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Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition
Abstract
Weight changes are accompanied by imbalances between calorie intake and expenditure. This fact is often misinterpreted to suggest that obesity is caused by gluttony and sloth and can be treated by simply advising people to eat less and move more. However, various components of energy balance are dynamically interrelated and weight loss is resisted by counterbalancing physiological processes. While low carbohydrate diets have been suggested to partially subvert these processes by increasing energy expenditure and promoting fat loss, our meta-analysis of 32 controlled feeding studies with isocaloric substitution of carbohydrate for fat found that both energy expenditure (26 kcal/d; p<0.0001) and fat loss (16g/d; p<0.0001) were greater with lower fat diets. We review the components of energy balance and the mechanisms acting to resist weight loss in the context of static, settling point, and set-point models of body weight regulation, with the set-point model being most commensurate with current data.
... The EBM of Hall et al. [9] differs from these formulations, with a primary focus on the control of food intake and less attention to energy expenditure. This new EBM implies, and related reviews explicitly state [2,[18][19][20], that all calories are metabolically alike in the model. For instance, Hall and Guo [19] assert that, "for all practical purposes, 'a calorie is a calorie' when it comes to body fat and energy expenditure differences between controlled isocaloric diets varying in the ratio of carbohydrate to fat." ...
... This new EBM implies, and related reviews explicitly state [2,[18][19][20], that all calories are metabolically alike in the model. For instance, Hall and Guo [19] assert that, "for all practical purposes, 'a calorie is a calorie' when it comes to body fat and energy expenditure differences between controlled isocaloric diets varying in the ratio of carbohydrate to fat." While acknowledging that dietary composition influences oxidation rates of respective macronutrients, the EBM holds that diet ultimately drives fat deposition by increasing total energy intake, not through calorie-independent effects on substrate partitioning. ...
... This concern about CIM revision contrasts with their acknowledgment that "development of the EBM [still] requires elucidation of the factors in the dynamic food environment that are most responsible for instigating obesity [and] the mechanisms by which these factors alter the brain circuits controlling food intake" [9]. Indeed, dietary targets of EBM-based recommendations have changed from calorie counting in the early twentieth century [186] to an overarching focus on dietary fat restriction in the late twentieth century [173][174][175][176][177]187], to the notion that all calories are alike [2,18,19], to the new formulation [9], subtitled "beyond calories in, calories out," that now blames a host of modern dietary factors. For scientific models to remain relevant, they must grow as knowledge accrues. ...
The obesity pandemic continues unabated despite a persistent public health campaign to decrease energy intake (“eat less”) and increase energy expenditure (“move more”). One explanation for this failure is that the current approach, based on the notion of energy balance, has not been adequately embraced by the public. Another possibility is that this approach rests on an erroneous paradigm. A new formulation of the energy balance model (EBM), like prior versions, considers overeating (energy intake > expenditure) the primary cause of obesity, incorporating an emphasis on “complex endocrine, metabolic, and nervous system signals” that control food intake below conscious level. This model attributes rising obesity prevalence to inexpensive, convenient, energy-dense, “ultra-processed” foods high in fat and sugar. An alternative view, the carbohydrate-insulin model (CIM), proposes that hormonal responses to highly processed carbohydrates shift energy partitioning toward deposition in adipose tissue, leaving fewer calories available for the body’s metabolic needs. Thus, increasing adiposity causes overeating to compensate for the sequestered calories. Here, we highlight robust contrasts in how the EBM and CIM view obesity pathophysiology and consider deficiencies in the EBM that impede paradigm testing and refinement. Rectifying these deficiencies should assume priority, as a constructive paradigm clash is needed to resolve long-standing scientific controversies and inform the design of new models to guide prevention and treatment. Nevertheless, public health action need not await resolution of this debate, as both models target processed carbohydrates as major drivers of obesity.
... Importantly, proponents of this model argue against the simplistic approach of the carbohydrate-insulin-model neglecting that several variables in the food environment influence energy intake and energy partitioning. For example, energy expenditure and energy intake are dynamically interrelated by physiological counteracting mechanisms (e.g., adaptive thermogenesis corresponding to a reduced energy expenditure if energy intake is decreased 65 ) that are nearly impossible to look at in an isolated fashion 66 . While data supporting a lower energy expenditure following low-fat diets exist, authors claim that these differences are so small that "a calorie is a calorie" 66 . ...
... For example, energy expenditure and energy intake are dynamically interrelated by physiological counteracting mechanisms (e.g., adaptive thermogenesis corresponding to a reduced energy expenditure if energy intake is decreased 65 ) that are nearly impossible to look at in an isolated fashion 66 . While data supporting a lower energy expenditure following low-fat diets exist, authors claim that these differences are so small that "a calorie is a calorie" 66 . Also, one must acknowledge that evidence from meta-analysis is currently lacking that an LCD (favoring the carbohydrate-insulinmodel) is more effective than a low-fat diet if calorie restriction is achieved (favoring the energy-balance-model) 37 . ...
Nutrition and dietary interventions are a central component in the pathophysiology, but also a cornerstone in the management of patients with non-alcoholic fatty liver disease (NAFLD). Summarizing our rapidly advancing understanding of how our diet influences our metabolism and focusing on specific effects on the liver, we provide a comprehensive overview of dietary concepts to counteract the increasing burden of NAFLD. Specifically, we emphasize the importance of dietary calorie restriction independently of the macronutrient composition together with adherence to a Mediterranean diet low in added fructose and processed meat seems to exert favorable effects beyond calorie restriction. Also, we discuss intermittent fasting as a type of diet specifically tailored to decrease liver fat content and increase ketogenesis, awaiting future study results in NAFLD. Finally, personalized dietary recommendations could be powerful tools to increase the effectiveness of dietary interventions in patients with NAFLD considering the genetic background and the microbiome, among others.
... Journal of Theoretical Biology xxx (xxxx) 111240 Data in the first four rows are simulation inputs. Energy expenditure (EE) is assumed to be similar among diets (Hall et al., 2016;Hall and Guo, 2017;Hall et al., 2019;Brehm et al., 2005) and to remain constant for 6 days. Numbers in the remaining rows were calculated by the following equations: Assuming nitrogen (N) balance, daily urinary nitrogen equals (Protein intake)/6.25; ...
... Avg. excretion = [(DXA fat loss) -(Equation (6) An immediate consequence of equation (7) is that insulin now emerges as a modulator of fat loss since the excretion of fatty acid derivatives is inversely related to levels of this hormone (e.g., ketone bodies). Consequently, a diet that elevates insulin secretion elicits fat loss mainly through net fat oxidation whereas a diet that decreases insulin secretion evokes fat loss largely by increasing the excretion of fatty acids derivatives with minimal impact on net fat oxidation since daily energy expenditure appears to be unaltered (Hall et al., 2015(Hall et al., , 2016Hall and Guo, 2017;Hall et al., 2019;Brehm et al., 2005). As a result, a more coherent interpretation of Hall et al. (2015) study is as follows: ...
Metabolic physiology asserts that body weight stability is achieved when over time the average absorbed energy intake equals the average expended energy. This principle, known as energy balance, justifies the design of numerous investigations that aim to elucidate the biology of obesity. The present work provides a mathematical analysis that demonstrates, nonetheless, that weight stability must coexist with a constant energy imbalance, i.e., the average absorbed energy intake and the average expended energy are significantly different during steady weight periods. This analytical finding is not in contradiction with the First Law of Thermodynamics since open systems can manifest a stable mass in the absence of energy equilibrium. The effect of caloric imbalance on weight fluctuations is thus the result of its underlying net mass flux. The energy balance theory is, consequently, an inconsistent paradigm; and as such, the data analysis and interpretation that follows from its postulates is expected to be erroneous.
... A first framework holds that body mass may not fall below a certain threshold since "thrifty genes" have evolved for efficient fat deposition when nutrition levels decline (Speakman, 2018). While ancestrally linked to famine conditions, this factor may also partly explain inconsistent results from dieting and weight-loss regimes Anderson et al., 2001;Hall & Guo, 2017;Murillo et al., 2018;Zigman et al., 2016). A "thrifty late" version of this model emphasizes that famines are a recent feature of evolutionary history, emerging during the development of agriculture about 12,000 years ago (Ayub et al., 2014). ...
... In other words, rather than gravitating toward individuallystable set points, obesity is simply a consequence of factors that promote greater food intake (or lower energy expenditure). However, studies of human dieting do not seem consistent with this framework (Hall & Guo, 2017). The preponderance of evidence, in other words, does suggest a stable body mass zone. ...
Objectives
This study tested whether genetically predicted trait-body mass index (trait-BMI) was linked to more general daily discrimination among older adults, and consequently to decline in their life satisfaction.
Methods
Data were from the Health and Retirement Study, nationally representative of U.S. adults over 50. Genetic prediction models were used to extract the trait component of BMI, which was then deployed in regression models for discrimination. A recently developed “regression with residuals” approach was used to test associations with subsequent change in life satisfaction.
Results
Genetically predicted trait-BMI was linked to more general discrimination reports. It also had negative associations with change in life satisfaction—linkages not consistently or strongly mediated by discrimination.
Conclusions
Trait-BMI—arguably resistant to sustained alteration through individual efforts—seems linked to decline in older adults’ life satisfaction. General daily discrimination, however, may not be an important mechanism.
... In 2016, it was estimated that 39% of the global adult population aged ≥ 18 years (39% of males and 40% of females) were overweight, and 13% were deemed obese [1]. Obesity is characterized by excessive adipose tissue accumulation due to an imbalance between high consumption and low energy expenditure [2]. The excessive adipose tissue is deposited as visceral adipose tissue, which is well-known to secrete pro-inflammatory cytokines, resulting in a low-grade inflammatory condition. ...
Obesity causes low-grade inflammation that results in the development of comorbidities. In people with obesity, exacerbation of gastric lesion severity and delayed healing may aggravate gastric mucosal lesions. Accordingly, we aimed to evaluate the citral effects on gastric lesion healing in eutrophic and obese animals. C57Bl/6 male mice were divided into two groups: animals fed a standard diet (SD) or high-fat diet (HFD) for 12 weeks. Gastric ulcers were induced using acetic acid (80%) in both groups. Citral (25, 100, or 300 mg/kg) was administered orally for 3 or 10 days. A vehicle-treated negative control (1% Tween 80, 10 mL/kg) and lansoprazole-treated (30 mg/kg) were also established. Lesions were macroscopically examined by quantifying regenerated tissue and ulcer areas. Matrix metalloproteinases (MMP-2 and-9) were analyzed by zymography. The ulcer base area between the two examined periods was significantly reduced in HFD 100 and 300 mg/kg citral-treated animals. In the 100 mg/kg citral-treated group, healing progression was accompanied by reduced MMP-9 activity. Accordingly, HFD could alter MMP-9 activity, delaying the initial healing phase. Although macroscopic changes were undetectable, 10-day treatment with 100 mg/kg citral exhibited improved scar tissue progression in obese animals, with reduced MMP-9 activity and modulation of MMP-2 activation.
... The most efficacious treatments target the hypothalamus and melanocortin system, specifically glucagon-like protein 1 receptor (GLP-1R) and melanocortin 4 receptor (MC4R) agonists [9][10][11]. While these new pharmacological treatments are encouraging, diet and exercise remain the safest and most common lifestyle interventions; however, results are often temporary and many individuals regain weight in less than 5 years [12][13][14][15][16][17][18]. Understanding obesogenic factors that alter CNS function may allow for development of interventions that 'reset' these mechanisms and promote sustained weight loss through reduced appetite. ...
Background/Objective
As the obesity epidemic continues, the understanding of macronutrient influence on central nervous system function is critical for understanding diet-induced obesity and potential therapeutics, particularly in light of the increased sugar content in processed foods. Previous research showed mixed effects of sucrose feeding on body weight gain but has yet to reveal insight into the impact of sucrose on hypothalamic functioning. Here, we explore the impact of liquid sucrose feeding for 12 weeks on body weight, body composition, caloric intake, and hypothalamic AgRP neuronal function and synaptic plasticity.
Methods
Patch-clamp electrophysiology of hypothalamic AgRP neurons, metabolic phenotyping and food intake were performed on C57BL/6J mice.
Results
While mice given sugar-sweetened water do not gain significant weight, they do show subtle differences in body composition and caloric intake. When given sugar-sweetened water, mice show similar alterations to AgRP neuronal excitability as in high-fat diet obese models. Increased sugar consumption also primes mice for increased caloric intake and weight gain when given access to a HFD.
Conclusions
Our results show that elevated sucrose consumption increased activity of AgRP neurons and altered synaptic excitability. This may contribute to obesity in mice and humans with access to more palatable (HFD) diets.
... A more scientific and balanced nutritional diet is the key to weight management. Scholars have conducted many studies, and found that various components of energy balance were dynamically interrelated and weight change was resisted by counterbalancing physiological processes (63). Unbalanced nutritional diet was characterized by low cereals, vegetables, fruits, micronutrient density, and excessive of highly processed, sweet, high-fat foods, red meat and derivatives, as well as extreme diets (64,65). ...
