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EXMD4743 > WK1 - Obesity > Flashcards

WK1 - Obesity Flashcards

1
Q

Obesity and being overweight has been stigmatised and causes people to be 6x more likely to have CVD. True or False?

A

T
We need to reduce stigmatisation.

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2
Q

How do we understand obesity?

A

Utilise a Person First Approach.
1. respect diversity and avoid stereotypes
2. use appropriate language and terminology
3. conduct balanced and accurate coverage of obesity
4. select appropriate pics and images of individuals affected by obesity.

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3
Q

What are the 5 obesity myths?

A
  1. body weight = calories in-calories out
  2. obesity is primarily caused by voluntary overeating and sedentary lifestyle
  3. obesity is a lifestyle choice
  4. severe obesity is usually reversible by voluntarily eating less and exercising more.
  5. obesity is a condtion, not a disease
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4
Q

Why is “body weight = calories in-calories out” a myth?

A

Energy intake is dependent on…
–> amount of food consumed
–> amount of food-derived energy absorbed
–> latter depends on digestive enzymes, bile acids, microbiota, gut hormones and neutral signals.

Energy output accounts for 30% of total daily energy expenditure, with 10% as thermic effect of feeding and metabolic rate accounting for 60-80%
–> this idea would only work for athletes

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5
Q

Why is “obesity is primarily caused by voluntary overeating and sedentary lifestyle” a myth?

A
  • genetics and epigenetic factors, foodborne factors, sleep deprivation nad circadian dysrhythmia, psychological stress, endocrine disruptors, meds, intrauterine and intergenerational effects can cause obesity
  • -ve ipact of media and public health strategies recommending “eat less and move more”, can cause voluntary overeating nad sedentary lifestyle
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6
Q

Why is “obesity is a lifestyle choice” a myth?

A
  • people with obesity recognise the severity of obesity as a health issue
  • more than 2/3 in ACTION Study consider obesity to be a serious/more serious disease than other health conditions, inc. high BP, T2DM and depression.
  • other -ve impact on QoL and decrease life expectancy, obesity is NOT a choice
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7
Q

Why is “obesity is a condition, not a disease” a myth?

A
  • WHO defined it as a disease
  • allows for Tx and policies to address stigma and bias
  • important to understand obesity as a disease based on med evidence, not sociologic implication - which would increase weight stigma and bias
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8
Q

Why is “severe obesity is usually reversible by voluntarily eating less and exercising more” a myth?

A
  • body weight nad fat mass are regulated by psychological mechanisms, past food intake, PA
  • decrease in fat mass will cause decrease in energy expendtiure, followed by resting energy expenditure and changes in signals that increase hunger and reduce satiety, promoting weight regain.
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9
Q

Who contributed to the consensus statement on obesity?

A
  1. The obesity Society (TOS)
  2. the obesity action coalition (OAC)
  3. the obesity Med association (OMA)
  4. the American Society for Metabolic and Bariatric Surgery (ASMBS)
  5. Academy of Nutrition and Dietetics (AAND)
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10
Q

Who contributed to the consensus statement on obesity?

A
  1. The obesity Society (TOS)
  2. the obesity action coalition (OAC)
  3. the obesity Med association (OMA)
    4.
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11
Q

What is the consensus statement on obesity?

A
  • obesity = highly prevalent disease - excessive fat accumulation/distribution. Obesity associated with T2DM, heart disease, and cancer
  • BMI screens obesity, doesn’t displace clinical judgement. BMI doesn’t measure body fat. Social determinants, race, ethnicity, age may modify risk
  • bias and stigmatisation directed at obese people contributes to poor health and impairs Tx.

*every person with obesity should have evidence-based Tx

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12
Q

What is the aetiology of obesity?

A

It is more than a simple imbalance between EI and energy expenditure. Involves a complex interplay between genetic, physiological, metabolic, soical, environmental and psychological factors.

  • Obesity Education Initiative, NIH, 1998
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13
Q

Which AUS state/cities have the high proportion of overweight/obese individuals?

