Weight management exam 1

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56 Terms

1
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What is the Office of Genetics and Disease Prevention’s definition of obesity?

Excess body fat that increases health risk; BMI ≥ 30.

2
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What is Bray & Champagne’s definition of obesity?

A chronic, relapsing disease from energy imbalance involving genetics, behavior, and environment.

3
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How does human evolution favoring energy conservation affect energy expenditure?

Lowers voluntary energy use; bodies resist burning extra calories.

4
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What is food procurement and why form memories/rewards around it?

Finding/obtaining food; memories and rewards motivate eating and ensure survival.

5
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What are today’s survival foods?

High-calorie, energy-dense foods (fast food, snacks, sugary drinks).

6
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What is energy set point and how does age affect it?

Body’s natural fat level; aging raises set point and slows metabolism.

7
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What’s the issue with “energy in vs. energy out”?

Ignores biology, hormones, and environment that affect weight.

8
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What is the Edmonton Obesity Staging System (EOSS)?

Ranks obesity Stage 0–4 by physical, mental, and functional health and not just BMI.

9
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Why should clinicians use the EOSS?

Gives a fuller picture of health risk and guides treatment beyond weight.

10
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What’s the “bottom line” on assessing obesity in adults?

Use BMI + waist size + health status to assess risk.

11
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Is there a direct link between obesity and mortality?

No direct link; risk depends on fitness, fat distribution, and health conditions.

12
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What are the 6 domains?

Economic stability, neighborhood & environment, education, food, community/social context, health care system.

13
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Examples of each domain? Economic Stability:

Having a steady job or enough money to pay bills

14
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Examples of each domain? Education:

Completing high school or attending college

15
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Examples of each domain? Food:

Access to grocery stores instead of only fast food.

16
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Examples of each domain? Community/Social

Volunteering or family time.

17
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Examples of each domain? Cultural/Security:

Family traditions, safe neighborhoods, mental health access

18
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Examples of each domain? Health Care:

Access to doctors or insurance.

19
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What are Adverse Childhood Experiences (ACEs)?

Traumatic events before 18 that harm health and development.

20
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Examples of ACEs?

Abuse, neglect, divorce, household violence, or substance abuse.

21
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How do ACEs influence obesity risk?

Increase stress hormones, promote emotional eating, and disrupt metabolism.

22
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Is there such a thing as food addiction?

Yes, some show addiction-like responses to highly processed foods (though not officially a disorder).

23
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Similarities to substance addiction?

Activates dopamine reward pathways, causes cravings, loss of control, withdrawal, and compulsive use.

24
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Differences from substance addiction?

Food is necessary, involves specific foods, has less severe consequences, and dependence is behavioral, not chemical.

25
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What’s the real cost of ultra-processed foods (UPFs) from subsidized sources?

They’re cheap to buy but costly to health, contributing to obesity and chronic disease.

26
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What are other harmful attributes of UPFs?

Low nutrients, high sugar/fat/salt, disrupt gut health, and encourage overeating.

27
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How does the interaction between SES and stress contribute to obesity?

Low SES increases chronic stress, which raises cortisol, disrupts metabolism, and leads to unhealthy eating as coping. Limited resources also reduce access to healthy food and exercise options, worsening obesity risk.

28
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What can cause dysregulation of metabolic brain function?

Chronic stress, inflammation, and poor diet disrupting hunger and satiety signals.

29
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How do leptin changes affect energy metabolism?

Low leptin increases hunger and lowers metabolism; high leptin with resistance fails to stop eating.

30
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What is adiponectin and what happens as obesity increases?

A hormone that improves insulin sensitivity and fat metabolism; levels decrease with obesity.

31
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What is resistin and what does it do?

A hormone that induces insulin resistance and inflammation.

32
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What is the risk of central obesity regardless of BMI?

Higher risk of cardiovascular disease and metabolic disorders.

33
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What might be a proximal cause of leptin resistance?

Chronic inflammation and high fat intake affecting brain leptin receptors.

34
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How does ghrelin interact with the hedonic brain?

Increases reward-driven eating and food cravings

35
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What is the gut-brain axis?

Communication system between gut microbes and the brain that regulates appetite and metabolism.

36
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How does dysbiosis impact weight regulation?

Gut bacteria imbalance leads to inflammation, poor nutrient metabolism, and weight gain.

37
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What is the impact of UPFs on gut and weight regulation?

Damage gut microbiota, increase inflammation, and disrupt hunger/satiety signals.

38
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What’s the bottom line on appetite mediators after weight loss?

Hormones promoting hunger stay elevated long-term, so they don’t fully return to pre-weight gain levels, encouraging weight regain.

39
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What can cause dysregulation of metabolic brain function?

Chronic stress, inflammation, poor diet, and disrupted hunger/satiety signaling in the hypothalamus.

40
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How do changes in leptin levels affect energy metabolism?

Low leptin increases hunger and lowers metabolism; high leptin with resistance fails to suppress appetite.

41
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What is adiponectin and what happens as obesity increases?

A hormone that improves insulin sensitivity and fat metabolism; its levels decrease as obesity increases.

42
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What is resistin and what does it do?

A hormone that induces insulin resistance and promotes inflammation.

43
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What is the risk associated with central obesity regardless of BMI?

Increased risk of cardiovascular disease, diabetes, and metabolic syndrome.

44
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What is epigenetics?

Changes in gene expression caused by environment or behavior, not DNA sequence.

45
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What is plasticity?

The body’s ability to adapt or change in response to environmental influences.

46
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What is the physiologic response to stress in kids?

Activation of the HPA axis → cortisol release → changes in metabolism and appetite.

47
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What is the impact of stress on epigenetics in children?

Alters gene expression related to stress and metabolism, increasing obesity risk

48
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What is the impact of Adverse Childhood Experiences (ACEs)?

Increases chronic stress, hormonal imbalance, emotional eating, and long-term obesity risk.

49
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How does a mother’s gut microbiome impact the fetal gut microbiome?

The baby’s gut bacteria are influenced by the mother’s microbiome during pregnancy and birth.

50
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How are epigenetic changes passed from mom to children?

Through the placenta, breast milk, and inherited epigenetic markers in eggs.

51
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Based on Miller & Lumen’s chart, how does early life stress affect child self-regulation and health behaviors?

Impairs self-control, increases emotional eating, and promotes unhealthy lifestyle habits.

52
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Are epigenetic effects reversible? If yes, how?

Yes—through healthy diet, exercise, stress reduction, and supportive environments.

53
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How does breastfeeding impact energy regulation and obesity risk?

Promotes healthy gut bacteria, supports appetite control, and lowers obesity risk later in life.

54
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What is the relationship between musculoskeletal disorders and obesity?

Excess weight increases strain on joints, causing low back pain, osteoarthritis, and soft tissue damage.

55
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What are orthopedic complications of obesity in young children?

Flat feet, bowed legs, hip deformities, and early joint pain.

56
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Who ultimately pays for the monetary costs of obesity?

Society as a whole—through higher insurance premiums, healthcare taxes, and lost productivity.