Passive Overconsumption Research Articles

Passive overconsumption? Limited evidence of compensation in meal size when consuming foods high in energy density: Two randomised crossover experiments

Passive overconsumption? Limited evidence of compensation in meal size when consuming foods high in energy density: Two randomised crossover experiments

Passive overconsumption? Limited evidence of compensation in meal size when consuming foods high in energy density: Two randomised crossover experiments

Research has drawn contradictory conclusions as to whether humans adjust meal size based on meal energy density (ED) or exhibit ‘passive overconsumption’. Recent observational research has suggested that meal EDs greater than 1.7–2 kcal/g are compensated for through consumption of smaller meal sizes. We tested the relationship between ED and meal size by examining energy intake of meals at three levels of ED: low (∼1.0 kcal/g), medium (1.7–2.0 kcal/g) and high (>3.0 kcal/g). Two randomised, crossover experiments were conducted with adult participants. In experiment 1 (n = 34, 62% female, mean age 37.4 years), participants were served a lunch including a familiar low, medium or high ED dessert to eat ad libitum. In experiment 2 (n = 32, 66% female, mean age 36.4 years), participants were served a lunch meal manipulated to be low, medium or high ED to eat ad libitum. For experiment 2, later energy intake (post-meal energy intake) was also measured. In experiment 1, participants consumed a similar amount of energy from the low vs. medium ED food. The high ED food was associated with an increased intake of approximately 240 kcals compared to medium (p < 0.001, Cohen’s d = 2.31) and low (p < 0.001, Cohen’s d = 4.42) ED foods. In experiment 2, there were no significant differences in meal size (grams) between ED meals, resulting in a largely linear relationship between meal ED and energy intake across the three ED conditions (‘passive overconsumption’). There were no differences in later energy intake between ED conditions. Contrary to recent suggestions, foods higher in ED were not associated with adjustments to meal size and were associated with increased energy intake across two experiments. Reformulation of foods high in ED may be an effective population level approach to reducing energy intake and obesity.Clinical trial registry number: NCT05744050; https://clinicaltrials.gov/ct2/show/NCT05744050.

The hedonic overdrive model best explains high-fat diet-induced obesity in C57BL/6 mice.

High-fat diets cause obesity in male mice; however, the underlying mechanisms remain controversial. Here, three contrasting ideas were assessed: hedonic overdrive, reverse causality, and passive overconsumption models. A total of 12 groups of 20 individually housed 12-week-old C57BL/6 male mice were exposed to 12 high-fat diets with varying fat content from 40% to 80% (by calories), protein content from 5% to 30%, and carbohydrate content from 8.4% to 40%. Body weight and food intake were monitored for 30 days after 7 days at baseline on a standard low-fat diet. After exposure to the diets, energy intake increased first, and body weight followed later. Intake then declined. The peak energy intake was dependent on both dietary protein and carbohydrate, but not the dietary fat and energy density, whereas the rate of decrease in intake was only related to dietary protein. On high-fat diets, the weight of food intake declined, but despite this average reduction of 14.4 g in food intake, they consumed, on average, 357 kJ more energy than at baseline. The hedonic overdrive model fit the data best. The other two models were not supported.

Exploring the short-term impact of swapping consumption from standard protein snacks to higher protein snacks on energy intake in social drinkers: Is protein worth a nudge?

Drinking alcoholic beverages stimulates food intake and contributes to the passive overconsumption of dietary energy. As protein is the most satiating of all the macronutrients, increased levels in snacks taken with alcohol have the potential to minimize excess energy consumption. We hypothesized that swapping consumption from retail-available standard protein (SP) snacks to higher protein (HP) snack foods would increase satiety and reduce acute food energy intake in social drinkers. A randomized single-blind crossover trial with 19 healthy participants aged 19-31 years was conducted. Participants attended two separate testing sessions, where they ingested white wine (30 g alcohol) and were offered adlibitum access to either HP snacks with a protein-fortified dip or SP snacks with a dip. There were no significant differences in mean food mass, food energy intake, or subjective appetite ratings between the high and SP snacks (all p > .05). Mean protein intake was significantly increased with HP snacks compared with standard snacks (p < .001). Plasma glucose median incremental area under the curve and mean peak were significantly higher with the SP snacks (all p < .05) but remained within the reference range. This study demonstrated that consumption of a higher amount of protein after a moderate alcohol dose does not result in a change in food mass and energy intake or promote satiety in healthy young adults. The potential for a simple swap to different snack types is unlikely to bring substantial benefits to social drinkers and reduce passive energy consumption.