Objective
The COVID-19 pandemic has become a major public health concern over the past 3 years, leading to adverse effects on front-line healthcare workers. This study aimed to develop a Body Mass Index (BMI) change prediction model among doctors and nurses in North China during the COVID-19 pandemic, and further identified the predicting effects of lifestyles, sleep quality, work-related conditions, and personality traits on BMI change.Methods
The present study was a cross-sectional study conducted in North China, during May-August 2022. A total of 5,400 doctors and nurses were randomly recruited from 39 COVID-19 designated hospitals and 5,271 participants provided valid responses. Participants’ data related to social-demographics, dietary behavior, lifestyle, sleep, personality, and work-related conflicts were collected with questionnaires. Deep Neural Network (DNN) was applied to develop a BMI change prediction model among doctors and nurses during the COVID-19 pandemic.ResultsOf participants, only 2,216 (42.0%) individuals kept a stable BMI. Results showed that personality traits, dietary behaviors, lifestyles, sleep quality, burnout, and work-related conditions had effects on the BMI change among doctors and nurses. The prediction model for BMI change was developed with a 33-26-20-1 network framework. The DNN model achieved high prediction efficacy, and values of R2, MAE, MSE, and RMSE for the model were 0.940, 0.027, 0.002, and 0.038, respectively. Among doctors and nurses, the top five predictors in the BMI change prediction model were unbalanced nutritional diet, poor sleep quality, work-family conflict, lack of exercise, and soft drinks consumption.Conclusion
During the COVID-19 pandemic, BMI change was highly prevalent among doctors and nurses in North China. Machine learning models can provide an automated identification mechanism for the prediction of BMI change. Personality traits, dietary behaviors, lifestyles, sleep quality, burnout, and work-related conditions have contributed to the BMI change prediction. Integrated treatment measures should be taken in the management of weight and BMI by policymakers, hospital administrators, and healthcare workers.
... Una de las teorías más utilizadas se basa en el modelo "calorías que entran-calorías que salen", que describe parcialmente la causa de la obesidad. Investigaciones recientes explican que, al momento de realizar una restricción calórica al cuerpo le cuesta más trabajo disminuir el peso debido al "Set point", momento en el que este percibe una "agresión" y trata de mantener su energía que se encuentra almacenada en forma de grasa y que es diferente en cada persona, por ello, se han desarrollado investigaciones a nivel celular para explicar la causalidad molecular en la obesidad (Hall y Guo, 2017). ...
Los hongos comestibles poseen compuestos bioactivos que ejercen efectos benéficos a la salud. Sin embargo, la transición alimentaria fomenta el abandono de la dieta tradicional mexicana, incluyendo los hongos comestibles. Esto ha incrementado la prevalencia de enfermedades metabólicas en la población mexicana, por ello, en el presente trabajo se analizó el estado nutricional, la calidad dietética y el consumo de hongos en las comunidades de San Miguel Tianguistenco y Santiago Coltzingo, Puebla; asimismo, por primera vez, se evaluó el efecto del consumo de los hongos Pleurotus ostreatus, Ustilago maydis y Ganoderma lucidum en tejido adiposo de ratas con obesidad inducida por dieta para diseñar una estrategia de alimentación saludable a nivel regional.
Para el alcance de la primera fase de este trabajo, se llevó a cabo un diagnóstico en 72 individuos mediante mediciones antropométricas, parámetros bioquímicos y presión
arterial. Se evaluó la ingesta energética de macronutrimentos y micronutrimentos. Para la segunda fase, se estudió el efecto de la ingesta de hongos comestibles en ratas Wistar alimentadas con una dieta alta en grasa en marcadores inflamatorios (adiponectina, TNF-α y JNK) y del estrés del retículo endoplásmico (BiP, ATF6, XBP-1, TANK y elF2α) en tejido adiposo.
Existe una alta prevalencia de sobrepeso, obesidad y riesgo cardiovascular en las
comunidades. Se observó un bajo consumo de alimentos recomendables y un alto
consumo de alimentos no recomendables, así como un bajo consumo de hongos. Sobre el estudio del modelo in vivo, se encontró que la adición de los hongos en la dieta redujó la hipertrofia de los adipocitos, la expresión de los marcadores inflamatorios y del estrés del retículo endoplásmico. La evidencia básica del efecto benéfico del consumo de los hongos contribuye al desarrollo de estrategias a nivel regional que promuevan e integren su consumo para prevenir la obesidad y sus complicaciones metabólicas asociadas.
... Obesity is a global and complex health concern (1, 2), with increasing prevalence (3,4) and severe socio-economic repercussions (1,2,5,6). The high availability of foods rich in sugar or fat is implicated in the obesity epidemic (1,7,8). Sugar, via its pre-and post-ingestive value (9)(10)(11)(12), acts in brain reward circuitries, inducing food preferences (10, 12) and food-seeking behaviors (11). ...
IntroductionWhile sweet taste perception is a potential determinant of feeding behavior in obesity, the supporting evidence is inconsistent and is typically associated with methodological limitations. Notably, possible associations between sweet taste perception and measures of food reward remain undetermined.Materials and methodsWe conducted a cross-sectional analysis comparing 246 individuals with severe obesity and 174 healthy volunteers using a validated method for taste perception assessment. We included gustatory variables, namely intensity and pleasantness ratings of sour, salt, sweet, and bitter tastants, and taste thresholds assessed by electrogustometry. Reward-related feeding behavior, including hedonic hunger, food addiction, feeding behavior traits, and acceptance of foods and alcohol, was evaluated using self-rated scales for comparison with gustatory measures.ResultIn logistic regressions adjusted for age, gender, educational level, and research center, we found that a greater likelihood of belonging to the obesity group was associated with higher sweet intensity ratings (OR = 1.4, P = 0.01), hedonic hunger, food addiction symptoms, restrained and emotional eating (1.7 < OR ≤ 4.6, all P ≤ 0.001), and lower alcohol acceptance (OR = 0.6, P = 0.0002). Using principal component analysis, we found that while hedonic hunger, food addiction, and emotional eating were strongly interrelated, they were not associated with sweet intensity perception that, in turn, had a closer relationship with alcohol acceptance and restrained eating.Conclusion
We found that individuals with obesity report higher sweet taste intensity ratings than healthy controls. Furthermore, while psychological measures of reward-related feeding behavior assess a common construct, sweet intensity perception may represent a different obesity-related dimension.
... Unsweetened nonalcoholic drinks, such as coffee, herbal tea, tea, and infusions, were allowed. Because micronutrients were not balanced in the treatment, one daily caplet of multimineral multivitamins (Multicentrum, GlaxoSmithKline S.p.A., Verona, Italy) was integrated into the nutritional intervention to avoid deficiencies [39] In addition, every patient was instructed to drink a minimum of two liters of water daily as part of the treatment plan and to take all the supplements, including potassium and magnesium, amounting to six tablets per day, giving a total of 300 mg of potassium and 113 mg of magnesium (Polase, GlaxoSmithKline S.p.A., Verona, Italy). Following the completion of the revised protein-sparing diet, each patient undertook a slow and gradual reintroduction of carbohydrates and lipids over a period of 8-12 weeks. ...
Effective nutrition therapy is a pressing issue in obesity and type 2 diabetes mellitus (T2DM) management. As such, this research aimed to determine the performance of a revised dietary strategy built on the protein-sparing diet in obesity and type 2 diabetes mellitus with regard to obtaining a rapid and stable improvement in glucometabolic control, body weight, body composition, and energy metabolism when applying the strategy in just twenty-one days. The revised protein-sparing diet differs from the traditional protein-sparing modified fast (PSMF) because it does not include foods. The daily calorie intake of this diet is exclusively derived from Isolate whey protein in addition to a formulation of Isolate whey protein enriched with essential amino acids in free form, with the addition of lipids such as extra virgin olive oil and coconut oil as a source of medium chain fatty acids, where the latter is taken for only the first four days of the diet, together with the use, for the same duration, of extended-release metformin, as the only antihyperglycemic allowed. Anthropometric measurements, bioimpedance analysis, indirect calorimetry, and blood chemistry assessments were conducted at the beginning of the study, time 0 (T0), and at the end, time 1 (T1), i.e., on the 21st day. The main outcomes of the revised protein-sparing diet after only twenty-one days were a reduction in body weight with the predominant loss of visceral atherogenic abdominal fat and, therefore, a possible contextual reduction in ectopic fat deposits together with a simultaneous reduction in insulin resistance and normalization of insulin levels, maintenance of free fat mass and basal metabolism, restoration of metabolic flexibility, and improvement of the glucometabolic and lipidic parameters. These results demonstrate the promising potential of the revised protein-sparing diet as an “etiologic tool” in the integrated nutritional treatment of metabolic diseases such as obesity and type 2 diabetes mellitus.
... Just restricting calories without adhering to the low-carbohydrate or low-fat instructions was not enough. Hall and Guo, in their review of the components of human energy balance, 24 discussed how some people might experience substantial changes in their energy intake and see the corresponding changes in their weight, and others will maintain a stable weight despite large caloric intake changes. There seem to be a variety of counterbalancing physiological processes to prevent weight loss. ...
To understand what determines the success of short- and long-term weight loss, we conduct a secondary analysis of dietary, metabolic, and molecular data collected from 609 participants before, during, and after a 1-year weight-loss intervention with either a healthy low-carbohydrate (HLC) or a healthy low-fat (HLF) diet. Through systematic analysis of multidomain datasets, we find that dietary adherence and diet quality, not just caloric restriction, are important for short-term weight loss in both diets. Interestingly, we observe minimal dietary differences between those who succeeded in long-term weight loss and those who did not. Instead, proteomic and gut microbiota signatures significantly differ between these two groups at baseline. Moreover, the baseline respiratory quotient may suggest a specific diet for better weight-loss outcomes. Overall, the identification of these dietary, molecular, and metabolic factors, common or unique to the HLC and HLF diets, provides a roadmap for developing individualized weight-loss strategies.
... They are supplied by the fat found in food, olive oil, olives, and avocados. (Hall et al., 2017) who reviewed 32 controlled trials, concluded that the reduction in total body fat was greater on lower fat diets compared to isocaloric diets. ...
Following a balanced diet is essential, not only for maintaining a good body shape, but it is also crucial for our health. By controlling our nutrition, we can reduce the symptoms and also the progression of many diseases such as diabetes, anemia, cardiovascular disease, movement disorders, and more. Of particular importance is the right proportion of the main energy sources - carbohydrates, proteins, and fats, which aim to reduce excess body fat and increase muscle mass. In search of an answer to whether a balanced diet is enough, we studied 20 volunteers to build a harmonious body. The present study focuses on the diagnosis and control of the main physical indicators of managed 20 to 30 years and how they are affected by 50 days balanced diet combined with and without strength training, divided into two groups - basic and experimental. Anthropometric parameters were measured using a body composition analyzer from the Japanese company TANITA. Based on the indicators of daily caloric intake and kilograms of muscle mass, the required daily intake of proteins, carbohydrates, and fats is calculated. In the main group, after 50 days, a decrease in body weight was reported on average by 5.87% (6.07 kg). What is concerning is the fact that body fat was reduced by only 1.8%, while muscle loss was 4.83% (3.73 kg). In the experimental group, which was on the same diet, but included strength training, the muscle mass was increased by 4.14% (3 kg) and a decrease in total fat by 3.05%. No significant differences are observed in total body weight - 0.89% (0.68 kg), due to the increase in muscle mass. After the research, we concluded that following a diet is not enough to build a harmonious body. This should be used in combination with a training process aimed at increasing muscle mass and lower in total body fat.
... Baltymai teigiamai veikia liesąją kūno masę tiek metant svorį, tiek norint svorio priaugti [15]. Žmogaus organizmas didžiąja dalimi yra sudarytas iš baltymų, kurių baltymų kiekis organizme nuolat kinta. ...
Mitybos nepakankamumas apibūdinamas kaip būsena, atsirandanti dėl maisto medžiagų trūkumo, dėl kurio pasikeičia kūno kompozicija (sumažėja raumeninė, riebalinė, kaulinė masė) bei kūno ląstelių masė, turinti įtakos fizinėms ir psichinėms asmens funkcijoms. Dėl mitybos nepakankamumo prastėja asmens gyvenimo kokybė, ekonominis produktyvumas, didėja gydymo išlaidos, auga žmogiškojo kapitalo nuostoliai. Mitybos nepakankamumo paplitimas Lietuvoje 2019 metais siekė 2,5 procento. Pasaulinės mitybos ataskaitos 2020 (angl. Global Nutrition Report 2020) duomenimis, vienas iš devynių žmonių pasaulyje yra alkanas arba jo mityba nepakankama. Tyrimo tikslas – įvertinti sveikatai palankios mitybos plano taikymo poveikį nepakankamos mitybos žmonių svoriui, kūno masės indeksui ir kūno kompozicijai. Mitybos plane, pagal kurį tiriamieji maitinosi tris mėnesius, maistinės makromedžiagos paskirstytos santykiu: baltymai 20 proc. (105 g), riebalai 30 proc. (70 g) ir angliavandeniai 50 proc. (262,50 g) paros energijos. Bendra dienos energinė vertė 2100 kcal. Valgymo režimas 5 kartai per dieną. Tyrime savanoriškai dalyvavo ir tris mėnesius pagal sudarytą mitybos planą maitinosi 10 tiriamųjų, kurių KMI tyrimo pradžioje buvo ≤ 18,5 kg/m2. Nepakankamos mitybos asmenims pritaikius sveikatai palankios mitybos planus, nustatytas svorio ir kūno masės indekso padidėjimas, tačiau kūno kompozicijos rodikliai pakito ne visi. Raumenų masė padidėjo visiems tiriamiesiems, kaulinė masė padidėjo pusei tyrimo dalyvių, penktadaliui tyrimo dalyvių sumažėjo riebalų masė, penktadaliui padidėjo metabolinis amžius, o visceralinių kūno riebalų masės pokyčių nenustatyta.
