Caloric Deprivation Research Articles

Integrative Review of Dietary Choice Revealed by fMRI: Considerations for Obesity Prevention and Weight-Loss Education.

Emerging findings from neuroimaging studies investigating brain activity associated with dietary behavior are illuminating the interaction of biological and behavioral mechanisms that have implications for obesity prevention. Globally, A total of 1.9 billion adults are overweight, and 650 million are obese. Obesity and being overweight are major risk factors for chronic illness and death. Behaviorally based health interventions have had limited success in curbing the obesity epidemic. Greater understanding of brain responses to food cues will contribute to new knowledge and shape public health efforts in obesity prevention. However, an integration of this knowledge for obesity prevention education has not been published. This study links evidence generated from brain activation studies generated in response to diet and food images and highlights educational recommendations for nurses engaged in obesity prevention and weight-loss education. An integrative review of the literature was conducted using the MeSH keywords "magnetic resonance imaging," "diet," and "food images" in PubMed, MEDLINE Complete, CINAHL, and Cochrane databases from their first appearance in 2006 through March 2018. Studies published in English and using functional magnetic resonance imaging to measure brain response to diet, and food images were initially identified. Animal models, those whose primary focus was a specific disease, and intervention studies were excluded. Of 159 studies identified, 26 met inclusion criteria. Findings from neuroimaging studies may help explain the relationship between brain mechanisms and behavioral aspects of dietary choice and inform patient education in obesity prevention. Awareness of this evidence is applicable to nursing education efforts. This review contributes several recommendations that should be considered by nurses providing individualized weight-loss education. Nurses engaged in patient education for obesity prevention should consider personalized interventions that cultivate internal awareness for dietary adherence, self-care, exercise, hydration, and mood state; avoid using caloric deprivation approaches, such as skipping breakfast, for weight-loss interventions; and note the importance of individualized obesity prevention and weight-loss education.

Nutritional status, poverty, and relative deprivation among socio-economic and gender groups in India: Is the growth inclusive?

India has witnessed high economics growth from the beginning of the new millennium. The agriculture and allied sector also recorded the highest growth during 2003–4 to 2012–13, coupled with marked improvement in production. It is now a food surplus and net-exporter country from food deficit since the mid-1990s. This should have result in lower incidence of poverty and calorie deprivation. However, the realisation of the growth went on the contrary to the general expectation by driving inequality and increasing deprivation. The prevalence of direct poverty remained high, which is a serious concern for achieving inclusive growth. This study examined nutritional status, direct and indirect poverty, and relative deprivation among socio-economic, and gender groups in India using national sample survey data. Albeit considering meals consumed outside the home, the results bespeak that nutritional status has been deteriorating. The incidence of nutritional poverty has been ascending since 2004–5 and adversely affected economic weaker sections and the marginalised socio-religious, and gender groups. They remained most deprive section of the society. The results are consistent and robust to use of alternate recommended dietary allowance and adjusted calorie intake, which takes into account under-reporting of food consumed away from home. Above findings question the inclusiveness of India’s high growth narrative.

Early caloric deprivation in preterm infants affects Bayley-III scales performance at 18–24 months of corrected age

BackgroundAdequate nutrition is essential for optimal neurodevelopment to preterm infants. Our aim was to evaluate the impact of caloric deprivation on Bayley-III scales performance at 18–24 months of corrected age, in a cohort of preterm infants. MethodsWe prospectively enrolled infants with gestational age <30 weeks and birth weight <1500 g. Apart from a whole cohort analysis, we performed a subgroup analysis between infants received inadequate calories (<85 Kcal/kg/day) during the first two weeks of age, compared to a standard nutrition group. All infants underwent a Bayley-III assessment at 18–24 months of corrected age. ResultsFrom the 63 preterm infants analysed, 25% had caloric deprivation compared to 75% with adequate nutrition. Caloric deprived infants were of lower gestational age and birth weight, and received a lower amount of enteral feeding during the first 14 days of age. There were no differences between the two groups regarding the common neonatal co-morbidities. Caloric deprived infants had significantly lower composite index scores at 18–24 months of corrected age. Caloric deprivation, late onset sepsis, necrotizing enterocolitis, and bronchopulmonary dysplasia were significant risk factors of neurodevelopmental impairment. ConclusionsSeveral neonatal factors affect the neurodevelopmental outcome of preterm infants, and nutrition may pose an important role.

