Highly Palatable Food Research Articles

An Overview of Livestock Role in Ensuring Food and Nutrition Security: The Case of Ethiopia

This review aimed to deliver and document summarized information on the contribution of livestock to food and nutrition security, both generally and specifically in the case of Ethiopia. Livestock have made both positive and negative contributions to food and nutrition security. Positively, they provide high biological value, palatable, and nutrient-dense food sources such as milk, meat, and eggs for human consumption. They also offer quick income, employment, source of fuel, social functions, raw materials for industry (hide and skin…. etc.), input for soil fertility (manure) and draft power, indirectly contributing to stable food cultivation. However, livestock also pose negative impacts on food and nutrition supply by competing with humans for grains, utilizing fodder crop lands, emitting greenhouse gases, and transmitting zoonotic diseases to humans. In Ethiopia, trends in livestock populations and food production levels reveal disparities between actual consumption and productivity compared to available resources. Energy, protein, and fat supply from the livestock sector has increased from 2010 to 2021. Yet, the country's per capita consumption of dairy, meat, and eggs remains below global averages, exacerbating undernutrition, particularly in rural areas. Livestock products are rich in high-quality protein and essential micronutrients crucial for growth and development, especially in children and infants. Enhancing nutritional outcomes in Ethiopia necessitates addressing barriers to livestock output and promoting the consumption of livestock-derived foods. Tackling underlying issues impeding livestock productivity is equally vital as efforts to enhance productivity and ensure access to livestock-based foods.

Repeated binge-like eating episodes in female rats alter adenosine A2A and dopamine D2 receptor genes regulation in the brain reward system.

Binge-eating disorder is an eating disorder characterized by recurrent binge-eating episodes, during which individuals consume excessive amounts of highly palatable food (HPF) in a short time. This study investigates the intricate relationship between repeated binge-eating episode and the transcriptional regulation of two key genes, adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R), in selected brain regions of rats. Binge-like eating behavior on HPF was induced through the combination of food restrictions and frustration stress (15 min exposure to HPF without access to it) in female rats, compared to control rats subjected to only restriction or only stress or none of these two conditions. After chronic binge-eating episodes, nucleic acids were extracted from different brain regions, and gene expression levels were assessed through real-time quantitative PCR. The methylation pattern on genes' promoters was investigated using pyrosequencing. The analysis revealed A2AAR upregulation in the amygdala and in the ventral tegmental area (VTA), and D2R downregulation in the nucleus accumbens in binge-eating rats. Concurrently, site-specific DNA methylation alterations at gene promoters were identified in the VTA for A2AAR and in the amygdala and caudate putamen for D2R. The alterations on A2AAR and D2R genes regulation highlight the significance of epigenetic mechanisms in the etiology of binge-eating behavior, and underscore the potential for targeted therapeutic interventions, to prevent the development of this maladaptive feeding behavior. These findings provide valuable insights for future research in the field of eating disorders. Using an animal model with face, construct, and predictive validity, in which cycles of food restriction and frustration stress evoke binge-eating behavior, we highlight the significance of epigenetic mechanisms on adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R) genes regulation. They could represent new potential targets for the pharmacological management of eating disorders characterized by this maladaptive feeding behavior.

Blunted orosensory perception of lipids during obesity: myth or reality?

Obesity is now considered as a disease requiring treatment and prevention efforts by reason of severe associated co-morbidities and its growing prevalence in worldwide population. Although origin of this “epidemic” situation is clearly multifactorial, recent changes in our life-style especially about our food supply with an easy access to low-cost energy-dense foods seem to play a significant causal role in this phenomenon. Studies also report that obesity is frequently associated with a preferential consumption of high palatable foods rich in fat and sugar. Since these foods are pleasant and have high hedonic quality, this obesogenic eating behavior change raises the possibility of an alteration of orosensory perception system as a consequence of obesity. This hypothesis has led to a recent literature on the relationship between obesity and sensory sensitivity, known to play a significant role in the food choice. The purpose of this mini-review, focused on the orosensory perception of dietary lipids (i.e. taste of fat), is to provide a short overview of what is observed in food-induced obese rodents as compared to what is found in patients with obesity. It tries to answer to the following basic question: is obesity associated with a loss of orosensory sensitivity to dietary lipids that leads to obesogenic food choices?