Time to revisit the passive overconsumption hypothesis? Humans show sensitivity to calories in energy-rich meals

ABSTRACTBackgroundA possible driver of obesity is insensitivity (passive overconsumption) to food energy density (ED, kcal/g); however, it is unclear whether this insensitivity applies to all meals.ObjectivesWe assessed the influence of ED on energy intake (kcal) across a broad and continuous range of EDs comprised of noncovertly manipulated, real-world meals. We also allowed for the possibility that the association between energy intake and ED is nonlinear.MethodsWe completed a secondary analysis of 1519 meals which occurred in a controlled environment as part of a study conducted by Hall and colleagues to assess the effects of food ultra-processing on energy intake. To establish the generalizability of the findings, the analyses were repeated in 32,162 meals collected from free-living humans using data from the UK National Diet and Nutrition Survey (NDNS). Segmented regressions were performed to establish ED “breakpoints” at which the association between consumed meal ED and mean centered meal caloric intake (kcal) changed.ResultsSignificant breakpoints were found in both the Hall et al. data set (1.41 kcal/g) and the NDNS data set (1.75 and 2.94 kcal/g). Centered meal caloric intake did not increase linearly with consumed meal ED, and this pattern was captured by a 2-component (“volume” and “calorie content” [biologically derived from the sensing of fat, carbohydrate, and protein]) model of physical meal size (g), in which volume is the dominant signal with lower energy-dense foods and calorie content is the dominant signal with higher energy-dense foods.ConclusionsThese analyses reveal that, on some level, humans are sensitive to the energy content of meals and adjust meal size to minimize the acute aversive effects of overconsumption. Future research should consider the relative importance of volume and calorie-content signals, and how individual differences impact everyday dietary behavior and energy balance.

The Metabolic Concept of Meal Sequence vs. Satiety: Glycemic and Oxidative Responses with Reference to Inflammation Risk, Protective Principles and Mediterranean Diet.

With increasing exposure to eating opportunities and postprandial conditions becoming dominant states, acute effects of meals are garnering interest. In this narrative review, meal components, combinations and course sequence were questioned vis-à-vis resultant postprandial responses, including satiety, glycemic, oxidative and inflammatory risks/outcomes vs. protective principles, with reference to the Mediterranean diet. Representative scientific literature was reviewed and explained, and corresponding recommendations discussed and illustrated. Starting meals with foods, courses and/or preloads high in innate/added/incorporated water and/or fibre, followed by protein-based courses, delaying carbohydrates and fatty foods and minimizing highly-processed/sweetened hedonic foods, would increase satiety-per-calorie vs. obesogenic passive overconsumption. Similarly, starting with high-water/fibre dishes, followed by high-protein foods, oils/fats, and delayed/reduced slowly-digested whole/complex carbohydrate sources, optionally closing with simpler carbohydrates/sugars, would reduce glycaemic response. Likewise, starting with foods high in innate/added/incorporated water/fibre/antioxidants, high monounsaturated fatty acid foods/oils, light proteins and whole/complex carbohydrate foods, with foods/oils low in n-6 polyunsaturated fatty acids (PUFA) and n-6:n-3 PUFA ratios, and minimal-to-no red meat and highly/ultra-processed foods/lipids, would reduce oxidative/inflammatory response. Pyramids illustrating representative meal sequences, from most-to-least protective foods, visually communicate similarities between axes, suggesting potential unification for optimal meal sequence, consistent with anti-inflammatory nutrition and Mediterranean diet/meal principles, warranting application and outcome evaluation.

A low-fat diet up-regulates expression of fatty acid taste receptor gene FFAR4 in fungiform papillae in humans: a co-twin randomised controlled trial.

