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NUTR*3090 > Final > Flashcards

Final Flashcards

1
Q

What is the definition of overweight/obesity?

A
  • Body weight above a defined standard relative to height
  • Abnormally high % of body fat which increases risk of health problems & mortality
  • A negative social label
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2
Q

What are the BMI classifications?

A
  • Underweight: < 18.5
  • Normal: 18.5 - 24.9
  • Overweight: 25.0 - 29.9
  • Obesity I: 30.0 - 34.9
  • Obesity II: 35.0 - 39.9
  • Obesity III: ≥ 40
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3
Q

What is the relationship between weight and mortality?

A
  • BMI inversely related to overall mortality (especially with respiratory disease and lung cancer)
  • Lowest mortality at 22.5-25 kg/m2
  • Each 5 kg/m2 higher BMI above 25 associated with 30% higher overall mortality
  • J-shaped curve between BMI and all-cause mortality
    • Underweight people are still at risk
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4
Q

What is the relationship between weight and CVD risk?

A
  • The higher your BMI, the higher your risk of CVD (major risk)
  • Obesity acts through hypertension and dyslipidemia
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5
Q

How much shorter is your lifespan if your BMI is higher than 25?

A
  • 25-27.5 = 0-1
  • 27.5-30 = 1-2
  • 30-35 = 2-4
  • 40-50 = 8-10 (comparable to smoking)
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6
Q

What may be a better predictor of mortality than BMI?

A
  • Some studies suggest that fitness and WC are better predictors of mortality than BMI
  • But most studies are focused on BMI
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7
Q

Which diseases have a greatly increased risk if you are obese?

A

Type 2 diabetes, gallbladder disease, dyslipidemia, insulin resistance, breathlessness, sleep apnea

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8
Q

Which diseases have a moderately increased risk if you are obese?

A

Coronary heart disease, hypertension, inflammation of joints (osteoarthritis, gout)

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9
Q

Which diseases have a slightly increased risk if you are obese?

A

Breast, endometrial and colon cancer, reproductive hormone problems, polycystic ovary syndrome, impaired fertility, low back pain, fetal defects due to maternal obesity

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10
Q

What are NOT good anthropometric indicators of obesity?

A
  • Height and waist-to-hip ratio (WHR) are not good predictors of obesity
  • BMI, WC, hip circumference, body adiposity index (BAI) is
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11
Q

What is the significance of the waist-to-height ratio to CVD risk?

A
  • Simple, low-cost measure of distribution of body fat
  • Higher values (> 0.5) indicate higher risk of obesity-related CVD
    • Cardiometabolic risk factors are significantly increased if WHtR ≥ 0.5 even among “healthy” BMI individuals
    • WHtR may identify risk earlier and more accurately than BMI (indicator of “early health risk”)
    • Clinicians should look further than BMI to assess CVD risk
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12
Q

What is the significance of the body adiposity index to risk? Mention what it is calculated with.

A
  • Calculated with hip circumference and height

- NOT a more accurate measure of adiposity than BMI, WC, or HC

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13
Q

What is epigenetics? Discuss causes.

A
  • The study of heritable and stable alterations in gene expression that are not caused by changes in DNA sequence
  • May be caused by:
    • Modifications at the level of histones (proteins that package DNA into chromosomes)
    • Interference with the transition of RNA to proteins
    • Methylation of DNA sequence
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14
Q

According to epigenetics, which mutations are associated with obesity? How and discuss limitations as a therapeutic strategy.

A
  • BDNF (brain-derived neurotrophic factor)
  • Produces protein in brain that regulates appetite, facilitates neuronal differentiation during development, and synaptic plasticity when mature
  • Mutations result in obesity insatiable appetite, and less energy expenditure
  • May be therapeutic strategy but ⟶ low bioavailability, short half-life, poor penetrability through blood-brain barrier
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15
Q

Discuss the window for interventions for obesity.

A
  • Major contributors to obesity development occur early in life
  • Significant changes in disease risk is achieved with early life interventions
  • The more delayed the interventions, the less change is produced for diseases later in life
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16
Q

What are 4 pathways of early-life determinants of obesity?

