Obesity Flashcards

1
Q

how is obesity like other metabolic conditions

A
  1. non-communicable disease (not contagious, due to lifestyle factors)
  2. assoc with increased susceptability to other metabolic conditions, cancer, dementia, and influenza and negative physical and mental health effects
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2
Q

definition of obesity and diagnosis

A
  1. excessive or abnormal adposity; is complex, progressive, and relapsing
  2. diagnosed through anthropometric measurement such as waist circumference, BMI, % body fat (goldS), and body fat location (goldS)
  3. in 2020 Canadian guidelines added that lack of anthropometric risk factors cannot be considered heathy since there is still increased risk of morbidity
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3
Q

epidemiology of obesity

A
  1. world obesity is rising sig in numbers and percentage since 1975
  2. higher risk for women due to biology
  3. more than 50% of Canadian and US population is obese and increase with age
  4. obesity is highly prevalent in children as well showing obesity is long term issue
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4
Q

difference in obesity and BMI
1. differences in ethnicity
2. differences in other demographics

A
  1. BMI measures obesity prevalence which is correlated with diabetes prevalence but not concurrent (occuring at same time) for some ethnicities (can have high obesity w/o diabetes risk); increased risk of diabetes occurs at different BMIs for different ethnicities, therefore different suggest cutoff for each ethnicity, why EDI important
  2. people with different body composition such as bodybuilders are not well rep by BMI; using waist to hip ratio or waist circumference is better measure since can differentiate risk between sexes since they carry adiposity differently in terms of amount and distribution but still need to consider ethnicity
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5
Q

risk factors for obesity
1. overview
2. socieconomic status
3. socioecological factors
4. genome studies

A
  1. complex, obesity risk beyond E intake v. expenditure
  2. socioeconomic status or occupational demands can put certain people at higher risk due to money and time req for healthy diet and exercise
  3. socioecological factors such as chem leeching and hormonal leeching can also increase obesity risk
  4. large scale genome wide assoc studies have id FTO locus responsible for leptin and leptin receptor (signals satiety by inhibiting ghrelin, hunger hormone) to have small effect on obesity susceptibility across many ethnicities comp to lifestyles and socioE factors
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6
Q

obesity as chronic health conditon
1. relation between BMI and mortality
2. comorbidity and classifications

A
  1. increased risk of mortality with both BMI extremes; increased risk with high visceral adiposity and neg lifestyle choices; decreased risks with low lvl of ectopic and visceral adiposity and healthy lifestyle choices
  2. obesity is a modifiable risk factor linked with many chronic diseases; combine BMI and waist circumference to add predictive values to each BMI class for better prediction for easy and cheap assessment but limited comp imaging techniques
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7
Q

type of fat and pathophysiology

A
  1. subQ (close to skin, less innervation and BF), ectopic (within muscle and liver, non-adaptive), and visceral fat (near omentum and organs with more innervation and BF, drains into portal veins, 2 kg increase signaling for hepatic insulin res, increasing T2D risk)
  2. subQ releases adipokines for anti-inflammatory effect against chronic diseases, does not promote obesity
  3. ectopic and visceral has increased adipocyte necrosis, pro-inflammation allows for growth factors to stay in local area and increase dmg by spreading fat cells, assoc with obesity
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8
Q

location of adiposity

A
  1. android obesity more common in males assoc with fat around abdomen for greater risk of chronic conditions
  2. gynoid obesity more common with females in lower extremity has lesser degree of downstream metabolic dysfunction due to less fat around essential organs
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9
Q

obesity paradox
1. overview
2. survival
3. fitness

A
  1. obesity not always assoc with morbidity; 20% obese adults have healthy biochem; 40% of normal weight adults have metabolic perturbations similar to those with chronic conditions
  2. for whole pop, J curve of obesity, obesity increases risk of disease and death but for those with CVD, obesity is protective possibly due to ability to provide more fuel but can also have higher BMI with greater % muscle
  3. being fit counteracts the increased risk assoc with overweight; fit obese people have much lower chance of dying than non-obese, non active people
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10
Q

severity of health impacts of obesity

A

obesity cannot be healthy due to comorbidities
1. stage 0 is normal weight with no apparent obesity related risk factors
2. stage 1 is presence of obesity releated subclinical risk factors where obesity can be fixed through lifestyle intervention but neg psychological relationship with food and eating habits begin (comorbidity) req psych interventions
3. stage 2-4 have obesity related conditions req pharmalogical intervention