A

SA
W NSW
W Vic
W Moreton

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14
Q

Which AUS state/cities have the 2nd highest proportion of overweight/obese people?

A
  • WA
  • N QLD
  • Central QLD, Wide Bay and Sunshine Coast
  • SE NSW
  • Murrary
  • Hobart
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15
Q

Which Aus state/city has the lowest proportion of overweight/obese people?

A
  • W QLD
  • Murrumbridge
  • Gippsland
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16
Q

What is the prevalence of obesity in Aus 2017-2018?

A

1 in 4 (25%) children and adolescents aged 2-17

2 in 3 (67%) adults
–>36% overweight but not obese
–>31% were obese

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17
Q

What does “not all fat is equal” mean?

A

Fat is distributed unevenly across the body.

60% men, 66% women –> waist circumference that indicated high risk of metabolic complications

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18
Q

What is VAT?

A

Visceral Adipose Tissue
* increased free fatty acid release
* inflammation
* insulin resistance and dyslipidemia

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19
Q

What are the complications of liver fat?

A
  • vascular dysfunction
  • non-calcified atherogenic plaque
  • aortic stiffness
  • coronary artery intima-media thickness
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20
Q

What is the indirect cost of obesity?

A

4.8bil

e.g. absenteeism, presentism, gov subsidies

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21
Q

What is the direct cost of obesity?

A

3.8bil

e.g. GP, ALP, specialist services, hospital care, pharmaceutical, weight loss interventions

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22
Q

What is the total cost of obesity?

A

8.6bil

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23
Q

How overweight/obese is Aus compared to other countries?

A
  • AUS is the 5th most overweight/obese country
  1. US
  2. mexico
  3. NZ
  4. Hungary
  5. Australia
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24
Q

What are the causes of obesity?

A
  • food and nutrition
  • physical inactivity
  • obesogenic environment - favouring weight gain

Other factors:
* psychological stress
* lower socioeconomic status
* genetic predisposition (20-90%)
* low plasma leptin levels
* SE of meds
* endocrine-disrupting chemicals
* areas of living (housing, safety, transport, parks, recreation, food availability

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25
Q

It is normal that body weight fluctuates throughout life. T or F?

A

T

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26
Q

What happens with weight loss?

A

Adaptive responses that drive weight regain are recruited due to energy gap

Increase hunger
- increase ghrelin, decrease GLP-1
- decrease PPY, decrease insulin
- decrease CCK, decrease leptin
this all = increase hunger, decrease satiety/satiation

Decrease energy expenditure
- decrease SNS activity, body mass, leptin
- increase energy efficiency
this all = decrease TDEE, TEF, RMR, PAEE

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27
Q

What is PYY?

A

peptide YY

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28
Q

What is CCK?

A

cholecystokinin

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29
Q

what is GLP-1?

A

glucagon-like peptide -1

30
Q

What is TDEE?

A

total daily energy expenditure

31
Q

What is TEF?

A

thermic effect of food

32
Q

What is RMR?

A

resting metabolic rate

33
Q

What is PAEE?

A

PA energy expenditure

34
Q

Metabolic slowing with massive weight loss despite preservation of fat-free mass. T or F?

A

T

Based on The Biggest Loser show

35
Q

Compare the difference in composition of weight in WK6 and WK30 from The Biggest Loser.

A
36
Q

Increased PA associated with less weight regain 6y after The Biggest Loser competition. T or F

A

T

Losing weight - sure!
But preventing weight regain is hard because it requires the individual to perform regular PA to prevent fat deposition.

We never lose the fat cells but we are able to reduce the size of these cells.

37
Q

What does a failure to see weight as biologically controlled lead to….?

A
  • blaming people for their weight in a way we do not blame people with high BP or T2DM
  • unrealistic views on what Tx of obesity is
  • persistence and growth of problem that is affecting health of country and productivity of workers
38
Q

Consider bidirectional causation. How do we relate it to obesity?

