Chapter 11, 12, and 13 review Flashcards
What do Robert Sapolksy’s studies with stress in baboons tell us about the role of social status in stress and health/sickness associated with stress?
What about the role of culture in social stress?
How does the baboon work coincide with what was observed in the Whitehall study of British civil servants of different seniority rankings?
Baboon Study Shows Why High Social Status Boosts Health
Ranking
Being at the bottom of the social ladder is generally a predictor of bad health: research shows that poor people die sooner and have more disease than rich people, even when you account for factors like lack of access to health care.
But the data on social hierarchy and health — including studies in primates other than humans — contains a paradox for males: high status is linked with high levels of testosterone, and high testosterone can in turn lower immunity and increase disease risk. So, why is high rank consistently associated with good health?
Scientists examined wild baboons living Kenya. The researchers looked specifically at the relationship between illness & injury and rank — that is, whether higher- or lower-ranking males fell ill or were hurt more frequently. Scientists also measured how fast the males recovered. (Females were not studied due to complexities related to their reproductive cycles and childbirth.)
There were significant differences, all favoring the higher-ranked animals. In fact, at any particular time, the odds of recovery from sickness/injury for a high-status animal were 3x’s greater than for a male at the bottom. The alpha males at the very top healed faster than all other males. And this outcome occurred even when the high-ranking males had high levels of glucocorticoids (stress hormones), as well as high levels of testosterone, both of which can suppress immunity.
Based on their stress & hormone levels, one would expect the males at the top to get sicker and recover from wounds more slowly than their low-on-the-totem-pole peers. In part, the findings can be explained by age: top-ranked males tend to be younger and healthier than lower-ranking animals. But age didn’t account for the differences completely. High status was a better predictor of healing than age was.
Alpha and low-ranking males seem to experience elevated glucocorticoids as a result of different stressors and over different periods of time. Such differences may alter the immunosuppressive effects of stress. Specifically, high glucocorticoids in alpha males probably are caused primarily by energetic stress, whereas high glucocorticoids in low-ranking males probably are caused largely by social stressors, such as high rates of received aggression, a lack of a sense of control, and few coping mechanisms.
In other words, the short-term stress experienced by alpha males tends to be “good” stress, the kind that comes from exercise or sex. It doesn’t last long, it doesn’t include feelings of loss of control, and it doesn’t involve a persistent threat to important social relationships. When you consistently win battles for dominance, you don’t worry much about how the losers will treat you.
In contrast, lower-ranked males experience ongoing, uncontrollable stress, which does affect their relationships, particularly the amount of bullying they face from higher-ranked males. Among baboons, “displacement” aggression is common, wherein the top guy kicks the guy below him when he’s pissed off and that guy kicks a lower-ranking dude, all the way down the chain. This leads to chronically elevated stress hormones in low-ranking members of the pack, which can be harmful.
The top animals also tend to get more social support. In baboons, this involves being groomed by others, which not only removes parasites, but more importantly, also calms the stress system and lowers the animal’s levels of glucocorticoids.
In the short term, then, elevated levels of testosterone and glucocorticoids seem to improve immunity; if they remain consistently high, however, they lower immunity and harm health. Social contact seems to be an important way to “turn down” the stress system.
The researchers note that the study cannot determine whether an animal’s high or low rank is caused by its health status in the first place, or vice versa — and these explanations aren’t mutually exclusive. Strong, resilient animals may rise through the ranks, and then their alpha position may reinforce their good health. Similarly, poor health may drive rank downward by impairing an animal’s performance. The authors write: “It is likely that both forces interact to shape differences in health and immune function.”
(MORE: How Bullying and Abuse May Age Children Prematurely)
In humans, decades worth of data suggest it is higher social status itself that improves health, and the chronic stress of low social status that harms it, particularly when this stress starts early in life.
As stress researcher Robert Sapolsky who has studied baboons in Amboseli, said: “When humans invented inequality and socioeconomic status, they came up with a dominance hierarchy that subordinates like nothing the primate world has ever seen before.”
There is a remedy for status stress that works even in the face of social inequality. While humans don’t typically groom each other like baboons, research finds that high levels of social support, esp. physical contact like hugs & massages, can mitigate the effects of stress for humans.
According to the video viewed in class, how does stress alter teleomeres on the chromosomes?
How does this impact health?
Chronic Stress is harming our DNA
Personality, stress processes, and environment affect our DNA
Money problems, a heavy work load, caregiving…. increasingly common pressures have helped make stress a part of modern life.
According to APA’s Stress survey, 42% of adults in the U.S. say their stress level has increased over the past 5 years.
Even teens reported stress rivaling adult levels.
