Tailoring pharmacotherapy to specific eating behaviours in obesity: Can recommendations for personalised therapy be made from the current data?

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Term Occurence Count Dictionary
phentermine 15 endocrinologydiseasesdrugs
type 2 diabetes mellitus 1 endocrinologydiseases
Liraglutide 14 endocrinologydiseasesdrugs
amphetamine 2 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
obesity 32 endocrinologydiseases
orlistat 2 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Liraglutide 9509 inhibitory control or reward responsivity, for these reasons it has not been included in this review. Liraglutide (Saxenda)Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist with long-lasting biological
Liraglutide 9530 reward responsivity, for these reasons it has not been included in this review.Liraglutide (Saxenda) Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist with long-lasting biological activities (half-life
Liraglutide 9772 comparison with endogenous GLP-1 which is rapidly degraded by the enzyme dipeptidyl peptidase-IV (DPP-IV). Liraglutide is approved for treatment of T2DM at the 1.8 mg dose, and recently attained FDA (2014) and EMA (2015)
Liraglutide 12178 data on the efficacy of liraglutide for weight loss come from the Satiety and Clinical Adiposity– Liraglutide Evidence (SCALE) studies. These studies suggest liraglutide 3.0 mg is effective at reversing prediabetes
Liraglutide 15524 significantly reduced at 1.8 mg liraglutide vs placebo (although how this was assessed is not reported). Liraglutide , therefore, appears to produce weight loss through homoeostatic mechanisms that boost satiety, leading
Liraglutide 16878 pharmacotherapiesDrugMechanism of actionEffect on appetite expression, eating behaviour or CNS activity Liraglutide GLP-1 receptor agonistReduced intake, reduced post-meal hunger, increased post-meal satiety and fullness.
Liraglutide 19143 studies included in reviewAuthors and yearDrugParticipantsAppetite effects/CNS activityInoue et al. 2011 Liraglutide 0.9 mg compared to oral glucose lowering medicationn = 20 (12 female), T2DMDecreased daily staple
Liraglutide 19387 non-staple food. Decreased external eating, reduced preference for fatty foodsHorrowitz et al. 2012 Liraglutide 1.8 mg, glimepiride and placebo, incomplete Latin square designn = 46 (19 female), T2DM, BMI 27–40 kg/m2Decreased
Liraglutide 19607 27–40 kg/m2Decreased fasting hunger, shorter meal duration. No significant effects on intakeFlint et al. 2013 Liraglutide 1.8 mg—randomised, placebo-controlled, double-blind, crossover designn = 18 (4 female), T2DM, BMI
Liraglutide 19956 nutrient intake or meal duration. Decreased mean 5 h postprandial hunger ratingsvan Can et al. 2014 Liraglutide 1.8 mg, 3 mg or placebo—randomised placebo-controlled, double-blind, incomplete crossover trialn = 49
Liraglutide 20264 satiety and fullness (post-meal), reduced prospective consumption (post-breakfast)Farr, et al. 2016a Liraglutide 1.8 mg—randomised, placebo-controlled, double-blind, crossover trial.n = 18 (9 female) T2DM, placebo
Liraglutide 36119 time meal, several hours following a fixed load breakfast (and overnight fast)Van Can (2014) [[31]]— Liraglutide Microstructure of eating and eating rateSatiety/rewardUniversal eating monitor used to measure total
Liraglutide 38121 (DEBQ)Inhibitory controlExternal, emotional and restrained eating patternsDe Boer et al. (2016) [[62]] Liraglutide The mindful eating scaleInhibitory controlKey environment stimuli associated with reduced control of
Liraglutide 38408 measures:fMRISatietyActivity in response to food cues in fed and fasted statesFarr et al. (2016) [[32]] Liraglutide 1.8 mgfMRI—reward systemRewardActivity and functional connectivity of reward system during receipt
amphetamine 31212 cardiovascular effects whilst having a synergistic effect on weight loss.Mechanism of actionThe atypical amphetamine derivative phentermine stimulates norepinephrine release in the CNS, with limited effects on dopamine
amphetamine 31612 loss for up to 6 months. However, despite the absence of addictive potential, due to its status as an amphetamine derivative, phentermine is presumed to increase blood pressure and heart rate (although there is evidence
orlistat 9099 four most recently available (FDA approved) mono and combination pharmacotherapies for obesity. Whilst orlistat (Xenical) has been approved as a pharmacological intervention for obesity since 1998, this is not a
orlistat 32922 [[27]] phentermine/topiramate produced the highest odds of achieving 5 and 10% weight loss compared to orlistat , liraglutide, lorcaserin and bupropion/naltrexone (moderate confidence in estimates) with no increased
phentermine 638 are European Medicines Agency and US Food and Drug Administration (FDA) approved, and lorcaserin and phentermine /topiramate, which have FDA approval only. Each of the six drugs, used singly or in combination, has
phentermine 30670 weight management in the obese and overweight with one or more weight related comorbidity (initial dose: phentermine 3.75 mg/topiramate 23 mg extended-release, maintenance dose: phentermine 7.5 mg/topiramate 46 mg
phentermine 30745 comorbidity (initial dose: phentermine 3.75 mg/topiramate 23 mg extended-release, maintenance dose: phentermine 7.5 mg/topiramate 46 mg extended-release). Phentermine is currently approved singly for short-term
phentermine 30981 topiramate is used in the treatment of epilepsy and migraine prevention [[50]]. The combination of phentermine /topiramate as a pharmacotherapy for obesity is understood to combine lower doses of each drug to reduce
phentermine 31235 whilst having a synergistic effect on weight loss.Mechanism of actionThe atypical amphetamine derivative phentermine stimulates norepinephrine release in the CNS, with limited effects on dopamine and serotonin [[51]].
