Obesity Flashcards
(111 cards)
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
2
Q
anorexigenic definition
A
appetite inhibiting
3
Q
iatrogenic definition
A
resulting from treatment
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
5
Q
orexigenic definition
A
appetite stimulating
6
Q
what is the primary determinant of REE?
A
lean body mass
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;
8
Q
To which demographic do EER values apply?
A
only to persons having a healthy weight
9
Q
What is the stimuli provoked by increased energy intake - anorexigenic or orexigenic?
A
anorexigenic
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
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.
12
Q
what is the predominant type of adipose tissue?
A
white
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
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
15
Q
Is normal BMI always a sign of health
A
no, if waste circumference is above the norm-> health risk
16
Q
Where is waist circumference measure done?
A
taken at the point yielding the maximum circumference around the hips or buttocks
17
Q
High-Risk Waist Circumference in Adult Males and Females cut-offs
A
Males >40 in (>102 cm)
Females >35 in (>88 cm)
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),
19
Q
Definition of overweight
A
excess body weight (fat, muscle, bone, water)
BMI: 25-29
20
Q
Definition of obesity for men and women
A
excess adiposity: body fat > 25% in men body fat > 35% in women
BMI>30
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
22
Q
Healthy BMI range
A
18.5-24.9
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
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
25
Relationship with economic development of countries and the prevalence of obesity
more developed countries show decrease in progression of obesity problem
in less developed countries obesity prevalence is still increasing
26
Obesity and overweight prevalence amongst men and womend
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)
27
What are the factors obesity is related to according to NHANES
obesity is related to socio-economic status: race, gender, education
28
In which demographic groups is prevalence of obesity lower
– Higher income groups
– More educated (college degree)
– Men (34%) vs. women (38%)
– Asians (12%, lowest) vs. African-American (48%, highest)
29
What 3 factors increase Cardiometabolic risk
Cardiovascular diseases
Hypertension
Diabetes
30
What are the main killers
CVD and cancer
31
Health consequences of obesity
* 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
32
How does increase in BMI related to an increase in risk hazard ratio
(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
33
What is the relationship between mortality and BMI
J-shape
| exponential increase above BMI of 30
34
What is the relationship between CHD and BMI
exponential relations
mild increase from 21 to 25
sharp increase of the risk from 25 to 29
35
What is the relationship between diabetes and BMI
risk of developing diabetes and BMI is almost linear
36
How s BMI and glucose intolerance connected?
BMI over 30+ high visceral fat-> highest intolerance to glucose
higher glucose intolerance in those with high visceral fat
37
Which cancers are increased in obese people
Women: Endometrium, Ovary
Cervix, Breast (postmenopausal)
Men: Prostate, Pancreas, Oesophagus
Both genders: colon, gallbladder, kidney, liver
38
Obesity and gallstone disorders
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
39
Obesity and liver disease
Abdominal obesity ↑ risk of non-alcoholic fatty liver disease (NAFLD)
– Steatosis-> steatohepatitis-> cirrhosis-> liver failure
- heaptosteatosis - accumulation of fat in the liver
40
Obesity and reproductive disorders in men
– Reduced testoterone, increased estrogens levels
| – Gynecomastia (breast development)
41
Obesity and reproductive disorders in women
– 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.
42
Etiology of obesity
* Energy balance
* Appetite and body weight regulation
* Genes
* Environmental factors
* Medical conditions and medications
* Other factors
43
Describe an Obesogenic environment
High fat, energy-dense foods Palatable, low cost, available foods
Large portion sizes
Sedentary behavior
↓ Work-related physical activity ↓ Activities of daily living
44
What are the normal % of components of TEE
15-30% Physical Activity Energy (PAE)
5-10% Thermic Effect of Feeding (TEF)
60-75% Resting Energy Expenditure (REE)
45
Proportions of component of TEE fo sedentary normal vs sedentary active
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
active vs sedentary obese TEE
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
Hunger vs satiety vs satiation vs appetite
• 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
Where and how does the central regulation of food intake occur?
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
Where and how does the peripheral regulation of food intake occur?
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
Describe leptin
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
How does chronic obesity affect hunger signals?
Creates disruption
52
Anorexigenic hormones of the hypothalamus
```
POMC
Nesfatin-1
TRH
CRH
Oxytocin
Serotonin
Histamine
Urocortin
```
53
Orexigenic hormones of the hypothalamus
```
Neuropeptide Y (NPY)
AgRP
Orexins
MCH
Endocannabicoids
Opiods
```
54
Anorexigenic hormones of the GI tract
```
CCK
GLP-1 (glucagon like peptide-1)
Peptide YY (PYY)
Oxyntomodulin
Enterostatin
Bombesin
Uroguanylin
```
55
Is obesity caused by one gene?