Fatty acid taste (FAT) perception is involved in the regulation of dietary fat intake, where impaired FAT is associated with increased fatty food intake. There are a number of FAT receptors identified on human taste cells that are potentially responsible for FAT perception. Manipulating dietary fat intake, and in turn FAT perception, would elucidate the receptors that are associated with long-term regulation of FAT perception. The present study aimed to assess associations between diet-mediated changes to FAT receptors and FAT perception in humans. A co-twin randomised controlled trial was conducted, where each matching twin within a pair were randomly allocated to either an 8-week low-fat (LF; <20 % energy fat) or an 8-week high-fat (HF; >35 % energy fat) diet. At baseline and week 8, fungiform papillae were biopsied in the fasted state and FAT receptor gene expressions (cluster of differentiation 36 (CD36), free fatty acid receptor 2 (FFAR2), FFAR4, G protein-coupled receptor 84 (GPR84) and a delayed rectifying K+ channel (K+ voltage-gated channel subfamily A member 2; KCNA2)) were measured using RT-PCR; and FAT threshold (FATT) was assessed using three-alternate forced choice methodology. Linear mixed models were fitted, adjusting for correlation between co-twins. Intake was compliant with the study design, with the LF and HF groups consuming 14·8 and 39·9 % energy from fat, respectively. Expression of FFAR4 increased by 38 % in the LF group (P = 0·023; time-diet interaction P = 0·063). ΔFFAR4 (Δ, week 8-baseline) was associated with Δfat intake (g) ( = -159·4; P < 0·001) and ΔFATT ( = -8·8; P = 0·016). In summary, FFAR4 is involved in long-term diet-mediated changes to FAT perception. Manipulating dietary fat intake, and therefore FFAR4 expression, might aid in reducing taste-mediated passive overconsumption of fatty foods.

Lycopene supplementation attenuates western diet-induced body weight gain through increasing the expressions of thermogenic/mitochondrial functional genes and improving insulin resistance in the adipose tissue of obese mice

This passive overconsumption of western diet has precipitated a steep rise in obesity and its comorbidities, and obesity has become one of the main threats to health worldwide. Thus, deciphering the molecular mechanisms leading to obesity is therefore of utmost importance to guide the search for novel therapeutic and preventive strategies. Lycopene (LYC), a major carotenoid present in tomato, has been regarded as a nutraceutical that has powerful anti-oxidant and anti-obesity bioactivities. Even though substantial progress has been made in deciphering the mechanism of how LYC affects obesity in recent years, whether thermogenic genes, mitochondrial function and insulin resistance are involved in the anti-obesity effect of LYC is yet to be elucidated. In the current study, we demonstrated that LYC remarkably suppressed HFFD-elevated mice body weight gain. LYC blocked lipid accumulation in adipose tissue by decreasing the expressions of lipogenesis genes and increasing the expressions of lipidolysis related genes, including thermogenic and mitochondrial functional genes. Moreover, LYC improved HFFD-induced insulin resistance in WATs via inhibiting the inflammation responses in WATs, decreasing circulating proinflammatory cytokines, suppressing gut leak and intestinal inflammation. Our study indicating that the supplementation of LYC might be a nutritional preventive strategy to combat obesity.

Informing a roadmap for cross-sectoral collaboration on portion size management as a national strategy to improve population nutrition - a Delphi study.