A
  1. Maternal undernutrition or unbalanced nutrition
    • Mismatch between genes and environment for fetus/baby
  2. Low birth weight
    • Mismatch between genes and environment for fetus/baby
  3. Maternal obesity, excessive gestational weight gain, and GDM
    • Hyperinsulinemia in the fetus/baby
    • Increased fat cell number in fetus/baby
  4. Postnatal nutrition (formula vs. breastfeeding, infant overfeeding)
    • Altered control of satiery/appetite
    • Increased fat cell number in fetus/baby
    • Acquisition of unhealthy food preferences in baby
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17
Q

What did studies show about fitness levels and weight on mortality?

A
  • Normal weight + fit had similar mortality risk as those who are overweight/obese + fit
  • Unfit individuals had much higher risk of mortality (9% normal weight, 20% overweight, 50% obese)
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18
Q

List the theories of over-nutrition.

A
  1. Genetic Theory
  2. Lipostatic Theory
  3. Thermogenetic Theory
  4. Diabetes-Associated Theory
  5. Psychological Causation Theory
  6. Volumetrics
  7. Sleep Deprivation
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19
Q

What is the principle behind the genetic theory on weight?

A
  • Many genes are involved in the regulation of food intake and weight
  • Polymorphisms (genetic mutations) predispose individuals to being overweight/obese
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20
Q

What is the principle behind the lipostatic theory on weight?

A
  • Obese individuals have a higher hypothalamic set-point; difficult to maintain weight loss
    • Hypothalamus regulates body weight at a defined set-point via a combo of hormonal and neural signals
    • Inhibits/activates feeding behaviour when signals reflecting body weight are higher/lower than set-point
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21
Q

What is the principle behind the thermogenetic theory on weight?

A

Obese individuals have fewer brown cells (release heat/energy; do not store energy like adipose) and cannot burn off excess energy

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22
Q

What is the principle behind the diabetes-associated theory on weight?

A
  • Excess food leads to high blood glucose levels, hyperinsulinemia, and therefore enhanced hypertrophy (size) and hyperplasia (#) of fat cells
  • This may explain why obese individuals have higher insulin levels
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23
Q

What is the principle behind the psychological causation theory on weight?

A

Obese individuals are more vulnerable to external cues to eat (eg. meal size, presence of friends, stress, smell)

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24
Q

What is the principle behind the volumetrics theory on weight?

A
  • People tend to eat the same volume routinely and do not sense caloric density very precisely
  • Obese individuals tend to overeat larger volumes ⟶ increased calories
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25
Q

What is the principle behind the sleep deprivation theory on weight?

A

Short sleep is associated with the release of appetite hormones and higher body weight

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26
Q

What is the energy balance equation?

A

Ein - Eout = Δ body weight

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27
Q

Explain the physiology of energy balance.

A
  • Short-term or long-term regulators circulate either in the blood (circulation) or released through nervous system (sagal and spinal)
    • GI nutrients, GI hormones + peptides, neurotransmitters
  • Regulators interact with the following structures:
    • Brain
    • Organs (pancreas, adipose, GI tract)
    • Autonomic nervous system
  • External cues (smell, taste, psychological factors) also influence the brain’s regulation
28
Q

What is the most important component of the brain for energy balance? Why?

A
  • Hypothalamus
  • Arcuate nucleus: important component of hypothalamus; situated at its base
  • Releases neurotransmitters (via neurons) to control hunger/satiety, energy expenditure, and growth/reproduction
29
Q

How does the autonomic nervous system regulate energy balance?

A
  • SNS ⟶ decreases food intake

- PNS ⟶ increases food intake (vagal nerve)

30
Q

What are the long-term energy signals? List them.

A
  • More precise and stable
  • Keep brain informed of the overall energy balance and adipose levels in the body
  • Insulin and leptin
31
Q

What are the short-term energy signals? List them.

A
  • Act quicker and are related to meals (initation/termination)
  • CCK, PYY, ghrelin
32
Q

Where is ghrelin secreted and what are its effects?

