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FNH 477 > Obesity > Flashcards

Obesity Flashcards

1
Q

Describe the issue of overweight & obesity.

A
  • Almost 60% of people are overweight
  • Of which nearly 25% are obese
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2
Q

What underpins the rise in being overweight? [4]

A
  • 50% of people have an unhealthy diet (measured against national guidelines)
  • 1 in 3 people do not do a sufficient amount of physical activity
  • 40% of waking time is spent in sedentary activities (e.g., video games, watching TV)
  • 2 in 5 individuals do not consume a sufficient amount of fruits and vegetables
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3
Q

Describe how the prevalence of obesity differs between men, women, and those 5-19 years of age.

A
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4
Q

In Canada, what is the overweight-attributable reduction in life expectancy?

A
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5
Q

In Canada, what are the overweight attributable cases of disease?

A

CVD - 23% of total cases
Diabetes - 79% of total cases
Dementia - 22% of total cases
Cancers - 13% of total cases

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6
Q

Describe the projected rates of obesity.

A

It is projected that by 2050 there will be around 92 million premature deaths from obesity- related diseases in OECD.

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7
Q

Describe health risk classification according to BMI.

A

Normal weight BMI - 18.5 - 24.9 has the least risk of developing health problems.

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8
Q

Obesity increases risk for: [12]

A
  • Coronary heart disease
  • Heart failure
  • Hypertension
  • Stroke
  • Type 2 diabetes
  • Some cancers
  • Osteoarthritis
  • Sleep apnea
  • Reproductive problems
  • Gall stones
  • Non-alcoholic fatty liver
  • Dementia
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9
Q
A

D. You cannot make any conclusions based on BMI alone.

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10
Q

How is BMI assesssed in children?

A
  • Up to age 19 y, defined using BMI-for-age
  • Pre-obese ≥ 85th percentile;< 95th
    percentile
  • Obese: ≥ 95th percentile
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11
Q

What is the adiposity rebound?

A

In general, BMI rapidly increases during the first year of life, then subsequently decreases and reaches a low point around 6 years of age. Thereafter, BMI increases again throughout childhood, and this second rise is referred to as the adiposity rebound.

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12
Q

What is the association between BMI and mortality?

A

U-shaped curve

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13
Q

Describe the RRs of death by activity level, controlling for sociodemographics and selected health-related behaviors in this study.

A

Stay active!

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14
Q

Describe the association of BMI with overall and cause-specific mortality in a population-based cohort study of 3.6 million adults in the UK.

A
  • BMI had J-shaped associations with overall mortality and most specific causes of death.
  • Lower BMI was associated with increased mortality, risk for mental and behavioural, neurological, and external causes.
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15
Q

Compare the expected age at death for a never-smoker aged 40 years by WHO BMI category, and estimated reduction in life expectancy compared with an individual of healthy weight.

A

Notice how the reduction in life expectancy is greater for those who are underweight versus those who are overweight.

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16
Q

What is BMI intended to tell you? [2]

A
  • Adiposity
  • Proxy for % body fat
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17
Q

What is a limitation of BMI?

A
  • Doesn’t necessarily tell us about adiposity.
Arnold here has BMI 33
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18
Q

Describe how not all fat is equal?

A

Visceral fat is more dangerous than subcutneous fat, but both are necessary for health.

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19
Q

What is a better predictor of visceral fat than BMI?

A
  • Waist circumference
  • If WC is larger than a particular cut-off number, risk for heart disease, hypertension, and diabetes increases
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20
Q

What are the possible links between obesity & chronic disease? [3]

A
  • Large size - increased strain on heart, joints, etc.
  • Adipose (particularly visceral) is metabolically active - plays a role in inflammation - obesity is associated with a pro-inflammatory state
  • Other metabolic effects of obesity/excess food intake - insulin resistance, altered serum lipids, hypertension
21
Q

What ‘causes’ obesity?

A
  • Energy imbalance - energy intake > energy expenditure (however, the body is able to regulate the imbalance within a certain range; i.e., energy expenditure decreases during underfeeding and increases (somewhat) during overfeeding)
  • Genetic factors may predispose individuals to have energy intake (poor appetite regulation) or lower energy expenditure
  • Environmental factors that increase energy intake and decrease energy expenditure = obesogenic
"The obesity pandemic is a result of underlying biologic susceptibilities to obesity within an obesogenic environment" - Polsky, Obesity: Epidemiology, Etiology, and Prevention
22
Q

What factors increase energy intake and decrease energy expenditure? [2]

A
  • Genetic factors
  • Environmental factors
23
Q

What is the ARC?