SummaryBackgroundAddressing food portion sizes is a key untapped opportunity to help tackle obesity. This study sought to inform the agenda of a national movement involving diverse sectors to manage portion sizes in packaged foods, restaurants, cafeterias and prepared foods in grocery stores.MethodsA Delphi study was conducted with representatives from public health, private‐sector food companies and academia that formed a panel of experts (n = 32). Three iterative rounds of surveys were administered over 3 months. The surveys gathered opinions on psychological mindsets affecting portion size choice, eating habits, portion perception and distortion, passive overconsumption and challenges and advantages of this tool to improve population nutrition. The survey also inquired about visions for a future food environment. After every round, responses were analysed and questions narrowed to reach group consensus on specific items in the subsequent round.ResultsAlthough many experts fear that portion size interventions might be perceived as paternalistic, 91% of respondents agreed stealth interventions were preferable. Seventy‐three per cent of experts believed that the most impactful portion size intervention was product reformulation while smaller packages were the most effective intervention according to only 28% of experts. The majority of the panel (59%) also believed that creating an artificial stopping point in packages was the best strategy to reduce food consumption. Finally, the study found that one of the most complex aspects of establishing a multi‐sector collaboration for obesity prevention was to ascertain trust in the private sector's ability to balance profit versus social responsibility.[Corrections added on 21 March 2019, after first online publication: The percentage of experts who believed that small packages were the most effective intervention has been changed from “16%” to “28%”.]ConclusionThis study informs the agenda of a cross‐sectoral, coordinated movement to tackle obesity through a combination of changing social norms, individual behaviours and industry practices around portion size. Although cross‐sectoral collaboration for non‐communicable disease prevention is encouraged by different organizations, strategic efforts to define a common agenda on portion size have been limited thus far. This research highlights important strategies in portion size interventions and steps needed for the success of such a movement, as part of a wider effort across sectors and stakeholders to halt and reverse obesity rates in the USA.

Homeostatic and non-homeostatic appetite control along the spectrum of physical activity levels: An updated perspective.

The current obesogenic environment promotes physical inactivity and food consumption in excess of energy requirements, two important modifiable risk factors influencing energy balance. Habitual physical activity has been shown to impact not only energy expenditure, but also energy intake through mechanisms of appetite control. This review summarizes recent theory and evidence underpinning the role of physical activity in the homeostatic and non-homeostatic mechanisms controlling appetite. Energy intake along the spectrum of physical activity levels (inactive to highly active) appears to be J-shaped, with low levels of physical activity leading to dysregulated appetite and a mismatch between energy intake and expenditure. At higher levels, habitual physical activity influences homeostatic appetite control in a dual-process action by increasing the drive to eat through greater energy expenditure, but also by enhancing post-meal satiety, allowing energy intake to better match energy expenditure in response to hunger and satiety signals. There is clear presumptive evidence that physical activity energy expenditure can act as a drive (determinant) of energy intake. The influence of physical activity level on non-homeostatic appetite control is less clear, but low levels of physical activity may amplify hedonic states and behavioural traits favouring overconsumption indirectly through increased body fat. More evidence is required to understand the interaction between physical activity, appetite control and diet composition on passive overconsumption and energy balance. Furthermore, potential moderators of appetite control along the spectrum of physical activity, such as body composition, sex, and type, intensity and timing of physical activity, remain to be fully understood.

Impact of physical activity level and dietary fat content on passive overconsumption of energy in non-obese adults

BackgroundPassive overconsumption is the increase in energy intake driven by the high-fat energy-dense food environment. This can be explained in part because dietary fat has a weaker effect on satiation (i.e. process that terminates feeding). Habitually active individuals show improved satiety (i.e. process involved in post-meal suppression of hunger) but any improvement in satiation is unknown. Here we examined whether habitual physical activity mitigates passive overconsumption through enhanced satiation in response to a high-fat meal.MethodsTwenty-one non-obese individuals with high levels of physical activity (HiPA) and 19 individuals with low levels of physical activity (LoPA) matched for body mass index (mean = 22.8 kg/m2) were recruited. Passive overconsumption was assessed by comparing ad libitum energy intake from covertly manipulated high-fat (HFAT; 50% fat) or high-carbohydrate (HCHO; 70% carbohydrate) meals in a randomized crossover design. Habitual physical activity was assessed using SenseWear accelerometers (SWA). Body composition, resting metabolic rate, eating behaviour traits, fasting appetite-related peptides and hedonic food reward were also measured.ResultsIn the whole sample, passive overconsumption was observed with greater energy intake at HFAT compared to HCHO (p < 0.01), without any differences between activity groups (p > 0.05). SWA confirmed that HiPA were more active than LoPA (p < 0.01). HiPA had lower body fat and greater fat-free mass than LoPA (p < 0.05 for both) but did not differ in resting metabolic rate, eating behaviour traits, appetite-related peptides or food reward (p > 0.05 for all).ConclusionsNon-obese individuals with high or low physical activity levels but matched for BMI showed similar susceptibility to passive overconsumption when consuming an ad libitum high-fat compared to a high-carbohydrate meal. This occurred despite increased total daily energy expenditure and improved body composition in HiPA. Greater differences in body composition and/or physical activity levels may be required to impact on satiation.

