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NUTR 344 > Obesity > Flashcards

Obesity Flashcards

1
Q

What is adaptive thermogenesis?

A

energy expenditure above and beyond the thermic effect of food and resting energy expenditure that is seen in response to overfeeding, traumatic injury, changes in hormonal status, and expo- sure to a cold environment

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2
Q

anorexigenic definition

A

appetite inhibiting

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3
Q

iatrogenic definition

A

resulting from treatment

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4
Q

Define NEAT

A

non-exercise activity thermogenesis- the energy expended through physical activity involved in performing the ordinary activities of daily life; it excludes energy expended in activities to obtain physical exercise or involving sports-like activity

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5
Q

orexigenic definition

A

appetite stimulating

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6
Q

what is the primary determinant of REE?

A

lean body mass

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7
Q

What is EER

A

estimated energy requirement (EER)—the average dietary energy intake that is predicted to maintain energy balance in a healthy adult of a defined age, gender, weight, height, and level of physical activity, consistent with good health;

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8
Q

To which demographic do EER values apply?

A

only to persons having a healthy weight

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9
Q

What is the stimuli provoked by increased energy intake - anorexigenic or orexigenic?

A

anorexigenic

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10
Q

How do proteins, monosac- charides, and fatty acids in the chyme affect hunger signals?

A

Proteins, monosac- charides, and fatty acids in the chyme (semi-liquid mass of partially digested food) leaving the stomach stimulate neural and endocrine receptors in the mucosa of the small intestine, resulting in neural signals to the brain that decrease appetite and food intake, and the release of the hormones cholecys- tokinin, glucagon-like peptide-1, and peptide YY, which also decrease appetite and food intake

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11
Q

What and when releases gherlin and what is it’s effect?

A

Ghrelin is a peptide hormone that is mainly produced by the stomach and stimulates appetite. Ghrelin levels are normally elevated during fasting, but immediately decline following food intake.

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12
Q

what is the predominant type of adipose tissue?

A

white

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13
Q

2 categories of body fat distribution in terms of health implication

A

(1) abdominal or central body fat dis- tribution and (2) lower body fat distribution

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14
Q

gynoid vs android

A

android-male type of fat distribution- accumulation of fat around abdominal area- apple shaped
gynoid- female type of fat accumulation at located primarily in the lower region of the body, particularly within the hips and thighs- pear shaped

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15
Q

Is normal BMI always a sign of health

A

no, if waste circumference is above the norm-> health risk

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16
Q

Where is waist circumference measure done?

A

taken at the point yielding the maximum circumference around the hips or buttocks

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17
Q

High-Risk Waist Circumference in Adult Males and Females cut-offs

A

Males >40 in (>102 cm)

Females >35 in (>88 cm)

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18
Q

What are factors affected by genetics that have an effect on body weight?

A

appetite, taste preferences, energy intake, resting energy expenditure, the thermic effect of food, non-exercise activity thermogenesis (NEAT),

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19
Q

Definition of overweight

A

excess body weight (fat, muscle, bone, water)

BMI: 25-29

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20
Q

Definition of obesity for men and women

A

excess adiposity: body fat > 25% in men body fat > 35% in women
BMI>30

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21
Q

Obesity is a __disease characterized by __ fat that can __

A

Progressive chronic disease characterized by excess or abnormal body fat that can impair health

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22
Q

Healthy BMI range

A

18.5-24.9

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23
Q

Least risk group in terms of BMI and waist circumference

A

Waist:
Men < 102 cm Women <88 cm
Healthy BMI: 18.5-24.9

anything above those values is a risk for health

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24
Q

BMI and waist guidelines for non-whites

A

Asian populations
BMI: overweight ≥23, obesity ≥27 kg/m2
Waist (↑ risk): ≥90 cm in men, ≥ 80 cm in women

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25
Q

Relationship with economic development of countries and the prevalence of obesity

A

more developed countries show decrease in progression of obesity problem
in less developed countries obesity prevalence is still increasing

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26
Q

Obesity and overweight prevalence amongst men and womend

A

more obese women, but more overweight men

Men tend to have excessive weight more than women this explains trend in T2DM prevalence (more common in men)

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27
Q

What are the factors obesity is related to according to NHANES

A

obesity is related to socio-economic status: race, gender, education

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28
Q

In which demographic groups is prevalence of obesity lower

A

– Higher income groups
– More educated (college degree)
– Men (34%) vs. women (38%)
– Asians (12%, lowest) vs. African-American (48%, highest)

