Is Weight Loss More Severe in Older People with Dementia?

2021 ◽  
pp. 1-17
Author(s):  
Alvin Surya Tjahyo ◽  
Joan Gandy ◽  
Judi Porter ◽  
Christiani Jeyakumar Henry

Weight loss, a hallmark feature of dementia, is associated with higher mortality in older people. However, there is a lack of consensus in the literature as to whether the weight loss commonly observed in older people with dementia results from reduced energy intake and/or increased energy expenditure. Understanding the cause of energy imbalance in older people with dementia would allow more targeted interventions to avoid detrimental health effects in this vulnerable group. In this paper, we review studies that have considered weight change, energy intake, and energy expenditure in older people with and without dementia. We critically assess the studies’ methodology and outline the various factors which may decrease and increase energy intake and expenditure respectively in older people with and without dementia. Current available literature does not support the view that there is a lower energy intake and/or a higher energy expenditure in older people with dementia when compared to those without dementia. The need for more high-quality studies is also highlighted in order to shed more light towards this issue which continues to elude researchers and clinicians alike.

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.


2017 ◽  
Vol 313 (4) ◽  
pp. R357-R371 ◽  
Author(s):  
Zachary S. Roberts ◽  
Tami Wolden-Hanson ◽  
Miles E. Matsen ◽  
Vitaly Ryu ◽  
Cheryl H. Vaughan ◽  
...  

Oxytocin (OT) administration elicits weight loss in diet-induced obese (DIO) rodents, nonhuman primates, and humans by reducing energy intake and increasing energy expenditure. Although the neurocircuitry underlying these effects remains uncertain, OT neurons in the paraventricular nucleus are positioned to control both energy intake and sympathetic nervous system outflow to interscapular brown adipose tissue (BAT) through projections to the hindbrain nucleus of the solitary tract and spinal cord. The current work was undertaken to examine whether central OT increases BAT thermogenesis, whether this effect involves hindbrain OT receptors (OTRs), and whether such effects are associated with sustained weight loss following chronic administration. To assess OT-elicited changes in BAT thermogenesis, we measured the effects of intracerebroventricular administration of OT on interscapular BAT temperature in rats and mice. Because fourth ventricular (4V) infusion targets hindbrain OTRs, whereas third ventricular (3V) administration targets both forebrain and hindbrain OTRs, we compared responses to OT following chronic 3V infusion in DIO rats and mice and chronic 4V infusion in DIO rats. We report that chronic 4V infusion of OT into two distinct rat models recapitulates the effects of 3V OT to ameliorate DIO by reducing fat mass. While reduced food intake contributes to this effect, our finding that 4V OT also increases BAT thermogenesis suggests that increased energy expenditure may contribute as well. Collectively, these findings support the hypothesis that, in DIO rats, OT action in the hindbrain evokes sustained weight loss by reducing energy intake and increasing BAT thermogenesis.


Obesity ◽  
2013 ◽  
Vol 22 (2) ◽  
pp. 363-370 ◽  
Author(s):  
James P. DeLany ◽  
David E. Kelley ◽  
Kazanna C. Hames ◽  
John M. Jakicic ◽  
Bret H. Goodpaster

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.


2014 ◽  
Vol 68 (5) ◽  
pp. 581-586 ◽  
Author(s):  
M Hopkins ◽  
C Gibbons ◽  
P Caudwell ◽  
P M Hellström ◽  
E Näslund ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nikita Sanjay Israni ◽  
Thomas Cassimatis ◽  
Laura A Fletcher ◽  
Brooks P Leitner ◽  
Courtney J Duckworth ◽  
...  

Abstract Design and rationale: Obesity results from energy intake exceeding energy expenditure (EE) over a prolonged period. Many anti-obesity drugs are designed to decrease energy intake. However, their potential impact on EE is not well documented. We designed a placebo-controlled, double-blind, randomized cross-over study to determine the acute effects of several FDA-approved anti-obesity drugs on basal metabolic rate (BMR) under well-controlled conditions. Protocol and inclusion criteria: This ongoing study is limited to healthy males of all ethnicities aged 18–35 years with a BMI of 18.5 to 25.0 kg/m2. Following an overnight stay in the Metabolic Clinical Research Unit, fasting subjects were measured from 8:00am to 12:00pm in a whole-room indirect calorimeter, which was maintained at a thermoneutral temperature (26.7±0.9°C) to prevent non-shivering thermogenesis. The six treatments include placebo, caffeine as the positive control (300 mg), phentermine (37.5 mg), topiramate (200 mg), Qsymia (phentermine 15 mg / topiramate 92 mg), and naltrexone (100 mg), with a 1-week outpatient washout period after each treatment. Drug-naïve subjects received a single dose of each drug to minimize potential metabolic adaptations that may occur with weight-loss or chronic use. The prespecified primary outcome was a ≥5% increase in BMR vs. placebo for each drug. This difference can be detected for 16 subjects with 0.83 power at α=0.05 allowing for ≤25% dropout. Secondary outcomes include respiratory quotient (RQ), heart rate (HR), mean arterial pressure (MAP), and self-reported hunger. Preliminary data: To date, 7 subjects were recruited and 6 have completed the study (26.1±4.3 years, BMI 23.1±1.4 kg/m2, body fat percentage 18.4±4.1%). Interim analysis using paired t-tests shows, compared to placebo, caffeine trended towards increasing EE (1.17±0.07 vs. 1.27±0.12 kcal/min; p=0.07) and increased MAP by 5.5±4.2% (88±2 vs. 93±4; p<0.05), but did not change heart rate (59±10 vs. 61±13 bpm). Naltrexone increased EE by 5.9±4.3% (p<0.05). No treatments altered resting RQ compared to placebo (0.83±0.05). Phentermine increased resting HR, both alone (15.7±7.9%, p<0.01) and in Qsymia (9.2±3.6%, p<0.05), compared to placebo. Of the five drug-treatments, only Qsymia reduced self-reported hunger scores compared to placebo. Summary and future directions: Anti-obesity drugs may increase energy expenditure by upregulating sympathetic nervous system activity. Combined with appetite suppression, the impact on energy balance can lead to weight loss. We aim to complete our study to determine whether these drugs can acutely increase EE with minimal cardiovascular side-effects and compare our findings with long-term interventions.