Free-choice high-fat diet consumption reduces lateral hypothalamic GABAergic activity, without disturbing neural response to sucrose drinking in mice.

Nutrition can influence the brain and affect its regulation of food intake, especially that of high-palatable foods. We hypothesize that fat and sugar have interacting effects on the brain, and the lateral hypothalamus (LH) is a prime candidate to be involved in this interaction. The LH is a heterogeneous area, crucial for regulating consummatory behaviors, and integrating homeostatic and hedonic needs. GABAergic LH neurons stimulate feeding when activated, and are responsive to consummatory behavior while encoding sucrose palatability. Previously, we have shown that glutamatergic LH neurons reduce their activity in response to sugar drinking and that this response is disturbed by a free-choice high-fat diet (fcHFD). Whether GABAergic LH neurons, and their response to sugar, is affected by a fcHFD is yet unknown. Using head-fixed two-photon microscopy, we analyzed activity changes in LHVgat neuronal activity in chow or fcHFD-fed mice in response to water or sucrose drinking. A fcHFD decreased overall LHVgat neuronal activity, without disrupting the sucrose-induced increase. When focusing on the response per unique neuron, a vast majority of neurons respond inconsistently over time. Thus, a fcHFD dampens overall LH GABAergic activity, while it does not disturb the response to sucrose. The inconsistent responding over time suggests that it is not one specific subpopulation of LH GABAergic neurons that is driving these behaviors, but rather a result of the integrative properties of a complex neural network. Further research should focus on determining how this dampening of LH GABAergic activity contributes to hyperphagia and the development of obesity.

Chronic Exposure to High Fat Diet Affects the Synaptic Transmission That Regulates the Dopamine Release in the Nucleus Accumbens of Adolescent Male Rats

Obesity is a pandemic caused by many factors, including a chronic excess in hypercaloric and high-palatable food intake. In addition, the global prevalence of obesity has increased in all age categories, such as children, adolescents, and adults. However, at the neurobiological level, how neural circuits regulate the hedonic consumption of food intake and how the reward circuit is modified under hypercaloric diet consumption are still being unraveled. We aimed to determine the molecular and functional changes of dopaminergic and glutamatergic modulation of nucleus accumbens (NAcc) in male rats exposed to chronic consumption of a high-fat diet (HFD). Male Sprague-Dawley rats were fed a chow diet or HFD from postnatal day (PND) 21 to 62, increasing obesity markers. In addition, in HFD rats, the frequency but not amplitude of the spontaneous excitatory postsynaptic current is increased in NAcc medium spiny neurons (MSNs). Moreover, only MSNs expressing dopamine (DA) receptor type 2 (D2) increase the amplitude and glutamate release in response to amphetamine, downregulating the indirect pathway. Furthermore, NAcc gene expression of inflammasome components is increased by chronic exposure to HFD. At the neurochemical level, DOPAC content and tonic dopamine (DA) release are reduced in NAcc, while phasic DA release is increased in HFD-fed rats. In conclusion, our model of childhood and adolescent obesity functionally affects the NAcc, a brain nucleus involved in the hedonic control of feeding, which might trigger addictive-like behaviors for obesogenic foods and, through positive feedback, maintain the obese phenotype.

Maternal Over- and Malnutrition and Increased Risk for Addictive and Eating Disorders in the Offspring

Evidence from human and animal studies has shown that maternal overnutrition and/or obesity are linked with neurobehavioral changes in the offspring. This fetal programming is characterized by adaptive responses to changes in the nutritional state during early life. In the past decade, an association has been made between overconsumption of highly-palatable food by the mother during fetal development and abnormal behaviors resembling addiction in the offspring. Maternal overnutrition can lead to alterations in the offspring's brain reward circuitry leading to hyperresponsiveness of this circuit following exposure to calorie-dense foods later in life. Given the accumulating evidence indicating that the central nervous system plays a pivotal role in regulating food intake, energy balance, and the motivation to seek food, a dysfunction in the reward circuitry may contribute to the addiction-like behaviors observed in the offspring. However, the underlying mechanisms leading to these alterations in the reward circuitry during fetal development and their relevance to the increased risk for the offspring to later develop addictive-like behaviors is still unclear. Here, we review the most relevant scientific reports about the impact of food overconsumption during fetal development and its effect on addictive-like behaviors of the offspring in the context of eating disorders and obesity.

