science of bodyweight lect 3 Flashcards

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1
Q

what are the 3 ways to reduce bodyweight

A

dieting (lifestyle modifications)
drugs
bariatric metabolic surgery

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2
Q

what is the historical development of dietary restrictions

A

dr george cheyne 1708
-reduced bodyweight by taking diet of milk with seeds, bread, mealy roots and fruit
-lost between 16 and 18 stone (102-114kg)
(strings 2019)

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3
Q

what are the findings of the WRAP trial

A

-1 year follow up assessed mean weight changes in groups
-brief intervention = loss of 3kg
-12 week programme = loss of 5kg
-52 week programme = loss of 7kg

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4
Q

what do the findings of the WRAP trial suggest

A

longer the intervention = greater weight loss
-difference between groups still significant after 2 years but NOT after 5 years
-most of weight lost in first year
-there is a problem maintaining weight

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5
Q

what does the research into duration of effect of dieting show

A

Crawford et al
-might yield results in the ST but not LT
-54% gained weight in first 12 months
-26% maintained weight over three years
-5% lost (after 1 year) and maintained weight successfully over the next 2 years

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6
Q

what happens when undertaking an energy restricted diet

A

Mars et al
-looked at leptin and appetite ratings
-44 healthy adult male pp (mean age of 43) (mean BMI = 27.3 = overweight category)
-measured over a 4 day diet (36% energy requirement provided)
-looked at fasting leptin cone and appetite levels

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7
Q

what are the findings of Mars’ study into an energy restricted diet

A

-after 4 days fasting leptin concentration decreases by 39%
-leptin levels are negatively correlated with hunger/desire to eat/total appetite (as leptin decreases, hunger increases)
-suggests leptin has an important role in bodyweight regulation (likely mediated through appetite)
-helps us to understand role of leptin

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8
Q

what happens when diet is nutrient targeted

A

wiegle et al
-looks into protein and weight loss
-19 pp
-2 week weight maintaining diet (15% protein)
-2 week iso-caloric diet (30% protein) (calorie controlled specific to indiv)
-12 week ad libitum (30% protein) (pp eat as many calories as the want)
-measured levels of insulin, ghrelin and leptin

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9
Q

what are the findings of wiegle nutrient controlled diet study

A

-satiety increased on iso caloric diet (less hunger) with no change to leptin
-ad libitum: energy intake decreased, bodyweight decreased by 4.9kg, decreased leptin and ghrelin
-decreased leptin = anorexigenic affect/ appetite suppressing

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10
Q

what are the basic drug mechanisms

A

1.decreasing appetite and caloric intake
2.increasing energy expenditure
3.decreasing fat absoption

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11
Q

what is an agonist

A

binds to receptor and produces an effect within the cell

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12
Q

what is an antagonist

A

binds to same receptor but does not produce response, instead it blocks that receptor from a natural agonist

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13
Q

what is an analogue

A

compound having structure similar to that of another compound but differing from in in respect to a certain component

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14
Q

lorcaserin

A

-serotonin agonist, decreasing caloric intake
-part of anorexigenic pathway
-humans fmri study
show pics e.g doughnuts
when taking drug = decreasing emotion and saliency related to activity or limbic system
decreases activity of parietal and visual cortices in response to highly palatable food

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15
Q

phentermine hydrochloric, deithylpropion, benzphetamine, phendimetrazine

A

-noradrenergic agonists suppress appetite
-humans: mechanism of action not completely understood
-rats: acting on homeostatic related hypothalamus and reward related nucleus accumbens

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16
Q

phentermine and topiramate

A

-combination of these suppresses appetite
-humans: mechanisms poorly understood
-phentermine: enhances release of serotonin, norepinephrine and dopamine
-topiramate: GABA agonist, glutamate antagonist and carbonic anhydrase inhibitor

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17
Q

naltrexone and bupropion

A

-both have weight loss as side effect
-work to increase POMC peptide production, regulate appetite and decrease food intake
-rats: bupropion act on POMC neurons and activates anorexigenic pathway
-humans: fmri showed change in response to food in hypothalamus

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18
Q

ciraglutide and semaglutide

A

-blood glucose regulation
-slows gastric emptying
-increases fullness
-acts on hypothalamus, reduces appetite/hunger etc
-rats: acts on reward system to reduce intake of highly palatable foods
-humans: altered activation in response to images of desirable foods, decreased hunger and increased fullness

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19
Q

orlistat

A

-inhibits gastrointestinal and pancreatic lipases
-reduced fatty acid absorption
-1/3 of fatty acids in foods not absorbed

20
Q

how does bariatric surgery work

A

weight loss via
-restricting amount of food stomach can hold
-malabsorption of nutrients
(or a combination of both)
(often causes hormonal changes)