... Regarding the RQ, it increased significantly (p = 0.005) in women after the intervention, reflecting an increase in the contribution of carbohydrates at rest 39,40 . The results differ from what was expected 41 since, after a period of energy deficit, the metabolism of fatty acids at rest would be favoured [42][43][44] . ...
Background:
Diet and exercise are the mainstay of weight reduction programs.
Aim:
To evaluate the effect of diet and exercise on body weight and composition and resting metabolic rate (RMR) in obese adults.
Material and Methods:
Twenty-eight obese adults aged 22 to 61 years (18 women) completed four months of diet and exercise. They attended monthly nutritional consultations, and two-three weekly exercise sessions. At baseline and the end of the intervention, anthropometry, body composition by bioimpedance and RMR by indirect calorimetry (IC) were measured. Metabolic adaptation, defined as a decrease in thermogenesis to an extent greater than predicted based on the change in body weight and composition, was calculated.
Results:
Significant reductions in body weight and fat mass were observed in both genders. Fat-free mass decreased in women and remained unchanged in men. RMR remained stable. Metabolic adaptation was observed in 11/27 participants. Fat mass change in participants with and without metabolic adaptation was 8 Kg and 4,4 kg, respectively (p = 0,018). In the linear regression analysis, male sex accounted for a higher RMR (247.80 Kcal, p = 0,006) than females. For each kg of fat and fat free mass, the RMR varies 7.25 Kcal, (p = 0.02) and 9.79 Kcal (p = 0,006), respectively.
Conclusions:
The intervention reduced body weight and fat mass and maintained RMR. Fat free mass decreased in women. Participants with metabolic adaptation showed greater changes in fat mass.
... The reduction in indirectly measured physical activity with carbohydrate restriction that has previously been observed [20], suggests that either the potential effects of carbohydrate restriction on physical activity occur in the longer-term, and(or) that components of energy expenditure other than physical activity and resting metabolic rate are decreased with carbohydrate restriction. There is debate around the propensity for carbohydrate restriction to alter total energy expenditure, with suggestions that duration might be an important factor [41,42]. Findings from the present study suggest physical activity is not a large contributor to potential changes in total energy expenditure in the initial 24 h, which agrees with findings from 5 days of carbohydrate-manipulated diet in overweight men [43]although not to ketogenic levels. ...
Purpose
To determine the effects of dietary sugar or carbohydrate restriction on physical activity energy expenditure, energy intake, and physiological outcomes across 24 h.
Methods
In a randomized, open-label crossover design, twenty-five healthy men ( n = 10) and women ( n = 15) consumed three diets over a 24-h period: moderate carbohydrate and sugar content (MODSUG = 50% carbohydrate [20% sugars], 15% protein, 35% fat); low sugar content (LOWSUG = 50% carbohydrate [< 5% sugars], 15% protein, 35% fat); and low carbohydrate content (LOWCHO = 8% carbohydrate [< 5% sugars], 15% protein, 77% fat). Postprandial metabolic responses to a prescribed breakfast (20% EI) were monitored under laboratory conditions before an ad libitum test lunch, with subsequent diet and physical activity monitoring under free-living conditions until blood sample collection the following morning.
Results
The MODSUG, LOWSUG and LOWCHO diets resulted in similar mean [95%CI] rates of both physical activity energy expenditure (771 [624, 919] vs. 677 [565, 789] vs. 802 [614, 991] kcal·d ⁻¹ ; p = 0.29] and energy intake (2071 [1794, 2347] vs. 2195 [1918, 2473] vs. 2194 [1890, 2498] kcal·d ⁻¹ ; P = 0.34), respectively. The LOWCHO condition elicited the lowest glycaemic and insulinaemic responses to breakfast ( P < 0.01) but the highest 24-h increase in LDL-cholesterol concentrations ( P < 0.001), with no differences between the MODSUG and LOWSUG treatments. Leptin concentrations decreased over 24-h of consuming LOWCHO relative to LOWSUG ( p < 0.01).
Conclusion
When energy density is controlled for, restricting either sugar or total dietary carbohydrate does not modulate physical activity level or energy intake over a 24-h period (~ 19-h free-living) despite substantial metabolic changes.
Clinical trials registration ID
NCT03509610, https://clinicaltrials.gov/show/NCT03509610
... The most e cacious treatments target the hypothalamus and melanocortin system, speci cally glucagon-like protein 1 receptor (GLP-1R) and melanocortin 4 receptor (MC4R) agonists [9][10][11]. While these new pharmacological treatments are encouraging, diet and exercise remain the safest and most common lifestyle interventions; however, results are often temporary and many individuals regain weight in less than 5 years [12][13][14][15][16][17][18]. Understanding obesogenic factors that alter CNS function may allow for development of interventions that 'reset' these mechanisms and promote sustained weight loss through reduced appetite. ...
As the obesity epidemic continues, the understanding of macronutrient influence on central nervous system function is critical for understanding diet-induced obesity and potential therapeutics, particularly in light of the increased sugar content in processed foods. Previous research showed mixed effects of sucrose feeding on body weight gain but has yet to reveal insight into the impact of sucrose on hypothalamic functioning. Here, we explore the impact of liquid sucrose feeding for 12 weeks on body weight, body composition, caloric intake, and hypothalamic AgRP neuronal function and synaptic plasticity. While mice given sugar-sweetened water do not gain significant weight, they do show subtle differences in body composition and caloric intake. When given sugar-sweetened water, mice show similar alterations to AgRP neuronal excitability as in high-fat diet obese models. Increased sugar consumption also primes mice for increased caloric intake and weight gain when given access to a HFD. Our results show that elevated sucrose consumption increased activity of AgRP neurons and altered synaptic excitability. This may contribute to obesity in mice and humans with access to more palatable (HFD) diets.
... However, the majority of individuals with obesity are not successful in maintaining weight loss over time: they regain the weight within a year or two after ending therapy (Nordmo et al., 2020). These results indicate that in most humans, the obese body weight is actively defended, which is one of the biggest hurdles in the treatment of obesity (Hall & Guo, 2017). ...
The mechanisms under body weight regulation are complex and involve different factors like homeostatic system, hedonic system, and interacting pathways. Obesogenic environment has been shown to impair various aspects of body weight regulatory system, contributing to the increasing obesity rates all over the world. In the face of obesogenic environment, primary prevention before the development of overweight or obesity, particularly in children and adolescents, is the first line of defense. Despite the explosion of obesogenic environment research within the last decade, consensus on the definition and components of obesogenic environment has not been reached. This presents a major challenge towards our understanding of environmental research for obesity and our development of evidence-based support action for curbing the obesity epidemic. Future research may utilize the aforementioned ANGELO framework to comprehensively assess the effects of obesogenic environment, filling the gaps in the literature—effects of macro-environments and the political and socio-cultural microenvironments.
... Instead, the 0.23 MJ . day -1 per lb rule has been suggested (Hall et al., 2017). Based on the revised estimate, the athlete would have required a daily energy surplus of 2.84 MJ . ...
The primary aim of this thesis was to evaluate the dietary intake, energy expenditure and energy balance of young professional male rugby league players across the season.
... [52][53][54][55] Intimately closed to the malfunction of thermogenesis, obesity is often described as a disorder of energy intake and expenditure. 56 Up to now, abundant evidence has proved the fact that impaired heat production can give rise to obesity. For example, inhibition of the key transcriptional factor PRDM16 or reduction of UCP1 which is both involved in the UCP1dependent pathway can drive obesity. ...
The incidence of metabolism-related diseases like obesity and type 2 diabetes mellitus has reached pandemic levels worldwide and increased gradually. Most of them are listed on the table of high-risk factors for malignancy, and metabolic disorders systematically or locally contribute to cancer progression and poor prognosis of patients. Importantly, adipose tissue is fundamental to the occurrence and development of these metabolic disorders. White adipose tissue stores excessive energy, while thermogenic fat including brown and beige adipose tissue dissipates energy to generate heat. In addition to thermogenesis, beige and brown adipocytes also function as dynamic secretory cells and a metabolic sink of nutrients, like glucose, fatty acids, and amino acids. Accordingly, strategies that activate and expand thermogenic adipose tissue offer therapeutic promise to combat overweight, diabetes, and other metabolic disorders through increasing energy expenditure and enhancing glucose tolerance. With a better understanding of its origins and biological functions and the advances in imaging techniques detecting thermogenesis, the roles of thermogenic adipose tissue in tumors have been revealed gradually. On the one hand, enhanced browning of subcutaneous fatty tissue results in weight loss and cancer-associated cachexia. On the other hand, locally activated thermogenic adipocytes in the tumor microenvironment accelerate cancer progression by offering fuel sources and is likely to develop resistance to chemotherapy. Here, we enumerate current knowledge about the significant advances made in the origin and physiological functions of thermogenic fat. In addition, we discuss the multiple roles of thermogenic adipocytes in different tumors. Ultimately, we summarize imaging technologies for identifying thermogenic adipose tissue and pharmacologic agents via modulating thermogenesis in preclinical experiments and clinical trials.
... There are checks in the homeostatic mechanism for balancing the calories obtained from diet by its expenditure through body's energy-consuming activities [8][9][10]. If the consumed calories are more than the rate of expenditure by body's energy-consuming activities, the homeostatic mechanism fails and then the extra calories remain stored in the body in the form of adipose tissue fat which increases body mass. ...
The present study has shown a parallel increase of triacylglycerol, cholesterol, and low density lipoprotein (LDL) along with an increase in body mass and BMI of human obese subjects. Conversely a fall in HDL concentration was observed. Plasma leptin level increased proportionately with increase of body weight as obesity advanced from obese to morbid type. A positive correlation was observed between leptin and insulin concentrations in obese subjects. A parallel increase of plasma glucose concentration was followed with decreased expression of insulin receptor, measured in adipose tissue, with the progress of obesity. The decreased insulin receptor concentration might be the reason for seen insulin resistance and increased insulin level which marked the positive correlation with associated liptin level in obese subjects.
... Also, there is no solid evidence to support a particular macronutrient composition of a hypocaloric diet unique for use in NAFLD patients. Independent of weight loss, a diet low in carbohydrates and higher in protein intake is associated with improvements of metabolic parameters in NAFLD patients [73,78]. A recent meta-analysis 32 controlled isocaloric feeding studies with a constant proportion of protein in the diet and varying ratios of carbohydrate and fat indicates that diet differences are too small, which implies the importance of caloric intake in NAFLD patients [79]. ...
The prevalence of nonalcoholic fatty liver disease (NAFLD) is rising worldwide, paralleling the epidemic of obesity. The liver is a key organ for the metabolism of proteins, fats and carbohydrates. Various types of fats and carbohydrates in isocaloric diets differently influence fat accumulation in the liver parenchyma. Therefore, nutrition can manage hepatic and cardiometabolic complications of NAFLD. Even moderately reduced caloric intake, which leads to a weight loss of 5%-10% of initial body weight, is effective in improving liver steatosis and surrogate markers of liver disease status. Among dietary patterns, the Mediterranean diet mostly prevents the onset of NAFLD. Furthermore, this diet is also the most recommended for the treatment of NAFLD patients. However, clinical trials based on the dietary interventions in NAFLD patients are sparse. Since there are only a few studies examining dietary interventions in clinically advanced stages of NAFLD, such as active and fibrotic steatohepatitis, the optimal diet for patients in these stages of the disease must still be determined. In this narrative review, we aimed to critically summarize the associations between different dietary patterns, obesity and prevention/risk for NAFLD, to describe specific dietary interventions' impacts on liver steatosis in adults with NAFLD and to provide an updated overview of dietary recommendations that clinicians potentially need to apply in their daily practice.
... More specifically, the bodyweight set point theory posits the existence of a tightly regulated and complex biological control system, which drives a dynamic feedback loop aimed at defending a predetermined relative or absolute amount of adiposity. 33 Support for this theory comes from evidence in adults demonstrating immediate and sustained alterations in levels of hormones driving appetite and satiety, perceptions of food palatability, and resting energy expenditure following attempts at weight loss. 34,35 Other biobehavioural factors such as poor sleep quality, adversity, stress, and medications (causing iatrogenic weight gain) can also serve to exacerbate dysfunction of the energy regulatory system favouring weight gain. ...
Background:
There is limited evidence regarding the experiences, challenges, and needs of adolescents living with obesity (ALwO), their caregivers, and healthcare professionals (HCPs).