Why are predator cues in the field not more evocative? A ‘real world’ assay elicits subtle, but meaningful, responses by wild rodents to predator scents

Mismatches between highly-standardized laboratory predatory assays and more realistic environmental conditions may lead to different outcomes. Understanding rodents’ natural responses to predator scents is important. Thus, field studies on the same and related species are essential to corroborate laboratory findings to better understand the contexts and motivational drives that affect laboratory responses to predator scents. However, there are too few field assays to enable researchers to study factors that influence these responses in genetically variable populations of wild rodents. Therefore, we placed laboratory-style chambers and remote-sensing devices near multiple colonies of two species of wild mice (Apodemus agrarius and Apodemus flavicollis) to test dual-motivational drives (appetitive and aversive) in a ‘familiar’, yet natural environment. A highly-palatable food reward was offered daily alongside scents from coyotes, lions, rabbits, and both wet and dry controls. In all but two instances (n = 264), animals entered chambers and remained inside for several minutes. Animals initiated flight twice, but they never froze. Rather, they visited chambers more often and stayed inside longer when predatory scents were deployed. The total time spent inside was highest for lion urine (380% longer than the dry control), followed by coyote scent (75% longer), dry control and lastly, herbivore scents (no difference). Once inside the chamber, animals spent more time physically interacting with predatory scents than the herbivore scent or controls. Our findings support the common assumption that rodents fail to respond as overtly to predatory scents in the field compared to what has been observed in the laboratory, possibly due to their varying motivational levels to obtain food. More time spent interacting with scents in the field was likely a function of ‘predator inspection’ (risk assessment) once subjects were in a presumed safe enclosure. We conclude this sort of chamber assay can be useful in understanding the contexts and motivational drives inherent to field studies, and may help interpret laboratory results. Our results also suggest more attention should be given to subtle behaviors such as scent inspection in order to better understand how, and when, environmental stimuli evoke fear in rodents.

More complex than you might think: Neural representations of food reward value in obesity

Obesity reached pandemic proportions and weight-loss treatments are mostly ineffective.The level of brain activity in the reward circuitry is proposed to be proportionate to the reward value of food stimuli, and stronger in people with obesity. However, empirical evidence is inconsistent. This may be due to the double-sided nature of high caloric palatable foods: at once highly palatable and high in calories (unhealthy).This study hypothesizes that, viewing high caloric palatable foods, a hedonic attentional focus compared to a health and a neutral attentional focus elicits more activity in reward-related brain regions, mostly in people with obesity. Moreover, caloric content and food palatability can be decoded from multivoxel patterns of activity most accurately in people with obesity and in the corresponding attentional focus.During one fMRI-session, attentional focus (hedonic, health, neutral) was manipulated using a one-back task with individually tailored food stimuli in 32 healthy-weight people and 29 people with obesity. Univariate analyses (p < 0.05, FWE-corrected) showed that brain activity was not different for palatable vs. unpalatable foods, nor for high vs. low caloric foods. Instead, this was higher in the hedonic compared to the health and neutral attentional focus. Multivariate analyses (MVPA) (p < 0.05, FDR-corrected) showed that palatability and caloric content could be decoded above chance level, independently of either BMI or attentional focus.Thus, brain activity to visual food stimuli is neither proportionate to the reward value (palatability and/or caloric content), nor significantly moderated by BMI. Instead, it depends on people's attentional focus, and may reflect motivational salience. Furthermore, food palatability and caloric content are represented as patterns of brain activity, independently of BMI and attentional focus. So, food reward value is reflected in patterns, not levels, of brain activity.