A

Physical inactivity <–> obesity

cause and consequence

39
Q

What is the “fat overflow hypothesis”?

A

Based on adipose tissue – endocrine organ

Chronic +ve energy balance (increased energy intake and/or reduced energy expenditure)
- reach limits of expansion capacity of adipose tissue
- lipid overflow

40
Q

What does VAT independently predict?

A
  • elevated BP
  • myocardial infarction
  • insuline resistance

As total body fact increases, insulin resistance increases

As total VAT increases, insulin resistance increases
- stronger relationship

41
Q

What are the health consequences of excess VAT?

A
  • insulin resistance
  • impaired glucose tolerance
  • T2DM
  • CVD
  • respiratory diseases
  • brain health
  • cancers
  • others
    –> reduced BMD
    –> polycystic ovary syndrome
    –> HIV infection and antiretroviral therapy
42
Q

What CVD are associated with excess VAT?

A
  • hypertension
  • heart failure
  • CHD, myocardial infarctions
  • valve diseases
  • arrhythmias
43
Q

What respiratory diseases are associated with excess VAT?

A
  • sleep apnoea
  • COPD
44
Q

What brain health consequences are associated with excess VAT?

A
  • stroke, necrosis
  • reduced brain size
  • reduced grey matter
  • reduced cognitive function
  • dementia
45
Q

What is the function of white adipose tissue (WAT)?

A
  • mechanical protection
  • thermal regulation
  • energy storage
  • secretion of adipokines for numerous functions.
46
Q

When in the lifecycle should we target intervention for obesity?

A

Pregnancy - infancy - childhood (habit formation) - adolscence -adulthood - pregnancy (genetic/epigenetics)

47
Q

How much weightloss is required to improve health?

A

-3% for blood glucose / triglycerides

-5% for HDL-C, S/DBP, hepatic steatosis (MRS), measures of feeling/function (urinary stress incontinence, sexual function, QoL)

-10% NASH Activity score (biopsy) and apnea-hypopnea index

-15-20% reduced CV events, mortlaity, remission of T2DM

48
Q

Why is modest weightloss beneficial?

A

10% weight loss = 30% VAT loss

Improves…
- lipid profile
- insulin sensitivity
- blood insulin / glucose
- risk markers for thrombosis
- inflammatory markers
- endothelial function

49
Q

What induces clinically significant weight loss? Order for highest to lowest.

A
  1. Roux-en-Y Gastric Bypass (30%)
  2. Sleeve Gastrectomy (25%)
  3. gastric banding )~13%)
  4. Older antiobeisty meds (phentermine/topiramate, liraglutide, bupropion/natrexone, gelesis-100, orlistat)

Lifestyle + exercise (10%)

50
Q

Dietary adherence is more important than diet type for weight loss. T or F?

A

T

51
Q

When is antiobesity med provided?

A

BMI >30 or >27 + >1complication

Obesity Tx guideline: med work to reinforce lifestyle change and should be Px as an adjuct to lifestyle interventions

Prescribed to <3% of eligible people

52
Q

What are the 5 C’s of choosing antiobesity meds?

A
  1. contraindications/cautions - assess pt Hx and risk/benefit
  2. comorbidities - select AOM that Tx obesity and improve other conditions
  3. Cues - consider appetite control Sx, adverse events, prefence on mode of Delivery
  4. Combinations - consider therapy with lifestyle interventions, other AOMs and surgical procedures
  5. Cost/coverage - insurance plan/med cost
53
Q

What are pipeline medications?

A
  • GLP-1/GIP RA
  • oral GLP-1 RA
  • GLP-1 RA/amylin analogue
  • PYY analogue
  • GDF-15 analogue
54
Q

What are off-label meds?

A
  • metformin
  • GLP-1RAs
  • SGLT2 inhibitors
  • topiramate
  • bupropion
  • other stimulants
55
Q

What meds target obesity via the brain?

A

Bupropion/naltrexone

phenterine/topiramate

phentermine

liraglutide

56
Q

what meds target obesity via the stomach?