Time-Restricted Eating to Prevent and Manage Chronic Metabolic Diseases.

Molecular clocks are present in almost every cell to anticipate daily recurring and predictable changes, such as rhythmic nutrient availability, and to adapt cellular functions accordingly. At the same time, nutrient-sensing pathways can respond to acute nutrient imbalance and modulate and orient metabolism so cells can adapt optimally to a declining or increasing availability of nutrients. Organismal circadian rhythms are coordinated by behavioral rhythms such as activity-rest and feeding-fasting cycles to temporally orchestrate a sequence of physiological processes to optimize metabolism. Basic research in circadian rhythms has largely focused on the functioning of the self-sustaining molecular circadian oscillator, while research in nutrition science has yielded insights into physiological responses to caloric deprivation or to specific macronutrients. Integration of these two fields into actionable new concepts in the timing of food intake has led to the emerging practice of time-restricted eating. In this paradigm, daily caloric intake is restricted to a consistent window of 8-12 h. This paradigm has pervasive benefits on multiple organ systems.

Two days of calorie deprivation impairs high level cognitive processes, mood, and self-reported exertion during aerobic exercise: A randomized double-blind, placebo-controlled study

Military personnel and emergency responders perform cognitively-demanding tasks during periods of sustained physical exertion and limited caloric intake. Cognitive function is preserved during short-term caloric restriction, but it is unclear if preservation extends to combined caloric restriction and physical exertion. According to the “reticular-activating hypofrontality” model, vigorous exertion impairs prefrontal cortex activity and associated functions. This double-blind, placebo-controlled, crossover study examined cognitive function during sustained exertion while volunteers were calorically-deprived. Twenty-three volunteers were calorie-depleted for two days on one occasion and fully-fed on another. They completed intermittent bouts of exercise at 40–65% VO2peak while prefrontal cortex-dependent tasks of cognitive control, mood, and perceived exertion were assessed. Calorie deprivation impaired accuracy on the task-switching task of set-shifting (p < .01) and decreased sensitivity on the go/no-go task of response inhibition (p < .05). Calorie deprivation did not affect risk taking on the Rogers risk task. During exercise, calorie deprivation, particularly on day 2, increased perceived exertion (p < .05) and impaired mood states of tension, depression, anger, vigor, fatigue, and confusion (all p < .01). Physical exertion during severe calorie deprivation impairs cognitive control, mood, and self-rated exertion. Reallocation of cerebral metabolic resources from the prefrontal cortex to structures supporting movement may explain these deficits.

Binge-Like Eating Is Not Influenced by the Murine Model of OPRM1 A118G Polymorphism.

Impairments in opioid receptor signaling have been implicated in disordered eating. A functional variant of the OPRM1 gene is a guanine (G) substitution for adenine (A) at the 118 position of exon 1 (A118G). The influence of the A118G variant on binge eating behaviors and the effectiveness of pharmacotherapies used to treat binge eating have not been characterized. Mice were generated with A to G substitution at the 112 position on exon 1 to produce a murine equivalent of the human A118G variant. Homozygous female mice (AA or GG) were exposed to intermittent access to a highly palatable sweet-fat food with or without prior calorie deprivation to promote dietary-induced binge eating. There were no genotype-dependent differences in the dietary-induced binge eating. However, GG mice exposed to intermittent calorie restriction (Restrict) had higher body weights compared with GG mice exposed to intermittent sweet fat-food (Binge) and ad libitum feeding (Naive). Acute oral dosing of lisdexamfetamine (0.15, 0.5, and 1.5 mg/kg) or sibutramine (0.3, 1, and 3 mg/kg) did not produce genotype-dependent differences in binge-like eating. In addition, no genotype-dependent differences in binge-like eating were observed with chronic (14-day) dosing of lisdexamfetamine (1.5 mg/kg/day) or sibutramine (3 mg/kg/day). In the chronic dosing, body weights were higher in the GG Restrict compared with AA Restrict. Our findings suggest that the A112G polymorphism does not influence binge eating behaviors or pharmacotherapies for treating binge eating.