A
  • X/A-like cells in gastric fundus
  • Orexigenic hormone (stimulates appetite)
    • Increase food intake
    • Decrease energy expenditure
33
Q

Where is insulin secreted and what are its effects?

A
  • Pancreatic β-cells

- Decrease food intake

34
Q

Where is leptin secreted and what are its effects?

A
  • Adipose

- Decrease food intake

35
Q

Where is CCK secreted and what are its effects?

A
  • I-cells of SI (and stomach)

- Decrease food intake

36
Q

Where is PYY secreted and what are its effects?

A
  • L-cells of distal ileum, colon, and rectum (and stomach)
  • Anorexigenic hormone (decreases appetite)
    • Decrease food intake
37
Q

Where is glucagon secreted and what are its effects?

A
  • Pancreatic α-cells
  • Decrease food intake
  • Increase energy expenditure
38
Q

Where is GLP-1 secreted and what are its effects?

A
  • L-cells of SI

- Decrease food intake

39
Q

What are the 2 neurons in the brain? What are their effects?

A
  1. Neuropeptide Y (NPY) and agouti-related peptide (AgRP) neurons
    - Release NPY + AgRP neurotransmitters
    - Increase food intake
    - Inhibits MSH receptors
  2. Proopiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) neurons
    - Release MSH (α melanocyte-stimulating hormone)
    - Decreases food intake + increases energy expenditure
40
Q

How does the brain respond to the regulators?

A
  • Leptin/insulin (increase in proportion to adipose) inhibits NPY/AgRP + activates POMC/CART neurons
    • Decrease in food intake
    • Many obese individuals have resistance to leptin/insulin!
  • Ghrelin increases NPY/AgRP
  • PYY inhibits NPY/AgRP
    • Does not directly activate POMC/CART
41
Q

What did studies show about breast-feeding on appetite hormones?

A

Infants who are exclusively breast-fed at 3 months had less adipose mass (lower leptin and insulin) and less appetite (lower ghrelin, higher PYY) than infants who are exclusively formula-fed

42
Q

What did studies show about whole milk on appetite hormones?

A
  • Whole milk has beneficial effects due to an interaction between its protein, lactose, and fat
  1. Appetite:
    - Decrease ghrelin
    - Increase PYY/CCK
  2. Blood glucose levels:
    - Delay gastric emptying (slow glucose absorption into blood)
    Increase insulin
43
Q

What did studies show about weight loss over the long-term on appetite hormones?

A

Weight loss will stimulate hormones to counteract over the long-term
• Increase ghrelin
• Decrease PYY/CCK/amylin

44
Q

What did studies show about bariatric surgery on appetite hormones?

A
  • Bariatric surgery (roux-en-Y gastric bypass) is more successful for weight loss in the long-term than the diet approach (overcomes hormonal counter-regulation)
    • Ghrelin levels didn’t increase much with bariatric surgery
    • PYY did not decrease much
45
Q

List of predictors of weight loss (no details).

A
  1. Patient
  2. Process
  3. Treatment
  4. Behaviour Changes
46
Q

What are the patient predictors of weight loss?

A

POSITIVE:

  • Higher body weight/BMI
  • Male (females have sex hormones that may interfere)
  • Higher RMR
  • Adipocyte hyperplasia (more fat cells to lose)
  • Self-efficacy (how well you can control your behaviour)
47
Q

What are the process predictors of weight loss?

A

POSITIVE:

  • Early weight loss
  • Attendance of counselling sessions

NEGATIVE:

  • Repeated previous dieting attempts (yo-yo diets; higher set-point)
  • Experience of perceived stress (stress fat cells and make them more likely to return to original size)
48
Q

What are the treatment predictors of weight loss?

A

POSITIVE:

  • Increased length of support
  • Social support
49
Q

What are the behaviour change predictors of weight loss?

A

POSITIVE:

  • Self monitoring
  • Goal-setting
  • Slowing rate of eating
  • Physical activity
50
Q

What are the mechanisms of weight regain?