High Endocannabinoid Tone In LFABP -/- Mice Drives Fat Intake and Preference

Abstract Objectives Our objective was to understand if LFABP -/- mice display a higher preference for a high fat, high palatable food over Wild-type (WT) mice and if this preference is due to alteration of oral fatty acid detection thresholds by endocannabinoids. Methods For the first experiment, 6 mice (3 WT and 3 LFABP -/-) were given access to a high-fat cake frosting (Crisco/sugar mixture) for 5 minutes and frosting intake was recorded. This was done at the same time each day and repeated 3 times. For the second experiment, we conducted a 24-hour 2 bottle preference test of a control versus stearic acid solution in 5 WT and 5 LFABP -/- mice. The 2 bottles were switched at 12 hours to minimize side-preference. Preference was defined as the percentage of intake of fatty acid solution over total intake. Results Our preliminary results showed that 1) the LFABP KO mice consumed more high-fat frosting during a brief access test and 2) the WT mice significantly preferred the control over the stearic acid solution, whereas the LFABP -/- mice showed no difference in preference between the two bottles. Conclusions These results suggest that elevated endocannabinoid tone contributes to preference for frosting, in part, by modulating oral fatty acid detection thresholds. Changes in oral detection thresholds of taste stimuli are known to affect consumption of the stimuli; the present data support this idea for ‘fat-taste’ as well. This has important implications for the overconsumption of highly palatable food in our society. Funding Sources This research was supported by NIH NIDCD R01 014286 to PASB Co-PI, USDA NJ Hatch NJ14120 to PASB and NIH NIDDK R01 38389 and USDA NJ Hatch NJ14115 to JS.

Orexin-A/Hypocretin-1 Controls the VTA-NAc Mesolimbic Pathway via Endocannabinoid-Mediated Disinhibition of Dopaminergic Neurons in Obese Mice

Disinhibition of orexin-A/hypocretin-1 (OX-A) release occurs to several output areas of the lateral hypothalamus (LH) in the brain of leptin knockout obese ob/ob mice. In this study, we have investigated whether a similar increase of OX-A release occurs to the ventral tegmental area (VTA), an orexinergic LH output area with functional effects on dopaminergic signaling at the mesolimbic circuit. By confocal and correlative light and electron microscopy (CLEM) morphological studies coupled to molecular, biochemical, and pharmacological approaches, we investigated OX-A-mediated dopaminergic signaling at the LH-VTA-nucleus accumbens (NAc) pathway in obese ob/ob mice compared to wild-type (wt) lean littermates. We found an elevation of OX-A trafficking and release to the VTA of ob/ob mice and consequent orexin receptor-1 (OX1R)-mediated over-activation of dopaminergic (DA) neurons via phospholipase C (PLC)/diacylglycerol lipase (DAGL-α)-induced biosynthesis of the endocannabinoid 2-arachidonoylglycerol (2-AG). In fact, by retrograde signaling to cannabinoid receptor type 1 (CB1R) at inhibitory inputs to DA neurons, 2-AG inhibited GABA release thus inducing an increase in DA concentration in the VTA and NAc of ob/ob mice. This effect was prevented by the OX1R antagonist SB-334867 (30 mg/Kg, i.p.), or the CB1R antagonist AM251 (10 mg/Kg, i.p.) and mimicked by OX-A injection (40 μg/Kg, i.p.) in wt lean mice. Enhanced DA signaling to the NAc in ob/ob mice, or in OX-A-injected wt mice, was accompanied by β-arrestin2-mediated desensitization of dopamine D2 receptor (D2R) in a manner prevented by SB-334867 or the D2R antagonist L741 (1.5 mg/Kg, i.p.). These results further support the role of OX-A signaling in the control of neuroadaptive responses, such as compulsive reward-seeking behavior or binge-like consumption of high palatable food, and suggest that aberrant OX-A trafficking to the DA neurons in the VTA of ob/ob mice influences the D2R response at NAc, a main target area of the mesolimbic pathway, via 2-AG/CB1-mediated retrograde signaling.

Glutamatergic projections from homeostatic to hedonic brain nuclei regulate intake of highly palatable food

Food intake is a complex behavior regulated by discrete brain nuclei that integrate homeostatic nutritional requirements with the hedonic properties of food. Homeostatic feeding (i.e. titration of caloric intake), is typically associated with hypothalamic brain nuclei, including the paraventricular nucleus of the hypothalamus (PVN). Hedonic feeding is driven, in part, by the reinforcing properties of highly palatable food (HPF), which is mediated by the nucleus accumbens (NAc). Dysregulation of homeostatic and hedonic brain nuclei can lead to pathological feeding behaviors, namely overconsumption of highly palatable food (HPF), that may drive obesity. Both homeostatic and hedonic mechanisms of food intake have been attributed to several brain regions, but the integration of homeostatic and hedonic signaling to drive food intake is less clear, therefore we aimed to identify the neuroanatomical, functional, and behavioral features of a novel PVN → NAc circuit. Using viral tracing techniques, we determined that PVN → NAc has origins in the parvocellular PVN, and that PVN → NAc neurons express VGLUT1, a marker of glutamatergic signaling. Next, we pharmacogenetically stimulated PVN → NAc neurons and quantified both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc and observed a robust and significant increase in extracellular glutamate and phospho-cFos expression. Finally, we pharmacogenetically stimulated PVN → NAc which decreased intake of highly palatable food, demonstrating that this glutamatergic circuitry regulates aspects of feeding.