The Neurocognitive Effects of Ghrelin-induced Signaling on the Hippocampus: A Promising Approach to Alzheimer's Disease.

The communication between the gastrointestinal tract and the central nervous system (CNS) allows for certain peptide hormones to influence neurocognitive function. Ghrelin, also known as the ‘hunger hormone,' has the unique ability to enter the CNS and interact with the growth hormone secretagogue receptor (GHS-R) within the hippocampus. Upon interaction with ghrelin, a conformational change in the receptor causes an increase in transcription factors to foster a wide array of physiologic changes in response to caloric deprivation. With the GHS-R in a relatively high concentration within the hippocampus, ghrelin can promote memory, spatial, learning, and behavioral effects. In fact, ghrelin appears to also have a neuroprotective and neuromodulatory response once active within the hippocampal dentate gyrus. Through the GHS-R, higher levels of ghrelin may alter cognitive circuitry and offer a possible link to the treatment of some pathologies implicated in neurological dysfunction. Alzheimer’s disease (AD) is already becoming a significant target for ghrelin neuroreceptor therapy. In such experimental models, ghrelin has been shown to combat this degenerative process by eliciting an ameliorative and regenerative response. Although trials and research are still ongoing, further studies are indicated as early research into this adjuvant therapy is promising.The research team explored the effects of ghrelin by reviewing the downstream signaling modifications of ghrelin's interaction with a specific CNS receptor, the GHS-R. Although the GHS-R is found in multiple locations within the CNS, the team investigated the role of the GHS-R within the hippocampus to focus solely on the neurocognitive implications of ghrelin. The team noted which signaling pathways in particular that ghrelin initiated and used this approach to determine whether ghrelin may have any therapeutic benefits. The team explored the possible therapeutic indications of ghrelin by looking at studies conducted with a specific neurodegenerative disease known to target the hippocampus.

The circulating metabolome of human starvation.

The human adaptive starvation response allows for survival during long-term caloric deprivation. Whether the physiology of starvation is adaptive or maladaptive is context dependent: activation of pathways by caloric restriction may promote longevity, yet in the context of caloric excess, the same pathways may contribute to obesity. Here, we performed plasma metabolite profiling of longitudinally collected samples during a 10-day, 0-calorie fast in humans. We identify classical milestones in adaptive starvation, including the early consumption of gluconeogenic amino acids and the subsequent surge in plasma nonesterified fatty acids that marks the shift from carbohydrate to lipid metabolism, and demonstrate findings, including (a) the preferential release of unsaturated fatty acids and an associated shift in plasma lipid species with high degrees of unsaturation and (b) evidence that acute, starvation-mediated hypoleptinemia may be a driver of the transition from glucose to lipid metabolism in humans.

Cell-Specific “Competition for Calories” Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-human Animals

The mammalian body is a complex physiologic “ecosystem” in which cells compete for calories (i.e., nutrient-energy). Axiomatically, cell-types with competitive advantages acquire a greater number of consumed calories, and when possible, increase in size and/or number. Thus, it is logical and parsimonious to posit that obesity is the competitive advantages of fat-cells (adipocytes) driving a disproportionate acquisition and storage of nutrient-energy. Accordingly, we introduce two conceptual frameworks. Asymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specific competition for calories that determines the partitioning of nutrient-energy to oxidation, anabolism, and/or storage; and Effective Caloric Intake which describes the number of calories available to constrain energy-intake via the inhibition of the sensorimotor appetitive cells in the liver and brain that govern ingestive behaviors. Inherent in these frameworks is the independence and dissociation of the energetic demands of metabolism and the neuro-muscular pathways that initiate ingestive behaviors and energy intake. As we demonstrate, if the sensorimotor cells suffer relative caloric deprivation via asymmetric competition from other cell-types (e.g., skeletal muscle- or fat-cells), energy-intake is increased to compensate for both real and merely apparent deficits in energy-homeostasis (i.e., true and false signals, respectively). Thus, we posit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesity and metabolic diseases is engendered by apparent deficits (i.e., false signals) driven by the asymmetric inter-cellular competition for calories and concomitant differential partitioning of nutrient-energy to storage. These frameworks, in concert with our previous theoretic work, the Maternal Resources Hypothesis, provide a parsimonious and rigorous explanation for the rapid rise in the global prevalence of increased body and fat mass, and associated metabolic dysfunctions in humans and other mammals inclusive of companion, domesticated, laboratory, and feral animals.