A

1) Weight loss-induced changes in energy expenditure (EE)
• EE is reduced after weight loss and returns to pre-weight loss level at about 24 months

2) Neuroendocrine pathways
• After weight loss, increased ghrelin and decreased satiety hormones for as much as 1 year later

3) Nutrient metabolism
• Weight regain differs to some extent by diet given
• High protein and low GI diet ⟶ takes longer to regain weight
• Low protein and high GI diet ⟶ very easy to regain weight

4) Gut physiology
• Delayed gastric emptying is often seen after weight loss
• Delay the release of satiety gut hormones ⟶ you eat more

5) Subjective appetite
• Preference and reward aspects for high kcal food both increase
• Has biochemical, mechanical, neurological, and psychological basis

51
Q

What are the 3 approaches to RD counselling for adult obesity?

A
  1. Dieting/Calorie Focus
    - Traditional approach
    - Focuses on counting calories, food records, and lowering calories (Very Low Calorie Diets)
    - Not the best approach (ignores disordered eating)
  2. Foods, Exercise, and Behaviour Modification
    - Better mix of strategies
    - Less focus on diet (still uses counting systems such as points/exchanges), but more lifestyle changes
    - Still have weight regain with this approach as well
  3. Health at Every Size
    - Overall healthy lifestyle approach; NO focus on weight
    - Improved self-esteem but minimal weight loss
    - Still diet-focused; mindful eating
52
Q

How do you assess for management of adult obesity?

A
  • “Diets” for weight loss only appropriate for some patients
  • Use ABCDE
  • Assess 4 Ms (contribute to experience of weight loss):
    • Mechanical (eg. sleep apnea)
    • Monetary/milieu (eg. family stressors, food environment)
    • Mental (eg. anxiety)
    • Metabolic (eg. T2DM, dyslipidemia)
  • Assess knowledge:
    • Obesity causes, diet role, options, goals (make sure realistic), importance of PA
53
Q

How do you determine a patient’s caloric needs?

A
  • Collect information on patient’s:
    • Current intake from food records or recall
    • Weight history
    • Knowledge of portion sizes / food
    • Dieting experience
  • Often use both DRI and individual data for first estimate!
54
Q

How large of a deficit do you need to manage obesity for a patient? If someone wants to lose 3 kg, how long will it take?

A
  • To lose 1 kg, need 5000-7000 kcal deficit
  • More deficit ⟶ faster weight loss BUT more hunger + greater decline in EE
    • 500-1000 kcal/d is in practice guidelines, but difficult to manage
    • 100-200 kcal/d is more manageable
  • If the person wants to lose 3 kg, it will take on average 3.5 months
    • 7000 kcal x 3 kg = ~21000 kcal / 200kcal/d deficit = 3.5
55
Q

What are some strategies to reduce calories in food?

A
  • High-intensity non-nutritive (0 calories) sweeteners
    • Common practice to give sweet taste
  • Sugar substitutes and bulking agents (eg. inulin, polyols, polydextrose)
    • Blended generally with high-intensity sweeteners as they provide little or no sweetness
    • Reduced calories; but not 0 calories
    • Replace the bulk, physical weight and volume lost when sugar is removed
    • Provide sensory properties such as texture, viscosity and mouthfeel
  • Increase fiber
  • Reduce energy from fats
    • Use less fats
    • Use fat replacers
    ‣ Olestra is heat-stable + has similar structure and taste of fat, but not absorbed (0 calories)
    ‣ BUT side effects (eg. diarrhea, malabsorption of fat-soluble vitamins)
56
Q

List the drugs to manage obesity.

A
  1. Pancreatic Lipase Inhibitors (Orlistat or Xenical)
  2. Metformin
  3. Saxenda (Liraglutide)
  4. Nasal PYY?
57
Q

How do pancreatic lipase inhibitors work to manage obesity? What are side effects?

A
  • Inhibit release of lipase from pancreas to absorb fat
  • Must be taken 3x/d around meals
  • Diet must have no more than 30% fat
    • Peak fecal fat excretion at 30% fat; more = start absorbing fat
  • Side effects ⟶ diarrhea, fatty stools
58
Q

How do metformin work to manage obesity? What are side effects?