A

hydrogel
- mixes with food to create a larger volume - feeling of fullness

semaglutide
- induces satiety, suppresses appetite

57
Q

What med targets obesity via the large intestines?

A

orlistat

58
Q

What med targets obesity via

A
59
Q

how does semaglutide work?

A

2.4mg SC once weekly
Dosage: 0.25, 0.5, 1, 1.7, 2.4
single-use pens
Dose increased every 4wks

Nausea 44%
Diarrhea 32%
Constipation 24%

Cost :$1400

17,500 participants - SELECT-COVT
>10% weightloss = 69.1% participants
>20% weightloss = 32%

60
Q

What is the efficacy of antiobesity meds?

A

sleeve gastrectomy 25%
semaglutide 16.9%
phentermine/topiramate 14.4%
liraglutide 9.2%
orlistat 8.8%
naltrexone/bupropion 8.1%
phentermine/monotherapy 7.4%

61
Q

Why is treating obesity like treating hypertension?

A

If you stop, the condition will return

62
Q

Despite a larger effect of diet on total body weight loss, exercise tends to have superior effects on reducing VAT. T or F

A

T

63
Q

How to discuss obesity with patient?

A
  • patient centred care
  • empathetic
  • unbiased - free of judgement, shame and guilt
  • focused on health rather than weight
  • appropriate terminology
  • share decision-making, provide practical options

Provide care that is respectful and responsive to preferences, eneds and values and ensure patient values guide all clinical decisions.

64
Q

What is the objective of management of people with obesity/overweight?

A
  • improve overall health/QoL
  • reduce comorbidities
  • reduce ectopic fat/central adiposity/weight
  • improve cardiometabolic fitness and weight-related behaviours
65
Q

What are the Ex recommendations for people with obesity?

A
  • mod/vig aerobic Ex 5-7days 300-420mins for weight loss
  • mod/vig aerobic Ex 3-7days (can be <300mins) for reducing central adiposity + RT >75% 1RM 3days
  • mod/vig/HIIT Ex 3-5days (can be <300min) for reducing ectopic weight
  • mod/vig Ex 5-7days >150mins to prevent weight gain
  • mod/vig 5-7days >60mins most days to prevent weight regain
66
Q

What is part of the Ask and Assess stage in practice?

A
  • Ax/monitor BMI and waist circumference
  • discuss weight Hx and health issues
  • identify comorbidities
  • Ax other factors (meds, smoking, social, stressors etc)
  • Ax current PA
67
Q

What is part of the Advise stage in practice?

A

Promote/explain
- healht benefits of PA
- benefits of weight managemet
- importance of energy expenditure for weight goals
- volume/type of PA required
- achiving MVPA intensity

Indicate
- benefit of PA and dietary interventions
- benefits of PA independent of weight loss

68
Q

What is part of the assist stage of practice?

A
  • agree on appropriate goals
  • incorporate therapeutic goals beyond weight change
  • use guidelines
  • tailor to individual circumstances
69
Q

What is part of the arrange stage in practice?

A
  • monitor client progress towards achieving PA goals
  • consider referral to other AHP
  • identify PA options within community for long-term adherence
70
Q

What are some special considerations for testing and prescription?

A
  • low work capacity - due to excess body weight
  • orthopaedic limitations
  • risk for CVD events - myocardial ischaemia
  • meds
  • accountability and staff support valued/enablers
71
Q

Summarise exercise training in obesity.

A
  • AT is an endocrine organ with certai nfat distributions particularly linked to cardiometabolic risk
  • “best” mode of exercise depends on therapeutic goal
  • prescription can and should be highly individualised
  • benefits - multifaceted and extend beyond weight loss
72
Q

Benefits of exercise. List some examples.

A

Improved…
- CRF, glucose control, fat oxidation, strength, muscle bulk, flexibiltiy, BMD, mood, energy levels, sleep, self-esteem/confidence

Decreased…
- BP
- insulin resistance
- VAT/overall fat
- anxiety/depression

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