Objectives:
The cross-sectional, survey-based global ACTION Teens study aimed to identify perceptions, attitudes, behaviours, and barriers to effective obesity care among ALwO, caregivers of ALwO, and HCPs.
Methods:
ALwO (aged 12 to <18 years; N = 5275), caregivers (N = 5389), and HCPs treating ALwO (N = 2323) from 10 countries completed an online survey (August-December 2021).
Results:
Most ALwO perceived their weight as above normal (76% vs. 66% of caregivers), were worried about its impact on their health (85% vs. 80% of caregivers), and recently made a weight loss attempt (58%). While 45% of caregivers believed ALwO would slim down with age, only 24% of HCPs agreed. Most commonly reported weight loss motivators for ALwO were wanting to be more fit/in better shape according to ALwO (40%) and caregivers (32%), and improved confidence/social life according to HCPs (69%). ALwO weight loss barriers included lack of hunger control (most commonly reported by ALwO/caregivers), lack of motivation, unhealthy eating habits (most commonly agreed by HCPs), and lack of exercise.
Conclusions:
Misalignment between ALwO, caregivers, and HCPs-including caregivers' underestimation of the impact of obesity on ALwO and HCPs' misperception of key motivators/barriers for weight loss-suggests a need for improved communication and education.
... Además, la genética, la influencia familiar, el entorno sociocultural, algunas enfermedades subyacentes y otros factores como el uso de determinados medicamentos, la falta de sueño, el estrés crónico, etc.; pueden conducir al desarrollo de sobrepeso y/u obesidad (Valk y col., 2019). En este sentido, el modelo actual de prevención de la obesidad, basado en el equilibrio entre la ingesta y el gasto energético, se considera un modelo simplista (Hall & Guo, 2017). Además, la prevalencia de sobrepeso y la obesidad en niños y adolescentes ha aumentado en países desarrollados y en desarrollo en un período de tiempo relativamente corto (Ng y col., 2014). ...
El estilo de vida de la sociedad actual es uno de los responsables del desequilibrio energético entre las calorías ingeridas y las gastadas, por lo que mejorar la educación nutricional de los ciudadanos y despertar la conciencia sobre la importancia del ejercicio podría revertir en parte esta situación. Para ello, una de las estrategias que se está llevando a cabo es el etiquetado con el método Actividad Física Equivalente al Gasto Calórico (PACE). El objetivo del estudio fue analizar la influencia del etiquetado según el método PACE sobre la elección de los productos que se consumen en una máquina expendedora tipo “vending” ubicada en un campus universitario. Estudiantes de diferentes Grados de una universidad privada (24 mujeres y 19 hombres, 20,77±2,42 años) respondieron a una encuesta mediante un código QR expuesto en un póster con el etiquetado PACE en una máquina “vending”. El 63% (n=27) de los participantes cambiaron su intención de compra al recibir las informaciones del etiquetado PACE. Al comparar entre sexos, el 75% (n=18) de las mujeres cambió de decisión frente al 47% (n=9) de los hombres. Presentar la información calórica de un producto de forma visual y relacionarla con el equivalente en actividad física con el método PACE puede tener un efecto positivo sobre la decisión de compra de los consumidores de una máquina “vending”. Además, este efecto positivo parece ser más destacado en las mujeres con respecto a los hombres.
... The underlying mechanisms leading to overweight and obesity are comprised of a vast array of often interrelated internal and external mechanisms including biological, medical, social, psychological, economic and infrastructural, amongst others [5]. Research has consistently shown that both weight loss success and adherence can be achieved with varying dietary approaches [6,7]. Behavioural interventions entailing dietary and physical activity protocols have shown to be particularly promising [8][9][10][11]. ...
Introduction
The long-term effects of interventions aiming to achieve substantial, sustainable weight loss maintenance have been disappointing. Most people regain their lost weight over time but some seem to be able to maintain their weight loss. We are following the experiences of patients over time prospectively. This study forms the baseline to provide insights into patient experiences prior to entering a primary care-led weight management intervention and their expectations going forward.
Materials and methods
We recruited 21 adult male and female patients of varying ethnicity with a BMI between 27.7kg/m2 and 48.4kg/m2 from a cohort of patients entering a primary care-led weight management intervention. Patients were offered video and audio interview options during the COVID-19 lockdown. In total, twenty chose the audio option, while one chose the video option. The interview format was semi-structured with room for individual exploration.
Discussion
We found that participants experienced feeling unable to control their weight and encountered a multitude of internal and external barriers to weight management. Some had supportive environments, while others experienced discouraging external influences. Though personal characteristics varied, motivations, goals and expected benefits were similar across this cohort. Most participants had previously experienced transient successful weight-loss attempts with varying approaches. COVID-19 was experienced as an opportunity or barrier for change.
Conclusion
This study illustrates the importance of gaining comprehensive insights into the diverse experiences patients encounter when trying to achieve weight loss. Personalized support taking into account individual experiences and circumstances may enhance long-term treatment outcomes. Future research into the complexities of weight management based on individual accounts can aid in the creation of improved treatment protocols.
... We also agree that there might be ranges of body fatness where the physiologic regulation is relatively weak (8). However, there is a wealth of data demonstrating that perturbations causing significant alterations in body weight are met by counteracting changes in energy expenditure and appetite (5), strongly suggesting that body weight is effectively a regulated variable. Body weight regulation might conceivably be an emergent phenomenon resulting from the regulation of more fundamental quantities such as cellular energy supply, status, and stores as depicted in the figure in our Perspective (1). ...
... Specifically, the differences in nutrients observed in the quinoa diet phase are attributable to the change in the pseudocereal and not to other dietary modifications since quinoa is rich, among other things, in unsaturated fats and protein, and poor in carbohydrates. In this line, the thermodynamic arguments imply that the number of calories is not the only determinant of body weight, but that the composition of the diet also plays a very important role [19]. Precisely, the difference in weight that we can observe is due to these three macronutrients. ...
This study aimed to observe if quinoa could produce a benefit on postprandial glycemia that would result in less progression to type 2 diabetes (T2D). A cross-over design pilot clinical study with a nutritional intervention for 8 weeks was performed: 4 weeks on a regular diet (RD) and 4 weeks on a quinoa diet (QD). Nine subjects aged ≥65 years with prediabetes were monitored during the first 4 weeks of RD with daily dietary records and FreeStyle Libre®. Subsequently, participants started the QD, where quinoa and 100% quinoa-based products replaced foods rich in complex carbohydrates that they had consumed in the first 4 weeks of RD. The glycemic measurements recorded by the sensors were considered as functions of time, and the effects of nutrients consumed at the intended time period were analyzed by means of a function-on-scalar regression (fosr) model. With QD participants, decreased body weight (−1.6 kg, p = 0.008), BMI (−0.6 kg/m2 p = 0.004) and waist circumference (−1.5 cm, p = 0.015) were observed. Nutrients intake changed during QD, namely, decreased carbohydrates (p = 0.004) and increased lipids (p = 0.004) and some amino acids (p < 0.05). The fosr model showed a reduction in postprandial glycemia in QD despite intrapersonal differences thanks to the joint action of different nutrients and the suppression of others consumed on a regular diet. We conclude that in an old age and high T2D-risk population, a diet rich in quinoa reduces postprandial glycemia and could be a promising T2D-preventive strategy.
... Given that this environment is the main cause of obesity in a majority of humans, bariatric surgery is only a symptomatic treatment but does not attack the root cause of obesity, which would require removal or neutralization of the obesogenic environment. However, the sustained effects on body weight after bariatric surgery are nothing but remarkable, considering that similar weight loss induced by dieting provokes very strong adaptive and counter-regulatory responses such as increased hunger and reduced metabolism [9,10]. Such counter-regulatory responses are by and large absent in bariatric surgery patients. ...
Background
Bariatric or weight loss surgery is currently the most effective treatment for obesity and metabolic disease. Unlike dieting and pharmacology, its beneficial effects are sustained over decades in most patients, and mortality is among the lowest for major surgery. Because there are not nearly enough surgeons to implement bariatric surgery on a global scale, intensive research efforts have begun to identify its mechanisms of action on a molecular level in order to replace surgery with targeted behavioral or pharmacological treatments. To date, however, there is no consensus as to the critical mechanisms involved.
Scope of Review
The purpose of this non-systematic review is to evaluate the existing evidence for specific molecular and inter-organ signaling pathways that play major roles in bariatric surgery-induced weight loss and metabolic benefits, with a focus on Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG), in both humans and rodents.
Major Conclusions
Gut-brain communication and its brain targets of food intake control and energy balance regulation are complex and redundant. Although the relatively young science of bariatric surgery has generated a number of hypotheses, no clear and unique mechanism has yet emerged. It seems increasingly likely that the broad physiological and behavioral effects produced by bariatric surgery do not involve a single mechanism, but rather multiple signaling pathways. Besides a need to improve and better validate surgeries in animals, advanced techniques, including inducible, tissue-specific knockout models, and the use of humanized physiological traits will be necessary. State-of-the-art genetically-guided neural identification techniques should be used to more selectively manipulate function-specific pathways.
... 4 Interventions commonly used to combat obesity try to establish a negative energy balance to promote weight loss, as this condition is seen as an imbalance between energy intake, which is excessive, and energy expenditure. 5 However, to establish a negative energy balance, the individual's energy expenditure needs to be measured. 6 Precise and validated techniques, such as calorimetry (direct or indirect) and doubly labeled water (DLW), are considered gold standard tools for establishing resting energy expenditure (REE) and total energy expenditure (TEE), respectively. ...
Context:
Energy expenditure predictive equations can generate inaccurate estimates for overweight or obese individuals.
Objective:
The objective of this review was to determine which predictive equations for resting energy expenditure (REE) and total energy expenditure (TEE) have the lowest bias and the highest precision in adults with overweight and obesity.
Data sources:
Searches were performed in January 2022 in MEDLINE, Web of Science, Scopus, CENTRAL, and the gray literature databases.
Data extraction:
Meta-analyses were performed with equations included in more than 1 study. The DerSimonian and Laird random-effects model and the I2 statistic were used to quantify heterogeneity in the quantitative analyses. The Egger test was performed to assess potential publication biases, and metaregressions were conducted to explore the heterogeneity. Findings were presented separated by participants' body mass index classification (overweight and obesity).
Data analysis:
Sixty-one studies were included. The FAO/WHO/UNU (1985) equation, which uses only body weight in its formula, showed the lowest bias in estimating REE (mean difference [MD] = 8.97 kcal; 95% CI = -26.99; 44.94). In the subgroup analysis for individuals with obesity, the Lazzer (2007) equation showed the lowest bias (MD = 4.70 kcal; 95% CI = -95.45; 104.86). The Harris-Benedict equation (1919) showed the highest precision values for individuals with overweight (60.65%) and for individuals with obesity (62.54%). Equations with body composition data showed the highest biases. The equation proposed by the Institute of Medicine (2005) showed the lowest bias (MD = -2.52 kcal; 95% CI = -125.94; 120.90) in estimating the TEE. Most analyses showed high heterogeneity (I2 > 90%). There was no evidence of publication bias.
Conclusion:
For individuals with overweight, the FAO/WHO/UNU (1985) and the Harris-Benedict equations (1919) showed the lowest bias and the highest precision in predicting the REE, respectively. For individuals with obesity, the Harris-Benedict equation (1919) showed the highest precision and the Lazzer equation (2007) showed the lowest bias. More studies are needed on predictive equations to estimate the TEE.
Systematic review registration:
PROSPERO registration no. CRD42021262969.
... Despite the multifactorial nature of obesity, it influences genetic and nutritional aspects and lack of physical activity [3]; however, the energy imbalance has been described as one of the main causes due to the dynamic interrelationship between various components of energy balance and compensatory physiological processes [4]. The resting metabolic rate (RMR) contributes as much as 60-75% of the total daily energy expenditure, and it plays a key role in energy balance and body weight control [5]. ...
Hormonal changes are caused by the menstrual cycle phases, which influence resting metabolic rate and eating behavior. The aim of the study was to determine resting metabolic rate (RMR) and its association with dietary intake according to the menstrual cycle phase in lean and obese Chilean women. This cross-sectional analytical study included 30 adult women (15 lean and 15 with obesity). Body composition was measured with a tetrapolar bioelectrical impedance meter. Nutritional status was determined by adiposity. A 24-h recall of three nonconsecutive days verifies dietary intake. The RMR was measured by indirect calorimetry. All measurements were performed in both the follicular and luteal phases of the menstrual cycle. Statistical analyses were performed with STATA software at a significance level, which was α = 0.05. The RMR (β = 121.6 kcal/d), temperature (β = 0.36 °C), calorie intake (β = 317.1 kcal/d), and intake of lipids (β = 13.8 g/d) were associated with the luteal phase in lean women. Only extracellular water (β = 1.11%) and carbohydrate consumption (β = 45.2 g/d) were associated in women with obesity. Lean women showed increased RMR, caloric intake, and lipid intake during the luteal phase. For women with obesity, carbohydrate intake increased but not RMR.
