Problem 6 - Genes vs Environment Flashcards
(36 cards)
Obesogenic environment
food:
- more highly palatable & energy-dense
- easier accessible and cheaper
- bigger portions
- incentives for buying larger quantities
Exercise:
- reduced physical activity in everyday life (transportation)
- increases in range of sedentary screen based entertainments
- -> reduced activity level
higher engird-intake that energy-expenditure
Gene-Environment Interaction
the more obseogenic the environment, the stronger the genetic effect on body weight
- studies found that genetic effects are moderated by environment
(found in twin studies)
Genetics
genes account for 50% - 90% for differences in BMI
- genome-wide associations have (GWAS) found 97 genetic variants (SNPs)
Behavioural Susceptibility Theory (BST)
Appetite mediates genetic risk of obesity
proposes that individuals who inherit a more avid appetite or lower sensitivity to satiety (‘obesity genes’)
–> they overeat in food environment
two important aspects
- eating onset
- eating offset
- theory proposes that genetic risk operates through these two traits
- they confer differential susceptibility to food environment
- -> idea that obesity genes work through effects on appetite
eating onset (BST)
responsiveness to signals to stark eating
–> ppl who are more responsive to food cues (smell, sight, taste) are more likely to eat in response to tempting opportunities
eating offset
responsiveness to stop signals
–> ppl who have weaker internal signalling from their gut once they start eating or are less aware go the signals (sensitivity to satiety) are likely to carry on eating for longer once they have started
Reward Sensitivity
personal risk factor
- explains individual differences in rewards motivation
- high –> more vulnerable to rewarding properties of food cues and generate approach behaviour
youth with high sensitivity show higher intakes of palatable, energy-dense foods & sugar-sweetened beverages - obese adults with binge eating appear to have greater responsiveness ness to food and a genotype related ti greater reward sensitivity
Reward Deficiency Syndrom (reward sensitivity)
addictive substances are used as a form of medication used to boost a sluggish or hypo-functionunfg reward system and to increase hedonic capacity
(Taq1a+ allele)
Hypersensitivity to rewards
contributes to increased vulnerability for overeating because of an enhanced motivation to engage in pleasurable activities
(opioid receptor gene OPRM1 in binge eating disorder patients)
Impulsivity
- failure to disinhibit inappropriate behaviour
- heightened sensitivity to reward (without appropriate sensitivity to punishment)
–> reward-based sensitivity
(has shown to be strongly associated with overeating and weight gain)
- impulsivity also part of poor decision-making, esp. when outcome of immediate action has future consequences
Attention Deficit/Hyperactivity Disorder ADHD
impulsivity * reward sensitivity converge as risk factors for obesity
- low mesolimbic dopamine availability (cause of ADHD symptoms)
- some cases of obesity may be the consequence of a food addiction38 that occurs, such as drug dependence, with greater prevalence in those with ADHD
Environmental Factors
- obesigenic environment
stable behavioural phenotypes that confer risk:
- food responsiveness, reinforcing value of food,
eating in absence of hunger,
habitual consumption of high fat diets, weak satiety, disinhibition
Genetic Factors
candidate gene variants presupposing to polygenic obesity generally relate to the regulation of energy intake and expenditure and include
- adrenergic receptors, uncoupling proteins, peroxisome proliferator-activated receptor (PPARG)
- proopoimelanocortin (POMC)
- melanocortin (MC4R)
Genetic Factors
candidate gene variants presupposing to polygenic obesity generally relate to the regulation of energy intake and expenditure and include
- adrenergic receptors, uncoupling proteins, peroxisome proliferator-activated receptor (PPARG)
- proopoimelanocortin (POMC)
- melanocortin (MC4R)
- and fat mass and obesity associated (FTO) genes
FTO
Candiate Gene Variants in Obesity Risk
- adults homozygous for the risk allele (in form of a SNP) weigh 3 kg and are more likely to be obese
- Frequency of the risk allele is estimated at ~39% in populations of European descent
- FTO gene is located on chromosome 16 + expressed mostly in brain, pancreatic islets,
adipose tissue and adrenal glands →HPA axis - FTO gene indicates higher risk for obesity that is conferred by differences in energy intake rather than expenditureA allele carriers:
- in children associated with lower satiety responsiveness
+ more EAH (= eating in absence of hunger), but no impact on reported activity measures
+ more consumption of energy-dense food
➔ Physical activity attenuates the genetic susceptibility to
overweight and obesity conferred by the A allele of FTO
precision medicine
tailoring of medical treatment to the individual characteristics of each patient & ability to classify individuals into subpopulations differing in susceptibility to particular disease , in biology or prognosis of disease or in response to specific treatment
–> seeks to maximise effectiveness by taking individual genetic variability into account
behavioural phenotypic
patterns of behaviour that are distinct, are quantifiable and measurable and result from interaction of genotype with environment
- individual appetitive traits combining to make up broader eating phenotype (can help to predict response to intervention & match prevention and treatment approaches)
Appetitive traits
self-regulation
Self-Regulation
some (not all) infants born with capacity to self-regulate energy intake
- can self-regulate at young age (unclear why differences)
- breastfed better able regulate energy intake and lower risk of weight gain
Individual differences in satiety (caloric compensation)
- individuals with obesity showing impaired sensitivity to internal satiety cues
- satiety value of food typically assessed by consuming it as compulsory first course (preload) at peak and measuring effect in ad libitum energy intake at subsequent main course (test meal)
- poorer energy compensation ability in children associated with higher child weight status, over age, racial/ethnic minority status, having mothers who use controlling/restrictive feeding practices
energy compensation
adjustments in intake in response to changes in energy density of compulsory preload –> measure of individual differences in satiety
food-seeking appetitive traits
eating in absence of hunger (EAH)
relative reinforcing value of food (RRVF)
reward sensitivity
eating rate
relative reinforcing value of food (RRVF)
- examines how hard individuals are willing to work to gain access to preferred food rather than appealing nonfood alternative (uses behavioural economics concept)
- sig interaction between children’s weight status, reinforcer type and schedule of reinforcement
- -> obese & overweight found food more reinforcing than nonfood & more motivate to work for food
eating in absence of hunger (EAH)
- eating beyond satiation when high energy-dense snack foods are there
eating rate
- rapid eating rate possible behavioural phenotype for childhood obesity
- rate of eating shown to be heritable
- emerges early in life
- may be risk factor for excess weight gain in children