phentermine 31474 norepinephrine is understood to produce its anorectic effects. A meta-analysis [[52]] suggests that monotherapy phentermine produces modest weight loss for up to 6 months. However, despite the absence of addictive potential,
phentermine 31636 However, despite the absence of addictive potential, due to its status as an amphetamine derivative, phentermine is presumed to increase blood pressure and heart rate (although there is evidence to contrary see Hendricks
phentermine 32341 respectively) [[55]].Efficacy, effects on behaviour and tailoring potentialEfficacy and safety of two doses of phentermine /topiramate were assessed in the phase III clinical trials CONQUER (2487 overweight or obese patients
phentermine 32484 phase III clinical trials CONQUER (2487 overweight or obese patients receiving placebo, once-daily phentermine 7.5 mg/topiramate 46.0 mg, or once-daily phentermine 15.0 mg/topiramate 92.0 mg) [[56]], SEQUEL
phentermine 32539 obese patients receiving placebo, once-daily phentermine 7.5 mg/topiramate 46.0 mg, or once-daily phentermine 15.0 mg/topiramate 92.0 mg) [[56]], SEQUEL (866 patients in continuation study from CONQUER) [[57]]
phentermine 32703 patients in continuation study from CONQUER) [[57]] and EQUIP (1267 obese patients receiving placebo, phentermine 3.75 mg/topiramate 23 mg extended or phentermine 15 mg/topiramate 92 mg) [[50]]. In a meta-analysis
phentermine 32754 and EQUIP (1267 obese patients receiving placebo, phentermine 3.75 mg/topiramate 23 mg extended or phentermine 15 mg/topiramate 92 mg) [[50]]. In a meta-analysis [[27]] phentermine/topiramate produced the highest
phentermine 32826 3.75 mg/topiramate 23 mg extended or phentermine 15 mg/topiramate 92 mg) [[50]]. In a meta-analysis [[27]] phentermine /topiramate produced the highest odds of achieving 5 and 10% weight loss compared to orlistat, liraglutide,
phentermine 33310 fMRI data to provide neurophysiological correlates of behaviour. Thus, the behavioural specificity of phentermine /topiramate remains unknown and effects on the psychological and motivational aspects which underlie
phentermine 34082 and real-world therapeutic benefits, i.e. proof of concept.Whilst there are no mechanistic data for phentermine /topiramate, other reviewed studies provide tentative evidence that liraglutide and lorcaserin produce
Select Disease Character Offset Disease Term Instance
diabetes mellitus 23211 between-group differences in neurocognitive testing (including inhibitory control SSRT)T2DM type 2 diabetes mellitus , BMI body mass index (kg/m2), GIP gastric inhibitory peptide, DLPFC dorsolateral prefrontal cortex,
obesity 84 Title: Acta DiabetologicaTailoring pharmacotherapy to specific eating behaviours in obesity : Can recommendations for personalised therapy be made from the current data?Carl A. RobertsPaul ChristiansenJason
obesity 410 (ppub): /2017Abstract Pharmacotherapy provides an adjunct to behaviour modification in the management of obesity . There are a number of new drug therapies purportedly targeting appetite; liraglutide, and bupropion/naltrexone,
obesity 926 action, thus the potential to provide defined therapeutic options to personalise the management of obesity . Yet, with regard to pharmacotherapy for obesity, we are far from true personalised medicine. We review
obesity 975 therapeutic options to personalise the management of obesity. Yet, with regard to pharmacotherapy for obesity , we are far from true personalised medicine. We review the limited mechanistic data with four mono and
obesity 1715 required to characterise responders for distinct pharmacotherapeutic options.IntroductionThe global obesity pandemic is a primary public health concern, due to prevalence (600 million obese, BMI ≥ 30, within
obesity 2029 weight has on physical, psychological and economic quality of life [[1]]. In the UK, the annual cost of obesity to the NHS is an estimated £5.1 billion, whilst total cost to the wider economy is an estimated £27
obesity 2208 wider economy is an estimated £27 billion [[2]]. Therefore, effective measures to tackle the burden of obesity , and obesity related diseases, are essential.Reducing energy intake through changes in eating behaviour,
obesity 2221 an estimated £27 billion [[2]]. Therefore, effective measures to tackle the burden of obesity, and obesity related diseases, are essential.Reducing energy intake through changes in eating behaviour, and increasing
obesity 2466 the state of negative energy balance required to lose weight. These are the principle components of obesity treatment and demand fundamental and sustained behavioural change. In the context of intervention, there
obesity 3749 IC (disinhibited eating, uncontrolled hunger) that comprise a susceptible behavioural phenotype for obesity . Thus, regulatory control of eating is undermined by reduced satiety and increased responsivity to food
obesity 4734 motivation.Heritability estimates of body weight are high. However, multiple common genetic variants belie obesity in the general population. Recent meta-analyses suggest that 97 BMI-associated genetic loci account
