation, despite normal intestinal fat absorption. Finally, STRs (T1r2/T1r3) were upregulated in the adipose tissue of WT mice in response to HF/LC diet, and their expression positively correlated with fat mass and glucose intolerance. The chemosensory receptor T1R2, plays an important role in glucose homeostasis during diet-induced obesity through the regulation of yet to be identified molecular mechanisms that alter energy disposal and utilization in peripheral tissues.

Increased Ghrelin Levels and Unchanged Adipocytokine Levels in Major Depressive Disorder.

One of the hypotheses of the pathophysiology of major depressive disorder (MDD) proposes that there is a relationship between adipocytokine and ghrelin levels and depression. Patients with major depression with a BMI ≤25 kg/m2 between the ages of 11 and 18 years (n = 30) were compared with a healthy control group (n = 30). Both groups were evaluated across a pretreatment period (MD-PT) and an improved period (MD-I). We measured serum leptin, adiponectin, resistin, and ghrelin levels and other parameters related to metabolic syndrome, such as glucose, insulin, insulin resistance (homeostasis model assessment [HOMA]), triglycerides (TG), and total cholesterol (TCHOL). Leptin, adiponectin, and resistin levels did not differ across groups; however, ghrelin levels were increased in the MD-I group compared with the control and MD-PT groups (p < 0.05). HOMA levels were also higher in the MD-PT group than in the control group (p < 0.05). After treatment, there was no difference in this measurement. The relationship between adipocytokines and major depression may be dependent on ghrelin levels as a result of antidepressant treatment and subsequent obesity.

Certified Nurse-Midwives’ Experiences with Gestational Weight Management

Excessive gestational weight gain is associated with fetal metabolic reprogramming and subsequent childhood obesity, as well as maternal recalcitrant obesity and its successive morbidities. We conducted a review of the literature and an explorative, descriptive study of the techniques and strategies used by a subset of certified nurse-midwives to help women achieve optimal gestational weight gain. We also identified barriers to this outcome. With more effective management approaches to gestational weight gain, adverse maternal and neonatal health outcomes could potentially be prevented. http://dx.doi.org/10.1016/j.nwh.2015.12.007

Can Optimal Complementary Feeding Improve Later Health and Development?

Nutrition and growth during early infancy influence later health and development, but most research has focused on the period of milk feeding, and the possibility that the timing, content or method of complementary feeding (CF) might have similar later effects has received less attention. Such effects are plausible, given that the CF period is one of rapid growth and development when infants are susceptible to nutrient deficiencies and excesses, and during which there are marked changes in diet with exposure to many new foods, tastes and feeding experiences. CF practices could influence later outcome by several potential mechanisms, including programming effects, but also direct effects on food preferences, appetite and eating behavior. Investigating these issues is challenging given the diversity and complexity of CF practices, which limit the feasibility and generalizability of randomized trials in this field. Available evidence relating CF practices to later health and development are currently limited in quantity and quality, but suggest that avoiding the introduction of solid foods before 4 months may reduce the risk of subsequent obesity and allergy. Whilst recommendations for different aspects of CF may be developed in the future based on broad principles, they will need to be tailored for different populations.

Déterminants précoces de l’obésité

The prevalence of childhood obesity has increased dramatically in the second half of the 20th century even in children before the age of 5 years. Many factors may interfere with early development, from the prenatal period to the first two years of life, and modulate susceptibility to subsequent obesity. Regarding the prenatal period, maternal BMI before pregnancy is a factor associated with adult obesity in a very reproducible way. Many studies are also consistent for gestational maternal weight gain and maternal smoking during pregnancy, after adjustment for major potential confounders. More recently, a meta-analysis concluded that caesarean delivery is also a risk marker. For the post natal period, the marker most consistently associated with adult obesity is rapid weight gain during the first months of life. Most studies are negative for breastfeeding. Advances in the genetics of obesity, epigenetics and new knowledge on intestinal microbiota should help decipher the mechanisms behind these associations. Many of these early markers become more frequent during the second half of the 20th century and they may have feed the obesity epidemic in children.

Fetal Growth, Obesity, and Atopic Disorders in Adolescence: a Retrospective Birth Cohort Study.