... Tam et al. [166] explored the responses of mice to perturbations of energy balance and concluded empirically that they did not have an SP control system for adiposity. In contrast, Hall and Guo [167] suggested that an SP was commensurate with current data in humans. In both cases, though a DIP was not explicitly considered. ...
People completely lacking body fat (lipodystrophy/lipoatrophy), and those with severe obesity, both show profound metabolic and other health issues. Regulating levels of body fat somewhere between these limits would therefore appear to be adaptive. Two different models might be contemplated. More traditional is a set-point where levels are regulated around a fixed level. Alternatively, is a system that tolerates fairly wide variation but is activated when critically high or low levels are breached - a dual intervention point (DIP) system. A DIP system seems to fit our experience much better than a set-point, and models suggest it is more likely to have evolved. A DIP system may have evolved because of two contrasting selection pressures. At the low end we may have been selected to avoid low levels of fat as a buffer against starvation, disease induced anorexia, and to support reproduction. At the upper end we may have been selected to avoid excess storage because of the elevated risks of predation. This upper limit of control seems to have malfunctioned because some of us deposit large fat stores, with important negative health effects. Why has evolution not protected us against this problem? One possibility is that because the system evolved as a protection against predation risks, then when we dramatically reduced the risk of being predated in our evolutionary history, the protective system slowly fell apart due to random mutations. By chance it fell apart more in some people than others, and these people are now unable to effectively manage their weight in the face of the modern food glut. To understand the evolutionary context of obesity it is important to separate the adaptive reason for storing some fat (i.e. the lower intervention point), from the non-adaptive reason for storing lots of fat (a broken upper intervention point). The DIP model has several consequences for how we understand the obesity problem and what happens when we attempt to treat it.
... And can we attribute this capacity to all organisms? For instance, 'balance' could track many things, such as getting enough nutrients or avoiding excesses, or it could be quantified through inputs and outputs in an energy equation-an old view still hotly debated (Hall et al. 2012;Hall and Guo 2017;Raubenheimer and Simpson 2019;Minderis et al. 2021;Ludwig et al. 2021). Balance might even suggest the platitude of eating 'everything in moderation', still generally promoted by nutritionists (Sizer and Whitney 2020) and public health researchers (Mente and Yusuf 2018). ...
While philosophers of science have marginally discussed concepts such as ‘nutrient’, ‘naturalness’, ‘food’, or the ‘molecularization’ of nutrition, they have yet to seriously engage with the nutrition sciences. In this paper, I offer one way to begin this engagement by investigating conceptual challenges facing the burgeoning field of nutritional ecology and the question of how organisms construct a ‘balanced’ diet. To provide clarity, I propose the distinction between nutrient balance as a property of foods or dietary patterns and nutrient balancing as an evolved capacity to regulate nutrient intake. This distinction raises conceptual and empirical issues, such as what properties constitute this capacity and whether they are the same in all organisms. Additionally, while scientists use the term ‘balancing’, its intension and extension need further clarification. Based on the literature, the properties of external nutrient detection, internal sensing of nutrient levels, and organismal regulation could provide a basic recipe for nutrient balancing. Next, using an evolutionary lens, I examine nutrient acquisition in some prokaryotes, slime molds, simple multicellular eukaryotes, and in the quirks of multicellular metabolism to raise questions about the origins and universality of balancing. Finally, I build on this explication of balance and balancing by considering how obesity and cancer might respectively elucidate problems of organismal nutrient imbalances versus disrupted cellular nutrient balancing. http://philsci-archive.pitt.edu/20344/
... However, they can cause adverse effects such as headache, insomnia, constipation, and steatorrhea [3]. Several exogenous factors, such as diet and lifestyle, can affect energy expenditure and are therefore also associated with the risk of developing obesity [4]. Therefore, it is important to explore safe and effective natural dietary phytochemicals as candidates for obesity prevention and to understand their underlying mechanisms of action. ...
Liquiritigenin (LQG) is a natural flavonoid from the herb Glycyrrhiza uralensis Fisch that exhibits multiple biological activities. However, its specific role in antiobesity and its related underlying molecular mechanisms remain unknown. The primary purpose of this study is to explore the effects and regulatory mechanisms of LQG on lipid accumulation in 3T3-L1 adipocytes. The results show that LQG significantly reduced triglyceride levels and downregulated the expression of transcription factors such as CCAAT/enhancer-binding protein � (C/EBP�) and peroxisome proliferator-activated receptor (PPAR) in 3T3-L1 adipocytes. Additionally, the expression of sterolregulatory element-binding protein 1c (SREBP1c), acetyl-CoA carboxylase 1 (ACC1), and fatty acid synthase (FASN) involved in lipogenesis was reduced by treatment with LQG. The protein expression levels of light chain 3B (LC3B), autophagy-related protein 7 (ATG7) and p62 were also modulated by LQG, leading to the suppression of autophagy. Further, LQG activated the phosphorylation of the mammalian target of rapamycin (mTOR), the inhibition of which was followed by the restored expression of autophagy-related proteins. Pretreatment with an mTOR inhibitor also reverted the expression of several genes or proteins involved in lipid synthesis. These results suggest that LQG inhibited lipid accumulation via mTOR mediated autophagy in 3T3-L1 white adipocytes, indicating the role of LQG as a potential natural bioactive component for use in dietary supplements for preventing obesity.
... The ketogenic diet is a high fat, low carbohydrate with moderate protein diet [18]. It has been used in multiple diseases, such as epilepsy, obesity, type2 diabetes, and so on [19][20][21][22][23][24][25][26]. Recent studies showed that the benefits of ketogenic diet were mostly due to the ability to regulate inflammation by the ketone body β-hydroxybutyrate (BHB) [18,[27][28][29][30]. ...
Background
Aseptic Loosening (AL) following periprosthetic osteolysis is the main long-term complication after total joint arthroplasty (TJA). However, there is rare effective treatment except for revision surgery, which is costly and painful to the patients. In recent years, the ketone body β-hydroxybutyrate (BHB) has attracted much attention and has been proved to be beneficial in many chronic diseases. With respect to the studies on the ketone body β-hydroxybutyrate (BHB), its anti-inflammatory ability has been widely investigated. Although the ketone body β-hydroxybutyrate has been applied in many inflammatory diseases and has achieved considerable therapeutic efficacy, its effect on wear particles induced osteolysis is still unknown.
Results
In this work, we confirmed that the anti-inflammatory action of β-hydroxybutyrate (BHB) could be reappeared in CoCrMo alloy particles induced osteolysis. Mechanistically, the ketone body β-hydroxybutyrate (BHB) deactivated the activation of NLRP3 inflammasome triggered by CoCrMo alloy particles. Of note, this inhibitory action was independent of Gpr109a receptor as well as histone deacetylase (HDAC) suppression. Furthermore, given that butyrate, one kind of short chain fatty acid (SCFA) structurally related to β-hydroxybutyrate (BHB), has been reported to be an inhibitor of osteoclast, thus we also investigate the effect of β-hydroxybutyrate (BHB) on osteoclast, which was contributed to bone resorption. It was found that β-hydroxybutyrate (BHB) did not only affect osteoclast differentiation, but also inhibit its function. Unlike the inflammasome, the effect of β-hydroxybutyrate (BHB) on osteoclast may mainly rely on histone deacetylase (HDAC) suppression.
Conclusions
In general, our study showed that the alleviation of osteolysis may owe to the effect of β-hydroxybutyrate (BHB) on inflammasome deactivation and osteoclast.
Graphical Abstract
... More specifically, the bodyweight set point theory posits the existence of a tightly regulated and complex biological control system, which drives a dynamic feedback loop aimed at defending a predetermined relative or absolute amount of adiposity. 33 Support for this theory comes from evidence in adults demonstrating immediate and sustained alterations in levels of hormones driving appetite and satiety, perceptions of food palatability, and resting energy expenditure following attempts at weight loss. 34,35 Other biobehavioural factors such as poor sleep quality, adversity, stress, and medications (causing iatrogenic weight gain) can also serve to exacerbate dysfunction of the energy regulatory system favouring weight gain. ...
This Review describes current knowledge on the epidemiology and causes of child and adolescent obesity, considerations for assessment, and current management approaches. Before the COVID-19 pandemic, obesity prevalence in children and adolescents had plateaued in many high-income countries despite levels of severe obesity having increased. However, in low-income and middle-income countries, obesity prevalence had risen. During the pandemic, weight gain among children and adolescents has increased in several jurisdictions. Obesity is associated with cardiometabolic and psychosocial comorbidity as well as premature adult mortality. The development and perpetuation of obesity is largely explained by a bio-socioecological framework, whereby biological predisposition, socioeconomic, and environmental factors interact together to promote deposition and proliferation of adipose tissue. First-line treatment approaches include family-based behavioural obesity interventions addressing diet, physical activity, sedentary behaviours, and sleep quality, underpinned by behaviour change strategies. Evidence for intensive dietary approaches, pharmacotherapy, and metabolic and bariatric surgery as supplemental therapies are emerging; however, access to these therapies is scarce in most jurisdictions. Research is still needed to inform the personalisation of treatment approaches of obesity in children and adolescents and their translation to clinical practice.
... Results from one meta-analysis showed a greater, but not clinically significant, body fat change (by 16 g/day) favoring lower fat diets compared to lower carbohydrate diets [138]. A systematic review in people with T2DM [139], several studies [140][141][142][143], and a metaanalysis [144] suggested that lowering total fat intake did not consistently improve glycemia or CVD risk factors in T2DM, but the benefit from a low-fat eating pattern appeared to be mostly related to weight loss and not to the eating pattern itself [145,146]. ...
As years progress, we are found more often in a postprandial than a postabsorptive state. Chrononutrition is an integral part of metabolism, pancreatic function, and hormone secretion. Eating most calories and carbohydrates at lunch time and early afternoon, avoiding late evening dinner, and keeping consistent number of daily meals and relative times of eating occasions seem to play a pivotal role for postprandial glycemia and insulin sensitivity. Sequence of meals and nutrients also play a significant role, as foods of low density such as vegetables, salads, or soups consumed first, followed by protein and then by starchy foods lead to ameliorated glycemic and insulin responses. There are several dietary schemes available, such as intermittent fasting regimes, which may improve glycemic and insulin responses. Weight loss is important for the treatment of insulin resistance, and it can be achieved by many approaches, such as low-fat, low-carbohydrate, Mediterranean-style diets, etc. Lifestyle interventions with small weight loss (7–10%), 150 min of weekly moderate intensity exercise and behavioral therapy approach can be highly effective in preventing and treating type 2 diabetes. Similarly, decreasing carbohydrates in meals also improves significantly glycemic and insulin responses, but the extent of this reduction should be individualized, patient-centered, and monitored. Alternative foods or ingredients, such as vinegar, yogurt, whey protein, peanuts and tree nuts should also be considered in ameliorating postprandial hyperglycemia and insulin resistance. This review aims to describe the available evidence about the effects of diet, chrononutrition, alternative dietary interventions and exercise on postprandial glycemia and insulin resistance.
Obesity is a serious, chronic disease that is associated with a range of adiposity‐based comorbidities, including cardiovascular disease, type 2 diabetes, and nonalcoholic fatty liver disease. In the United States, obesity is a public health crisis, affecting more than 40% of the population. Obesity disproportionately affects Latinx people, who have a higher prevalence of obesity and related comorbidities (such as cardiovascular disease, type 2 diabetes, and nonalcoholic fatty liver disease) compared with the general population. Many factors, including genetic predisposition, environmental factors, traditional calorie‐dense Latinx diets, family dynamics, and differences in socioeconomic status, contribute to the increased prevalence and complexity of treating obesity in the Latinx population. Additionally, significant heterogeneity within the Latinx population and disparities in health care access and utilization between Latinx people and the general population add to the challenge of obesity management. Culturally tailored interventions have been successful for managing obesity and related comorbidities in Latinx people. Antiobesity medications and bariatric surgery are also important options for obesity treatment in Latinx people. As highlighted in this review, when managing obesity in the Latinx population, it is critical to consider the impact of genetic, dietary, cultural, and socioeconomic factors, in order to implement an individualized treatment strategy.
Purpose
This study aims to evaluate the carbohydrate content, ingredient profile and degree of processing of supposedly “low-carb” foods in the Brazilian market.
Design/methodology/approach
Information was collected from physical supermarkets in Divinópolis, Minas Gerais and on websites throughout Brazil between July and September/2020. The carbohydrate content was assessed in g/100 g, and ingredient lists were investigated for the presence of carbohydrate-rich ingredients. The degree of processing of the products was evaluated by NOVA classification to determine whether the term “low carb” had been translated into Portuguese.
Findings
This study evaluated a total number of 164 products, the most frequent were bakery products (34.7%), granola and cereal bars (19.5%) and candies and desserts (14.0%). This claim was also found in low-carb foods such as cheese and chicken. Most food products evaluated (56.0%) were classified as ultra-processed, with the group having the highest carbohydrate content (20.0; 3.0–47.5g/100g), compared to products classified as processed foods ( p < 0.01). The ingredient lists showed items rich in carbohydrates, such as cassava and corn derivatives. In 162 products, a low-carb claim was displayed without translation into Portuguese. These data demonstrate that most of these products are ultra-processed and have a high glycidic content.
