Time to Correctly Predict the Amount of Weight Loss with Dieting

Thomas, Diana M.; Gonzalez, Maria Cristina; Pereira, Andréa Z; Redman, Leanne M.; Heymsfield, Steven B.

doi:10.1016/j.jand.2014.02.003

Cited by 44 publications

(34 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The same processes occur in free-living humans in positive caloric imbalance e namely, they gain weight until or unless these well-understood caloric costs of a larger body bring them back into caloric balance [77,81,82,84]. None of these processes requires the induction of intracellular metabolic pathways that specifically waste energy.…”

Section: Postprandial Effects Of Insulin On De-novo Lipogenesis (Dnl)mentioning

confidence: 99%

“…This is the "3500 kcal per pound rule" e that is, whenever excess intake totals 3500 kcal, you will have gained a pound; when it reaches 7700 kcal, you have gained a kilogram; and decreased intake causes the same amounts of weight loss, kilogram after kilogram. Thomas et al briefly summarize the history of linear models [77].…”

Section: Chronic Positive Caloric Imbalance Is the Cause Of Obesity Ementioning

confidence: 99%

“…This last item remains quantitatively significant, even taking into account chronically lower levels of NEAT in the obese [66], e.g., just moving from chair to chair takes more energy. Thus, experimentally overfed subjects or free-living humans who overeat by a defined amount each day will reliably increase their body weight until it plateaus when a new energy balance is achieved [77,81,82,84]. In other words, careful attention to thermodynamics indicates that a fixed, sustained increase in daily caloric intake, with no change in purposeful exercise, does not increase human weight linearly without limit.…”

Section: Chronic Positive Caloric Imbalance Is the Cause Of Obesity Ementioning

confidence: 99%

“…Taken together, the insights from thermodynamically correct mathematical models of human weight change significantly aid the management of patients' expectations [77], improve our ability to estimate the potential benefits of policy proposals such as new labels or taxes on sugar-sweetened beverages [82,88], and advance our understanding of obesity in terms of quantitative caloric fluxes.…”

Section: Chronic Positive Caloric Imbalance Is the Cause Of Obesity Ementioning

confidence: 99%

See 3 more Smart Citations

Imbalanced insulin action in chronic over nutrition: Clinical harm, molecular mechanisms, and a way forward

Williams

2016

Atherosclerosis

View full text Add to dashboard Cite

The growing worldwide prevalence of overnutrition and underexertion threatens the gains that we have made against atherosclerotic cardiovascular disease and other maladies. Chronic overnutrition causes the atherometabolic syndrome, which is a cluster of seemingly unrelated health problems characterized by increased abdominal girth and body-mass index, high fasting and postprandial concentrations of cholesterol- and triglyceride-rich apoB-lipoproteins (C-TRLs), low plasma HDL levels, impaired regulation of plasma glucose concentrations, hypertension, and a significant risk of developing overt type 2 diabetes mellitus (T2DM). In addition, individuals with this syndrome exhibit fatty liver, hypercoagulability, sympathetic overactivity, a gradually rising set-point for body adiposity, a substantially increased risk of atherosclerotic cardiovascular morbidity and mortality, and--crucially--hyperinsulinemia. Many lines of evidence indicate that each component of the atherometabolic syndrome arises, or is worsened by, pathway-selective insulin resistance and responsiveness (SEIRR). Individuals with SEIRR require compensatory hyperinsulinemia to control plasma glucose levels. The result is overdrive of those pathways that remain insulin-responsive, particularly ERK activation and hepatic de-novo lipogenesis (DNL), while carbohydrate regulation deteriorates. The effects are easily summarized: if hyperinsulinemia does something bad in a tissue or organ, that effect remains responsive in the atherometabolic syndrome and T2DM; and if hyperinsulinemia might do something good, that effect becomes resistant. It is a deadly imbalance in insulin action. From the standpoint of human health, it is the worst possible combination of effects. In this review, we discuss the origins of the atherometabolic syndrome in our historically unprecedented environment that only recently has become full of poorly satiating calories and incessant enticements to sit. Data are examined that indicate the magnitude of daily caloric imbalance that causes obesity. We also cover key aspects of healthy, balanced insulin action in liver, endothelium, brain, and elsewhere. Recent insights into the molecular basis and pathophysiologic harm from SEIRR in these organs are discussed. Importantly, a newly discovered oxide transport chain functions as the master regulator of the balance amongst different limbs of the insulin signaling cascade. This oxide transport chain--abbreviated 'NSAPP' after its five major proteins--fails to function properly during chronic overnutrition, resulting in this harmful pattern of SEIRR. We also review the origins of widespread, chronic overnutrition. Despite its apparent complexity, one factor stands out. A sophisticated junk food industry, aided by subsidies from willing governments, has devoted years of careful effort to promote overeating through the creation of a new class of food and drink that is low- or no-cost to the consumer, convenient, savory, calorically dense, yet weakly satiating. It is past time for the rest of us ...

show abstract

Section: Postprandial Effects Of Insulin On De-novo Lipogenesis (Dnl)mentioning

confidence: 99%

Section: Chronic Positive Caloric Imbalance Is the Cause Of Obesity Ementioning

confidence: 99%

Section: Chronic Positive Caloric Imbalance Is the Cause Of Obesity Ementioning

confidence: 99%

Section: Chronic Positive Caloric Imbalance Is the Cause Of Obesity Ementioning

confidence: 99%

See 2 more Smart Citations

Imbalanced insulin action in chronic over nutrition: Clinical harm, molecular mechanisms, and a way forward