Developmental status at birth and subsequent obesity have been implicated in the development of childhood atopic dermatitis (AD) and allergic rhinitis (AR). The current study analysed the cohort data of 74 688 junior high school students from a national retrospective birth cohort study in Taiwan. A random 10% sample was selected from singleton livebirths with complete data on the analytical variables of interest. Atopic disorders, including AD and AR, were assessed by questionnaires (International Study of Asthma and Allergies in Childhood). Logistic regression analyses were applied with adjustments for related risk factors. Among subjects mainly 13-15 years of age, the estimated prevalence was 7.6% for AD and 22.4% for AR. While the role of fetal growth in allergic disorders was less evident, the risk of developing AD and AR were both influenced by a combination of fetal growth status and adolescent body mass index (BMI). Compared with those with normal fetal growth and school-aged BMI, the risk of developing AD increased 64% among adolescents with both restricted fetal growth and high BMI (odds ratio 1.64, 95% confidence interval 1.37, 1.97). The risk for this combination was higher than that for either restricted fetal growth or high BMI alone. Nevertheless, the overall interaction between BMI and fetal growth status on atopic disorders did not reach statistical significance. Excessive weight gain could be an important risk factor related to developing atopic dermatitis and allergic rhinitis during adolescence, especially among infants born small for gestational age.

The Healthy Core Metabolism: A New Paradigm for Primary Preventive Nutrition.

Research in preventive nutrition aims at elucidating mechanism by which our diet helps us to remain in good health through optimal physiological functions. However, despite decades of accumulated data in human nutrition and regular subsequent nutritional recommendations, obesity and type 2 diabetes epidemics continue to progress worldwide each year leading to a regular decrease of the Healthy Life Years, notably in Western countries. Such a paradox may be explained by the Nutrition Transition, the extreme application of the reductionist paradigm in nutrition research, the lack of nutritional education and a too strong focus on curative nutrition in at risk/ill subjects. In this position paper, we hypothesized that researchers should focus more on healthy subjects, from birth until maturity. Rather than exploring what differentiates healthy and at risk/ill subjects, we propose to thoroughly study what characterizes a healthy state and its underlying metabolism. We define it as the Healthy Core Metabolism which remains stable whatever energy inputs (diets) and outputs (exercise), genetic background and external/internal stress, e.g., temporary illnesses. As a basis for Healthy Core Metabolism investigation, we observed that main physiological and ubiquitous functions of human organism, i.e., the neuro-vasculo-sarco-osteoporotic system, tend to follow a concave curve with common phases of growth, optimum, and decline. Finally, we hypothesized that true primary preventive nutrition should focus on the growth phase to reach the maximum capital of a given physiological function so that - whatever the further decline -, Healthy Life Years may approach or coincide with theoretical Life Expectancy.

PP.19.20

Objective: Dietary sugar and fat contribute to adiposity and are deleterious to cardiovascular heath. In addition, high dietary fructose in the absence of dietary fat induces leptin resistance and exacerbates subsequent HF-induced obesity. In addition, augmented leptin is associated with arterial stiffness. Thus, we hypothesized that a high-fat/high-fructose (HF/F) diet would have more severe consequences than a high-fat (HF) or chow diet on cardiovascular health. Design and method: Male Sprague Dawley rats were fed either with chow, HF (30%) or HF/F (30%/44%) diets for 12 weeks (N = 8-10/group) and adiposity, basilar artery reactivity, basilar artery wall thickness, heart weight, and biochemical parameters assessed. Basilar artery was cannulated in a pressurized system (90 cm H2O). Results: Vascular contractile responses to KCl (30-120 mM) were unchanged whereas both HF and HF/F diets decreased relaxation responses to papaverin (10-10-10-4 M, direct smooth muscle); acetylcholine (ACh) (10-10-10-4 M, endothelium dependent); and diethylamine (DEA)-NONO-ate (10-10-10-4 M, endothelium independent) relaxation compared to chow. The log EC50 values were -5.84, chow; -4.87, HF; -4.98, HF/F, p < .05 for papaverin; -6.48, chow; -5.65, HF; 5.79HF/F, p < 0.05 for Ach) and -5.94, chow; -4.45, HF; -4.49, HF/F, p < .05 for DEA. Artery wall thickness was increased only in HF group (27 ± 1.6 μm) compared with chow (22 ± 1.2, p < .05) and eNOS immunofluroescence was decreased by 50% in HF and HF/F diets (arbitrary units, p < .05). Adipose tissue weights (10.7 ± .5 HF; 12.7 ± .8 HF/F vs 7.8 ± .3 chow, p < .05) and total adiposity by TDNMR were elevated by the same degree in both HF and HF/F diets. Blood triglycerides (157 ± 32 mg/dl) and leptin (10.4 ± 1.8ng/ml) were greater with HF/F diet than with HF (65 ± 15; 6.6 ± .6) or chow diet (63 ± 14; 4.1 ± .3). Conclusions: In conclusion, both HF diets impaired basilar artery relaxation, and increased heart weight potentially due to decreased eNOS synthesis. Although, leptin and triglycerides were greater with HF/F diet only the HF increased wall thickness. These data suggest that the presence of high fructose in a HF diet does not exacerbate the detrimental consequences of a HF diet on cardiovascular health.

