Obesity: A Game of Inches

PEDIATRICS ◽  
1995 ◽  
Vol 95 (1) ◽  
pp. 131-132
Author(s):  
Rudolph L. Leibel

Obesity, like baseball, is a game of inches. Weight gain cannot occur unless energy intake exceeds energy expenditure. Such positive energy balance is a sine qua non for normal growth in the child, and for obesity in the adult. Very small excesses of intake over expenditure can make a big difference if present over a long period of time. Consider the children in the study reported by Klesges et al1 elsewhere in this journal (pages 126-130). At about 4½ years of age, these children were estimated (by diet history) to have been ingesting about 2000 kcal per day. This is almost certainly an overestimate of the actual caloric intake of these children (see below).

2015 ◽  
Vol 75 (3) ◽  
pp. 319-327 ◽  
Author(s):  
David J. Clayton ◽  
Lewis J. James

The belief that breakfast is the most important meal of day has been derived from cross-sectional studies that have associated breakfast consumption with a lower BMI. This suggests that breakfast omission either leads to an increase in energy intake or a reduction in energy expenditure over the remainder of the day, resulting in a state of positive energy balance. However, observational studies do not imply causality. A number of intervention studies have been conducted, enabling more precise determination of breakfast manipulation on indices of energy balance. This review will examine the results from these studies in adults, attempting to identify causal links between breakfast and energy balance, as well as determining whether consumption of breakfast influences exercise performance. Despite the associations in the literature, intervention studies have generally found a reduction in total daily energy intake when breakfast is omitted from the daily meal pattern. Moreover, whilst consumption of breakfast supresses appetite during the morning, this effect appears to be transient as the first meal consumed after breakfast seems to offset appetite to a similar extent, independent of breakfast. Whether breakfast affects energy expenditure is less clear. Whilst breakfast does not seem to affect basal metabolism, breakfast omission may reduce free-living physical activity and endurance exercise performance throughout the day. In conclusion, the available research suggests breakfast omission may influence energy expenditure more strongly than energy intake. Longer term intervention studies are required to confirm this relationship, and determine the impact of these variables on weight management.


2003 ◽  
Vol 62 (2) ◽  
pp. 539-543 ◽  
Author(s):  
Jonathan Webber

The current epidemic of human obesity implies that whilst energy balance appears to be regulated, the extent of this regulatory process is being overwhelmed in large numbers of the population by environmental changes. Clearly, the shift towards positive energy balance reflects both alterations in energy intake and decreases in physical activity. Increased energy intake and, in particular, the rising proportion of energy from fat is linked with obesity. However, on a population level reduced levels of activity probably play the predominant role. It is apparent that individual susceptibility to weight gain varies enormously. The factors underlying this susceptibility are an area of intense research interest. Variations in BMR from that predicted appear to be linked to the propensity to gain weight. The genes responsible for this variation may include uncoupling proteins-2 and -3, with a number of studies showing a link with obesity. However,in vivostudies of these proteins have not yet demonstrated a physiological role for them that would explain the link with obesity. Non-exercise activity thermogenesis may also protect from weight gain, but the regulation of this type of thermogenesis is unclear, although the sympathetic nervous system may be important. A profusion of hormones, cytokines and neurotransmitters is involved in regulating energy intake, but whilst mutations in leptin and the melanocortin-3 receptor are responsible for rare monogenic forms of obesity, their wider role in common polygenic obesity is not known. Much current work is directed at examining the interplay between genetic background and environmental factors, in particular diet, that both lead to positive energy balance and seem to make it so hard for many obese subjects to lose weight.


2020 ◽  
Vol 26 (3) ◽  
pp. 197-202
Author(s):  
David R. Gater ◽  
Craig Bauman ◽  
Rachel Cowan

Physiological changes that occur after spinal cord injury (SCI) are profound and affect almost every organ system in the human body. Energy balance is significantly altered due to motor paralysis, spasticity or flaccidity, neurogenic sarcopenia, neurogenic osteopenia, sympathetic nervous system disruption, and blunted anabolism. Energy expenditure is markedly reduced, whereas hypothalamic control of appetite and satiety is diminished, resulting in discordant energy intake. Ultimately, neurogenic obesity ensues as the result of a positive energy balance. Even though nutritional guidelines for persons with SCI have been available since 2009, the necessity for body composition assessment and total daily energy expenditure was insufficiently addressed such that most individuals with SCI continued in positive energy balance despite “adherence” to the guidelines. Macronutrients must be carefully assessed to optimize caloric intake, while micronutrient consumption may need to be supplemented in order to meet recommended daily allowances. Such a diet would emphasize foods with low caloric yet high nutrient density. This article reviews current literature regarding nutritional requirements for SCI and provides a straightforward plan for implementing more rigorous dietary interventions meant to address the obesity crisis in this especially vulnerable population.