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29
Q

What 3 factors increase Cardiometabolic risk

A

Cardiovascular diseases
Hypertension
Diabetes

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30
Q

What are the main killers

A

CVD and cancer

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31
Q

Health consequences of obesity

A
  • Obesity increases all-cause mortality
  • hypertension
  • Diabetes
  • Cancer
  • Breathing problems: sleep apnea and asthma
  • Arthritis
  • Hepatobiliary disorders
  • Reproductive and obstetrical complications
  • Surgical risk and complications
  • Psychosocial and emotional consequences
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32
Q

How does increase in BMI related to an increase in risk hazard ratio

A

(BMI 25-30), but there isn’t a high increase in health risk
risk of hazard increases significantly from BMI>30
BMI of 35-40 is the highest risk group

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33
Q

What is the relationship between mortality and BMI

A

J-shape

exponential increase above BMI of 30

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34
Q

What is the relationship between CHD and BMI

A

exponential relations
mild increase from 21 to 25
sharp increase of the risk from 25 to 29

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35
Q

What is the relationship between diabetes and BMI

A

risk of developing diabetes and BMI is almost linear

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36
Q

How s BMI and glucose intolerance connected?

A

BMI over 30+ high visceral fat-> highest intolerance to glucose
higher glucose intolerance in those with high visceral fat

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37
Q

Which cancers are increased in obese people

A

Women: Endometrium, Ovary
Cervix, Breast (postmenopausal)
Men: Prostate, Pancreas, Oesophagus
Both genders: colon, gallbladder, kidney, liver

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38
Q

Obesity and gallstone disorders

A

Obesity ↑ risk of formation of gallstones (cholelithiasis)
– Prevalence of gallstones >3X in BMI>30 compared to healthy BMI (NHANES III)
– More related to abdominal obesity, more in women than men (related to higher levels of lipid and cholesterol)
– Risk is also increased with rapid weight loss due to increased liberation of fat in the liver

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39
Q

Obesity and liver disease

A

Abdominal obesity ↑ risk of non-alcoholic fatty liver disease (NAFLD)
– Steatosis-> steatohepatitis-> cirrhosis-> liver failure
- heaptosteatosis - accumulation of fat in the liver

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40
Q

Obesity and reproductive disorders in men

A

– Reduced testoterone, increased estrogens levels

– Gynecomastia (breast development)

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41
Q

Obesity and reproductive disorders in women

A

– Polycystic ovary syndrome (PCOS) in 5-10% of women:
àirregular cycles, acne, excess body hair, infertility
– During pregnancy: ↑ risk gestational diabetes, preeclampsia (high blood pressure), labor and deliveries complications, fetal and maternal death.

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42
Q

Etiology of obesity

A
  • Energy balance
  • Appetite and body weight regulation
  • Genes
  • Environmental factors
  • Medical conditions and medications
  • Other factors
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43
Q

Describe an Obesogenic environment

A

High fat, energy-dense foods Palatable, low cost, available foods
Large portion sizes

Sedentary behavior
↓ Work-related physical activity ↓ Activities of daily living

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44
Q

What are the normal % of components of TEE

A

15-30% Physical Activity Energy (PAE)
5-10% Thermic Effect of Feeding (TEF)
60-75% Resting Energy Expenditure (REE)

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45
Q

Proportions of component of TEE fo sedentary normal vs sedentary active

A

Sedentary normal will have a lower proportion of of REE as an obese individual spends more energy caring the weight

obese individual burns more energy overall

46
Q

active vs sedentary obese TEE

A

active would burn more energy and most of it will be due to higher PAE, but will have a lower proportion coming from REE

47
Q

Hunger vs satiety vs satiation vs appetite

A

• Hunger: physical sensation indicating need or intense desire for food
• Satiety: feeling of fullness after eating
• Satiation: state of being satisfactorily full associated with length of time between meals
• Appetite: desire to eat (greek “orexis”)
– Homeostatic control
– Hedonic control: influence of environmental factors, emotional, social

48
Q

Where and how does the central regulation of food intake occur?

A

central regulation of food intake takes place in hypothalamus, in arcuate nucleus where there are 2 main pathways of opposing functions:
has 2 pathways of opposing functions
1) NPY- with AgRP stimulates appetite
2) POMC neurones decrease appetite
the balance between the 2 dictates the regulation of appetite

49
Q

Where and how does the peripheral regulation of food intake occur?