The Melanocortin System behind the Dysfunctional Eating Behaviors.

The dysfunction of melanocortin signaling has been associated with obesity, given the important role in the regulation of energy homeostasis, food intake, satiety and body weight. In the hypothalamus, the melanocortin-3 receptor (MC3R) and melanocortin-4 receptor (MC4R) contribute to the stability of these processes, but MC3R and MC4R are also localized in the mesolimbic dopamine system, the region that responds to the reinforcing properties of highly palatable food (HPF) and where these two receptors seem to affect food reward and motivation. Loss of function of the MC4R, resulting from genetic mutations, leads to overeating in humans, but to date, a clear understanding of the underlying mechanisms and behaviors that promote overconsumption of caloric foods remains unknown. Moreover, the MC4R demonstrated to be a crucial modulator of the stress response, factor that is known to be strictly related to binge eating behavior. In this review, we will explore the preclinical and clinical studies, and the controversies regarding the involvement of melanocortin system in altered eating patterns, especially binge eating behavior, food reward and motivation.

Go/no-go for food: Attention bias and intention to eat unhealthy food

ObjectiveThe current research evaluated whether Go/No-go training for highly palatable (HP) food affected attention bias for HP food (an automatic/implicit outcome) and intention to eat unhealthy food (a controlled/explicit outcome). MethodA sample of Australian adults representative for age, gender and Body Mass Index (BMI) (N = 561, Mage = 46.31 years, SD = 16.75, 52.3% women, MBMI = 27.11, SD = 6.34) completed self-report measures of dietary psychological constructs and food image modified Stroop tasks as measures of pre- and post-test attention bias for HP food. After random assignment of participants to two conditions, a Go/No-go intervention was used to train HP food targeted inhibitory control in the experimental group, or general inhibitory control in the control group. All research tasks were delivered online. ResultsThe experimental, HP food inhibitory control training group reported intention to eat less unhealthy food than the control group, F (1, 637) = 4.81, R2 = 0.09, p = .029. Counter to expectations, the experimental group exhibited a heightened attention bias to HP food images after the training, F (1, 637) = 9.48, R2 = 0.39, p = .002. ConclusionGo/No-go training for food may improve both top-down and bottom-up inhibitory control, using both automatic and controlled processes. Further, it may not be effective in lowering attention bias for HP food, but may be effective in lowering unhealthy food intake despite raising attention bias for HP food. Further research that tests these effects using varied reaction time tasks is needed to confirm these results and to explore possible alternative explanations.

Nutritious or Delicious?

Unhealthy eating habits involving the consumption of highly-palatable energy-dense foods are a major contributor to weight gain its associated health conditions. Consumption of these “unhealthy” items continues to be common despite ongoing efforts for promoting healthy-eating behavior. However, relatively little is known about the factors that lead to the consumption of unhealthy foods. Prior research has shown that states of hunger influence the desire to eat without changing the perception or enjoyment of food items. The present study utilized an online-survey which asked participants to rate foods according to the items’ palatability, likelihood of being consumed, and healthiness. Demographic and bodily state information was also collected. The results of this study demonstrate that, in college students, a state of hunger biases the selection (“wanting”) of foods toward highly-palatable (“tasty”) food items. However, this finding was not observed in data gathered from a sample of older adults affiliated with a health and fitness organization. Collectively, this may suggest that age, education, or increased health-awareness can influence the preference for high-palatable foods that occurs when individuals are hungry.&#x0D;

Food craving, cortisol and ghrelin responses in modeling highly palatable snack intake in the laboratory