2018 ◽  
Vol 79 (4) ◽  
pp. 191-195 ◽  
Author(s):  
Leticia C.R. Pereira ◽  
Sarah A. Elliott ◽  
Linda J. McCargar ◽  
Rhonda C. Bell ◽  
Carla M. Prado

Purpose: Energy metabolism is at the core of maintaining healthy body weights. Likewise, the assessment of energy needs is essential for providing adequate dietary advice. We explored differences in energy metabolism of a primigravid woman (age: 30 years) at 1 month prepregnancy (“baseline”), during pregnancy (33 weeks), and at 3 and 9 months postpartum. Measured versus estimated energy expenditure were compared using equations commonly used in clinical practice. Methods: Energy metabolism was measured using a state-of-the-art whole body calorimetry unit (WBCU). Body composition (dual-energy X-ray absorptiometry), energy intake (3-day food records), physical activity (Baecke questionnaire), and breastmilk volume/breastfeeding energy expenditure (24-hours of infant test–retest weighing) were assessed. Results: This case report is the first to assess energy expenditure in 3 different stages of a woman’s life (prepregnancy, pregnancy, and postpartum) using WBCU. We noticed that weight and energy needs returned to prepregnancy values at 9 months postpartum, although a pattern of altered body composition emerged (higher fat/lean ratio) without changes in physical activity and energy intake. For this woman, current recommendations for energy overestimated actual needs by 350 kcal/day (9 months postpartum). Conclusion: It is likely that more accurate approaches are needed to estimate energy needs during and postpregnancy, with targeted interventions to optimize body composition.


2020 ◽  
Vol 105 (4) ◽  
pp. e1601-e1611 ◽  
Author(s):  
Jasper Most ◽  
Abby D Altazan ◽  
Marshall St. Amant ◽  
Robbie A Beyl ◽  
Eric Ravussin ◽  
...  

Abstract Context This study was designed to understand causes and critical periods for postpartum weight retention by characterizing changes in body composition, energy intake, energy expenditure and physical activity in women with obesity during pregnancy and postpartum. Design In this prospective, observational cohort study, body composition (plethysmography), energy expenditure (doubly labeled water, whole-body room calorimetry), physical activity (accelerometry), metabolic biomarkers, and eating behaviors were measured. Energy intake was calculated by the intake-balance method for pregnancy, and for 2 postpartum periods (0 to 6 months and 6 to 12 months). Results During the 18-month observation period, weight loss occurred in 16 (43%) women (mean ± SEM, −4.9 ± 1.6 kg) and weight retention occurred in 21 (57%) women (+8.6 ± 1.4 kg). Comparing women with postpartum weight loss and weight retention, changes in body weight were not different during pregnancy (6.9 ± 1.0 vs 9.5 ± 0.9 kg, P = 0.06). After pregnancy, women with postpartum weight loss lost −3.6 ± 1.8 kg fat mass whereas women with weight retention gained 6.2 ± 1.7 kg fat mass (P < 0.001). Women with postpartum weight loss reduced energy intake during the postpartum period (compared with during pregnancy) by 300 kcal/d (1255 kJ/d), while women with weight retention increased energy intake by 250 kcal/d (1046 kJ/d, P < 0.005). There were no differences in the duration of breastfeeding, eating behavior, or metabolic biomarkers. Conclusions Postpartum weight gain was the result of increased energy intake after pregnancy rather than decreased energy expenditure. Dietary intake recommendations are needed for women with obesity during the postpartum period, and women should be educated on the risk of overeating after pregnancy.


2012 ◽  
Vol 37 (5) ◽  
pp. 893-899 ◽  
Author(s):  
David P. Bradley ◽  
Roger Kulstad ◽  
Natalie Racine ◽  
Yoram Shenker ◽  
Melissa Meredith ◽  
...  

Exenatide is a medication similar in structure and effect to native glucagon-like peptide-1, an incretin hormone with glucose-lowering properties. The aim of the study was to measure the change in total energy expenditure (TEE) and body composition during exenatide administration and by deduction the relative contributions of energy expenditure and energy intake to exenatide-induced weight loss. Forty-five obese (body mass index, 30–40 kg·m–2) subjects were identified. After exclusion criteria application, 28 subjects entered into the study and 18 subjects (12 female, 6 male) completed the study, which consisted of 6 visits over 14 weeks and injection of exenatide for an average of 84 ± 5 days. Respiratory gas analysis and doubly labeled water measurements were performed before initiation of exenatide and after approximately 3 months of exenatide administration. The average weight loss from the beginning of injection period to the end of the study in completed subjects was 2.0 ± 2.8 kg (p = 0.01). Fat mass declined by 1.3 ± 1.8 kg (p = 0.01) while the fat-free mass trended downward but was not significant (0.8 ± 2.2 kg, p = 0.14). There was no change in weight-adjusted TEE (p = 0.20), resting metabolic rate (p = 0.51), or physical activity energy expenditure (p = 0.38) and no change in the unadjusted thermic effect of a meal (p = 0.37). The significant weight loss because of exenatide administration was thus the result of decreasing energy intake. In obese nondiabetic subjects, exenatide administration did not increase TEE and by deduction the significant weight loss and loss of fat mass was due to decreased energy intake.


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