Perspectives on resilience for military readiness and preparedness: Report of an international military physiology roundtable

Modern warfare operations often occur in volatile, uncertain, complex, and ambiguous (VUCA) environments accompanied by physical exertion, cognitive overload, sleep restriction and caloric deprivation. The increasingly fast-paced nature of these operations requires military personnel to demonstrate readiness and resiliency in the face of stressful environments to maintain optimal cognitive and physical performance necessary for success. Resiliency, the capacity to overcome the negative effects of setbacks and associated stress on performance, is a complex process involving not only an individual’s physiology and psychology, but the influence of factors such as sex, environment, and training. The purpose of this moderated roundtable was to address five key domains of resiliency in a point/counterpoint format: physiological versus psychological resiliency, sex differences, contributions of aerobic and strength training, thermal tolerance, and the role of nature versus nurture. Each speaker was given three minutes to present and the moderator facilitated questions and discussion following the panel’s presentation. The interconnectedness of the five domains highlights the need for an interdisciplinary approach to understand and build resilience to enhance military performance.

Nutritional Deprivation at the Household Level in Rural India:Causes and Concerns

The aim of the paper is to quantify the proportion of undernourished households in rural India without relying on any particular calorie cut-off point. For that, mean RDA (Recommended Dietary Allowance) has been estimated at the household level, after adjusting for age and gender distribution of the sedentary household members. The two NSS rounds that pertain to the years 2004-05 and 2011-12 are used here. The results confirmed that it was among the lowest expenditure group that seems to have reported the highest increase in RDA between 2004-05 and 2011-12. An investigation of the determinants of calorie deprivation leads us to the finding that poor ST and OBC households, regular wage and self-employed in non-agriculture and Christians have the greater probability of being calorie deprived.

The paradox of marrow adipose tissue in anorexia nervosa.

Anorexia nervosa (AN) is a psychiatric disorder characterized by inappropriate nutrient intake resulting in low body weight. Multiple hormonal adaptations facilitate decreased energy expenditure in this state of caloric deprivation including non-thyroidal illness syndrome, growth hormone resistance, and hypogonadotropic hypogonadism. Although these hormonal adaptations confer a survival advantage during periods of negative energy balance, they contribute to the long-term medical complications associated with AN, the most common of which is significant bone loss and an increased risk of fracture. In recent years, marrow adipose tissue (MAT) has emerged as an important potential determinant of the low bone mass state characteristic of AN. Unlike subcutaneous and visceral adipose tissue depots which are low in AN, MAT levels are paradoxically elevated and are inversely associated with BMD. In this review, we discuss what is known about MAT in AN and the proposed hormonal determinants of this adipose tissue depot.

Pyruvate induces torpor in obese mice

Mice subjected to cold or caloric deprivation can reduce body temperature and metabolic rate and enter a state of torpor. Here we show that administration of pyruvate, an energy-rich metabolic intermediate, can induce torpor in mice with diet-induced or genetic obesity. This is associated with marked hypothermia, decreased activity, and decreased metabolic rate. The drop in body temperature correlates with the degree of obesity and is blunted by housing mice at thermoneutrality. Induction of torpor by pyruvate in obese mice relies on adenosine signaling and is accompanied by changes in brain levels of hexose bisphosphate and GABA as detected by mass spectroscopy-based imaging. Pyruvate does not induce torpor in lean mice but results in the activation of brown adipose tissue (BAT) with an increase in the level of uncoupling protein-1 (UCP1). Denervation of BAT in lean mice blocks this increase in UCP1 and allows the pyruvate-induced torpor phenotype. Thus, pyruvate administration induces torpor in obese mice by pathways involving adenosine and GABA signaling and a failure of normal activation of BAT.