A

peripheral system will also regulate appetite
1) vagus nerve- lines our GI tract
distention of the stomach will signal to our brain that we ate
drinking water can thus decrease appetite -. causes distention
2) peripheral hormones and peptides will also signal the brain - stimulate or inhibit appetite

50
Q

Describe leptin

A

leptin is secreted by the adipose tissue
leptin is secreted in proportion of amount of adipocytes that we have
inhibits hunger
with time people develop resistance to leptin

51
Q

How does chronic obesity affect hunger signals?

A

Creates disruption

52
Q

Anorexigenic hormones of the hypothalamus

A 
POMC
Nesfatin-1
TRH
CRH
Oxytocin 
Serotonin
Histamine
Urocortin
53
Q

Orexigenic hormones of the hypothalamus

A 
Neuropeptide Y (NPY)
AgRP
Orexins
MCH
Endocannabicoids
Opiods
54
Q

Anorexigenic hormones of the GI tract

A 
CCK
GLP-1 (glucagon like peptide-1)
Peptide YY (PYY)
Oxyntomodulin
Enterostatin
Bombesin
Uroguanylin
55
Q

Is obesity caused by one gene?

A

Obesity is a polygenic disease: multiple genes having relatively small effect on predisposition vs. environment

56
Q

Susceptibility to obesity is __ and __ determined

A

Susceptibility to obesity is genetically and epigenetically determined

57
Q

is BMI predicted more by the BMI of biological or adopted parents?

A

biological

58
Q

Describe Gene Wide Associated studies (GWAS)

A

Genome wide association studies (GWAS)
– Leptin receptor(LEPR), pro opiomelanocortin (POMC), pro-hormone
convertase 1 (PC1), brain derived neurotropic factor (BDNF),…
– Fat mass and obesity-associated gene(FTO) and melanocortin-4 receptor (MCR4) genes are major contributors (6%) of cases

many gene SNPs were identified but all of them had a small impact after all, thus it was the combination of genes that led to overall effect

59
Q

Which portion of fat in the body did genetic factors have a higher effect?

A

genes affect total fat and it’s distribution more compared to their effect on BMI an the quantity of subcutaneous fat

60
Q

What is an obesogenic environment?

A

physical, social, cultural and economic factors that promote weight gain and are barriers to weight loss

61
Q

What are some of neuroendocrine disorders that promote weight gain/ conservation

A

Cushing’s disease- High levels of cortisol result in a redistribution of fat, especially to the chest and stomach, along with a rounding of the face.
Hypothyrodism

62
Q

What are the types of medical conditions and pharmacological agents that participate in weight gain

A
  • congenital causes
  • neuroendocrine disorders
  • pharmacological agents (especially psychiatric medications lead to weight gain)
63
Q

How do corticosteroid affect our weight?

A

lead to water retention

64
Q

How are pre-natal exposures associated with obesity?

A

too low or too high birthweight, high maternal BMI and pregnancy weight gain-> increased risk of OB in a child

65
Q

Sleep deprivation and obesity connection

A

Sleep deprivation is associated with OB in children and young adults

66
Q

OB and breast feeding link

A

Breast-feeding might be protective

67
Q

Smoking cessation and OB

A

smokers have higher metabolism and less desire to eat

smoking cessation increases the risk of weigth gain

68
Q

OB and Viruses

A

Virus AD-36 is associated with weight gain

69
Q

OB and toxins

A

endocrine disruptor-> metabolism disturbances

some chemicals are stored in fat . when weight is lost, those are liberated and become toxic

70
Q

When do transferrin, albumin, prealbumin and RBP levels decrease?

A

transferrin, albumin, prealbium, RBP concentrations will decrease in concentration when there’s not enough protein in the diet ass there’s n AA to make those proteins
in inflammation, their levels will also decrease even if there’s enough protein
however, in high inflammation the synthesis of albumin in cachexia are not lower, but levels in the blood are lower due to increased exit of albumin form the concentration due to increased permeability of the wall of capillaries
this also contributes to oedema

71
Q

Which serum protein is the most affected by various conditions? Why?

A

albumin is the most affected as it is the most abundant

72
Q

Obesity is __c disease recognized across the life-span resulting from __ with development of excess __ that over time leads to __, __, and __.

A

Obesity is a multi-causal chronic disease recognized across the life-span resulting from long-term positive energy balance with development of excess adiposity that over time leads to structural abnormalities, physiological derangements, and functional impairments.

73
Q

Which types of disease occurrence is associated with obesity?