Mystification and obfuscation in portion sizes in UK food products

Concern has been expressed as to how obesity is framed as an individual responsibility easily solved with common sense. Such research has questioned the appropriateness of a size-based emphasis to public health. Moving away from the emphasis on the individual, this paper critically reviews consumer marketing techniques in the presentation of portion sizes, given what is known about human cognitive and physical limitations around food choice. Through a micro study of portion size in three products, cereals, cereal bars and yogurts, claims are made regarding marketing techniques of obfuscation in portion size presentation that at a macro level link to earlier critiques of marketing mystification. Findings suggest a number of specific obfuscators that could lead to passive overconsumption. The paper concludes that regulators should shift their emphasis away from the individual to examining marketing mystification and techniques of obfuscation. Information presentation should be more appropriate and consistent across brands within a product category.

Salt Promotes Passive Overconsumption of Dietary Fat in Humans

Background: Excess fat consumption has been linked to the development of obesity. Fat and salt are a common and appetitive combination in food; however, the effect of either on food intake is unclear. Fat taste sensitivity has been negatively associated with dietary fat intake, but how fat taste sensitivity influences the intake of fat within a meal has, to our knowledge, not yet been investigated.Objectives: Our objectives were, first, to investigate the effects of both fat and salt on ad libitum food intake and, second, to investigate the effects of fat taste sensitivity on satiation responses to fat and whether this was affected by salt.Methods: Forty-eight healthy adults [16 men and 32 women, aged 18–54 y, body mass index (kg/m2): 17.8–34.4] were recruited and their fat taste sensitivity was measured by determination of the detection threshold of oleic acid (18:1n–6). In a randomized 2 × 2 crossover design, participants attended 4 lunchtime sessions after a standardized breakfast. Meals consisted of elbow macaroni (56%) with sauce (44%); sauces were manipulated to be 1) low-fat (0.02% fat, wt:wt)/low-salt (0.06% NaCl, wt:wt), 2) low-fat/high-salt (0.5% NaCl, wt:wt), 3) high-fat (34% fat, wt:/wt)/low-salt, or 4) high-fat/high-salt. Ad libitum intake (primary outcome) and eating rate, pleasantness, and subjective ratings of hunger and fullness (secondary outcomes) were measured.Results: Salt increased food and energy intakes by 11%, independent of fat concentration (P = 0.022). There was no effect of fat on food intake (P = 0.6), but high-fat meals increased energy intake by 60% (P < 0.001). A sex × fat interaction was found (P = 0.006), with women consuming 15% less by weight of the high-fat meals than the low-fat meals. Fat taste sensitivity was negatively associated with the intake of high-fat meals but only in the presence of low salt (fat taste × salt interaction on delta intake of high-fat − low-fat meals; P = 0.012).Conclusions: The results suggest that salt promotes passive overconsumption of energy in adults and that salt may override fat-mediated satiation in individuals who are sensitive to the taste of fat. This trial was registered at the Australian New Zealand Clinical Trials Registry (www.anzctr.org.au) as ACTRN12615000048583.

The home food environment of overweight gatekeepers in the Netherlands.

The aim of the present study was to gain insight into (i) processed snack-food availability, (ii) processed snack-food salience and (iii) the size of dinnerware among households with overweight gatekeepers. Moreover, associations between gatekeepers' characteristics and in-home observations were determined. A cross-sectional observation of home food environments was conducted as part of a baseline measurement of a larger study. Home food environments of overweight and obese gatekeepers in the Netherlands. Household gatekeepers (n 278). Mean household size of the gatekeepers was 3.0 (SD 1.3) persons. Mean age of the gatekeepers was 45.7 (SD 9.2) years, 34.9% were overweight and 65.1% were obese. Of the gatekeepers, 20.9% had a low level of education and 42.7% had a high level of education. In 70% of the households, eight or more packages of processed snack foods were present. In 54% of the households, processed snack foods were stored close to non-processed food items and in 78% of households close to non-food items. In 33% of the households, processed snack foods were visible in the kitchen and in 15% of the households processed snack foods were visible in the living room. Of the dinnerware items, 14% (plates), 57% (glasses), 78% (dessert bowls), 67% (soup bowls) and 58% (mugs) were larger than the reference norms of the Netherlands Nutrition Centre Foundation. Older gatekeepers used significantly smaller dinnerware than younger gatekeepers. Environmental factors endorsing overconsumption are commonly present in the home environments of overweight people and could lead to unplanned eating or passive overconsumption.

