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Clinical nutrition > Obesity part 1 > Flashcards

Obesity part 1 Flashcards

1
Q

what is the def of obesity

A

obesity is a chronic progressive and relapsing disease characterized by excess or abnormal adiposity that impairs health and social well being

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2
Q

patterns of body fat distribution in man vs woman

A

men : apple shape
woman: pear shaped

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3
Q

what is the advantage of beige/brown depots

A

people who have more are less prone to be obese

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4
Q

hin a fat molecule what are the 2 things it could arrive for an accumulation and lipotoxicity

A
  • hypertrophy ( bigger in size)
  • hyperplasia ( higher in number)
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5
Q

how can a fat molecule increase in number

A

de novo

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6
Q

the increase in number and size can lead to

A

inflammariob, fibrosis which can lead to insulin resistance

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7
Q

the waist circumference cut off depends on ethnicity. Which ethnicity has a higher waist circumference and which has a lower

A

higher : caucasian europe, US,
lower : african

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8
Q

what happened to the prevalence of obesity from 1980 to 2011

A

it has doubled

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9
Q

the difference of the prevelance of obesity between man and women

A

men are more overweight and obese class 1, than women. However, women are more obese class 3 than men

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10
Q

before obesity was a condition of

A

people who were rich. They had money so they ate more

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11
Q

now obesity is related to

A

socio-economic status: ethinicity, sex/gender, education

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12
Q

obesity is lower on what type of groups

A
  • higher income groups
  • more educated
  • women more than men
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13
Q

what are the 3 most related increases cause of mortality in people who have obesity

A
  • cardiovascular disease
  • hypertension
  • diabetes
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14
Q

BMI and cause of mortality

A

lower BMI has an increase risk of mortality
lowest risk is the normal BMI
after an BMI of 25 the increase of mortality increases almost linear

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15
Q

true or false
mortality, Coronary Heart Disease and diabetes increase as the BMI increase

A

true

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16
Q

intra-abdominal fat is a predictor of what in men

A

predictor of all-cause mortality

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17
Q

an increase of 500grams increases how much in terms of risk of death

A

2x risk
20%

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18
Q

intra abdominal fat increase what in premenopausal women

A

increase the risk of type 2 diabetes

19
Q

in a graphic where it shows 3 curbs of nonobese women, obese with low intra abdominal fat, and obese with a high intra abdominal fat what would the curbs be if we give a drink that has sugar

A

normal: the glucose will go up, but after it would go down

obese low abdo fat: the glucose will go up but it will not go down completely (insulin will be high)

obese with high abdo fat: a big spike of glucose in the blood and it would not go down complete ( insulin resistance)

20
Q

what is insulin resistance and where do we see insulin resistant people

A

insulin resistance is when the person cannot respond to insulin, so they would have a high glucose sugar because the glucose is not going into the cell. However the body is still making insulin but the body is not responding

21
Q

obesity increases what types of cancer in females/males and both

A

females: endometrium, ovary, cervix and breast

male: prostate, pancreas, oesophagus

both: colon, gallbladder, kidney and liver

22
Q

obesity and hepatobiliary disorder

A

abdominal obesitity can increase non alcoholic fatty liver disease

23
Q

what are the process of a non alcoholic fatty liver disease

A

steatosis-> seteatohepatitis -> cirrhoris -> liver failure

24
Q

what is the risk of obesity and gallstones

A

the risk increases when the person has a BMI over 30 and if the person has a rapid weight loss it can also increase the risk

25
Q

what are the risk of obesity and reproductive disorders in male and women

A

risk in males are: reduced testosterone and increased estrogen levels. Plus Gynecomastia ( bigger breast)

risk in women: Polyastric ovary syndrome. Plus during pregnancy, they can have gestational diabetes/ labor and delivery complication/ fetal and maternal death

26
Q

what is the etiology (causes ) of obesity

A
  • energy balance
  • appetite and body weight regulation
  • genes
  • env factors
  • medical conditions and medication
27
Q

how is our physiology not prepared for the modern world

A

our genes and metabolism evolved in a context of starvation, to conserve and store energy - critical to survive. Therefore, our body is not apt to the amount of food and the sedentarism- our body wants to keep and store that energy

28
Q

how is the energy balance of a person who is obese

A

high energy intake: high fat, energy dense foods, low cost, available foods and large portion sizes

low energy expenditure : sedentary behaviours - less work related physical activity and less activities of daily living

29
Q

energy expenditure components in sedentary obese

A

they have a higher resting energy expenditure. They have a bigger body and more fat free mass therefore they will expand more energy

30
Q

what is the difference between satiety, satiation and appetite

A

satiety: feeling of fullness after eating

satiation: state of being satisfactorily full associated with the length of time between meals

appetite: desire to eat

31
Q

which pathways in the hypothalamus stimulates appetite and decrease appetite

A

NPY, AgRP : stimulates
CART,aplhaMSH : inhibits

32
Q

what are the hormones that stimulate hunger and the hormones that inhibit hunger

A

stimulates: ghrelin
inhibits: gut - CCP , fat : leptin (some people ar resistant to this), insulin, amulin

33
Q

how are genes and obesity related to

A

obesity is a polygenic disease : multiple genes have small effect on predisposition

34
Q

how can gene affect obesity

A

genes may affect is several aspects : regulation of appetite, metabolism and distribution of fat

35
Q

Explain some studies of how are genes related to obesity in identical twin

A

in identical twin they have 50-80% of their BMI is explained by genetic.

36
Q

true or false
antidepressants are widely used to different conditions and they an lead to obesity

A

true

37
Q

what are some things in the environmental factors that won’t let a person lose weight ( promote a sedentary life and high cal food)

A

obesogenic env : physcal, social cultural and econimic factors that promote weight gain and barriers to weight loss

  • neighbourhood, workplace, transported and screen time can promote a sedetary life
  • accessibility to food at low cost, large portion and energy dense food - high caloric
38
Q

true or false
is sleep deprivation associated with obesity

A

true

39
Q

how do we assess obesity

A
  • dietary history and habits
  • physical act
  • medical, psychosocial, cultural
  • behavioural aspects
40
Q

give examples of how dietary history and habits affect obesity

A
  • weight history and diet can affect the metabolism
  • food intake
  • patterns of meals (what time food is consumed, with whom, what reason)
  • ability to cook
  • allergies, intolerances
  • medications
  • emotional eating - eat to punish yourself
41
Q

what is the number of physical activity level when it is
- low
- moderate
-high

A

low : 1.3
moderate: 1.5
high: 1.8

42
Q

examples of medical, psychosocial, cultural aspects for people with obesity

A
  • physical examination, blood pressure, lab test
  • complications with diabtetes
  • pregnancy, age
  • psychological disorders
  • practices and belies
  • patient’s readiness
43
Q

what are some aspect of behavioural aspects

A

readiness to change (right time, social support, long term changes)

Clinical nutrition (11 decks)

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