Williams

2016

Atherosclerosis

View full text Add to dashboard Cite

show abstract

“…They will also show weight gain plateaus (weight gain ceasing and stabilising despite constant food intake) because their carbon dioxide retention will eventually cause sufficiently high levels of carbon dioxide that will eventually cause their less responsive CO 2 SCs to respond by increasing ventilation which then enhances their carbon dioxide excretion such that weight stabilisation occurs. But when they diet they will be disappointed because their ‘diets fail’ and their prescribed weight loss is far less than expected5 because low carbon inputs from diets will reduce their CO 2 initiated respiratory drive, there will then be compensatory carbon retention and weight loss will plateau thus explaining why (sensible, non-anorexic) diets often fail. Indeed the number and variety of calorie restricted diets on offer are perhaps the best testaments to the fact that not one is particularly effective in the long term.…”

Section: Four Consequencesmentioning

confidence: 99%

Why diets fail: a hypothesis for discussion

Welsby¹

2016

Postgraduate Medical Journal

View full text Add to dashboard Cite

Weight regulation depends on the difference between weights of absorbed and metabolised carbon and excretion of the end products of metabolism, calories and carbon dioxide, which can be independently and variably excreted. Calories can be variably excreted as heat by vasoconstriction or vasodilation and carbon dioxide can be excreted variably as exhaled carbon dioxide (the major route of carbon excretion). Unless there are changes in ventilatory carbon excretion, 'metabolism,' 'genetic factors,' 'hormones' or 'exercise' do not provide complete explanatory mechanisms for weight changes, obesity and failure of diets. Low sensitivity of respiratory centres to carbon dioxide may cause overweight and dietary failures after initial weight loss.

show abstract

Effect of a Personalized Diet to Reduce Postprandial Glycemic Response vs a Low-fat Diet on Weight Loss in Adults With Abnormal Glucose Metabolism and Obesity

Popp¹,

Hu²,

Kharmats³

et al. 2022

JAMA Netw Open

View full text Add to dashboard Cite

ImportanceInterindividual variability in postprandial glycemic response (PPGR) to the same foods may explain why low glycemic index or load and low-carbohydrate diet interventions have mixed weight loss outcomes. A precision nutrition approach that estimates personalized PPGR to specific foods may be more efficacious for weight loss.ObjectiveTo compare a standardized low-fat vs a personalized diet regarding percentage of weight loss in adults with abnormal glucose metabolism and obesity.Design, Setting, and ParticipantsThe Personal Diet Study was a single-center, population-based, 6-month randomized clinical trial with measurements at baseline (0 months) and 3 and 6 months conducted from February 12, 2018, to October 28, 2021. A total of 269 adults aged 18 to 80 years with a body mass index (calculated as weight in kilograms divided by height in meters squared) ranging from 27 to 50 and a hemoglobin A1c level ranging from 5.7% to 8.0% were recruited. Individuals were excluded if receiving medications other than metformin or with evidence of kidney disease, assessed as an estimated glomerular filtration rate of less than 60 mL/min/1.73 m2 using the Chronic Kidney Disease Epidemiology Collaboration equation, to avoid recruiting patients with advanced type 2 diabetes.InterventionsParticipants were randomized to either a low-fat diet (&lt;25% of energy intake; standardized group) or a personalized diet that estimates PPGR to foods using a machine learning algorithm (personalized group). Participants in both groups received a total of 14 behavioral counseling sessions and self-monitored dietary intake. In addition, the participants in the personalized group received color-coded meal scores on estimated PPGR delivered via a mobile app.Main Outcomes and MeasuresThe primary outcome was the percentage of weight loss from baseline to 6 months. Secondary outcomes included changes in body composition (fat mass, fat-free mass, and percentage of body weight), resting energy expenditure, and adaptive thermogenesis. Data were collected at baseline and 3 and 6 months. Analysis was based on intention to treat using linear mixed modeling.ResultsOf a total of 204 adults randomized, 199 (102 in the personalized group vs 97 in the standardized group) contributed data (mean [SD] age, 58 [11] years; 133 women [66.8%]; mean [SD] body mass index, 33.9 [4.8]). Weight change at 6 months was −4.31% (95% CI, −5.37% to −3.24%) for the standardized group and −3.26% (95% CI, −4.25% to −2.26%) for the personalized group, which was not significantly different (difference between groups, 1.05% [95% CI, −0.40% to 2.50%]; P = .16). There were no between-group differences in body composition and adaptive thermogenesis; however, the change in resting energy expenditure was significantly greater in the standardized group from 0 to 6 months (difference between groups, 92.3 [95% CI, 0.9-183.8] kcal/d; P = .05).Conclusions and RelevanceA personalized diet targeting a reduction in PPGR did not result in greater weight loss compared with a low-fat diet at 6 months. Future studies should assess methods of increasing dietary self-monitoring adherence and intervention exposure.Trial RegistrationClinicalTrials.gov Identifier: NCT03336411

show abstract

Time to Correctly Predict the Amount of Weight Loss with Dieting

Cited by 44 publications

References 16 publications

Imbalanced insulin action in chronic over nutrition: Clinical harm, molecular mechanisms, and a way forward

Imbalanced insulin action in chronic over nutrition: Clinical harm, molecular mechanisms, and a way forward

Why diets fail: a hypothesis for discussion

Effect of a Personalized Diet to Reduce Postprandial Glycemic Response vs a Low-fat Diet on Weight Loss in Adults With Abnormal Glucose Metabolism and Obesity

Contact Info

Product

Resources

About