scholarly journals How Strongly Does Appetite Counter Weight Loss? Quantification of the Feedback Control of Human Energy Intake

Obesity ◽  
2016 ◽  
Vol 24 (11) ◽  
pp. 2289-2295 ◽  
Author(s):  
David Polidori ◽  
Arjun Sanghvi ◽  
Randy J. Seeley ◽  
Kevin D. Hall
2016 ◽  
Author(s):  
David Polidori ◽  
Arjun Sanghvi ◽  
Randy Seeley ◽  
Kevin D. Hall

AbstractObjectiveTo quantify the homeostatic feedback control of energy intake in response to long-term covert manipulation of energy balance in free-living humans.MethodsWe used a validated mathematical method 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. We analyzed the relationship between the body weight time course and the calculated energy intake changes using principles from engineering control theory. ResultsWe discovered that weight loss leads to a proportional homeostatic drive to increase energy intake above baseline by ~100 kcal/day per kg of lost weight – an amount more than 3-fold larger than the corresponding energy expenditure adaptations.ConclusionsWhile energy expenditure adaptations are often thought to be 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.FundingThis research was supported by the Intramural Research Program of the NIH, National Institute of Diabetes & Digestive & Kidney Diseases, using data from a study sponsored by Janssen Research & Development, LLC.DisclosureD.P. is a full-time employee of Janssen Research & Development, LLC. K.D.H. reports patent pending on a method of personalized dynamic feedback control of body weight (US Patent Application No. 13/754,058; assigned to the NIH) and has received funding from the Nutrition Science Initiative to investigate the effects of ketogenic diets on human energy expenditure. R.S. is a paid consultant for Janssen, Novo Nordisk, Takeda, Daichii Sankyo, Novartis, Pfizer, Nestle, Circuit Therapeutics and Ethicon. R.S., also has received research support from Novo Nordisk, Ethicon, Sanofiand Boehringer Ingelheim. A.S. reports no conflicts of interest.What is already known about this subject?Human body weight is believed to be regulated by homeostatic feedback control of both energy intake and energy expenditure.Adaptations of energy expenditure to weight loss have been well-established, but the homeostatic control of energy intake has yet to be quantified.What this study addsWe provide the first quantification of the homeostatic control of energy intake in free-living humans.The increase in energy intake per kg of weight lost is several-fold larger than the known energy expenditure adaptations.Homeostatic control of energy intake is likely the primary reason why it is difficult to achieve and sustain large weight losses.


Appetite ◽  
2021 ◽  
pp. 105273
Author(s):  
Sasha Fenton ◽  
Tracy L. Burrows ◽  
Clare E. Collins ◽  
Elizabeth G. Holliday ◽  
Gregory S. Kolt ◽  
...  

2009 ◽  
Vol 69 (1) ◽  
pp. 34-38 ◽  
Author(s):  
C. R. Hankey

Treatments to induce weight loss for the obese patient centre on the achievement of negative energy balance. This objective can theoretically be attained by interventions designed to achieve a reduction in energy intake and/or an increase in energy expenditure. Such ‘lifestyle interventions’ usually comprise one or more of the following strategies: dietary modification; behaviour change; increases in physical activity. These interventions are advocated as first treatment steps in algorithms recommended by current clinical obesity guidelines. Medication and surgical treatments are potentially available to those unable to implement ‘lifestyle interventions’ effectively by achieving losses of between 5 kg and 10 kg. It is accepted that the minimum of 5% weight loss is required to achieve clinically-meaningful benefits. Dietary treatments differ widely. Successful weight loss is most often associated with quantification of energy intake rather than macronutrient composition. Most dietary intervention studies secure a weight loss of between 5 kg and 10 kg after intervention for 6 months, with gradual weight regain at 1 year where weight changes are 3–4 kg below the starting weight. Some dietary interventions when evaluated at 2 and 4 years post intervention report the effects of weight maintenance rather than weight loss. Specific anti-obesity medications are effective adjuncts to weight loss, in most cases doubling the weight loss of those given dietary advice only. Greater physical activity alone increases energy expenditure by insufficient amounts to facilitate clinically-important weight losses, but is useful for weight maintenance. Weight losses of between half and three-quarters of excess body weight are seen at 10 years post intervention with bariatric surgery, making this arguably the most effective weight-loss treatment.


2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson’s disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.


Author(s):  
Nakamura T ◽  

Background and Aims: Patients with Alzheimer’s Disease (AD) frequently develop weight loss. However, little is known about the energy and protein thresholds that cause weight loss. The purpose of this study was to determine the threshold of daily energy and protein requirements to prevent weight loss in patients with AD. Methods: We included 75 Japanese long-term care hospital patients with probable AD (22 men and 53 women, aged 65–101 years) in an interventional study. After a one-week survey using weighed food records weighed food records, the relationship between the obtained energy and protein intake and weight loss after three months was examined. Multiple regression analysis was used to examine the daily determinants of weight loss. Subsequently, receiver operating characteristic curves were used to examine the threshold for discriminating weight loss. Results: Sixty-one (81.3%) patients were malnourished or at risk of malnutrition. Twenty patients (26.7%) had >5% weight loss. The significant associations with weight loss were Mini Nutritional Assessment (MNA) point, energy intake, and protein intake; with a MNA point at cutoff of 17.25, an energy intake at cutoff of 29.93kcal/kg, and a protein intake at cutoff of 1.122g/kg. Conclusion: To prevent weight loss in AD patients, it is important to prevent malnutrition and administer more than 30kcal/kg energy intake and more than 1.1g/kg protein intake. Future studies with a larger sample size are needed to determine the threshold of daily energy and protein requirements to prevent weight loss.


2019 ◽  
Vol 29 (12) ◽  
pp. 3874-3881 ◽  
Author(s):  
Louella A. H. M. Schoemacher ◽  
Abel B. Boerboom ◽  
Monique M. R. Thijsselink ◽  
Edo O. Aarts

Sign in / Sign up

Export Citation Format

Share Document