Alcohol, appetite and energy balance: Is alcohol intake a risk factor for obesity?

The increased recognition that the worldwide increase in incidence of obesity is due to a positive energy balance has lead to a focus on lifestyle choices that may contribute to excess energy intake, including the widespread belief that alcohol intake is a significant risk factor for development of obesity. This brief review examines this issue by contrasting short-term laboratory-based studies of the effects of alcohol on appetite and energy balance and longer-term epidemiological data exploring the relationship between alcohol intake and body weight. Current research clearly shows that energy consumed as alcohol is additive to that from other dietary sources, leading to short-term passive over-consumption of energy when alcohol is consumed. Indeed, alcohol consumed before or with meals tends to increase food intake, probably through enhancing the short-term rewarding effects of food. However, while these data might suggest that alcohol is a risk factor for obesity, epidemiological data suggests that moderate alcohol intake may protect against obesity, particularly in women. In contrast, higher intakes of alcohol in the absence of alcohol dependence may increase the risk of obesity, as may binge-drinking, however these effects may be secondary to personality and habitual beverage preferences.

Targeting abdominal obesity and the metabolic syndrome to manage cardiovascular disease risk

Almost every week there is an article published in a major national newspaper on the epidemic proportions reached by obesity in various countries. The pathophysiology of obesity is complex and...

Early life exposure to a high fat diet promotes long-term changes in dietary preferences and central reward signaling

Overweight and obesity in the United States continues to grow at epidemic rates in large part due to the overconsumption of calorically-dense palatable foods. Identification of factors influencing long-term macronutrient preferences may elucidate points of prevention and behavioral modification. In our current study, we examined the adult macronutrient preferences of mice acutely exposed to a high fat diet during the third postnatal week. We hypothesized that the consumption of a high fat diet during early life would alter the programming of central pathways important in adult dietary preferences. As adults, the early-exposed mice displayed a significant preference for a diet high in fat compared to controls. This effect was not due to diet familiarity as mice exposed to a novel high carbohydrate diet during this same early period failed to show differences in macronutrient preferences as adults. The increased intake of high fat diet in early exposed mice was specific to dietary preferences as no changes were detected for total caloric intake or caloric efficiency. Mechanistically, mice exposed to a high fat diet during early life exhibited significant alterations in biochemical markers of dopamine signaling in the nucleus accumbens, including changes in levels of phospho–dopamine and cyclic AMP-regulated phosphoprotein, molecular weight 32 kDa (DARPP-32) threonine-75, ΔFosB, and cyclin-dependent kinase 5. These results support our hypothesis that even brief early life exposure to calorically-dense palatable diets alters long-term programming of central mechanisms important in dietary preferences and reward. These changes may underlie the passive overconsumption of high fat foods contributing to the increasing body mass in the western world.

Support for Benefit of Physical Activity on Satiety, Weight Control, and Diabetes Risk