An Empirical Investigation into Measurement and Determinants of Food Security

ABSTRACTWe examine the association between calorie-based indicators and experiential indicators of food security using data from slum households of Kolkata surveyed in 2010–2011. Experiential indicator is constructed following the United States Household Food Security Survey Module. Calorie based indicator is constructed using household-specific calorie norms. Modelling techniques take account of potential endogeneity in the relationship. The two indicators are aligned in the same direction implying more accurate targeting. However, there is a lack of one-to-one correspondence between the two measures and the drivers of calorie deprivation and food insecurity also differ, suggesting a one-size-fits-all policy cannot address both concerns simultaneously.

Effects of Anorexia Nervosa on the Endocrine System.

Anorexia nervosa (AN) is characterized by severe undernutrition associated with alterations in multiple endocrine axes, which are primarily adaptive to the state of caloric deprivation. Hormonal changes include growth hormone (GH) resistance with low insulin like growth factor-1 (IGF-1) levels, hypothalamic hypogonadism, relative hypercortisolemia and changes in appetite regulating hormones, including leptin, ghrelin, and peptide YY. These alterations contribute to abnormalities in bone metabolism leading to low bone mass, impaired bone microarchitecture, and increased risk for fracture, and may also negatively impact cognition, emotions and mood. The best strategy to improve all biologic outcomes is weight and menstrual recovery. Physiological estrogen replacement improves bone accrual rates and measures of trait anxiety in adolescents with AN. Other therapies including testosterone and IGF-1 replacement, and use of DHEA with oral estrogen-progesterone combination pills, bisphosphonates and teriparatide have also been studied to improve bone outcomes.

Two Days of Calorie Deprivation Induced by Underfeeding and Aerobic Exercise Degrades Mood and Lowers Interstitial Glucose but Does Not Impair Cognitive Function in Young Adults

In studies assessing the effects of acute undernutrition on cognitive function, volunteers are sedentary and findings are equivocal, even though glucose concentrations fall substantially. However, military personnel and endurance athletes often are underfed when physical demands, and consequently energy expenditure, are substantial. The objective of this study was to determine whether 2 d of near-total calorie deprivation combined with aerobic exercise degraded cognitive performance and mood. A double-blind, placebo-controlled, crossover design was used. Twenty-three volunteers [17 men (mean ± SD age: 20.5 ± 0.7 y) and 6 women (mean ± SD age: 23.3 ± 1.4 y); mean ± SD body mass index (in kg/m2): 25 ± 3] participated for 68 h, including a 51-h inpatient phase in a calorie-deprived or fully fed state during which behavioral testing was conducted and interstitial glucose was monitored continuously. Mood and cognitive performance, including psychomotor and visual vigilance, visual match-to-sample, repeated acquisition (motor learning), N-back (working memory), and grammatical reasoning, were repeatedly assessed. During each condition, individual daily energy intake and expenditure were controlled. During calorie deprivation, volunteers consumed 266 ± 61 kcal/d; during full feeding, they consumed 3935 ± 769 kcal/d. Participants engaged in identical exercise sessions for 4 h/d at 40-65% of peak volume of oxygen uptake attained. Calorie deprivation did not affect any aspect of cognitive performance, but produced robust effects on mood measured by the Profile of Mood States, including increased tension (P < 0.001), fatigue (P < 0.001), and total mood disturbance (from -0.80 ± 5.1 to 20.1 ± 6.1; P < 0.001), and decreased vigor (P = 0.002), as indicated by treatment × trial (time) effects on ANOVA. Interstitial glucose concentrations were lower during calorie deprivation than in the fully fed condition (P = 0.002, treatment × trial interaction) and declined to 61 mg/dL by the end of the treatment condition. In healthy young men and women, 2 d of severe calorie deprivation in combination with substantial aerobic exercise adversely affects multiple aspects of mood, but not cognition, in spite of substantial reductions in interstitial glucose concentrations. This trial was registered at clinicaltrials.gov as NCT01603550.

