Lec 7 - Obesity Flashcards

1
Q

How to calculate BMI and how does it define obesity and overweight

A

Bmi is weight divided by height squared

Overweight is defined as a BMI>=25 and <30 kg/m². Obesity is defined as a BMI >=30 kg/m².

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2
Q

as well as BMI, what are other measurements?

A

Computerised tomography/MRI/Ultrasound
Skinfold thickness
Waist/hip ratio
Underwater weighing

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3
Q

how many obese related deaths in US a year?

how many obese people in Scotland? and what age and sex has highest percentage?

which country hasnt increased in prevalance of obesity?

what was found in havana?

A

Approximately 280,000 obesity-related adult deaths in the US per annum.

Approx one third of middle aged people obese in Scotland, most aged 55-64 females in 2003

Neverthalands

obesity rates dropped after soviet union

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4
Q

Bhatnagar et al study (migrants in west london vs punjab in india)

A

This study looked genetically related individuals by comparing coronary risk factors in a randomly selected group of migrants from the Indian subcontinent of Punjabi origin living in West London and 117 of their siblings living in the Punjab in India

=The West London cohort had a greater BMI, systolic blood pressure, serum cholesterol, apolipoprotein B, lower high-density lipoprotein cholesterol and higher fasting blood glucose than their siblings in the Punjab.

Increases in serum cholesterol after migration from India lead to increased coronary risk conferred by high serum lipoprotein (a) concentrations and greater insulin resistance.

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5
Q

leptin vs ghrelin

A
  • Leptin – fat signal = Leptin is resistant in obese people, so they become resistant to inhibitory effects of leptin.
  • Ghrelin (gastric hormone) = Ghrelin is down regulated in obesity, and is form of neg feedback. It stimulates hunger and reward
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6
Q

who found the ob gene in mice? and what does it do?

A

Zang
The ob gene encodes for a hormone that inhibits food intake, ‘Leptin’, this provides negative feedback from adipose tissue. The obgene that codes for the hormone leptin, controls food intake via leptin receptors in the hypothalamus.

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7
Q

explain leaky barallel model

A

The amount of water entering the hose is analogous to the amount of available food.
The water pressure at the nozzle is the incentive value of available food
The amount of water entering the barrel is analogous to the amount of consumed energy.
The water level is the level of body fat.
The amount of water leaking is the amount of energy expended
The weight of the barrel on the hose (at the bottom) is the strength of the satiety signal
Water level can go up or down, there are many things that influence this, for example the pressure of water entering hose determines if tap is on or off, so food availability.
As water in barrel increases then the pressure on hose increases which will limit the amount of water entering barrel in first place. So there is no specific set point that the barrel is trying to attain but simply operates to a settling point over time.

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8
Q

Prentice & Jebb - carbs and fat proportion of overall intake over time
and energy expenditure over time

A

over 50 years..
Carbohydrates level decreased over time. Fat intake increased.
Crude measures of physical activity. Data fit better that there is a reduction in energy expenditure. (more cars and tv viewing)

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9
Q

What did Westerter argue?

A

Daily energy expenditure in Europe and North America is not sig different. They conclude that physical active expenditure in modern man is in line with those in wild mammals.

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10
Q

name the corresponding theory
- OBESE BY DESIGN
– OBESE BY ACCIDENT
– OBESE BY NECESSITY

A

Thrifty-gene hypothesis – OBESE BY DESIGN

Drift-gene hypothesis – OBESE BY ACCIDENT

Protein-leverage hypothesis – OBESE BY NECESSITY
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11
Q

Explain Thrifty gene hypothesis

A

(Neel)
Evolutionary model
‘Thrifty’ in the sense of being exceptionally efficient in the intake and/or utilization of food.
A ‘thrifty’ genotype would have been advantageous for hunter-gatherer populations. Eat food whenever it is available or encountered.
Fatter individuals carrying the thrifty genes would survive times of famine.

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12
Q

Limitations of Thrifty Gene hypothesis (and who?)

A

Speakman argues:

  1. Famines were irregular and quite rare
  2. Modern hunter/gathers are not obese – if there is a strong selection pressure then they should have a high BMI
  3. Why are we all not obese? 30% are obese in the US – if there was a strong selection pressure then why not 100%?
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13
Q

Drifty Gene hypothesis

A

Speakman
The genetic drift occurs when the mutant alleles in question are not under selection but selectively neutral. Thus genes predisposing to obesity are NOT under any positive selection. Random mutations occur in the genes and the frequencies of these mutant alleles drift at random. These genes may then be called ‘drifty genes’, and it is due to their influence that some of us are unfortunate in the genetic lottery and inherit a predisposition to conditions that in our modern society have such devastating effects

Around two million years ago predation was removed as a significant factor by the development of social behaviour, weapons, and fire. The absence of predation led to a change in the population distribution of body fatness due to random mutations and drift

The key aspect of this ‘‘drift’’ scenario is that the genetic predisposition to obesity is not interpreted to be an advantageous characteristic favored by the process of natural selection (as in the thrifty gene hypothesis). eg a fat animal has less chance of running from predator

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14
Q

Obesity prevalence in the US in 1890 was 3%. This reflects about 10% of the population having free access to abundant food. If 100% have access then 30% should be obese – around what we see in the US today… what theory does this fit with?

A

Drifty Gene hypothesis - obese by accident

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15
Q

explain protein leverage hypothesis

A

Protein matters because of amino acids that are building blocks. To increase overall protein we increase overall intake.
We are adapted to show specific interest in protein. Protein is the most satiating macronutrient group for humans
Obesity therefore can come about when there is a shift towards a diet containing a higher percentage of carbohydrate and fat. This could occur where fat- and/or carbohydrate-rich foods are more accessible, more affordable, in greater variety, or more palatable than alternatives, leading to people effectively being trapped on a suboptimal diet where under such circumstances, maintaining the amount of P eaten requires over-consumption of C + F.

in support of this Protein intake has decreased in the USA – 14% to 12.5% since 1961

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16
Q

Support for thrifty gene hypothesis

A

Comes from early development
uterine programming- Individuals exposed to famine during gestation have poor glucose tolerance and higher blood pressure (in second WW in Neverthalands)
babies were programmed to expect famine enviro, but instead they experienced energy rich enviro and so were more likely to be obese.

17
Q

chaotic eating

A

those who ate erratically (9 meals a day) had increased hunger and blunted postprandial thermogenic response. whereas regular eating improves insulin response to carb load

18
Q

the insurance hypothesis

A

Nestle -The IH is rooted in adaptive evolutionary thinking: the function of storing fat is to provide a buffer against shortfall in the food supply. Thus, individuals should store more fat when they receive cues that access to food is uncertain. Applied to humans, this implies that an important proximate driver of obesity should be food insecurity rather than food abundance per se.

obesity is associated with low SES
Although becoming obese increases cost expenditure. A high BMI may protect against periods of food shortage, so the reason people eat in relation to low SES is because it is an adaptive behaviour.

So do food insecure populations in low-income countries want to be fatter? Yes

19
Q

3 risk factors

A

Early development, chaotic eating and food insecurity