Is the Relationship between Common Mental Disorder and Adiposity Bidirectional? Prospective Analyses of a UK General Population-Based Study.

The direction of the association between mental health and adiposity is poorly understood. Our objective was to empirically examine this link in a UK study. This is a prospective cohort study of 3 388 people (men) aged ≥ 18 years at study induction who participated in both the UK Health and Lifestyle Survey at baseline (HALS-1, 1984/1985) and the re-survey (HALS-2, 1991/1992). At both survey examinations, body mass index, waist circumference and self-reported common mental disorder (the 30-item General Health Questionnaire, GHQ) were measured. Logistic regression models were used to compute odds ratios (OR) and accompanying 95% confidence intervals (CI) for the associations between (1) baseline common mental disorder (QHQ score > 4) and subsequent general and abdominal obesity and (2) baseline general and abdominal obesity and re-survey common mental disorders. After controlling for a range of covariates, participants with common mental disorder at baseline experienced greater odds of subsequently becoming overweight (women, OR: 1.30, 1.03 – 1.64; men, 1.05, 0.81 – 1.38) and obese (women, 1.26, 0.82 – 1.94; men, OR: 2.10, 1.23 – 3.55) than those who were free of common mental disorder. Similarly, having baseline common mental health disorder was also related to a greater risk of developing moderate (1.57, 1.21 – 2.04) and severe (1.48, 1.09 – 2.01) abdominal obesity (women only). Baseline general or abdominal obesity was not associated with the risk of future common mental disorder. These findings of the present study suggest that the direction of association between common mental disorders and adiposity is from common mental disorder to increased future risk of adiposity as opposed to the converse.

Hepatoprotective Effect of Herb Formula KIOM2012H Against Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is a hepatic ailment with a rapidly increasing incidence due to dietary hypernutrition and subsequent obesity. Fatty liver disease can lead to steatohepatitis, fibrosis, cirrhosis, and even cancer, which is associated with various complications. Discovering effective natural materials and herbs can provide alternative and complementary medical treatments to current chemical pharmaceuticals. To develop an effective natural agent for NAFLD, we formulated a combination of four herb mixtures (KIOM2012H) and observed lipid-lowering efficacy. The inhibitory effects of KIOM2012H on free fatty acid-induced lipid accumulation, triglyceride contents, and gene expressions were analyzed in HepG2 cells. Using high fat diet-fed mice, body weight changes, gross liver appearances, hepatic triglyceride contents, and gene expressions were evaluated. KIOM2012H dose-dependently inhibited lipid accumulation and gene expressions involved in lipogenesis and related regulators. Experimental animals also showed a decrease in body weight changes and lipid-associated physiological parameters. This study shows that KIOM2012H has an alleviating effect on fatty acid and lipid accumulation, and therefore can be applied for development of new therapeutic pharmaceuticals for treatment of NAFLD using natural products and herbs.

Abstract 167: High Dietary Fructose Does not Exacerbate the Detrimental Consequences of a HF Diet on Basilar Artery Function

