science of bodyweight lect 2 Flashcards

1
Q

what is an obesogenic environment

A

environment that promotes gaining weight and is not conducive to weight loss

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2
Q

context to weight gain in history (environmental milestones)

A

-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

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3
Q

features of obesogenic environment

A

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

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4
Q

changes in energy dense variety

A

-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

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5
Q

ultra processed foods and relation to bodyweight
barbara roll’s model

A

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

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6
Q

does the proportion of fresh ingredients relate to obesity

A

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

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7
Q

what is processed food vs ultra processed

A

processed: anything we do before eating e.g cooking, blending etc

ultraprocessed: unable to do in kitchen at home e.g make a wotsit

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8
Q

what is multi component food

A

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

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9
Q

what is habituation

A

-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

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10
Q

epstein demonstrating habituation to taste

A

-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

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11
Q

food variety study

A

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

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12
Q

strength for pleasantness liking research

A

-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

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13
Q

what is sensory complexity

A

perception of multiple sensations within a single mouthful fof food/drink as well as across an eating/drinking experience as a whole

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14
Q

what is the optimal arousal theory

A

dember and earl 1957
-e.g drinking wine
-liking for complex wine increases but too complex may cause disliking
(bell shaped curve)

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15
Q

what is gene environment interaction

A

different effect of environmental exposure on disease risk in persons with diff genotypes

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16
Q

pima people study

A

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

17
Q

genotype reactions to lifestyle interventions

A

-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

18
Q

leptin and weight

A

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

19
Q

research into leptin and mice

A

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)

20
Q

leptin and humans research

A

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)

21
Q

what does leptin do in humans

A

-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

22
Q

what does leptin deficiency lead to

A

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

23
Q

other monogenic causes for obesity

A

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

24
Q

what is polygenic and monogenic

A

polygenic = more than 1 gene
monogenic = 1 gene

25
Q

polygenic risk and bodyweight

A

Genome wide association study
polygenic risk score (how many trait relevant SNPs a person has and their strength of influence

26
Q

polygenic risk scores

A

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)

27
Q

konttinen et al study of genes and bodyweight

A

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
-

28
Q

mechanisms identified in konttinen study

A

-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

29
Q

how does environment affect obesity in children

A

children with good appetites and genetic risk were placed in non obesogenic environment which acted as a buffer for genetic predisposition

30
Q

hormone related to obesity

A

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)

31
Q

expression of ghrelin

A

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

32
Q

ghrelin and weight loss

A

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

33
Q

is weight regulation symmetrical

A

no it is assymetrical