2018 ◽  
Vol 30 (4) ◽  
pp. 506-515 ◽  
Author(s):  
Keren Susan Cherian ◽  
Ashok Sainoji ◽  
Balakrishna Nagalla ◽  
Venkata Ramana Yagnambhatt

Purpose: To evaluate energy expenditure, energy intake, and nutrient adequacy of Indian junior soccer players. Method: Forty junior national-level soccer players (Under-12 and Under-16 age groups) were assessed for 3-day weighed food records and 3-day energy expenditure. Energy and nutrient intake was analyzed from food records, and energy expenditure was measured using a portable metabolic analyzer and activity records. Nutrient adequacy was determined by comparing intake with prevailing recommendations. Results: Players exhibited no significant difference between energy intake (boys = 3062 [340.9] and girls = 2243 [320.3] kcal·d−1) and expenditure (boys = 2875 [717.3] and girls = 2442 [350.3] kcal·d−1). Across age groups, the Under-12 boys showed positive energy balance as against energy deficits in Under-16. Girls showed energy deficits, although not significant. There were 58% of girls showing energy availability <30 kcal·kg−1 fat-free mass, of which 37% were Under-16 players. Carbohydrates contributed to >60% of energy expenditure among 95.2% boys and 73.7% girls. Among 52.4% boys and 47.4% girls, <25% of energy expenditure was contributed by fat. More than 95% players consumed <1 g·kg−1 carbohydrates pretraining and 100% of them consumed >1.2 g·kg−1 carbohydrates posttraining. Conclusion: Junior soccer players consumed more than recommended carbohydrates in the diet, although not aligning with the pretraining, during training, and posttraining meal requirements. Considering the energy deficits observed among Under-16 players, a suitable dietary modification is warranted.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.


2001 ◽  
Vol 280 (6) ◽  
pp. R1680-R1687 ◽  
Author(s):  
S. Renee Commerford ◽  
Michael J. Pagliassotti ◽  
Christopher L. Melby ◽  
Yuren Wei ◽  
James O. Hill

Obesity results from positive energy balance and, perhaps, abnormalities in lipid and glycogen metabolism. The purpose of this study was to determine whether differences in lipogenesis, retention of dietary fat, and/or glycogenesis influenced susceptibility to dietary obesity. After 1 wk of free access to a high-fat diet (HFD; 45% fat by energy) rats were separated on the basis of 1 wk body weight gain into obesity-prone (OP; ≥48 g) or obesity-resistant groups (OR; ≤40 g). Rats were either studied at this time (OR1, OP1) or continued on the HFD for an additional 4 wk (OR5, OP5). Weight gain and energy intake were greater ( P ≤ 0.05) in OP vs. OR at both 1 (53 ± 2 vs. 34 ± 1 g; 892 ± 27 vs. 755 ± 14 kcal) and 5 (208 ± 7 vs. 170 ± 7 g; 4,484 ± 82 vs. 4,008 ± 72 kcal) wk, respectively. Rats were injected with 3H2O and were either provided free access to an HFD meal containing labeled fatty acids (fed; n = 10 or 11/group) or were fasted ( n = 10/group) overnight. The amount of food or 14C tracer eaten overnight was equivalent between OP and OR rats. In liver, the fraction of 3H retained in glycogen or lipid was not significantly different between OR and OP groups. Retention of dietary fat in the liver was not increased in OP rats. In adipose tissue, retention of3H was ∼49% greater ( P ≤ 0.05) in OP1 vs. OR1 and ∼30% greater in OP5 vs. OR5, but retention of dietary fat was not elevated in OP vs. OR. At the same time, fat pad weight (sum of epididymal, retroperitoneal, mesenteric) was 49% greater in OP1 rats vs. OR1 rats and 65% greater in OP5 vs. OR5 rats ( P ≤ 0.05). Thus a greater capacity for lipogenesis or retention of dietary fat does not appear to be included in the OP phenotype. The characteristic increase in energy intake associated with OP rats appears to be necessary and critical to accelerated weight and fat gain.


2009 ◽  
Vol 28 (3) ◽  
pp. 260-265 ◽  
Author(s):  
H.C. Reinbach ◽  
A. Smeets ◽  
T. Martinussen ◽  
P. Møller ◽  
M.S. Westerterp-Plantenga

2017 ◽  
Vol 49 (06) ◽  
pp. 472-479
Author(s):  
Tássia Borba ◽  
Lígia Galindo ◽  
Kelli Ferraz-Pereira ◽  
Raquel da Silva Aragão ◽  
Ana Toscano ◽  
...  