Originality/value
To the best of the authors’ knowledge, the study was a pioneer investigation of the ingredients of “low-carb” foods, their carbohydrate composition and their degree of processing based on the NOVA classification.
The antiobesity efficacy and underlying mechanisms of polysaccharides extracted from Fu brick tea (FBTP) were investigated. An 8-week administration of FBTP dose-dependently inhibited increases in body weight and weights of the epididymal-, retroperitoneal- and inguinal-white adipose tissues and stimulated beige-fat development and brown adipose tissue-derived nonshivering thermogenesis in high-fat diet-induced obese mice. FBTP protected against obesity-associated abnormality in serum adiponectin and leptin, indicating its positive regulation of energy metabolism. FBTP reversed gut dysbiosis by enriching beneficial bacteria, for example, Lactobacillus, Parabacteroides, Akkermansia, Bifidobacterium, and Roseburia. Results from the fecal microbiota transplantation further confirmed that FBTP-induced microbial shifts contributed to adipose browning and thermogenesis, thereby alleviating host adiposity, glucose homeostasis, dyslipidemia, and its related hepatic steatosis. Our study demonstrates the great potential of FBTP with prebiotic-like activities in preventing diet-induced obesity and its related metabolic complications via gut microbiota-derived enhancement of fat burning and energy expenditures.
Both scientific evidence and popular diet trends have sought to identify the ideal diet for weight loss with strategies focused on either restricting carbohydrates or fat. While there is a strong physiologic rationale for either carbohydrate restriction or fat restriction to achieve a calorie deficit needed for weight loss, evidence from randomized controlled trials suggest either type of diet is effective for weight loss. The level of adherence, rather than macronutrient content, is the driver of successful weight loss.
Fu brick tea is one of the most famous microbially fermented teas that has received considerable attention owing to its promising anti-obesity capacity; however, the underlying mechanisms of its action remain largely unexplored. Herein, an eight-week oral administration of Fu brick tea aqueous extract (FTE) was observed to dose-dependently reduce body weight and abnormal fat accumulation for inguinal white adipose tissue, stimulate beige-fat development and thermogenesis in the brown adipose tissue of mice fed with a high-fat diet (HFD) (p < 0.05). FTE ameliorated HFD-induced gut dysbacteriosis and improved the microbiome ecology such that it exhibited an increased capacity to reduce the host adiposity, abnormal glycometabolism, and hepatic steatosis. FTE increased the abundance of beneficial bacteria strains, e.g., Lactobacillus, Roseburia, Bifidobacterium, Akkermansia, Parabacteroides, and Prevotella, accompanied with the improved production of short-chain fatty acids (p < 0.05). Moreover, the PICRUSt pathway analysis revealed that FTE upregulated genes enriched in pathways of the carbohydrate metabolism, signaling molecules and immune system. As a rising star of post-fermented teas with the low cost, high accessibility and confirmed health benefits, our findings indicate the beneficial impacts of Fu brick tea on the promotion of adipose browning and thermogenesis in association with gut microbiota reconstructions, paving the way to restrict obesity and its associated metabolic diseases.
Callerya speciosa ("Niu Dali" in Chinese) is a well-known edible plant in Southeast China. C. speciosa roots contain a high level of polysaccharides, which have been reported to show multiple health-promoting effects. In the current study, the anti-obesity effects of a crude extract of C. speciosa polysaccharides (NP) and its underlying mechanisms of action are investigated. C57BL/6 mice were divided into three groups and fed either a standard diet or a high-fat diet (HFD). The HFD + NP group mice received oral administration of NP (100 mg per kg per day) every other day for 10 weeks. NP supplementation alleviated HFD-induced diabetic biomarkers including body weight gain, hyperlipidemia, liver steatosis, and adipocyte hypertrophy. Western blot and RT-PCR analyses revealed that NP inhibited hepatic de novo lipogenesis and adipogenesis (i.e. decreased expression of Srebp1c, Fas, Cebpα, and Pparγ), stimulated adipocyte lipolysis (enhanced mRNA expression of Hsl and Mgl), and attenuated HFD-induced hepatic inflammation (decreased expression of TNF-α and NF-κB p65). Furthermore, 16S rDNA and GC-MS analyses showed that NP supplementation restored the Firmicutes/Bacteroidetes proportion, elevated colon-derived SCFAs, especially acetic acid content, and increased the relative abundance of genera associated with SCFA production in HFD-fed mice. Findings from this study suggest that NP alleviated HFD-induced obesity in a mouse model, which was possibly due to its ameliorative effects on diet-induced gut dysbiosis. Polysaccharides from C. speciosa are promising prebiotics and they may be further developed as functional foods for the management of obesity.
Purpose
Nutrition is an important lifestyle modification used in the treatment of obesity. The purpose of this review is to highlight different dietary interventions used to promote weight loss in both adults and children.
Methods
A search using PubMed was performed for articles on topics related to nutrition and management and/or treatment of obesity in adults adolescents and children. The literature was reviewed and pertinent sources were used for this narrative review.
Discussion
There are many effective nutrition interventions used to treat obesity, including altering macronutrient composition, implementing different dietary patterns, and changing meal timing. Although these interventions can induce weight loss in adults, management of obesity in children is more difficult given their varied nutrition needs in growth and development. The use of food as medicine in obesity treatment is individualized based on patient's age, food preference, and concurrent medical conditions.
Implications
Given the multifactorial etiology of obesity, treatment requires multidisciplinary care beyond nutrition intervention.
Obesity is currently one of the most serious health problems, affecting 13% of the world's adult population. Obesity is characterized by persistent low‐grade chronic inflammation that assumes systemic proportions and triggers several associated metabolic diseases. Furthermore, obesity has been associated with an increased occurrence of central disorders such as impaired cognitive function, reward system dysfunction, and depression. In summary, there is a quantitative reduction in the release of neurotransmitters in depression. Postsynaptic cells capture lower concentrations of neurotransmitters, which leads to a functional reduction in the central nervous system (CNS). Globally, approximately 15–65% of women experience depressive symptoms during pregnancy, depending on their location. Depressive symptoms persist in some women, leading to postpartum depression (PPD). Thus, obesity may be considered a risk factor for PPD development. This study aimed to synthesize studies on the impact of obesity‐related neuroinflammation and PPD. We conducted a narrative review of the relevant literature. The search was performed in electronic databases, specifically PubMed, selecting articles in English published from 2014 to 2021 using the narrative review methodology.
Obesity has become a major health crisis in the past ∼50 years. The fat mass and obesity-associated (FTO) gene, identified by genome-wide association studies (GWAS), was first reported to be positively associated with obesity in humans. Mice with more copies of the FTO gene were observed to be obese, while loss of the gene in mice was found to protect from obesity. Later, FTO was found to encode an m⁶A RNA demethylase and has a profound effect on many biological and metabolic processes. In this review, we first summarize recent studies that demonstrate the critical roles and regulatory mechanisms of FTO in obesity and metabolic disease. Second, we discuss the ongoing debates concerning the association between FTO polymorphisms and obesity. Third, since several small molecule drugs and micronutrients have been found to regulate metabolic homeostasis through controlling the expression or activity of FTO, we highlight the broad potential of targeting FTO for obesity treatment. Improving our understanding of FTO and the underlying mechanisms may provide new approaches to treating obesity and metabolic diseases.
Accumulating evidence suggests that maternal overnutrition can result in a higher development risk of obesity and renal disease in the offspring’s adulthood. The present study tested different lipid levels in the maternal diet during pregnancy and lactation and its repercussions on the offspring of Wistar rats. Offspring of 1, 7, 30 and 90-d-old were divided into the following groups: Control (CNT) – offspring of dams that consumed a standard chow diet (3.5% of lipids); Experimental 1 (EXP1) – offspring of dams exposed to a high-fat diet (HFD) (28% of lipids); and Experimental 2 (EXP2) – offspring of dams exposed to a HFD (40% of lipids). Regarding maternal data, there was a decrease in the amount of diet ingested by EXP2. Daily caloric intake was higher in EXP1, while protein and carbohydrate intakes were lower in EXP2. While lipid intake was higher in the experimental groups, EXP1 consumed more lipids than EXP2, despite the body weight gain being higher in EXP2. Adult offspring from EXP1 presented higher blood glucose. Regarding morphometric analysis, in both experimental groups, there was an increase in the glomerular tuft and renal corpuscle areas, but an increase in the capsular space area only in EXP1. There was a decrease in the glomerular filtration rate (GFR) in EXP1, in contrast to an increase in GFR of EXP2, along with an increase in urinary protein excretion. In conclusion, the maternal HFDs caused significant kidney damage in offspring, but had different repercussions on the type and magnitude of recorded change.
Polysaccharide from Enteromorpha prolifera (EPP) has therapeutic and nutraceutical potential for obesity management due to its high hypolipidaemic activity. However, the metabolic mechanism by which EPP mediates anti-adiposity effects are not fully understood. This study aimed to evaluate the effects of EPP on insulin signaling and adaptive thermogenesis in high-fat diet (HFD)-fed obese mice, and further explore the underlying mechanisms. C57BL/6 male mice were fed a control diet or an HFD diet with or without 5% EPP for 12 weeks. The insulin signaling and thermogenic program in adipose tissue, and energy expenditure, as well as involvement of PPARγ coactivator-1α (PGC-1α)-fibronectin type 3 domain-containing protein 5 (FNDC5)/irisin pathway were assessed. EPP alleviated diet-induced adiposity, and decreased inflammatory response and improved insulin signaling in white adipose tissue (WAT) of HFD mice. Moreover, EPP administration increased oxygen consumption, carbon dioxide production and heat production in HFD mice, as reflected by the increased thermogenesis observed in brown fat and inguinal WAT. Meanwhile, EPP increased serum irisin concentration and activated PGC-1α/FNDC5/adenosine monophosphate-activated protein kinase α (AMPKα) pathway. These results suggested that dietary EPP improved insulin signaling and whole-body energy metabolism in obese mice, likely by activating the PGC-1α-FNDC5/irisin pathways.
Accurate measurement of free-living energy intake (EI) over long periods is imperative for understanding obesity and its treatment. Unfortunately, traditional methods rely on self-report and are notoriously inaccurate. Although EI can be indirectly estimated by the intake-balance method, this technique is prohibitively labor-intensive and expensive, requiring repeated measures of energy expenditure via doubly labeled water (DLW) along with multiple dual-energy X-ray absorptiometry (DXA) scans to measure changes in body energy stores.
Our objective was to validate a mathematical method to measure long-term changes in free-living energy intake.
We measured body weight and EI changes (ΔEI) over 4 time intervals by using the intake-balance method in 140 individuals who underwent 2 y of caloric restriction as part of the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy study. We compared the ΔEI values calculated by using DLW/DXA with those obtained by using a mathematical model of human metabolism whose only inputs were the initial demographic information and repeated body weight data.
The mean ΔEI values calculated by the model were within 40 kcal/d of the DLW/DXA method throughout the 2-y study. For individual subjects, the overall root mean square deviation between the model and DLW/DXA method was 215 kcal/d, and most of the model-calculated ΔEI values were within 132 kcal/d of the DLW/DXA method.
Accurate and inexpensive estimates of ΔEI that are comparable to the DLW/DXA method can be obtained by using a mathematical model and repeated body weight measurements. This trial was registered at clinicaltrials.gov as NCT00427193.
© 2015 American Society for Nutrition.
Over the past 20 y, higher-protein diets have been touted as a successful strategy to prevent or treat obesity through improvements in body weight management. These improvements are thought to be due, in part, to modulations in energy metabolism, appetite, and energy intake. Recent evidence also supports higher-protein diets for improvements in cardiometabolic risk factors. This article provides an overview of the literature that explores the mechanisms of action after acute protein consumption and the clinical health outcomes after consumption of long-term, higher-protein diets. Several meta-analyses of shorter-term, tightly controlled feeding studies showed greater weight loss, fat mass loss, and preservation of lean mass after higher-protein energy-restriction diets than after lower-protein energy-restriction diets. Reductions in triglycerides, blood pressure, and waist circumference were also reported. In addition, a review of the acute feeding trials confirms a modest satiety effect, including greater perceived fullness and elevated satiety hormones after higher-protein meals but does not support an effect on energy intake at the next eating occasion. Although shorter-term, tightly controlled feeding studies consistently identified benefits with increased protein consumption, longer-term studies produced limited and conflicting findings; nevertheless, a recent meta-analysis showed persistent benefits of a higher-protein weight-loss diet on body weight and fat mass. Dietary compliance appears to be the primary contributor to the discrepant findings because improvements in weight management were detected in those who adhered to the prescribed higher-protein regimen, whereas those who did not adhere to the diet had no marked improvements. Collectively, these data suggest that higher-protein diets that contain between 1.2 and 1.6 g protein · kg(-1) · d(-1) and potentially include meal-specific protein quantities of at least ∼25-30 g protein/meal provide improvements in appetite, body weight management, cardiometabolic risk factors, or all of these health outcomes; however, further strategies to increase dietary compliance with long-term dietary interventions are warranted.
© 2015 American Society for Nutrition.
