science of bodyweight lect 3 Flashcards by lilly ruffle

what are the 3 ways to reduce bodyweight

dieting (lifestyle modifications)
drugs
bariatric metabolic surgery

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what is the historical development of dietary restrictions

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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what are the findings of the WRAP trial

-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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what do the findings of the WRAP trial suggest

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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what does the research into duration of effect of dieting show

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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what happens when undertaking an energy restricted diet

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

-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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what happens when diet is nutrient targeted

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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what are the findings of wiegle nutrient controlled diet study

-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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what are the basic drug mechanisms

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

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what is an agonist

binds to receptor and produces an effect within the cell

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what is an antagonist

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

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what is an analogue

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

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lorcaserin

-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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phentermine hydrochloric, deithylpropion, benzphetamine, phendimetrazine

-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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phentermine and topiramate

-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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naltrexone and bupropion

-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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ciraglutide and semaglutide

-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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orlistat

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

how does bariatric surgery work

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

gastric bypass

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

sleeve gastrectomy

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

adjustable gastric band

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

biliopancreatic diversion with duodenum switch

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

procedures around the world

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

success of bariatric metabolic surgery

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

bariatric surgery and ghrelin

-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

bariatric surgery and leptin

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

other hormones and bariatric surgery

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

variability evidence after bariatric surgery

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

effects/co morbidities associated with obesity

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

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

Prickett et al

supportive links with bodyweight and cog

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

no links between bodyweight and cog

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

mixed evidence for bodyweight and cog

-visual memory -verbal memory -complex attention -inhibition

weaknesses of studies into bodyweight and cog

-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

leptin and cog functions

-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

inflammation

-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

balter research

-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

can losing weight improve cog fucntion

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

is food addiction a valid concept

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

what are the behavioural and clinical features of food addiction

-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

what is an addictive substance (food addiction)

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

is there a neural basis for food addiction

-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

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

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