Overeating of highly palatable (HP) foods in the ubiquitous HP food cue environment and under stress is associated with weight gain and contributes to the global obesity epidemic. However, subjective and biobehavioral processes that may increase HP overeating are not clear. Using a novel experimental approach, we examined HP food motivation and intake and neuroendocrine responses in the context of food cues, stress and a control neutral relaxing cue exposure in healthy individuals. Methods: Twenty individuals (12 M; 8F; ages 18–45) with body mass index (BMI) in the lean (LN: N = 8; 3/8 female BMI: 18–24.9) or overweight/obese (OW: N = 12; 5/12 female; BMI: 25–37) range were enrolled in a controlled, hospital-based, 3-day laboratory experiment. On each day, subjects were exposed to a brief 5-min individualized guided imagery of stress, food cue or an active neutral-relaxing control cue script, followed by a food snack test (FST), with one imagery condition per day and order of imagery exposure randomized and counterbalanced across subjects. Subjective HP food craving and caloric intake, anxiety, cortisol and total ghrelin was assessed repeatedly during each test day. Results: Significant condition and condition × group effects for food craving, anxiety and HP calorie intake were observed, with food cue relative to neutral condition increasing HP food craving and intake across all subjects (p < .001), but stress relative to neutral condition increased HP food craving and intake in the OW but not LN group (p < .01). Pre-snack increases in food craving after exposure to food cues and to stress predicted greater subsequent HP food intake (p's < 0.01). Furthermore, ghrelin increased in the food cue and stress conditions (p < .01), but stress-induced increases in ghrelin was associated with HP food intake only in the OW/OB condition (p < .01). Finally, cortisol increased during food cue exposure and increased cortisol responses were associated with greater HP food caving and with intake (p's < 0.05). Conclusions: These findings, while preliminary, validate a laboratory model of HP food motivation and intake and identify specific subjective and neuroendocrine responses that may play a role in HP snacking with implications for weight gain and obesity risk. (342 words).

VIPergic neurons of the infralimbic and prelimbic cortices control palatable food intake through separate cognitive pathways.

The prefrontal cortex controls food reward seeking and ingestion, playing important roles in directing attention, regulating motivation towards reward pursuit, and the assignment of reward salience and value. The cell types that mediate these behavioral functions, however, are not well described. We report here that optogenetic activation of vasoactive peptide expressing (VIP) interneurons in both the infralimbic (IL) and prelimbic (PL) divisions of the medial prefrontal cortex in mice is sufficient to reduce acute, binge-like intake of high calorie palatable food in the absence of any effect on low calorie rodent chow intake in the sated animal. In addition, we discovered that the behavioral mechanisms associated with these changes in feeding differed between animals that underwent either IL or PL VIPergic stimulation. While IL VIP neurons showed the ability to reduce palatable food intake, this effect was dependent upon the novelty and relative value of the food source. In addition, IL VIP neuron activation significantly reduced novel object- and novel social investigative behavior. Activation of PL VIP neurons, however, produced a reduction in high calorie palatable food intake that was independent of food novelty. Neither IL nor PL VIP excitation changed motivation to obtain food reward. Our data show how neurochemically-defined populations of cortical interneurons can regulate specific aspects of food reward-driven behavior, resulting in a selective reduction in intake of highly valued food.

Baseline and postprandial concentrations of cortisol and ghrelin in companion dogs with chronic stress-related behavioural problems: A preliminary study

Ghrelin has been proposed as an essential element regulating the stress response in both humans and rodents. The aim of this work was to study the relation between cortisol and ghrelin in companion dogs showing chronic stress-related behaviour problems and the effect of the administration of high energy palatable food on these hormones. Baseline and post-prandial serum concentrations of both hormones were analyzed in a group of stressed companion dogs (n = 16) showing social conflict-related aggression (SCA, n = 10) or separation anxiety (SA, n = 6), and in a group of non-stressed control companion dogs (n = 16). Significant differences (p < 0.05) between groups emerged for post-prandial levels, with SCA dogs showing higher cortisol than the control group. The change in cortisol levels (%) after eating in this group was positive, differing from the SA and control groups, which decreased their cortisol after food consumption. Ghrelin also decreased significantly in SA dogs after eating. Taking together, these findings suggest that a parallel meal-induced decrease in both cortisol and ghrelin occurred in the SA group, but not in the SCA group, pointing towards a failure to suppress ghrelin (and cortisol) after intake in the latter. Thus, even though SCA and SA were considered chronic stress-related behaviour problems, their different nature may affect animals in their stress response to the administration of palatable food. The possible alleviatory effect of food consumption, particularly “comfort foods”, after the owner is back home in SA dogs, as well as the changes in dogs’ eating behaviour in response to emotional states or stress (“emotional eating”) will require further studies.