A
  • Hypothalamic arcuate nucleus (ARC)
    • Pro-opiomelanocortin (POMC) appetite-inhibiting neurons
    • Neuropeptide Y (NPY) and agouti-related peptide (AgRP) appetite-stimulating co-experssing neurons
24
Q

Define: Orexigenic

A

Appetite increasing

25
Q

Define: anorexigenic

A

Appetite suppressing

26
Q

Which gut peptides are anorexigenic? [4]

A
  • Cholecystokinin (CCK)
  • Glucagon-like peptide (GLP)
  • Bombesin
  • Peptide YY
27
Q

What gut peptides are orexigenic? [1]

A

Ghrelin

28
Q

Where is leptin secreted from?

A

Adipose tissue

29
Q

Describe the function of the hormone leptin.

A
  • Binds to leptin receptor in hypothalamus
    • Inhibits orexigenic NPY/AgRP neurons
    • Stimulates anorexigenic POMC-expressing neurons
      • Leads to decreased appetite
30
Q

What accounts for 3% of individuals with severe obesity?

A
  • Genetic disorders (e.g., leptin deficiency and leptin receptor deficiency)
  • Causes severe obesity in the first few months of life
  • Affected individuals are normal weight at birth; but quickly gain weight
  • Affected individuals experience extreme hunger and chronic excessive eating, develop abnormal eating behaviours
31
Q

Describe leptin deficiency.

A
  • Due to polymorphisms/mutations in the Ob gene that encodes for leptin protein.
  • Characterized by undetectable circulating leptin concentrations.
  • Leptin therapy available
32
Q

Describe leptin receptor deficiency.

A
  • Due to polymorphisms/mutations in the LEPR gene that encodes for leptin receptor.
  • Characterized by extremely elevated circulating leptin concentrations.
  • Leptin therapy DOES NOT work.
  • No effective therapy available.
33
Q

Leptin therapy DOES NOT work for leptin deficiency.
True or False?

A

False.
Leptin therapy does work for leptin deficiency.

34
Q

Leptin therapy DOES NOT work for leptin receptor deficiency.
True or False?

A

True.

35
Q

Leptin therapy is available for leptin receptor deficiency.
True or False?

A

False.
Leptin therapy DOES NOT work for leptin receptor deficiency. No effective therapy is available.

36
Q

Leptin therapy is available for leptin deficiency.
True or False?

A

True.

37
Q

Describe the function of insulin.

A
  • Decreases appetite through inhibition of NPY/AgRP co-expressing neurons
38
Q

Describe environmental factors that influence caloric intake [4].

A
  • Food availability - cost & convenience
  • Portion sizes
  • Dietary diversity (sensory specific satiety)
  • Food composition - energy dense, high in added sugars, high in fat etc.
39
Q

What is sensory specific satiety?

A

Sensory specific satiety (SSS) describes the decline in pleasantness associated with a food as it is eaten relative to a food that has not been eaten (the ‘eaten’ and ‘uneaten’ foods, respectively).

40
Q

Describe healthy eating habits.

A
  • Be mindful of your eating habits (take time to eat; notice when you are hungry and when you are full)
  • Cook more often (plan what you eat; involve others in planning and preparing meals)
  • Enjoy your food (culture and traditions can be a part of heatlhy eating)
  • Eat meals with others
41
Q

Discuss why the energy density of foods matters.

A
  • Theory: eat the same volume of food, regardless of caloric content, so when food is more energy dense, we eat more calories
42
Q

Describe what fibre contributes to food nutrient composition. [4]

A
  • No energy
  • Increases bulk
  • Speeds transit time
  • Can decrease absorption of nutrients
43
Q

Describe how sugar-sweetened beverages contribute to weight gain.

A
  • Issue - if additional kCal consumed in beverages, we do not seem to compensate for this with reduced food intake (so, overall caloric intake goes up)
  • Contains high-fructose corn syrup - fructose is not under the same metabolic control as glucose, may be more easily converted to triacylglyceride (fat)
Recall that fructose bypasses the second regulatory step of glycolysis at phosphofructokinase.
44
Q

What can basal metabolic rate (and possibly thermic effect of food) be influenced by? [2]

A

Genetics and lean tissue mass

45
Q
A

Answer: Muscle

46
Q

Describe how physical activity impacts energy expenditure.

A
  • Daily activities (walking to work, cleaning, etc.)
  • Work-related activities
  • Leisure activity (sports)
47
Q

Describe some socioeconomic factors that impact energy intake and expenditure. [4]

A
  • Income
  • Access to grocery stores
  • Walkability of neighborhoods
  • Proximity to fitness facilities, parks, etc.
48
Q

There is convincing evidence that [2] decreases risk of obesity.

A
  • Regular physical activity
  • High dietary intake of dietary fibre
49
Q

There is convincing evidence that […]increases risk of obesity. [2]

A
  • Sedentary lifestyles
  • High intake of energy-dense micronutrient-poor foods

FNH 477 (11 decks)

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