A

The disease of obesity increases the risk of developing other chronic diseases and is associated with premature mortality

74
Q

Is there just one type of obesity and treatment

A

no, As with other chronic diseases, obesity is distinguished by multiple phenotypes, clinical presentations, and treatment responses

75
Q

What are the 5 components of assessment for obese patients

A
  • Dietary habits
  • Physical activity
  • Medical, psychosocial aspects • Behavioral aspects
76
Q

What are the components of dietary history and habits assessment

A
  • Weight history, previous diets
  • Food intake (24h-recall or other method)
  • Patterns of meals.
  • Ability to cook, access to food, budget
  • Allergies, intolerances, beliefs about foods
  • Use of vitamin/mineral supplements, herbs, natural products
  • Medications
77
Q

Which factor doesn’t physical activity assessment capture

A

Does not capture fidgeting and intensity of PA

78
Q

What can be used to measure step count?

A

pedometers

79
Q

What are accelerometers

A

Accelerometers are movement monitors that have the ability to capture intensity of physical activity.

80
Q

What is an advantage of an am band accelroemter

A

also captures the heat aspect

81
Q

Which type of accelerometers is more accurate?

A

tri-axial

82
Q

define physical activity

A

ALL leisure & non-leisure body movement resulting in a substantial increase in EE.

83
Q

Define exercise

A

a form of leisure time PA that is planned, structured, and repetitive. Its main objective is to improve or maintain physical fitness.

84
Q

Define physical fitness

A

a set of attributes that are either health or performance (skill) related. The ability to carry out daily tasks with vigor and alertness, without undue fatigue, and with ample energy to enjoy leisure time pursuits and to meet unforeseen emergencies

85
Q

define active living

A

when physical activities are an integral part of daily living.

86
Q

What are the low, moderate and high indexes fo PAL

A

Physical Activity Level (PAL) Low- 1.3
Moderate- 1.5
High -1.8

87
Q

What is MET?

A

Metabolic equivalent task: energy cost of physical activities
• 1 MET = 3.5 mL O2 uptake/kg BW/minute
• 1MET=1kcal/kg BW/hour (sitting or lying quietly)

88
Q

What are some common METs

A

– Sleeping = 0.9 METs-> the only one that is less than 1 met, but all the other activities are more than 1
– Walking slowly = 2.5 METs
– Vacuuming = 3.5 METs
– Swimming = 7.0 METs

89
Q

WHat are Medical & psychological aspects of an assessment of obesity

A

• presence of uncommon causal disease (eg., hypothyroidism)
• psychological disorder, especially bulimia, anorexia,
depression
• complications of obesity
• age < 16, pregnancy, lactation, morbid obesity (BMI > 40)
• previous approaches to weight control, to help assess the persons judgment
• patients readiness to change

90
Q

What are the stages of Change theory?

A

https://ighhub.org/sites/default/files/CH-graphics-stagesofchange.png

91
Q

How does Percentage of energy expenditure at rest differs from active state

A

during activity, skeletal muscle will start consuming more energy
the brain, however, will still consume the same amount (all the time)- the proportion will be lower

92
Q

Largest consumers of energy at rest to lowest

A 
Skeletal muscle (22%)
Liver (21%)
Brain (20%)
Heart (9%)
Kidneys (8%)
Adipose tissue (4%)

remainder (16%)

93
Q

What are the largest fuel stores to lowest

A

adipose-> protein-> CHO

94
Q

100 kcal from fat vs 100 kcal from protein/ CHO

A

100 kcal of glycogen= 20g of glycogen which is stored with 80 g of water
same ratio for protein
1g of fuel per 4 g of water
adipose tissue is not really stored with water
thus when we are burning fat, we don’t loose water weight with it

when you use glycogen and protein for energy, you weight decreases more
when you burn 100 kcal of fat, you will only loose 10g-> more weight is lost if you use glycogen and protein for energy

95
Q

The fed signals

A

fed signal: ingesting glucose-> insulin secretion
insulin regulates all events after a meal
insulin is required for acting on adipocytes-> will stimulate storage of excess energy
insulin is also essential for muscles to take up glucose and replenishing glycogen
glucose will move to the liver, replenish glycogen and excess will be converted to TG-> VLDL-> circulation-> storage in adipose tissue

96
Q

Which tissues require insulin for function and which are affected by it?