Though the hunger-reduction phenomenon reported during ketogenic diets is well-known, the underlying molecular and cellular mechanisms remain uncertain. Ketosis has been demonstrated to exert an anorexigenic effect via cholecystokinin (CCK) release while reducing orexigenic signals e.g., via ghrelin. However, ketone bodies (KB) seem to be able to increase food intake through AMP-activated protein kinase (AMPK) phosphorylation, gamma-aminobutyric acid (GABA) and the release and production of adiponectin. The aim of this review is to provide a summary of our current knowledge of the effects of ketogenic diet (KD) on food control in an effort to unify the apparently contradictory data into a coherent picture.
Energy intake (EI) and physical activity energy expenditure (PAEE) are key modifiable determinants of energy balance, traditionally assessed by self-report despite its repeated demonstration of considerable inaccuracies. We argue here that it is time to move from the common view that self-reports of EI and PAEE are imperfect, but nevertheless deserving of use, to a view commensurate with the evidence that self-reports of EI and PAEE are so poor that they are wholly unacceptable for scientific research on EI and PAEE. While new strategies for objectively determining energy balance are in their infancy, it is unacceptable to use decidedly inaccurate instruments, which may misguide health care policies, future research, and clinical judgment. The scientific and medical communities should discontinue reliance on self-reported EI and PAEE. Researchers and sponsors should develop objective measures of energy balance.International Journal of Obesity accepted article preview online, 13 November 2014. doi:10.1038/ijo.2014.199.
BACKGROUND: Differences in biological changes from weight loss by energy restriction and/or exercise may be associated with differences in long-term weight loss/regain.
OBJECTIVE: To assess the effect of weight loss method on long-term changes in weight, body composition and chronic disease risk factors.
DATA SOURCES: PubMed and Embase were searched (January 1990-October 2013) for studies with data on the effect of energy restriction, exercise (aerobic and resistance) on long-term weight loss. Twenty articles were included in this review.
STUDY ELIGIBILITY CRITERIA: Primary source, peer reviewed randomized trials published in English with an active weight loss period of >6 months, or active weight loss with a follow-up period of any duration, conducted in overweight or obese adults were included.
STUDY APPRAISAL AND SYNTHESIS METHODS: Considerable heterogeneity across trials existed for important study parameters, therefore a meta-analysis was considered inappropriate. Results were synthesized and grouped by comparisons (e.g. diet vs. aerobic exercise, diet vs. diet + aerobic exercise etc.) and study design (long-term or weight loss/follow-up).
RESULTS: Forty percent of trials reported significantly greater long-term weight loss with diet compared with aerobic exercise, while results for differences in weight regain were inconclusive. Diet+aerobic exercise resulted in significantly greater weight loss than diet alone in 50% of trials. However, weight regain (∼55% of loss) was similar in diet and diet+aerobic exercise groups. Fat-free mass tended to be preserved when interventions included exercise.
The obesity epidemic is believed to be driven by a food environment that promotes consumption of inexpensive, convenient, high-calorie, palatable foods. Individual differences in obesity susceptibility or resistance to weight loss may arise because of alterations in the neurocircuitry supporting food reward and eating habits. In particular, dopamine signaling in the ventromedial striatum is thought to encode food reward and motivation, whereas dopamine in the dorsal and lateral striatum orchestrates the development of eating habits. We measured striatal dopamine D2-like receptor binding potential (D2BP) using positron emission tomography with [(18)F]fallypride in 43 human subjects with body mass indices (BMI) ranging from 18 to 45 kg m(-)(2). Opportunistic eating behavior and BMI were both positively associated with D2BP in the dorsal and lateral striatum, whereas BMI was negatively associated with D2BP in the ventromedial striatum. These results suggest that obese people have alterations in dopamine neurocircuitry that may increase their susceptibility to opportunistic overeating while at the same time making food intake less rewarding, less goal directed and more habitual. Whether or not the observed neurocircuitry alterations pre-existed or occurred as a result of obesity development, they may perpetuate obesity given the omnipresence of palatable foods and their associated cues.Molecular Psychiatry advance online publication, 9 September 2014; doi:10.1038/mp.2014.102.
DE JONGE, LILIAN, GEORGE BRAY. The thermic effect of food and obesity: A critical review.
This review has examined the factors that influence the thermic effect of food (TEF) by evaluating 49 studies that have compared subjects who are obese with those who are lean. Meal size, meal composition, the nature of the previous diet, insulin resistance, physical activity, and ageing influence TEF. In the studies of individuals who are obese or lean, of those who used intravenous glucose infusions, all but one found an impaired thermic response. A total of 29 out of 49 studies of individuals of normal weight or with obesity were identified where there was no difference in age between the groups, and where the subjects who were “overweight” were clearly obese. Of these 29, 22 reported a statistically significant reduction in TEF, 3 studies were not designed to look primarily at the effect of obesity on TEF, and the other 4 may not have had sufficiently palatable meals. From this review, we conclude that the reduction of TEF in obesity is related to the degree of insulin resistance, which may be influenced by a low level of sympathetic activity.
The study of human appetite and eating behaviour has become increasingly important in recent years due to the rise in body weight dysregulation through both obesity and eating disorders. Adequate control over appetite is paramount for the control of body weight and in order to understand appetite, it is necessary to measure eating behaviour accurately. So far, research in this field has revealed that no single experimental design can answer all research questions. Each research question posed will require a specific study design that will limit the findings of that study to those particular conditions. For example, choices will be made among the use of laboratory or free-living studies, time period for examination, specific measurement techniques and investigative methodologies employed. It is important that these represent informed decisions about what design and which methodology will provide the most meaningful outcomes. This review will examine some of the 'gold standard' study designs and methodologies currently employed in the study of human appetite and eating behaviour.
Clinicians and policy makers need the ability to predict quantitatively how childhood bodyweight will respond to obesity interventions.
We developed and validated a mathematical model of childhood energy balance that accounts for healthy growth and development of obesity, and that makes quantitative predictions about weight-management interventions. The model was calibrated to reference body composition data in healthy children and validated by comparing model predictions with data other than those used to build the model.
The model accurately simulated the changes in body composition and energy expenditure reported in reference data during healthy growth, and predicted increases in energy intake from ages 5-18 years of roughly 1200 kcal per day in boys and 900 kcal per day in girls. Development of childhood obesity necessitated a substantially greater excess energy intake than for development of adult obesity. Furthermore, excess energy intake in overweight and obese children calculated by the model greatly exceeded the typical energy balance calculated on the basis of growth charts. At the population level, the excess weight of US children in 2003-06 was associated with a mean increase in energy intake of roughly 200 kcal per day per child compared with similar children in 1976-80. The model also suggests that therapeutic windows when children can outgrow obesity without losing weight might exist, especially during periods of high growth potential in boys who are not severely obese.
This model quantifies the energy excess underlying obesity and calculates the necessary intervention magnitude to achieve bodyweight change in children. Policy makers and clinicians now have a quantitative technique for understanding the childhood obesity epidemic and planning interventions to control it.
Many questions must be considered with regard to consuming food, including when to eat, what to eat and how much to eat. Although eating is often thought to be a homeostatic behaviour, little evidence exists to suggest that eating is an automatic response to an acute shortage of energy. Instead, food intake can be considered as an integrated response over a prolonged period of time that maintains the levels of energy stored in adipocytes. When we eat is generally determined by habit, convenience or opportunity rather than need, and meals are preceded by a neurally-controlled coordinated secretion of numerous hormones that prime the digestive system for the anticipated caloric load. How much we eat is determined by satiation hormones that are secreted in response to ingested nutrients, and these signals are in turn modified by adiposity hormones that indicate the fat content of the body. In addition, many nonhomeostatic factors, including stress, learning, palatability and social influences, interact with other controllers of food intake. If a choice of food is available, what we eat is based on pleasure and past experience. This article reviews the hormones that mediate and influence these processes.
Overweight and obesity affects more than 66% of the adult population and is associated with a variety of chronic diseases. Weight reduction reduces health risks associated with chronic diseases and is therefore encouraged by major health agencies. Guidelines of the National Heart, Lung, and Blood Institute (NHLBI) encourage a 10% reduction in weight, although considerable literature indicates reduction in health risk with 3% to 5% reduction in weight. Physical activity (PA) is recommended as a component of weight management for prevention of weight gain, for weight loss, and for prevention of weight regain after weight loss. In 2001, the American College of Sports Medicine (ACSM) published a Position Stand that recommended a minimum of 150 min wk(-1) of moderate-intensity PA for overweight and obese adults to improve health; however, 200-300 min wk(-1) was recommended for long-term weight loss. More recent evidence has supported this recommendation and has indicated more PA may be necessary to prevent weight regain after weight loss. To this end, we have reexamined the evidence from 1999 to determine whether there is a level at which PA is effective for prevention of weight gain, for weight loss, and prevention of weight regain. Evidence supports moderate-intensity PA between 150 and 250 min wk(-1) to be effective to prevent weight gain. Moderate-intensity PA between 150 and 250 min wk(-1) will provide only modest weight loss. Greater amounts of PA (>250 min wk(-1)) have been associated with clinically significant weight loss. Moderate-intensity PA between 150 and 250 min wk(-1) will improve weight loss in studies that use moderate diet restriction but not severe diet restriction. Cross-sectional and prospective studies indicate that after weight loss, weight maintenance is improved with PA >250 min wk(-1). However, no evidence from well-designed randomized controlled trials exists to judge the effectiveness of PA for prevention of weight regain after weight loss. Resistance training does not enhance weight loss but may increase fat-free mass and increase loss of fat mass and is associated with reductions in health risk. Existing evidence indicates that endurance PA or resistance training without weight loss improves health risk. There is inadequate evidence to determine whether PA prevents or attenuates detrimental changes in chronic disease risk during weight gain.
Insufficient energy compensation after a preload (meal, snack, or beverage) has been associated with excess energy intake, but experimental studies have used heterogeneous methodologies, making energy compensation difficult to predict. The aim of this systematic review was to analyze the relative contributions of two key variables, preload physical form and intermeal interval (IMI), to differences in energy compensation. Forty-eight publications were included, from which percent energy compensation (%EC) data were extracted for 253 interventions (121 liquid, 69 semisolid, 20 solid, and 43 composite preloads). Energy compensation ranged from -370% (overconsumption, mostly of liquids) to 450% (overcompensation). A meta-regression analysis of studies reporting positive energy compensation showed that IMI (as the predominant factor) together with preload physical form and energy contributed significantly to %EC differences, accounting for 50% of the variance, independently from gender and BMI. Energy compensation was maximized when the preload was in semisolid/solid form and the IMI was 30-120 min. These results may assist in the interpretation of studies assessing the relative efficacy of interventions to enhance satiety, including functional foods and weight management products.
International Journal of Obesity is a monthly, multi-disciplinary forum for papers describing basic, clinical and applied studies in biochemistry, genetics and nutrition, together with molecular, metabolic, psychological and epidemiological aspects of obesity and related disorders
Background:
Diet-induced weight loss is accompanied by adaptive thermogenesis, ie, a disproportional or greater than expected reduction of resting metabolic rate (RMR).
Objective:
The aim of this study was to investigate whether adaptive thermogenesis is sustained during weight maintenance after weight loss.
Design:
Subjects were 22 men and 69 women [mean ± SD age: 40 ± 9 y; body mass index (BMI; in kg/m(2)): 31.9 ± 3.0]. They followed a very-low-energy diet for 8 wk, followed by a 44-wk period of weight maintenance. Body composition was assessed with a 3-compartment model based on body weight, total body water (deuterium dilution), and body volume. RMR was measured (RMRm) with a ventilated hood. In addition, RMR was predicted (RMRp) on the basis of the measured body composition: RMRp (MJ/d) = 0.024 × fat mass (kg) + 0.102 × fat-free mass (kg) + 0.85. Measurements took place before the diet and 8, 20, and 52 wk after the start of the diet.
Results:
The ratio of RMRm to RMRp decreased from 1.004 ± 0.077 before the diet to 0.963 ± 0.073 after the diet (P < 0.001), and the decrease was sustained after 20 wk (0.983 ± 0.063; P < 0.01) and 52 wk (0.984 ± 0.068; P < 0.01). RMRm/RMRp was correlated with the weight loss after 8 wk (P < 0.01), 20 wk (P < 0.05), and 52 wk (P < 0.05).
Conclusion:
Weight loss results in adaptive thermogenesis, and there is no indication for a change in adaptive thermogenesis up to 1 y, when weight loss is maintained. This trial was registered at clinicaltrials.gov as NCT01015508.
In many interventions that are based on an exercise program intended to induce weight loss, the mean weight loss observed is modest and sometimes far less than the individual expected. The individual responses are also widely variable, with some individuals losing a substantial amount of weight, others maintaining weight, and a few actually gaining weight. The media have focused on the sub-population that loses little weight, contributing to a public perception that exercise has limited utility to cause weight loss. The purpose of the symposium was to present recent, novel data that help explain how compensatory behaviors contribute to a wide discrepancy in exercise-induced weight loss. The presentations provide evidence that some individuals adopt compensatory behaviors, i.e. increased energy intake and/or reduced activity, that offset the exercise energy expenditure and limit weight loss. The challenge for both scientists and clinicians is to develop effective tools to identify which individuals are susceptible to such behaviors, and to develop strategies to minimize their impact.