There is a strong correlation between the consumption of sugar- or fructose-enriched products and obesity. Moreover, high dietary fructose without added fat and in the absence of obesity induces leptin resistance and exacerbates subsequent HF-induced obesity. Elevated leptin is associated with arterial stiffness. Thus, we hypothesized that the consequences of a high-fat/high-fructose (HF/F) diet would be more detrimental than a high-fat (HF) or chow diet on functional and structural changes in the basilar arteries. Male Sprague Dawley rats were fed either with chow, HF (30%) or HF/F (30%/44%) diets for 12 weeks (N=8-10/group). The basilar artery was cannulated in a pressurized system (90cm H2O) and vascular contractile responses to KCl (30-120 mM) and endothelin (10-11-10-7 M), and relaxation to acetylcholine (ACh) (10-10-10-4 M), and diethylamine (DEA)-NONO-ate (10-10-10-4 M) evaluated and artery wall thickness and eNOS immunofluroescence determined. At death, leptin, blood lipids, and asymetricaldiamethyl arginine level (ADMA) were assayed in serum. Basilar artery contractility was unchanged, but both HF and HF/F diets resulted in decreased relaxation responses compared with chow to endothelium dependent (Ach logEC50: -6.48, chow; -5.65, HF; 5.79HF/F, p&lt;0.05) and endothelium independent relaxation (DEA: -5.94;-4.45;-4.49, p&lt;.05). Increased basilar artery wall thickness was observed only in HF group (22±1.2 vs 27±1.6μm, p&lt;.05). Both diets increased serum ADMA levels (.36±.03 HF; .42±.05 HF/F vs .26±.02 chow, p&lt;.05), 50% decreased eNOS immunofluorescence (arbitrary units, p&lt;.05), and increased adipose tissue (10.7±.5 HF; 12.7±.8 HF/F vs 7.8±.3 chow, p&lt;.05). HF/F increased triglycerides (157±32 mg/dl) and leptin (10.4±1.8ng/ml) greater than with HF (65±15; 6.6±.6) or chow diet (63±14; 4.1±.3). In conclusion, both HF diets impaired basilar artery relaxation, potentially due to decreased eNOS synthesis and increased ADMA. Although, leptin and triglycerides were greater with HF/F diet only the HF increased wall thickness. These data suggest that the presence of high fructose in a HF diet does not exacerbate the detrimental consequences of a HF diet on basilar artery function.

Hepatoprotective effect of herb formula KIOM2012H against nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a hepatic ailment with a rapidly increasing incidence due to dietary hypernutrition and subsequent obesity. Fatty liver disease can lead to steatohepatitis, fibrosis, cirrhosis, and even cancer, which is associated with various complications. Discovering effective natural materials and herbs can provide alternative and complementary medical treatments to current chemical pharmaceuticals. To develop an effective natural agent for NAFLD, we formulated a combination of four herb mixtures (KIOM2012H) and observed lipid-lowering efficacy. The inhibitory effects of KIOM2012H on free fatty acid-induced lipid accumulation, triglyceride contents, and gene expressions were analyzed in HepG2 cells. Using high fat diet-fed mice, body weight changes, gross liver appearances, hepatic triglyceride contents, and gene expressions were evaluated. KIOM2012H dose-dependently inhibited lipid accumulation and gene expressions involved in lipogenesis and related regulators. Experimental animals also showed a decrease in body weight changes and lipid-associated physiological parameters. This study shows that KIOM2012H has an alleviating effect on fatty acid and lipid accumulation, and therefore can be applied for development of new therapeutic pharmaceuticals for treatment of NAFLD using natural products and herbs.

Even transient rapid infancy weight gain is associated with higher BMI in young adults and earlier menarche.

BackgroundEarly postnatal rapid “catch-up” weight gain has been consistently associated with subsequent higher obesity risk and earlier pubertal development. In many low- and middle-income countries, infancy catch-up weight gain is transient and often followed by growth faltering. We explored the hypothesis that even transient catch-up weight gain during infancy is associated with later obesity risk and earlier puberty.Methods2352 (1151 male, 1201 female) black South African children in the Birth to Twenty (Bt20) prospective birth cohort study (Johannesburg-Soweto) underwent serial measurements of body size and composition from birth to age 18 years. At age 18 years, whole-body fat mass and fat-free mass were determined using dual energy x-ray absorptiometry. Pubertal development was assessed by the research team between ages 9 and 10 years, and recorded annually from age 11 years using a validated self-assessment protocol.ResultsCatch-up weight gain from birth to age 1 year, despite being followed by growth faltering between ages 1 and 2 years, was associated greater mid-upper arm circumference (p=0.04) and skin fold thickness (p=0.048) at age 8 years, and with higher weight (p<0.001) and BMI (p=0.001) at age 18 years after adjustment for sex, age, smoking during pregnancy, birth order, gestational age, formula-milk feeding and household socio-economic status. Infancy catch-up weight gain was also associated with younger age at menarche in girls (p<0.001). This association persisted after adjustment for smoking during pregnancy, birth order, gestational age, formula-milk feeding and household socio-economic status (p=0.005).ConclusionTransient catch-up weight gain from birth to age 1 year among children born in a low-income area of South Africa was associated with earlier menarche and greater adiposity in early adulthood. This observation suggests that modifiable determinants of rapid infancy weight gain may be targeted in order to prevent later obesity and consequences of earlier puberty in girls.

