science of bodyweight lect 2 Flashcards
what is an obesogenic environment
environment that promotes gaining weight and is not conducive to weight loss
context to weight gain in history (environmental milestones)
-12,000 yrs ago: advent of agriculture (move towards planting crops expecting growth and eating them)
-early 17th century: slave trade (accessibility to sugar increased, 1660 = 1200 barrels of sugar imported, 1700 = 50,000 barrels imported)
-speakman 2016: rising obesity in last 50 yrs
features of obesogenic environment
1.large portions
2.energy dense foods
3.highly palatable foods (tasty)
4.eating opportunities are abundant
5.food variety
these 5 interact with each other to create obesogenic environment
changes in energy dense variety
-as low energy dense variety increases, benefit increases e.g bell peppers in yellow red green etc
-as high energy dense variety increases, benefit tailors off e.g no benefit to eating strawberry, chocolate or vanilla ice cream
ultra processed foods and relation to bodyweight
barbara roll’s model
low cost and high convenience combined with ultra processed foods
causes increased eating rate, increased energy density and increased palatability
this causes increased intake
leading to weight gain
does the proportion of fresh ingredients relate to obesity
1980: 58% of food spent on fresh ingredients = 7% adults obese
2000: 25% of food spent on fresh ingredients = 20% adults obese
Now: 57% of food is ultraprocessed
what is processed food vs ultra processed
processed: anything we do before eating e.g cooking, blending etc
ultraprocessed: unable to do in kitchen at home e.g make a wotsit
what is multi component food
food involving more than one food class being brought together usually via processing of some kind in order to make a single food product (street 1995) e.g choc chip cookie/rocky road
each bite may taste diff
what is habituation
-basic form of learning
-we have a diminishing response to a repeated stimulus
-most known in terms of smell e.g nose blind but also applies to taste and eating
-two types: food variety and sensory complexity
epstein demonstrating habituation to taste
-measured by salivation of pp who received lemon or lime juice
-1-10 habituating trials of same juice, salivation decreases as trials go on
-trial 11 = new flavour, salivation increases again
-habituation = getting used to flavour in initial 10 trials
food variety study
hetherington
-measured pleasantness rating
-pleasantness goes down when same taste is presented repeatedly
-congruent = savoury food, savoury food
-incongruent = savoury food, sweet food
-food consumption higher when there was variety
strength for pleasantness liking research
-rolls: pp ate chicken and rated pleasantness, half of pp then ate plate of chicken and liking went down, others had a plate of something else and liking for chicken was preserved
-rolls: looked at firing rates of cells in monkeys, high levels responded for peanuts, then exposed to glucose on repeat (firing goes down), monkeys like flavour not just eating
-embling et al: meta analysis for variety effect shows the effect is robust
what is sensory complexity
perception of multiple sensations within a single mouthful fof food/drink as well as across an eating/drinking experience as a whole
what is the optimal arousal theory
dember and earl 1957
-e.g drinking wine
-liking for complex wine increases but too complex may cause disliking
(bell shaped curve)
what is gene environment interaction
different effect of environmental exposure on disease risk in persons with diff genotypes
pima people study
schulz
-2 areas: arizona and mexico
-same genes, diff environment
-high prevalence of type II diabetes in pima people (51%)
-females, pima = 78% were obese
-females, mexico = 19.8% obese
exercise difference is not enough to explain large differences here
genotype reactions to lifestyle interventions
-Moran: d allele = increased fat thickness, association strongest in women
-yoskida: intervention = low calorie diet and exercise, certain alleles cause people to lose less weight than someone with diff alleles
leptin and weight
leptin is a hormone (protein)
-coded for by ob gene (chromosome 7 in humans)
-produced by adipose tissue (fat cells)
-can cross blood brain barrier to reach neuronal targets (hypothalamus)
-influences appetite and energy expenditure
research into leptin and mice
ob/ob mice: recessive mutation of gene (responsible for leptin production) so cannot produce leptin
-mice eats rapidly and gains weight over lifetime
-leptin administration = reversal of weight gain (Halaas)
leptin and humans research
leptins should correlate positively with body fat
-case reports of children with congenital leptin deficiency resulted in:
hyperphagia (always hungry)
severe obesity
-leptin administered and weight loss seen (Farooqi)
what does leptin do in humans
-circulating levels reflect: amount of stored energy in fat and acute changes in calorie intake
-leptin binds to specific receptors in brain and peripheral tissues
-acts on brain to regulate appetite( activates either: anorexigenic-appetite diminishing or orexigenic-appetite stimulating neural circuitry)
-interacts with mesolimbic dopamine system (motivation and reward)
-effect in nucleus of solitary tract of brainstem
what does leptin deficiency lead to
its a monogenic cause for obesity
However: unlikely to be cause of obesity epidemic as mutation is very very rare
-most people with obesity have high leptin levels
other monogenic causes for obesity
rare mutations in MC4R were found in 5-6% of patients with severe early onset obesity (stutzmann et al) - such small % has low explanatory power
what is polygenic and monogenic
polygenic = more than 1 gene
monogenic = 1 gene
polygenic risk and bodyweight
Genome wide association study
polygenic risk score (how many trait relevant SNPs a person has and their strength of influence
polygenic risk scores
meta analysis of studies on BMI
-97 BMI associated SNPs
-SNP= single nucleotide polymorphisms
-explain 2.7% of BMI variation (more we dont know as systems are complex)
konttinen et al study of genes and bodyweight
Finland cohort study
-5024 pp took part
-genotyping done on each pp
-used 90/97 snips used on previous meta analysis to calculate polygenic risk score
-
mechanisms identified in konttinen study
-appetite traits: uncontrolled eating and emotional eating
-each pp had polygenic risk score (PRS), BMI, score for uncontrolled eating and emotional eating
-PRS is predictor of BMI
-PRS is genetic so uncontrollable
-put uncontrollable eating as mediator to see if PRS affected this and then in turn BMI
-uncontrollable eating controlled by PRS so there is genetic link here
-repeated with emotional eating as mediator and found same results
how does environment affect obesity in children
children with good appetites and genetic risk were placed in non obesogenic environment which acted as a buffer for genetic predisposition
hormone related to obesity
ghrelin (hunger hormone)
-peaks at meal times
-doesnt act in isolation (insulin)
-insulin rises just after meal times
-leptin less correlated with meals (increases most at night)
expression of ghrelin
mainly by stomach (gastric fundus), duodenum, lung, heart, pancreas etc
ghrelin secreted by stomach, reaches brain by crossing brain blood barrier and transmits signal through vagal nerve
ghrelin and weight loss
ghrelin could be responsible for weight loss
zigman 2005: looked at mice without ghrelin gene or receptor
-when they eat normally, they maintain body weight
-do not gain weight when fed a high fat palatable diet
is weight regulation symmetrical
no it is assymetrical