Síndrome de realimentação em idosos: estudo de uma série de cinco casos

INTRODUCTION: Undernourishment is a common health problem among elderly individuals, and its prevalence grows among frail patients, which makes nutritional support a priority, especially in acute diseases. However, providing nutritional support to undernourished patients or to those under acute caloric deprivation may lead to electrolyte disturbances associated with neurological, respiratory, and cardiac symptoms, including cardiac arrest. These disturbances occur a few days after receiving nutritional support, and characterize the refeeding syndrome. METHODOLOGY: Five elderly patients hospitalized for clinical reasons and who developed refeeding syndrome during the duration of the stay, were retrospectively evaluated. RESULTS: All patients analyzed were malnourished and frail, of whom four were women. The age group ranged between 82 and 85 years, and food deprivation time ranged between 7 to 15 days. Three patients had severe dementia and were admitted with hypoactive delirium. Hypophosphatemia occurred in 100% of the sample, followed by hypokalemia (60%) and hypomagnesemia (40%). Four patients developed peripheral edema, two developed metabolic ileus and three elderly persons (who had lower phosphorus values) died during the hospital stay. CONCLUSION: All refeeding syndrome patients developed hypophosphatemia, with fatal outcome among those whose phosphorus values were lower. The development of peripheral edema and metabolic ileus was frequent. Owing to the lack of data in literature, new researches on refeeding syndrome are extremely important. Electrolyte evaluation before and after nutritional support in patients at risk, is indispensable to facilitate recognition and treatment of this severe condition.

Interstitial Glucose Concentrations In Response To Acute Caloric Deprivation And Increased Exercise

Interstitial Glucose Concentrations In Response To Acute Caloric Deprivation And Increased Exercise

50 Years Ago in TheJournal ofPediatrics: Perinatal Stress and the Premature Neonate. II. Effect of Fluid and Calorie Deprivation on Blood Glucose

50 Years Ago in TheJournal ofPediatrics: Perinatal Stress and the Premature Neonate. II. Effect of Fluid and Calorie Deprivation on Blood Glucose

Management of Hyperglycemia in Diabetic Kidney Disease.

The growing incidence and prevalence of diabetes has made a significant impact on the development of diabetic kidney disease (DKD) (1). DKD is among the most frequent complications of diabetes; indeed, diabetes accounts for ∼50% of all cases of end-stage renal disease (ESRD) in developed countries (2). Patients often have comorbid diabetes and chronic kidney disease (CKD). Although intensive glycemic management has been shown to delay the onset and progression of increased urinary albumin excretion and reduced estimated glomerular filtration rate (eGFR) in diabetes patients (3), conservative dose selection and adjustment of antidiabetic medications is necessary to balance glycemic control with safety. A1C has limitations related to its precision and interpretation in the CKD population (4), with erythrocyte turnover being a major cause of A1C imprecision in this population. Red blood cell survival times become shorter as eGFR falls, resulting in a reduction in measured A1C. Treatment with erythrocyte-stimulating agents lowers A1C further, perhaps because of changes in hemoglobin concentrations (5,6). Observational data support the notion that higher A1C levels in nondialysis diabetes patients with CKD stages 3–5 (eGFR levels <60 mL/min/1.73 m2) are associated with worse outcomes, including progression of kidney disease (7). However, these patients are at higher risk for hypoglycemic events (8). Factors that may contribute to this increased risk can include slowed elimination of hypoglycemic agents, alcohol intake, chronic malnutrition, acute caloric deprivation, and decreased renal gluconeogenesis as kidney function declines (8–10). In the ACCORD (Action to Control Cardiovascular Risk in Diabetes) study, when compared with patients with normal renal function, those with baseline serum creatinine of 1.3–1.5 mg/dL had a 66% increased risk of severe hypoglycemia (11). A U-shaped relationship between A1C and mortality has been demonstrated, suggesting that hypoglycemia may be one reason for higher mortality in those …