Dieting Increases the Likelihood of Subsequent Obesity and BMI Gain: Results from a Prospective Study of an Australian National Sample.

Diet is a major determinant of obesity; however, findings from the studies examining how dieting to lose weight affects weight gain have been inconclusive. Our aim was to examine the longitudinal association of frequency of dieting for weight loss with (a) obesity status and (b) body mass index (BMI) change. We used data from Waves 9 (2009) and 10 (2010) of the Household Income and Labour Dynamics in Australia (HILDA) survey. Binominal logistic regression estimated the association of frequency of dieting in 2009 on probability of obesity in 2010. Multinomial logistic regression estimated the association of frequency of dieting in 2009 on the probability of BMI gain versus BMI maintenance and BMI loss between 2009 and 2010. The analysis sample size was 8824. Compared to those who were never on a diet in the previous year, the odds of obesity were 1.9, 2.9, and 3.2 times higher among those who were on a diet once, more than once, and always, respectively. Similarly, the odds of BMI gain versus BMI maintenance and also versus BMI loss were higher among those who dieted than those who did not. Dieting to lose weight can contribute to the risk of future obesity and weight gain. Losing weight requires a commitment to change one's lifestyle and a sustained effort to maintain a healthy diet and engage in physical activity.

Do we have to leave obesity treatment to the surgeons?

The comparison of the largest bariatric surgery study (Swedish Obese Subjects, SOS) with almost 4000 surgical and conservatively treated patients and its conservative counterpart, the LookAHEAD study (Action for Help in Diabetes) with more than 5000 obese patients (average BMI 36 kg/m(2)) with type 2 diabetes showed that although both studies resulted in improved cardiovascular risk factors (bodyweight, HbA1c, HDL/LDL, blood pressure, sleep apnoe syndrome) only the SOS study and subsequent obesity surgery studies could verify their primary outcome hypothesis (significant reduction of the incidence of both cardiovascular deaths, non-fatal infarctions and strokes and hospitalization angina). Furthermore the SOS study could demonstrate a decreased mortality compared to the Look-AHEAD study. Despite a high psychological co-morbidity of obesity surgery patients the majority of studies also with follow-ups of more than 5 years demonstrates an improvement in mental functioning and quality of life. In contrast, there seems to be an increased risk for suicide about 3-4 years after the surgical intervention. Thus, while the majority of obesity surgery patients seems to benefit both physically and mentally, there is a minority that risks to take at least psychologically serious damage.

Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes.

Diabetic foot ulcerations have been extensively reported as vascular complications of diabetes mellitus associated with a high degree of morbidity and mortality. Diabetic foot syndrome (DFS), as defined by the World Health Organization, is an "ulceration of the foot (distally from the ankle and including the ankle) associated with neuropathy and different grades of ischemia and infection". Pathogenic events able to cause diabetic foot ulcers are multifactorial. Among the commonest causes of this pathogenic pathway it's possible to consider peripheral neuropathy, foot deformity, abnormal foot pressures, abnormal joint mobility, trauma, peripheral artery disease. Several studies reported how diabetic patients show a higher mortality rate compared to patients without diabetes and in particular these studies under filled how cardiovascular mortality and morbidity is 2-4 times higher among patients affected by type 2 diabetes mellitus. This higher degree of cardiovascular morbidity has been explained as due to the observed higher prevalence of major cardiovascular risk factor, of asymptomatic findings of cardiovascular diseases, and of prevalence and incidence of cardiovascular and cerebrovascular events in diabetic patients with foot complications. In diabetes a fundamental pathogenic pathway of most of vascular complications has been reported as linked to a complex interplay of inflammatory, metabolic and procoagulant variables. These pathogenetic aspects have a direct interplay with an insulin resistance, subsequent obesity, diabetes, hypertension, prothrombotic state and blood lipid disorder. Involvement of inflammatory markers such as IL-6 plasma levels and resistin in diabetic subjects as reported by Tuttolomondo et al confirmed the pathogenetic issue of the a "adipo-vascular" axis that may contribute to cardiovascular risk in patients with type 2 diabetes. This "adipo-vascular axis" in patients with type 2 diabetes has been reported as characterized by lower plasma levels of adiponectin and higher plasma levels of interleukin-6 thus linking foot ulcers pathogenesis to microvascular and inflammatory events. The purpose of this review is to highlight the immune inflammatory features of DFS and its possible role as a marker of cardiovascular risk in diabetes patients and to focus the management of major complications related to diabetes such as infections and peripheral arteriopathy.

