Week 5 Flashcards

1
Q

What are the 4 evolutionary perspectives on developmental plasticity?

A
  1. Fetal programming
  2. Predictive adaptive response
  3. Thrifty phenotype
  4. Capacity-load model
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2
Q

Describe the fetal programming hypothesis

A

If a fetus does not receive proper nutrition, it will react by altering its metabolism. These changes are permanent, and affect chronic disease predisposition

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3
Q

What is a key flaw of the fetal programming hypothesis?

A

Does not factor in adult lifestyle into chronic disease predisposition, which we know plays some role in long-term health

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4
Q

How might a fetus alter its metabolism in response to undernutrition? (3)

A
  1. Redistribution of blood
  2. Change in oxidation rates of nutritions
  3. Altered sensitivity to certain hormones/altered secretions of hormones
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5
Q

Name 5 factors which might result in fetal undernutrition

A
  1. Maternal body composition: low energy stores
  2. Low maternal dietary intake
  3. Suboptimal uteroplacental blood flow
  4. Placental transfer
  5. Mutations in the fetal genome
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6
Q

Describe the predictive-adaptive response

A

A fetus with a given genotype will predict what its environment will be like and make adjustments to its metabolism accordingly. When the environment is richer (or just different) than predicted, the metabolism will be ill-suited to an environment, resulting in higher rates of chronic disease

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7
Q

What are the key problem with the predictive-adaptive response? (2)

A
  1. The fetus is never actually exposed to the environment: mom buffers the environment
  2. Does not explain why there are high rates of chronic disease in countries where malnutrition is rare
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8
Q

Describe the difference in the thrifty phenotype hypothesis and the fetal programming hypothesis

A

The difference is in the mechanism

Fetal programming: Change overall metabolism
Thrifty phenotype: Divert metabolism, normal brain and malfunction in less important organs

They have the overall same result but the way that they are proposed to happen is slightly different

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9
Q

Describe the thrifty phenotype hypothesis

A

Adaptive growth restriction: Fetal undernutrition causes the body to divert resources to the most important organs (like the brain) at the expense of lesser organs – protect the brain at all costs

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10
Q

Other than the brain, which organs does the body tend to spare in cases of fetal undernutrition? (3)

A

Liver, pancreas, spleen

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11
Q

What organ gets sacrificed and when is largely dependent on… (2)

A

Age and circumstance

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12
Q

True or false: the duration of hyperplasic growth is the same for different organs during fetal growth

A

False: differs between organs, hence why some organs may be sacrificed based on age and circumstance

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13
Q

What were the results of the Minnesota starvation study? How much total body weight was lost? What percentage of this loss was muscle? What percentage of this loss was fat?

A

Participants lost 25% of their body weight
70% Fat loss
10% Muscle loss
These were only men participating in the study!

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14
Q

Why might some people favour fat or muscle loss over the other?

A

In humans, can very generally be explained by biological sex: Women will lose muscle and men will lose fat – both are beneficial for reproduction but exceptions exist

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15
Q

How is muscle reproductively advantageous for human males?

A

Muscle helps you compete for mates

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16
Q

Describe the relative losses in lean and fat mass in men and women during tuberculosis?

A

Males will preferentially lose lean mass (muscle) and women will preferentially lose fat mass - men and women sacrifice their reproductive stores to run the immune system upon TB infection

17
Q

What is the issue with the observed health data which the thrifty phenotype hypothesis cannot explain?

A

If fetal birth weight is a predictor of adult health, why is it that there is not a threshold for chronic disease risk?

18
Q

In a study of 8600 Finnish babies, those who were born with low birth weight and later went on to have normal BMI and coronary heart disease displayed what pattern in prepubertal growth?

A

Huge spike in growth rate from ages 2-11 (hypertrophic growth)

19
Q

Describe the capacity load model

A

Metabolic load which exceeds the capacity which was established during hyperplasic growth is what predisposes a person to chronic disease

20
Q

Define metabolic load

A

Lifestyle traits which challenge the capacity for homeostasis (e.g. lack of exercise, high glycemic load-diet)

21
Q

Metabolic growth develops during (hyperplasic/hypertrophic) growth

A

Hypertrophic

22
Q

Metabolic capacity develops during (hyperplasic/hypertrophic) growth

A

Hyperplasic

23
Q

Define metabolic capacity

A

Traits which enhance the ability to maintain homeostasis (e.g. beta cell count, cardiac structure)

24
Q

Typically (smaller/larger) babies have greater metabolic capacity. Why?

A

Larger

Larger, more productive organs

25
Q

True or false: metabolic capacity can be altered with healthy lifestyle changes

A

False: metabolic capacity is set for life

26
Q

Why is obesity a risk factor which increases metabolic load?

A

An obese person has a lot of tissue which requires a lot of energy – demanding to keep up, increases oxidative stress

27
Q

The penalty for high metabolic load is greatest in individuals who…

A

Have diminished metabolic capacity

28
Q

Birth weight is lost primarily in this tissue

A

Lean mass (muscle and organ mass) – visceral fat mass is usually preserved

29
Q

Low birthweight babies tend to have (low/high) lean mass and (low high) abdominal fat mass compared to normal birth weight babies

A

Low lean mass
High abdominal/visceral fat mass

30
Q

How much (%) less lean tissues (muscle and organs) do low birthweight babies tend to have?

A

25%

31
Q

Why do babies lose lean mass over visceral fat mass?

A

Fat mass is an energy reserve for immediate survival

32
Q

How does early life undernutrition affect oxidative stress? (increase/decrease)

A

Increases oxidative stress

Fewer systems in place to manage physiological demands of body’s tissues - fewer B-cells = greater stress, etc.

33
Q

How does early exposure to irreversible oxidative stress influence a fetus’ telomerase?

A

Accelerates telomerase shortening - result in chromosomal damage sooner

34
Q

In high-income countries, what does the gradient in height look like between high and low status individuals?

A

Low: shorter
High: taller

35
Q

What model best explains the social gradients in height in high-income countries?

A

Capacity-load model

36
Q

Describe the relative heights of person 1: Born poor and became rich, and person 2: Born rich and became poor. Who is taller?

What is the overall message of these data?

A

Born rich and became poor = taller on average

Early life matters in overall adult health

37
Q

In high-income versus low-income countries, are chronic disease rates more an issue of load or capacity?

A

In high-income: capacity matters, poorer members have the lowest birthweights
In low-income: load matters, richer members have the highest load

38
Q

How can both slow and rapid infant growth elevate the risk for the same diseases?

A

Slow growth: penalty to capacity
Rapid growth: penalty to load