Background: It is currently unclear whether altering the carbohydrate-to-protein ratio of low-fat, energy-restricted diets augments weight loss and cardiometabolic risk markers.
Objective: The objective was to conduct a systematic review and meta-analysis of studies that compared energy-restricted, isocaloric, high-protein, low-fat (HP) diets with standard-protein, low-fat (SP) diets on weight loss, body composition, resting energy expenditure (REE), satiety and appetite, and cardiometabolic risk factors.
Design: Systematic searches were conducted by using MEDLINE, EMBASE, PubMed, and the Cochrane Central Register of Controlled Trials to identify weight-loss trials that compared isocalorically prescribed diets matched for fat intake but that differed in protein and carbohydrate intakes in participants aged ≥18 y. Twenty-four trials that included 1063 individuals satisfied the inclusion criteria.
Results: Mean (±SD) diet duration was 12.1 ± 9.3 wk. Compared with an SP diet, an HP diet produced more favorable changes in weighted mean differences for reductions in body weight (−0.79 kg; 95% CI: −1.50, −0.08 kg), fat mass (FM; −0.87 kg; 95% CI: −1.26, −0.48 kg), and triglycerides (−0.23 mmol/L; 95% CI: −0.33, −0.12 mmol/L) and mitigation of reductions in fat-free mass (FFM; 0.43 kg; 95% CI: 0.09, 0.78 kg) and REE (595.5 kJ/d; 95% CI: 67.0, 1124.1 kJ/d). Changes in fasting plasma glucose, fasting insulin, blood pressure, and total, LDL, and HDL cholesterol were similar across dietary treatments (P ≥ 0.20). Greater satiety with HP was reported in 3 of 5 studies.
Conclusion: Compared with an energy-restricted SP diet, an isocalorically prescribed HP diet provides modest benefits for reductions in body weight, FM, and triglycerides and for mitigating reductions in FFM and REE.
Western lifestyles differ markedly from those of our hunter-gatherer ancestors, and these differences in diet and activity level are often implicated in the global obesity pandemic. However, few physiological data for hunter-gatherer populations are available to test these models of obesity. In this study, we used the doubly-labeled water method to measure total daily energy expenditure (kCal/day) in Hadza hunter-gatherers to test whether foragers expend more energy each day than their Western counterparts. As expected, physical activity level, PAL, was greater among Hadza foragers than among Westerners. Nonetheless, average daily energy expenditure of traditional Hadza foragers was no different than that of Westerners after controlling for body size. The metabolic cost of walking (kcal kg(-1) m(-1)) and resting (kcal kg(-1) s(-1)) were also similar among Hadza and Western groups. The similarity in metabolic rates across a broad range of cultures challenges current models of obesity suggesting that Western lifestyles lead to decreased energy expenditure. We hypothesize that human daily energy expenditure may be an evolved physiological trait largely independent of cultural differences.
In lean humans, increasing dietary fat intake causes an increase in whole-body fat oxidation and changes in genes that regulate fat oxidation in skeletal muscle, but whether this occurs in obese humans is not known. We compared changes in whole-body fat oxidation and markers of muscle oxidative capacity differ in lean (LN) and obese (OB) adults exposed to a 2-day high-fat (HF) diet. Ten LN (BMI = 22.5±2.5 kg/m², age = 30±8 yrs) and nine OB (BMI = 35.9±4.93 kg/m², 38±5 yrs, Mean±SD) were studied in a room calorimeter for 24hr while consuming isocaloric low-fat (LF, 20% of energy) and HF (50% of energy) diets. A muscle biopsy was obtained the next morning following an overnight fast. 24h respiratory quotient (RQ) did not significantly differ between groups (LN: 0.91±0.01; OB: 0.92±0.01) during LF, and similarly decreased during HF in LN (0.86±0.01) and OB (0.85±0.01). The expression of pyruvate dehydrogenase kinase 4 (PDK4) and the fatty acid transporter CD36 increased in both LN and OB during HF. No other changes in mRNA or protein were observed. However, in both LN and OB, the amounts of acetylated peroxisome proliferator-activated receptor γ coactivator-1-α (PGC1-α) significantly decreased and phosphorylated 5-AMP-activated protein kinase (AMPK) significantly increased. In response to an isoenergetic increase in dietary fat, whole-body fat oxidation similarly increases in LN and OB, in association with a shift towards oxidative metabolism in skeletal muscle, suggesting that the ability to adapt to an acute increase in dietary fat is not impaired in obesity.
The role of diet composition in response to overeating and energy dissipation in humans is unclear.
To evaluate the effects of overconsumption of low, normal, and high protein diets on weight gain, energy expenditure, and body composition.
A single-blind, randomized controlled trial of 25 US healthy, weight-stable male and female volunteers, aged 18 to 35 years with a body mass index between 19 and 30. The first participant was admitted to the inpatient metabolic unit in June 2005 and the last in October 2007.
After consuming a weight-stabilizing diet for 13 to 25 days, participants were randomized to diets containing 5% of energy from protein (low protein), 15% (normal protein), or 25% (high protein), which they were overfed during the last 8 weeks of their 10- to 12-week stay in the inpatient metabolic unit. Compared with energy intake during the weight stabilization period, the protein diets provided approximately 40% more energy intake, which corresponds to 954 kcal/d (95% CI, 884-1022 kcal/d).
Body composition was measured by dual-energy x-ray absorptiometry biweekly, resting energy expenditure was measured weekly by ventilated hood, and total energy expenditure by doubly labeled water prior to the overeating and weight stabilization periods and at weeks 7 to 8.
Overeating produced significantly less weight gain in the low protein diet group (3.16 kg; 95% CI, 1.88-4.44 kg) compared with the normal protein diet group (6.05 kg; 95% CI, 4.84-7.26 kg) or the high protein diet group (6.51 kg; 95% CI, 5.23-7.79 kg) (P = .002). Body fat increased similarly in all 3 protein diet groups and represented 50% to more than 90% of the excess stored calories. Resting energy expenditure, total energy expenditure, and body protein did not increase during overfeeding with the low protein diet. In contrast, resting energy expenditure (normal protein diet: 160 kcal/d [95% CI, 102-218 kcal/d]; high protein diet: 227 kcal/d [95% CI, 165-289 kcal/d]) and body protein (lean body mass) (normal protein diet: 2.87 kg [95% CI, 2.11-3.62 kg]; high protein diet: 3.18 kg [95% CI, 2.37-3.98 kg]) increased significantly with the normal and high protein diets.
Among persons living in a controlled setting, calories alone account for the increase in fat; protein affected energy expenditure and storage of lean body mass, but not body fat storage.
clinicaltrials.gov Identifier: NCT00565149.
The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the 'obesity epidemic'--the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models--the general intake model and the dual intervention point model--that address this issue and might offer better ways to understand how body fatness is controlled.
Objective:
To quantify the feedback control of energy intake in response to long-term covert manipulation of energy balance in free-living humans.
Methods:
A validated mathematical method was used to calculate energy intake changes during a 52-week placebo-controlled trial in 153 patients treated with canagliflozin, a sodium glucose co-transporter inhibitor that increases urinary glucose excretion, thereby resulting in weight loss without patients being directly aware of the energy deficit. The relationship between the body weight time course and the calculated energy intake changes was analyzed using principles from engineering control theory.
Results:
It was discovered that weight loss leads to a proportional increase in appetite resulting in eating above baseline by ∼100 kcal/day per kilogram of lost weight-an amount more than threefold larger than the corresponding energy expenditure adaptations.
Conclusions:
While energy expenditure adaptations have often been considered the main reason for slowing of weight loss and subsequent regain, feedback control of energy intake plays an even larger role and helps explain why long-term maintenance of a reduced body weight is so difficult.
Background:
The carbohydrate-insulin model of obesity posits that habitual consumption of a high-carbohydrate diet sequesters fat within adipose tissue because of hyperinsulinemia and results in adaptive suppression of energy expenditure (EE). Therefore, isocaloric exchange of dietary carbohydrate for fat is predicted to result in increased EE, increased fat oxidation, and loss of body fat. In contrast, a more conventional view that "a calorie is a calorie" predicts that isocaloric variations in dietary carbohydrate and fat will have no physiologically important effects on EE or body fat.
Objective:
We investigated whether an isocaloric low-carbohydrate ketogenic diet (KD) is associated with changes in EE, respiratory quotient (RQ), and body composition.
Design:
Seventeen overweight or obese men were admitted to metabolic wards, where they consumed a high-carbohydrate baseline diet (BD) for 4 wk followed by 4 wk of an isocaloric KD with clamped protein. Subjects spent 2 consecutive days each week residing in metabolic chambers to measure changes in EE (EEchamber), sleeping EE (SEE), and RQ. Body composition changes were measured by dual-energy X-ray absorptiometry. Average EE during the final 2 wk of the BD and KD periods was measured by doubly labeled water (EEDLW).
Results:
Subjects lost weight and body fat throughout the study corresponding to an overall negative energy balance of ∼300 kcal/d. Compared with BD, the KD coincided with increased EEchamber (57 ± 13 kcal/d, P = 0.0004) and SEE (89 ± 14 kcal/d, P < 0.0001) and decreased RQ (-0.111 ± 0.003, P < 0.0001). EEDLW increased by 151 ± 63 kcal/d (P = 0.03). Body fat loss slowed during the KD and coincided with increased protein utilization and loss of fat-free mass.
Conclusion:
The isocaloric KD was not accompanied by increased body fat loss but was associated with relatively small increases in EE that were near the limits of detection with the use of state-of-the-art technology. This trial was registered at clinicaltrials.gov as NCT01967563.
Objective:
To measure long-term changes in resting metabolic rate (RMR) and body composition in participants of "The Biggest Loser" competition.
Methods:
Body composition was measured by dual energy X-ray absorptiometry, and RMR was determined by indirect calorimetry at baseline, at the end of the 30-week competition and 6 years later. Metabolic adaptation was defined as the residual RMR after adjusting for changes in body composition and age.
Results:
Of the 16 "Biggest Loser" competitors originally investigated, 14 participated in this follow-up study. Weight loss at the end of the competition was (mean ± SD) 58.3 ± 24.9 kg (P < 0.0001), and RMR decreased by 610 ± 483 kcal/day (P = 0.0004). After 6 years, 41.0 ± 31.3 kg of the lost weight was regained (P = 0.0002), while RMR was 704 ± 427 kcal/day below baseline (P < 0.0001) and metabolic adaptation was -499 ± 207 kcal/day (P < 0.0001). Weight regain was not significantly correlated with metabolic adaptation at the competition's end (r = -0.1, P = 0.75), but those subjects maintaining greater weight loss at 6 years also experienced greater concurrent metabolic slowing (r = 0.59, P = 0.025).
Conclusions:
Metabolic adaptation persists over time and is likely a proportional, but incomplete, response to contemporaneous efforts to reduce body weight.
Current obesity prevention strategies recommend increasing daily physical activity, assuming that increased activity will lead to corresponding increases in total energy expenditure and prevent or reverse energy imbalance and weight gain [1-3]. Such Additive total energy expenditure models are supported by exercise intervention and accelerometry studies reporting positive correlations between physical activity and total energy expenditure [4] but are challenged by ecological studies in humans and other species showing that more active populations do not have higher total energy expenditure [5-8]. Here we tested a Constrained total energy expenditure model, in which total energy expenditure increases with physical activity at low activity levels but plateaus at higher activity levels as the body adapts to maintain total energy expenditure within a narrow range. We compared total energy expenditure, measured using doubly labeled water, against physical activity, measured using accelerometry, for a large (n = 332) sample of adults living in five populations [9]. After adjusting for body size and composition, total energy expenditure was positively correlated with physical activity, but the relationship was markedly stronger over the lower range of physical activity. For subjects in the upper range of physical activity, total energy expenditure plateaued, supporting a Constrained total energy expenditure model. Body fat percentage and activity intensity appear to modulate the metabolic response to physical activity. Models of energy balance employed in public health [1-3] should be revised to better reflect the constrained nature of total energy expenditure and the complex effects of physical activity on metabolic physiology.
Dietary carbohydrate restriction has been purported to cause endocrine adaptations that promote body fat loss more than dietary fat restriction. We selectively restricted dietary carbohydrate versus fat for 6 days following a 5-day baseline diet in 19 adults with obesity confined to a metabolic ward where they exercised daily. Subjects received both isocaloric diets in random order during each of two inpatient stays. Body fat loss was calculated as the difference between daily fat intake and net fat oxidation measured while residing in a metabolic chamber. Whereas carbohydrate restriction led to sustained increases in fat oxidation and loss of 53 ± 6 g/day of body fat, fat oxidation was unchanged by fat restriction, leading to 89 ± 6 g/day of fat loss, and was significantly greater than carbohydrate restriction (p = 0.002). Mathematical model simulations agreed with these data, but predicted that the body acts to minimize body fat differences with prolonged isocaloric diets varying in carbohydrate and fat.
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