AbstractThe obesity epidemic has been the target of several studies to understand its etiology. The pathophysiological processes that take to obesity generally relate to the rupture of energy balance. This imbalance can result from environmental and/or endogenous events. Among the endogenous events, the hypothalamic-pituitary-adrenal axis, which promotes stress response via glucocorticoid activity, is considered a modulator of energy balance. However, it remains controversial whether the increase in plasma levels of glucocorticoids results in a positive or negative energy balance. Furthermore, there are no studies comparing different routes of administration of glucocorticoids in this context. Here, we investigated the effects of intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of a specific agonist for glucocorticoid receptors on food intake and energy expenditure in rats. Sixty-day old rats were treated with i.p. or i.c.v. dexamethasone. Food intake and satiety were evaluated, as well as locomotor activity in order to determine energy expenditure. Both i.p. and i.c.v. dexamethasone increased food intake and decreased energy expenditure. Moreover, i.c.v. dexamethasone delayed the onset of satiety. Together, these results confirm that central glucocorticoid signaling promotes a positive energy balance and supports the role of the glucocorticoid system as the underlying cause of psychological stress-induced obesity.


1994 ◽  
Vol 77 (1) ◽  
pp. 366-372 ◽  
Author(s):  
M. I. Goran ◽  
J. Calles-Escandon ◽  
E. T. Poehlman ◽  
M. O'Connell ◽  
E. Danforth

This study was designed to examine effects of alterations in energy balance on adaptive changes in components of total energy expenditure (TEE). Nineteen young healthy males were studied during a 10-day sedentary energy balance baseline period and then randomly assigned to one of four 10-day treatment groups: 1) no change in energy intake (EI) or physical activity (PA; energy balance at low energy flux), 2) EI increased by 50% with no change in PA (positive energy balance), 3) TEE increased by 50% by increasing PA, matched by a 50% increase in EI (energy balance at high energy flux), and 4) TEE increased by 50% by increasing PA with no change in EI (negative energy balance). TEE was measured with doubly labeled water, resting metabolic rate (RMR) by indirect calorimetry, and thermic response to feeding (TEF) by indirect calorimetry; energy expenditure of physical activity (EEPA) was estimated by subtracting RMR, TEF, and prescribed PA from TEE. TEE was significantly increased by PA (by design) but not EI. There was a significant main effect of intake and a significant intake-by-activity interaction for changes in RMR. In post hoc analysis, RMR was significantly increased during positive energy balance and energy balance at high energy flux relative to change in RMR when energy balance was maintained at low energy flux. A significant increase in RMR was also noted during negative energy balance after adjustment for change in fat-free mass. There was no significant difference in change in RMR among the three treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 319 (3) ◽  
pp. E472-E484
Author(s):  
Kikumi D. Ono-Moore ◽  
Jennifer M. Rutkowsky ◽  
Nicole A. Pearson ◽  
D. Keith Williams ◽  
Justin L. Grobe ◽  
...  

Obesity and its metabolic sequelae are implicated in dysfunction of the somatosensory, sympathetic, and hypothalamic systems. Because these systems contribute to integrative regulation of energy expenditure (EE) and energy intake (EI) in response to ambient temperature (Ta) changes, we hypothesized that diet-induced obesity (DIO) disrupts Ta-associated EE-EI coupling. C57BL/6N male mice were fed a high-fat diet (HFD; 45% kcal) or low-fat diet (LFD; 10% kcal) for ∼9.5 wk; HFD mice were then split into body weight (BWT) quartiles ( n = 8 each) to study DIO-low gainers (Q1) versus -high gainers (Q4). EI and indirect calorimetry (IC) were measured over 3 days each at 10°C, 20°C, and 30°C. Responses did not differ between LFD, Q1, and Q4; EI and BWT-adjusted EE increased rapidly when transitioning toward 20°C and 10°C. In all groups, EI at 30°C was not reduced despite lower EE, resulting in positive energy balance and respiratory exchange ratios consistent with increased de novo lipogenesis, energy storage, and relative hyperphagia. We conclude that 1) systems controlling Ta-dependent acute EI/EE coupling remained intact in obese mice and 2) rapid coupling of EI/EE at cooler temperatures is an important adaptation to maintain energy stores and defend body temperature, but less critical at thermoneutrality. A post hoc analysis using digestible EI plus IC-calculated EE suggests that standard IC assumptions for EE calculation require further validation in the setting of DIO. The experimental paradigm provides a platform to query the hypothalamic, somatosensory, and sympathetic mechanisms that drive Ta-associated EI/EE coupling.


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