The prevalence of food addiction as assessed by the Yale Food Addiction Scale: A systematic review

Obesity is a global issue and it has been suggested that an addiction to certain foods could be a factor contributing to overeating and subsequent obesity. Only one tool, the Yale Food Addiction Scale (YFAS) has been developed to specifically assess food addiction. This review aimed to determine the prevalence of food addiction diagnosis and symptom scores, as assessed by the YFAS. Published studies to July 2014 were included if they reported the YFAS diagnosis or symptom score and were published in the English language. Twenty-five studies were identified including a total of 196,211 predominantly female, overweight/obese participants (60%). Using meta-analysis, the weighted mean prevalence of YFAS food addiction diagnosis was 19.9%. Food addiction (FA) diagnosis was found to be higher in adults aged >35 years, females, and overweight/obese participants. Additionally, YFAS diagnosis and symptom score was higher in clinical samples compared to non-clinical counterparts. YFAS outcomes were related to a range of other eating behavior measures and anthropometrics. Further research is required to explore YFAS outcomes across a broader spectrum of ages, other types of eating disorders and in conjunction with weight loss interventions to confirm the efficacy of the tool to assess for the presence of FA.

The inheritance of obesity

Syndromic adiposity appears to have a predisposition to run in families suggesting a hereditary element in its transmission. Purely genetic defects and DNA sequence variants have been directly associated with the development of adiposity; however, these account for a very small proportion of cases. A stronger association has been made between the intrauterine and early childhood nutritional environment of the foetus and young child and the predisposition of childhood and subsequent adulthood obesity. The nutritional environments include both a situation of nutritional deprivation or excess working through the interplay of epigenetic changes, and pancreatic and hypothalamic development. This is further compounded by the nutritional and lifestyle attitudes of the particular at-risk family. Adiposity prevention measures must include reenforced intervention strategies stating with lifestyle education schemes during pregnancy followed through until infancy and early childhood especially in those families/individuals identified as being at a risk of developing significant adiposity.

The Prevalence of Food Addiction as Assessed by the Yale Food Addiction Scale: A Systematic Review

Obesity is a global issue and it has been suggested that an addiction to certain foods could be a factor contributing to overeating and subsequent obesity. Only one tool, the Yale Food Addiction Scale (YFAS) has been developed to specifically assess food addiction. This review aimed to determine the prevalence of food addiction diagnosis and symptom scores, as assessed by the YFAS. Published studies to July 2014 were included if they reported the YFAS diagnosis or symptom score and were published in the English language. Twenty-five studies were identified including a total of 196,211 predominantly female, overweight/obese participants (60%). Using meta-analysis, the weighted mean prevalence of YFAS food addiction diagnosis was 19.9%. Food addiction (FA) diagnosis was found to be higher in adults aged >35 years, females, and overweight/obese participants. Additionally, YFAS diagnosis and symptom score was higher in clinical samples compared to non-clinical counterparts. YFAS outcomes were related to a range of other eating behavior measures and anthropometrics. Further research is required to explore YFAS outcomes across a broader spectrum of ages, other types of eating disorders and in conjunction with weight loss interventions to confirm the efficacy of the tool to assess for the presence of FA.

Effect of diet on preference and intake of sucrose in obese prone and resistant rats.

Increased orosensory stimulation from palatable diets and decreased feedback from gut signals have been proposed as contributing factors to obesity development. Whether altered taste functions associated with obesity are common traits or acquired deficits to environmental factors, such as a high-energy (HE)-diet, however, is not clear. To address this, we examined preference and sensitivity of increasing concentrations of sucrose solutions in rats prone (OP) and resistant (OR) to obesity during chow and HE feeding and measured lingual gene expression of the sweet taste receptor T1R3. When chow-fed, OP rats exhibited reduced preference and acceptance of dilute sucrose solutions, sham-fed less sucrose compared to OR rats, and had reduced lingual T1R3 gene expression. HE-feeding abrogated differences in sucrose preference and intake and lingual T1R3 expression between phenotypes. Despite similar sucrose intakes however, OP rats consumed significantly more total calories during 48-h two-bottle testing compared to OR rats. The results demonstrate that OP rats have an innate deficit for sweet taste detection, as illustrated by a reduction in sensitivity to sweets and reduced T1R3 gene expression; however their hyperphagia and subsequent obesity during HE-feeding is most likely not due to altered consumption of sweets.