A
  • Decrease hepatic glucose synthesis, increase uptake of glucose in target cells, decrease glucose absorption in the gut
    • May help with weight loss in individuals with diabetes or PCOS
  • Side effects ⟶ GI (eg. nausea)
    • Hypoglycemia not an issue
59
Q

How do saxenda work to manage obesity? What are side effects?

A
  • GLP-1 receptor agonist
    • Activates GLP-1 receptors in place of GLP-1 (satiety hormone)
  • One-daily, self-injectable
  • Side effects ⟶ nausea, diarrhea, increased risk of thyroid tumours
60
Q

Discuss nasal PYY to manage obesity.

A
  • Study tested using PYY through the nose to increase satiety
  • But NOT efficient
61
Q

What are the types of bariatric surgery? Be sure to mention gastric plication.

A
  1. Adjustable Gastric Band (AGB)
    - Band around stomach (restriction)
  2. Sleeve Gastrectomy (SB)
    - Remove portion of stomach (restriction)
    - Irreversible
    • Gastric plication: folding stomach inwards and stapling (reversible)
  3. Roux-en-Y Gastric Bypass (RYGB)
    - Most common (both)
    - Create small pouch from stomach, and bypass part of the GI tract
  4. Biliopancreatic Diversion with Duodenal Switch (BPD/DS)
    - Remove portion of stomach; link it and pancreas to end of the GI tract (both)
    • Path from stomach to gut has no pancreatic enzymes to digest food
    • Only small common channel with pancreas and gut together
    - Irreversible
62
Q

What are the effects of bariatric surgery? Which has the most effects?

A
  • Weight loss
  • Metabolic effects
  • Improved morbidity and mortality
    • Resolve hypertension, diabetes, dyslipidemia
  • Nutrient deficiencies

• BPD/DS is the surgery with most effects

63
Q

Discuss pre-surgical care before bariatric surgery.

A
  • Treat deficiencies prior to surgery
    Discuss expectations, complications, and lifestyle changes afterwards
  • Optifast: high protein nutritionally balanced shake to encourage weight loss before surgery/stage 1 to reduce risk of complications
64
Q

Discuss post-operation care for bariatric surgery.

A
  1. Diet progression
    - Clear liquids ⟶ full fluids ⟶ pureed ⟶ soft ⟶ solids
    - Usually takes 4-8 weeks to move from stage 1 to 5 but varies
    - Some patients go back and forth from stages
    - Assess fluid, macro/micronutrient needs
    - Vitamin supplements may be needed for life
    - Protein supplements may be needed early on
  2. Long-term complications
    - Surgical
    - Dumping syndrome and reactive hypoglycemia
    • Small amounts eaten at any one time
    • Separate fluids and solid foods
    • Limitation on sugars (sugar attracts water to GI tract)
    • Higher protein and fibre (slow down movement to GI)
    • Limit alcohol (and caffeine)
    - Gallstones
    • Less bile acid production to dissolve cholesterol (forms stones)
    • Treat:
    • Ursidiol (bile acid that prevents cholesterol formation in liver and absorption by small intestine)
    • Cholecystectomy (remove gallbladder)
    - Nutrient deficiencies (high risk)
65
Q

Why does dumping syndrome occur after bariatric surgery? What are the symptoms?

A
  • Because of bypass, food arrives to GI tract in large amounts
  • Carbs are absorbed and insulin increases rapidly
  • Symptoms ⟶ GI (diarrhea), vasomotor (dizziness, palpitations, flushing) after high CHO meals
66
Q

What are the common nutrient deficiencies for each type of bariatric surgery?

A
  • AGB ⟶ iron, B12, calcium, vit D
  • SG ⟶ iron, B12, calcium, vit D, copper
  • RYGB ⟶ iron, B12, calcium, vit D, copper, B1, selenium, zinc
  • BPD/DS ⟶ iron, B12, calcium, vit ADEK, copper, B1, selenium, zinc

NUTR*3090 (4 decks)

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