Obesity and Eating Disorders Flashcards

1
Q

What is obesity?

A

It is abnormal or excessive fat accumulation, presenting a risk to health. BMI: 25+ = OW. BMI: 30+ = Obese.

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2
Q

How does exercise reduce obesity?

A

It increases cellular AMPK increasing GLUT 4 activation, glucose uptake and mitochondrial activity with enhanced ATP production.

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3
Q

How does sleep increase weight gain?

A

Reduced glucose tolerance and insulin sensitivity, disrupting the balance of ghrelin and leptin.

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4
Q

How does Chronobiology drive obesity?

A

Shift work, sleep deprivation and exposure to light at night increase weight gain prevalence.
Dysregulation of triglycerides and cholesterol, abdominal obesity and T2DM.

Late night eating causes higher peak post-prandial glucose levels, reduced lipolysis, circadian rhythm misalignment.

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5
Q

How does processed food drive obesity?

A

Strong dopamine stimulators (fat, salt, starch alcohol, caffeine) activate rewarding brain circuits to trigger anticipatory cravings for more.

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6
Q

How does long-term high cortisol exposure play a role in obesity?

A

Cortisol levels are elevated in obese people and associated with fat deposition.
Factors influencing HPA-Axis include high GI consumption, chronic stress, chronic pain, alcohol, sleep dep.

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7
Q

How does the microbiome drive obesity?

A

Gut flora produces carbohydrate-active enzymes to digest complex polysaccharides = produces SCFA = fuel for intestinal cells. Low plant fibre foods shift gut flora to a mucous-utilising bacteria with a lack of Akkermansia linked to obesity.

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8
Q

How do genetics play a role in obesity?

A

SNPs in fat mass and obesity-associated gene is a strong predictor of obesity.
VDR SNPs play a role in obesity associated with ongoing inflammation.

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9
Q

What is adipose tissue?

A

Metabolically active organ which regulates whole-body energy homeostasis.

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10
Q

What is ‘white adipose tissue’

A

Long term energy storage - subcutaneous adipose tissue sits under the skin. (SAT) Visceral adipose tissue (VAT) is intra-abdominal (angry).

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11
Q

What is ‘brown adipose tissue’

A

BAT abundant in early life

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12
Q

What happens when you have energy surplus?

A

WAT grows.
Chronic energy imbalances with increased storage result in increased adipocyte no.s (hyperplasia) and size (hypertrophy) which is associated with T2DM, NAFLD.

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13
Q

What is satiety?

A

The physiological state at the end of a meal when further eating is inhibited by fullness.

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14
Q

What are the mechanical factors involved in satiety?

A
  1. Stretch of the stomach via the vagus nerve
  2. Adipocyte hormones: Gherlin, Leptin,
  3. Hormone and peptides: GLP-1 and CCK
  4. Neuropeptides and neurotransmitters
  5. Other hormones e.g. thyroid/cortisol/insulin.
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15
Q

What is the name of the satiety hormone produced by adipocytes?

A

Leptin

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16
Q

What is leptin resistance?

A

Reduced sensitivity / failure in response of the brain to leptin.

17
Q

What is gherlin?

A

Appetite stimulating signal.

18
Q

What does Adiponectin do?

A

increases glucose uptake and oxidation of fats.

19
Q

What causes insulin resistance?

A
  1. High oxidative stress
  2. Reduced physical activity
  3. Chronic stress
  4. Mitochondria dysfunction
  5. Poor methylation
  6. Dysbiosis
20
Q

What is the naturopathic approach to IR?

A
  1. Stabilize blood sugars
  2. Reduce inflammation
  3. Optimise insulin sensitivity
21
Q

How can you reduce obesity?

A

Smaller portions
Protein at every meal
Simple meals
Fasting
Chewing & Mindful eating
Address micronutrient deficiency
Exercise

22
Q

What happens when you restrict calories?

A

Reduced leptin during weight loss tells the brain to increase eating and reduce energy expenditure
Increase in fat storage
Changes in circulating gut hormones involved in homeostatic regulation of body weight.

23
Q

Which nutrients can reduce obesity?

A
  1. 5-HTP (50-100 mg)
    Increases feeling of satiety
    Promotes sleep by enhancing melatonin
    Free radical scavenging activities
  2. Green Tea (600-900 mg)
    Polyphenols (EGCG) stimulate thermogenesis and fat oxidation
  3. L’Carnitine (2000 mg)
    Oxidises fatty acids in mitochondria
    Essential for utilization of fats for energy
    Improves leptin resistance
  4. Chromium (200-1000 mg)
    Lowers body weight yet increases lean body mass via increased insulin sensitivity
    Can reduce carb cravings.
24
Q

Name three types of clinical eating disorders

A
  1. Anorexia Nervosa
  2. Bulimia Nervosa
  3. Feeding/Eating Disorders (Orthorexia/Compulsive eating/binge eating
25
Q

Describe Anorexia Nervosa

A

When body is deprived of nutrients it changes the brain chemistry = depression and anxiety due to tryptophan depletion.
Starvation, vomiting, purges and laxatives
Self induced vomiting/dehydration

26
Q

What are pyrroles?

A

A byproduct of haemoglobin synthesis with no known function in the body and should be excreted in the urine.
They block receptor sites for B6 and Zinc
Symptoms: nervousness, anxiety, depression, memory problems and anger.

27
Q

What is the serotonin - oestrogen link?

A

Aromatase is expressed in adipose tissue
Adipose tissue is a key site for production and metabolism of oestrogen
Oestrogen deficiency reduces serotonin
Low serotonin = low mood, anxiety, depression, sleep problems
Carb consumption, acting via insulin secretion increases serotonin release.
This is why a lot of anorexics are on antidepressants

28
Q

Which supplement should be included in any therapeutic protocol for anorexia?

A

Zinc

29
Q

What precipitates a binge?

A

Food deprivation patterns
Stress and stress responses
Adaptions within t