Dear Editor: Several recent articles in the Journal 1-3 examined different, complementary facets of the relationship between physical activity, dietary choices, obesity risk and risk of diabetes mellitus. We believe that taken together, the articles provide important support for the importance of regular exercise as a short-term influence on satiety and long-term influence on diabetes risk. Tinker and her associates 1 concluded that three randomized controlled diabetes prevention trials reduced diabetes risk whereas the Womens Health Initiative-DMT did not, in part because the three previous trials had included physical activity in the lifestyle intervention wherease the WHT-DMT did not. Why should increasing physical activity make such a difference in the impact of dietary modification on risk of diabetes? One reason is that increased physical activity appears to improve the healthfulness of food preferences, thereby reducing passive overconsumption of energy.4 This is evidenced by the dose-response pattern observed by Palmer and her associates 2 between an increasing proportion of study participants reporting at least 1 hour per week of physical activity and decreasing consumption of sugar-sweetened soda beverages (goodness of fit chi square(2) = 205.4, p < .0001). Total beverage intake usually increases with increasing physical activity; it is therefore striking to see average sugar-sweetened soda beverage consumption actually decrease with increasing proportion of study participants reporting physical activity. Previous research has demonstrated that long bouts of aerobic physical activity increase the perceived sweetness of beverages.4 If we assume that commercial soda beverages have a sweetness optimized for a sedentary population, it is then likely that heavy exercisers will dislike these commercial beverages because of their perceived excessive sweetness. Harding and her associates 3 furthermore reported a dose-response relationship between an increasing proportion of subjects who were physically active and quintile of plasma vitamin C concentration. Plasma vitamin C is a useful biomarker for fruit and vegetable intake because 90% of vitamin C intake derives from fruit and vegetable intake. The intake of minimally processed fruit and vegetables, in turn, is becoming recognized as a sustainable way of increasing satiety with fewer calories,5 thereby leading to the kind of sustained weight loss that should, in turn, reduce risk of diabetes. Intervention trials are needed to confirm the nature and quantity of physical activity needed to motivate adherence to the healthier, high-satiety food choices that these articles have demonstrated can protect healthy adults from lifetime risk of diabetes.

Hidden Fat Facilitates Passive Overconsumption

Food intake regulation may be disturbed when sensory signals from foods are disconnected from their metabolic properties. Consumption of high-fat, energy-dense foods may stimulate passive overconsumption, because these foods do not provide sensory signals in accordance with the actual nutrient content. We examined the effects of perception of fat on energy intake in adults after overfeeding (Study 1) and on energy intake during a meal (Study 2). In study 1, 57 participants consumed 6 mandatory lunches differing in energy level (100, 200, and 300% of a standard lunch intake) and fat condition (visible fat and hidden fat). Ad libitum energy intake was measured during subsequent meals. In Study 2, 51 participants consumed 2 lunches that were high in visible or hidden fats. We measured ad libitum energy intake during lunch. In Study 1, the energy intake at dinner was 8% higher in the hidden fat condition than in the visible fat condition (P = 0.0046). A main effect was also found for the energy level of the lunch (P < 0.0001), with the highest intake following the 100% energy level and the lowest intake following the 300% energy level. In Study 2, the energy intake was 9% higher in the hidden fat condition than in the visible fat condition (P = 0.013). Perception of fat influences energy intake. In the presence of visible fats, energy intake was lower than in the presence of hidden fats, suggesting that hidden fats may contribute to overconsumption. Appropriate sensory signals may be important in preventing overconsumption.

Appetite-Related Gut Peptides in Obesity and Binge Eating Disorder.

The worldwide increase in obesity prevalence is a result of positive energy balance, with energy intake exceeding expenditure. The eating behavior in obesity ranges from mild passive overconsumption to excessive overeating with loss of control observed in binge eating disorder (BED). The signaling systems that underlie appetite control in BED are complex and, at this point, not well understood. The present review highlights the current knowledge of key components of the gut peptide system and examines evidence of defects in signaling that differentiate obese binge eaters from obese non-binge eaters. The signaling network underlying hunger, satiety, and metabolic status includes leptin and insulin from energy stores and cholecystokinin, glucagon-like peptide-1, peptide YY(3-36), and ghrelin from the gastrointestinal tract. Of the many gastrointestinal peptides, ghrelin is the only established appetite-stimulating one, whereas cholecystokinin, glucagon-like peptide-1, and peptide YY(3-36) promote satiety. Adipose tissue provides hormonal signals via leptin and insulin to the brain about energy stores and likely from adiponectin and resistin. Binge eating has been related to a dysfunction in the ghrelin signaling system. Moreover, the larger gastric capacity observed in BED may further reduce satiety signals and contribute to overeating.