obesity 5058 that a standardised personalised medicine approach of targeting key genes with pharmacotherapy for obesity would, on its own, be inadequate. However, the fat mass and obesity-associated gene (FTO) has the largest
obesity 5126 genes with pharmacotherapy for obesity would, on its own, be inadequate. However, the fat mass and obesity -associated gene (FTO) has the largest effect size of BMI-associated genetic variants, whereby adults
obesity 6211 suggest that differences in behaviour are critical in mediating the association between genetic risk and obesity .In order to personalise pharmacotherapy for obesity in adults, it is critical that behavioural issues
obesity 6263 mediating the association between genetic risk and obesity.In order to personalise pharmacotherapy for obesity in adults, it is critical that behavioural issues associated with obesity are targeted. How does drug
obesity 6337 personalise pharmacotherapy for obesity in adults, it is critical that behavioural issues associated with obesity are targeted. How does drug therapy impact appetite (within a meal and throughout the day), portion
obesity 6844 behaviours?Personalised therapySpecialised adult weight management services provide person-centred care, for treatment of obesity , assisting patients to make lasting lifestyle changes. In this setting, access to distinct pharmacotherapies
obesity 7229 recommends a specialist multidisciplinary team approach (including pharmacotherapy) for treatment of severe obesity [[20]]. Pharmacotherapy has the potential to improve weight loss outcomes in primary care and specialised
obesity 8515 producing a cycle whereby ability to control behaviour and self-efficacy is undermined. However, anti- obesity drugs can mitigate some of the effects of dieting by reducing hunger and food cue responsiveness, leading
obesity 9083 modification with the four most recently available (FDA approved) mono and combination pharmacotherapies for obesity . Whilst orlistat (Xenical) has been approved as a pharmacological intervention for obesity since 1998,
obesity 9174 pharmacotherapies for obesity. Whilst orlistat (Xenical) has been approved as a pharmacological intervention for obesity since 1998, this is not a centrally acting drug and is not regarded as having direct behavioural effects
obesity 16011 (360 mg/day) and opioid antagonist naltrexone (32 mg/day) (Table 1) is approved for the management of obesity in sustained release form by the FDA and the EMA. Bupropion is an atypical antidepressant, which is
obesity 16427 demonstrate modest weight loss [[35], [36]]. Naltrexone has also been investigated as monotherapy for obesity , but although it affects food choice and palatability, it is not associated with weight loss [[37]].
obesity 30858 7.5 mg/topiramate 46 mg extended-release). Phentermine is currently approved singly for short-term obesity management, and topiramate is used in the treatment of epilepsy and migraine prevention [[50]]. The
obesity 31029 and migraine prevention [[50]]. The combination of phentermine/topiramate as a pharmacotherapy for obesity is understood to combine lower doses of each drug to reduce undesired cardiovascular effects whilst
obesity 35801 connectivity, dynamic causal modelling) will provide powerful evidence to assess the mechanisms by which anti- obesity drugs work.Table 3Methodological platform for assessing drug actionComponent assessedSpecific methodsAs
obesity 37893 (2010) [[39]] Bupropion/naltrexonePower of foodInhibitory controlA tool developed to assess effects of obesity treatments on feelings of being controlled by foodCapelleri et al. (2009) [[61]]Dutch eating Behaviour
obesity 38875 inhibitory control taskBatterink et al. (2010) [[65]]In order to deliver personalised treatment with anti- obesity medication, it is necessary to characterise drug effects on phenotypic traits associated with increased
obesity 39096 intake. However, to date eating behaviour has not been studied in sufficient detail with current anti- obesity drugs. A methodological platform for assessment of drug effects on appetite regulation is provided in
obesity 39304 in Table 3.Clinical response to pharmacotherapy can vary greatly, as such future research with anti- obesity drugs should seek to assess sub-populations of patients who respond well to drug treatment and are successful
obesity 39834 successful outcomes (e.g. Hauner et al. [[58]]) will help enable personalisation of pharmacotherapy for obesity . The goal of pharmacogenetics is to help identify patients who may benefit most from drug therapies
obesity 39997 patients who may benefit most from drug therapies and is currently underused in drug development of anti- obesity drugs. Similarly categorising sub-populations by behavioural risk factors (susceptible phenotypes) and
type 2 diabetes mellitus 23204 intake. No between-group differences in neurocognitive testing (including inhibitory control SSRT)T2DM type 2 diabetes mellitus , BMI body mass index (kg/m2), GIP gastric inhibitory peptide, DLPFC dorsolateral prefrontal cortex,

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