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11
Q

obesity management
1. obesity management recommendations
2. negative E balance

A
  1. WHO recommends 5-10% reduction in BW as treatment but BW not always a good measure since SM and AT weigh differently
  2. achieved thorough pharamacological medication or surgery such as gastric bypass which ties off part of stomach or small intestine to reduce consumption but to be eligible for surgery must meet strict criteria about BMI and be motivated to change lifestyle with a multidisciplinary team
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12
Q

exercise and obesity management
1. exercise as form of obesity management
2. considerations of exercise prescription

A
  1. few to no symptoms but can have high mech stress due to more weight and thermal stress since fat is insulator; have decreased aerobic exercise capacity due to metabolic limitation due to greater O2 radicles from excessive fat; but should not prevent starting exercise but should start slow and build up
  2. goals, capabailty, socioecomic standard, tolerance for exercise, orthopedic concerns, exercise exp, current PA, medications or conditions
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13
Q

exercise on obesity
1. aerobic
2. resistance and high intensity
3. regular PA

A
  1. fat loss, reduction in abdominal VAT and ectopic fat even without weight loss, weight maintenance after weight loss, maintenence of (most) SM during weight loss, increase to cardioresp fitness and mobility
  2. res training offer weight maintenance and increase SM; higher intensity increase cardioresp fitness with less time
  3. improve cardiometabolic risk factors, increase QoL, improve mood disorders, and body image; PA good for phys and mental health
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14
Q

exercise v. diet on obesity
1. exercise training vs. hypocaloric diet
2. weight vs. VAT loss
3. CSEP guidelines for exercise programming
4. ACSM CDD4 recommendations for exercise programming

A
  1. both diet and exercise decreased VAT; hypocaloric diet has greater effect on weight loss (exercise lose fat but gain SM) while exercise has greater effect on VAT; exercise training without weight loss is 6% reduction in VAT but diet w/o weight loss is no change
  2. total body weight loss does not always reflect change in VAT thus is poor marker of benefits of lifestyle intervention, supervision recommended if disability or high comorbidity
  3. 150+ mins mod/vigorous PA, 2+ days RT, goal of 250+ mins per week
  4. 150-300 mod PA, goal of 250+ min/week, supervision of exercised specialist advised
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15
Q

challenges of weight loss
1. neg E balance
2. exercise
4. set point theory

A
  1. hypocaloric diet triggers compensatory mech such as low metabolic rate and increased appetite
  2. body shape mindset focus on tangible results such as body shape or weight can make it hard to stick with exercise since it is seen as a chore; non-body shape focus postitive outlook on exercise for well-being makes it easier to continue with exercise
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16
Q

overview of influences on E balance

A

weight loss and weight gain is extremely complex, many influences of E intake and expenditure
1. E intake influenced macronutrient comp of food (nutrition), internal cues and psychological aspects of food, physiological episodic short term appetite signals and tonic long term appetite signals
2. E expenditure influenced by nutritional influences, behaviours such as physical activity and exercise, and physiological use of E differ between organs, depends on body comp, demographic factors, etc

17
Q

set point theory

A

body tries to maintain weight within a homeostatic set range; false as fat mass is highly plastic and doesn’t explain many cases such as freshman 15, differences between eastern and western pop, socioeco status, etc

18
Q

leptin function on E balance
1. overview
2. weight gain
3. weight loss
2. exercise on leptin

A
  1. an adipokine acting on Lepr to activate catabolism to facilitate growth, EE, glycemic control, and repro and inhibit food intake and corticosteroids (stress response, increases food intake)
  2. leptin not regulated, increase leptin and increase leptin res (increases food intake)
  3. leptin decrease and stim feeding and anabolism (making it harder to maintain weight loss since it stims hunger)
  4. positive regulation of Lepr, chronic training decreases leptin res in hypothalamus and decreases leptin returning homeostatic set point to normal, allowing increase in satiety for longer periods and increase leptin sensitivity so that only small amounts needed to gen hunger
19
Q

effects of exercise VAT and muscle mass in obesity

A

adipokines near organs released by VAT increase inflammation and risk of adipocyte necrosis which increases adipokines and increases dmg around organs; exercise release IL-6 and other myokines from skeletal muscle act on VAT to increase mitochondria efficiency in VAT, increase muscle mass increase mitochondria and metabolism

20
Q

exercise and obesity on microbiome

A
  1. obesity increases wrong types of bacteria in microbiome; microbiome has high impact on whole body metabolism, psychology, and organ function
  2. exercise increase beneficial bacteria such as SCFA (butyrates), products of microbial fermentation reducing inflammation and influencing colonic absorption, increasing lean BMI and metabolic health