Correlates of Sugar Consumption Among High School Students and Faculty

The majority of Americans are overweight or obese, putting them at increased risk for high blood pressure, stroke, heart disease, type 2 diabetes, cancer, and other adverse outcomes. Multiple factors contribute to this trend, including the increased availability and portion size of Highly Palatable Food (HPF), which is defined by the combination of sugar, fat, and/or salt. Food addiction theory describes a cycle of ingesting sugary food, followed by insulin and dopamine responses that lead to increased cravings for HPF. With repeated exposure to HPF, some individuals become chronic over-consumers with a strong drive for this type of reward-based eating. This study sought to characterize the relationships between Reward-based Eating Drive (RED), consumption of HPF, cravings for sugary beverages, and knowledge of sugar’s effects on the brain and body in male and female high school students and faculty. Survey questions were uploaded to Surveymonkey and a link to the survey was sent to the listservs for all individuals with an email account at the high school. 176 anonymous responses were received. The results showed that reward-based eating drive was related to consumption and to cravings. For females, knowledge of sugar’s effects was significantly and inversely associated with consumption of sugary food. This finding suggests that public health interventions to increase knowledge of sugar’s adverse effects may be an avenue to decreasing consumption of HPF, ultimately decreasing the proportion of overweight and obese individuals, especially in young women.

What Children Eat in Developing Countries: Diet in the Etiology of Undernutrition?

We live in a world of paradoxes: one half of the world is overweight or obese with abundant access to food and the other half undernourished due to poor food access. It has been estimated that nearly 36% of children in Asia are stunted. Worldwide, approximately 1 in 4 children under the age of 5 years shows stunted growth, making the number of stunted children to 155 million; 52 million children under 5 years are wasted, of which 17 million are severely wasted. Given the wide-scale nature of global malnutrition and its long-term consequences, why has this scar in our consciousness not being addressed systematically? The Asian enigma underscores the observation that unlike other regions of the world, economic growth does not appear to keep pace with the eradication of undernutrition. Exclusive breastfeeding is capable of maintaining adequate growth in infants in the first 3-6 months of life. Human breast milk contains the lowest protein content than any other homoeothermic animal. Despite the very low protein content of the breast milk, the protein content is sufficient for adequate infant growth. Protein deficiency is, therefore, not the cause of undernutrition in children. Most weaning foods in developing countries are of very low energy density, high viscosity, and poor palatability. This paper suggests that it is the poor energy density of weaning food that is in part responsible for the stunting and wasting pandemic seen in developing countries. Using the concept of developing ready-to-use therapeutic food, the paper proposes an urgent need to develop high energy, low viscosity, and palatable foods. Processed foods at the village community level or on a large scale will remain one of the solutions to produce palatable and energy-dense foods. Without this intervention, our world will continue to see the ravage of malnutrition which plagues our conscience.

Do Obese Bacteria Make us “Want them”? Intestinal Microbiota, Mesocorticolimbic Circuit and Non-Homeostatic Feeding

Highly palatable foods (HPF) have rewarding effects, and their consumption induces gut dysbiosis. Because intestinal microbes communicate bidirectionally with the brain, we reviewed the literature in order to link the effects of HPF on the brain reward system and on gut microbiota. Additionally, we propose these alterations contribute to the pathophysiology of obesity. Non-homeostatic consumption of HPF programs the brain to seek these foods from early-life. Fatty food induces gut dysbiosis, which might alter communications to the brain. Additionally, prebiotic fibre and short-chain fatty acids affect the neurochemistry of the rodent mesocorticolimbic circuit. Consumption of HPF might start a vicious cycle by (1) activating the mesocorticolimbic circuit, leading to (2) non-homeostatic feeding, affecting the host’s metabolism and (3) altering gut microbes. The latter might impact the brain’s reward system, which becomes reinforced by signals from gut symbionts, thus contributing to the pathophysiology of obesity.