21
Q

gastric bypass

A

Roux- en - Y gastric bypass
- small stomach pouch created
-beginning of small intestine divided and one part brought up to reach new stomach pouch

22
Q

sleeve gastrectomy

A

-laparoscopic sleeve gastrectomy ‘The sleeve’
-removal of about 80% of stomach
-creates tubular pouch
-effect on gut hormones

23
Q

adjustable gastric band

A

-small stomach pouch via inflatable band around upper part of stomach
-port allows for filling of band with saline

24
Q

biliopancreatic diversion with duodenum switch

A

-first part similar to sleeve gastrectomy
-second part involves bypassing of large section of small intestine

25
Q

procedures around the world

A

-23 countries
-311,441 procedures registered
-61% sleeve gastrectomy procedures

26
Q

success of bariatric metabolic surgery

A

Sjostrom (swedish obese study)
-all pp lost weight but struggled to maintain it

27
Q

bariatric surgery and ghrelin

A

-ghrelin decreased
-removal of gastric fundus = main source of ghrelin
-variability due to differential exclusion
-ghrelin changes might underpin post surgery decrease in liking of palatable food, new food dislikes and changes in taste

28
Q

bariatric surgery and leptin

A

-leptin decreases after surgery = in line with weight loss
-adipose tissue secretes leptin, as volume of adipose tissue decreases so does leptin

29
Q

other hormones and bariatric surgery

A

-GLP-1, increases after surgery (anorexigenic pathway)
-post prandial levels increase after surgery
-effects seem to by LT

30
Q

variability evidence after bariatric surgery

A

Hollanda 2015
-looked at people after surgery
-1 year more weight loss, maintained for some but not all

31
Q

effects/co morbidities associated with obesity

A

-cardio vascular disease (ortega 2016)
-type II diabetes (mokdad 2003)
-some cancers (Font Burgada 2016)

32
Q

who reviewed the relationship between obesity and cog functions by using reaction times

A

Prickett et al

33
Q

supportive links with bodyweight and cog

A

-intellectual functioning
-psychomotor performance and speed
-visual construction
-decision making

34
Q

no links between bodyweight and cog

A

-general cog performance
-time judgement
-working memory
-verbal fluency

35
Q

mixed evidence for bodyweight and cog

A

-visual memory
-verbal memory
-complex attention
-inhibition

36
Q

weaknesses of studies into bodyweight and cog

A

-many studies fail to account for cofounds e.g age, education, depression
-many studies do not use exclusion criteria (people included who have cog deficits)
-lack of comparison groups
-publication bias (sig effects published)
-quality of assessment tools varied
-lack of broad assessment of cog domains

37
Q

leptin and cog functions

A

-leptin associated with impaired cog function
-higher bodyweight = higher adipose tissue = higher leptin = lower cog function
-leptin influences hippocampul dependent learning and memory
-anti depressant properties

38
Q

inflammation

A

-inflammation related with immune system is associated with obesity
-increase of adipose tissue = cell death = inflammatory marker
-inflammation causes neuronal dysfunction
-associated with subtle cog deficits

39
Q

balter research

A

-reaction time test for people with high and low BMI for diff ages
-older and high BMI had worst reaction time
-higher reaction time for high BMI due to inflammation

40
Q

can losing weight improve cog fucntion

A
  • yes attention and memory improved
    -veronese: overall there is an improvement in cog function when people lose weight
41
Q

is food addiction a valid concept

A

fletcher and kenny
-not enough support (fletcher)
-there is enough support (kenny)

42
Q

what are the behavioural and clinical features of food addiction

A

-addiction from DSM 5 has 11 criteria e.g taking substance in large amounts, craving it, wanting to stop etc

-Yale food addiction scale (Gearhardt et al 2009)
-self report questionnaire
-symptom count: how many of 11 criteria points to food addiction
-limited predictive power
-does not give clear pic about behavioural and clinical signs

-concept of food addiction does not directly map onto DSM 5

43
Q

what is an addictive substance (food addiction)

A

-many studies on sugar addiction are with animal studies
-not generalisable to humans
-more evidence needed
-no consistent evidence for sugar addiction

44
Q

is there a neural basis for food addiction

A

-overlapping neural substrates
-dopamine released when drugs taken and when we anticipate or eat food
-sensitisation seen over time (robinson and berridge) leading to increased wanting of food/drugs
-food lacks the motivational intensity of drugs
-reduction of D2 binding in substance addiction and obesity

45
Q

what are the 3 things we need to establish in food addiction

A

1.behavioural and clinical characteristics
2.the addictive substance
3.neural mechanism