Obesity is a polygenic disease: multiple genes having relatively small effect on predisposition vs. environment
56
Susceptibility to obesity is __ and __ determined
Susceptibility to obesity is genetically and epigenetically determined
57
is BMI predicted more by the BMI of biological or adopted parents?
biological
58
Describe Gene Wide Associated studies (GWAS)
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
Which portion of fat in the body did genetic factors have a higher effect?
genes affect total fat and it’s distribution more compared to their effect on BMI an the quantity of subcutaneous fat
60
What is an obesogenic environment?
physical, social, cultural and economic factors that promote weight gain and are barriers to weight loss
61
What are some of neuroendocrine disorders that promote weight gain/ conservation
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
What are the types of medical conditions and pharmacological agents that participate in weight gain
- congenital causes
- neuroendocrine disorders
- pharmacological agents (especially psychiatric medications lead to weight gain)
63
How do corticosteroid affect our weight?
lead to water retention
64
How are pre-natal exposures associated with obesity?
too low or too high birthweight, high maternal BMI and pregnancy weight gain-> increased risk of OB in a child
65
Sleep deprivation and obesity connection
Sleep deprivation is associated with OB in children and young adults
66
OB and breast feeding link
Breast-feeding might be protective
67
Smoking cessation and OB
smokers have higher metabolism and less desire to eat
| smoking cessation increases the risk of weigth gain
68
OB and Viruses
Virus AD-36 is associated with weight gain
69
OB and toxins
endocrine disruptor-> metabolism disturbances
| some chemicals are stored in fat . when weight is lost, those are liberated and become toxic
70
When do transferrin, albumin, prealbumin and RBP levels decrease?
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
Which serum protein is the most affected by various conditions? Why?
albumin is the most affected as it is the most abundant
72
Obesity is __c disease recognized across the life-span resulting from __ with development of excess __ that over time leads to __, __, and __.
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
Which types of disease occurrence is associated with obesity?
The disease of obesity increases the risk of developing other chronic diseases and is associated with premature mortality
74
Is there just one type of obesity and treatment
no, As with other chronic diseases, obesity is distinguished by multiple phenotypes, clinical presentations, and treatment responses
75
What are the 5 components of assessment for obese patients
* Dietary habits
* Physical activity
* Medical, psychosocial aspects • Behavioral aspects
76
What are the components of dietary history and habits assessment
* 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
Which factor doesn't physical activity assessment capture
Does not capture fidgeting and intensity of PA
78
What can be used to measure step count?
pedometers
79
What are accelerometers
Accelerometers are movement monitors that have the ability to capture intensity of physical activity.
80
What is an advantage of an am band accelroemter
also captures the heat aspect
81
Which type of accelerometers is more accurate?
tri-axial
82
define physical activity
ALL leisure & non-leisure body movement resulting in a substantial increase in EE.
83
Define exercise
a form of leisure time PA that is planned, structured, and repetitive. Its main objective is to improve or maintain physical fitness.
84
Define physical fitness
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
define active living
when physical activities are an integral part of daily living.
86
What are the low, moderate and high indexes fo PAL
Physical Activity Level (PAL) Low- 1.3
Moderate- 1.5
High -1.8
87
What is MET?
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
What are some common METs
– 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
WHat are Medical & psychological aspects of an assessment of obesity
• 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
What are the stages of Change theory?
https://ighhub.org/sites/default/files/CH-graphics-stagesofchange.png
91
How does Percentage of energy expenditure at rest differs from active state
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
Largest consumers of energy at rest to lowest
```
Skeletal muscle (22%)
Liver (21%)
Brain (20%)
Heart (9%)
Kidneys (8%)
Adipose tissue (4%)
```
remainder (16%)
93
What are the largest fuel stores to lowest
adipose-> protein-> CHO
94
100 kcal from fat vs 100 kcal from protein/ CHO
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
The fed signals
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
Which tissues require insulin for function and which are affected by it?
adipocytes and muscles require insulin
| CNS, RBC and liver are affected by insulin
97
What is a refeeding syndrome, when and how fast does it occur
syndrome that is a short-term syndrome that will bring metabolic consequences rapidly when refeeding someone
-> occurs in the first few days
98
What are the causes of refeeding syndrome
- 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
Symptoms of refeeding syndrome
Fatigue, lethargy, dizziness, muscle weakness, arrhythmia, hemolysis, edema due to excess water and sodium retention in the cells due to electrolyte imbalances
100
What are the physiological changes during repletion in refeeding syndrome
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
what is the nitrogen balance in stravation?
negative
102
WHat are the steps in refeeding?
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
How to assess whether excessive liquid is being conserved in refeeding syndrome?
conduction of fluid balance test: write down all inputs and outputs
104
Physiological changes after diet-induced weight loss that result in an increased energy storage
• 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
Physiological changes after diet-induced weight loss that result in an increased food intale
* 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
How long can physiological changes persist after diet-induced weight loss
changes may persist >1 year after weight loss
107
How is energy expenditure affected by weight loss
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
How is appetite affected by weight loss
* ↑soon during energy deficit and persists >1y
| * with accompanying hormonal adaptations
109
why might in be harder to control appetite after weight loss?
• Improved food reward, palatability and olfaction
110
What are the changes in the levels of PYY and gherlin after weight loss
gherlin levels increase, PYY levels decrease-> increased hunger
111
anorexigenic hormones of pnacreas
insulin
amylin
Pancreatic peptide (PP)