A

adipocytes and muscles require insulin

CNS, RBC and liver are affected by insulin

97
Q

What is a refeeding syndrome, when and how fast does it occur

A

syndrome that is a short-term syndrome that will bring metabolic consequences rapidly when refeeding someone
-> occurs in the first few days

98
Q

What are the causes of refeeding syndrome

A
  • shift back to glucose as the main fuel from using FA and ketones
  • Rapid fluxes of insulin due to CHO load
  • Rapid shift of electrolytes and intracellular anions and cations to intracellular space (PO4, K, Mg) due to Na-K ATPase utilization of those for energy production and they are also used for glucose transport
  • Sodium and water retention
    hyphophosphatemia - major cause of the symptoms in the refeeding system
    hypocalcemia- decrease of calcium in the circulation as it is being driven into cell
99
Q

Symptoms of refeeding syndrome

A

Fatigue, lethargy, dizziness, muscle weakness, arrhythmia, hemolysis, edema due to excess water and sodium retention in the cells due to electrolyte imbalances

100
Q

What are the physiological changes during repletion in refeeding syndrome

A

ECF expansion
- Edema from increased Na intake and electrolyte imbalances
Glycogen synthesis to restore glycogen stores and produce ATP ->further imbalances in phosphate and K levels
- May lower serum PO4 and K concentration
Increased REE
- Due to reversal of starvation and LBM rebuilding
Increased insulin secretion from CHO intake
- Fed signal is now present and uptake into cells resumes § Stimulates N retention
- Stimulates cell synthesis, growth, and rehydration

101
Q

what is the nitrogen balance in stravation?

A

negative

102
Q

WHat are the steps in refeeding?

A

Primary goal” Normalize fluid and electrolyte imbalances
- PO4, K and Mg using supplementation; IV infusion in severe cases
- Limit Na and fluid in the first few days to avoid oedema
Provide a mixed diet at maintenance energy levels: hypocaloric diet to meet REE needs, not TEE needs
gradual increase in calories
- To establish tolerance and avoid refeeding syndrome
- Aim for 100-150g glucose to stop LBM breakdown but start with 25% of dose and increase gradually
- Thiamine (or multivitamin) supplementation: thiamin and vit B6 are cofactors of CHO metabolism and will be highly used upon the metabolism of CHO-> may result in deficiency, thus supplements are needed
Provide protein at 1.5-2 g/kg current body wt/d
- Start with 20 g/day due to urea cycle enzyme adaptation, as the enzyme activity is suppressed during starvation (minimum amount of urea is produced during starvation
- To replenish LBM
Monitor serum electrolytes, weight, intake, output- if you see rapid weight gain-> not normal-> limit sodium and water intake as water retention conduction of fluid balance test: write down all inputs and outputs occurring

103
Q

How to assess whether excessive liquid is being conserved in refeeding syndrome?

A

conduction of fluid balance test: write down all inputs and outputs

104
Q

Physiological changes after diet-induced weight loss that result in an increased energy storage

A

• Decreased energy expenditure - when we loose weight, we loose LBM as well (about 25%)-> decreased REE
decreased body mass-> less weight to carry-> less calories burned and lower REE
there are also adaptation mechanisms-> further decreased in REE, independently of decrease in mass
• Decreased fat oxidation after the weight loss; during the weight loss, however, the rates of fat oxidation are high as it used for energy
• Decreased thyroid hormones, thus decreased energy expenditure
• Increased cortisol (will go back to normal over time)

105
Q

Physiological changes after diet-induced weight loss that result in an increased food intale

A
  • Decreased leptin> increased hunger; less leptin is secreted due to the lower amount of adipose tissue which is leptin’s secretory organ
  • Decreased PYY
  • Decreased amylin
  • Decreased insulin
  • Increased ghrelin, appetite
  • altered neural activation
106
Q

How long can physiological changes persist after diet-induced weight loss

A

changes may persist >1 year after weight loss

107
Q

How is energy expenditure affected by weight loss

A

Decreased energy expenditure:
• REE↓≅15 kcal per kg lost: more than expected from changes in body weight and composition
• Usual decrease in physical activity, more with severe restriction
• Decrease in TEF, from lower E intake
• Persists> 1 y after weight loss, perhaps permanently

108
Q

How is appetite affected by weight loss

A
  • ↑soon during energy deficit and persists >1y

* with accompanying hormonal adaptations

109
Q

why might in be harder to control appetite after weight loss?

A

• Improved food reward, palatability and olfaction

110
Q

What are the changes in the levels of PYY and gherlin after weight loss

A

gherlin levels increase, PYY levels decrease-> increased hunger

111
Q

anorexigenic hormones of pnacreas

A

insulin
amylin
Pancreatic peptide (PP)

NUTR 344 (22 decks)

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