Chronic stress damage starts before we’re even conceived and cuts into our very cells.
Studies link stress with shorter telomeres, a chromosomal component that’s associated with cellular aging and risk for heart disease, diabetes, and cancer.
Telomeres are a protective casing at the end of a strand of DNA.
Each time a cell divides, it loses a bit of its telomeres.
Telomerase enzyme can replenish it, but chronic stress and cortisol exposure decrease your supply.
When the telomere is too diminished, the cell often dies or becomes pro-inflammatory.
This sets the aging process in motion, along with associated health risks.
How does stress rank in terms of factors that affect telomere length?
The 2 biggest factors are chronological aging and genetics, but stress is now on the map as one of the most consistent predictors of shorter telomere length.
The type of stress determines how big its effect is.
Exposures to multiple early life adversities, such as child neglect, have the largest effects, since they track through to late adulthood, or they set in place persistent mechanisms that maintain short telomeres throughout life, such as exaggerated stress reactivity and poor health behaviors.
Stressors such as caregiving in late life also have an effect. This relationship between stress and cell aging spans a lifespan, and it’s fundamental to how we’re built.
When we expose our bodies to years of chronic stress arousal, we see effects that override normal aging, making our telomeres look like they are from a significantly older person.
People with psychiatric disorders related to dysregulated emotional responses (esp. depression) consistently have shorter telomeres than controls who have never experienced these disorders.
According to the video viewed in class, how does stress in non-human primates alter blood vessels, cardiovascular health, risk for stroke and heart attacks, as well as feelings of pleasure and dopamine sensitivity in the brain?
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How do the studies of the Dutch famine winter suggest that stress experienced by mothers can influence the development and health of the fetus?
Famine is never a good thing, particularly if you’re a developing fetus.
While the role of maternal diet in fetal programming is not new to the world of DNA methylation, there’s still a lot to be learned about the subtle variations.
When it comes to growth & metabolism, timing of the environmental exposure appears is important, whether it be the seasonal diet differences at conception affecting methyl donor avalibility or, as in today’s case, which trimester the mother experienced famine.
DNA methylation signatures link prenatal famine exposure to later abnormalities in growth & metabolism.
By using RRBS (Reduced representation bisulfite sequencing) on blood from 24 sibling pairs discordant for prenatal famine exposure (from the Dutch Hunger Winter Cohort), the team made interesting observations in the children:
There are a number prenatal famine exposure-related DMRs that occur in regulatory regions of intermediate levels of DNA methylation.
There is differential DNA methylation in growth & metabolic pathways from 1st trimester famine exposure.
But, surprisingly, these individuals were born with a normal birthweight, in stark contrast to those exposed to famine in the later trimesters, who are born with a signficantly lower birthweight.
The team was able to “pin point” the sensitive developmental period to right after conception, and think it is occurring just after implantation, since that is when major methylation remodelling goes down.
Adding function to finding, their experiments showed that DNA methylation in INSR was associated with birthweight, while CPT1A has a criminal association with cholesterol with both DMRs showing strong enhancer activity in vitro.
Ultimately, prenatal exposure to famine sets up a long-lasting metabolic and growth-related program, with variation coming from the timing of exposure.
“Individuals conceived in the Dutch Hunger Winter may have survived this horrendous period of WW2 thanks to many small epigenetic differences in growth & developmental pathways a few weeks after fertilization.
These changes may be somewhat unfavourable for them as adults, as they seem slightly more at risk to obesity & diabetes.
But overall they are a genomic testament for human resilience.
It is no mean feat for a tiny foetus to grow, when mum gets less than 25% of the minimum caloric.
The Dutch Hunger Winter children, now in their seventies, offer a rare window on how the early environment may leave a lasting imprint on our epigenetic make-up.”
What is the definition of stress?
Stressor?
Stress response?
Stress is a state of threatened homeostasis or disruption in homeostatic balance.
The thing responsible for the imbalance is the stressor.
The body’s response to the imbalance is the stress-response
What are the 2 main hormonal systems that comprise the stress response?
SYMPATHETIC NERVOUS SYSTEM
HYPOTHALAMIC-PITUITARY-ADRENAL AXIS
What hormones does the sympathetic nervous system stimulate the release of?
Where from?
What portion of the stress response does this induce?
The Sympathetic NS stimulates the release of norepinephrine & epinephrine from the adrenal medulla
“Fight or flight”
What are the hormones and endocrine organs that are part of the HPA axis?
Know how the HPA axis is turned on during a stressor, and turned off once the stressor ends.
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What other hormones are released in response to stress?
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What is the difference between an acute and a chronic stress?
Which is adaptive and which is maladaptive and why?
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What is the metabolic response to acute stress?
What is the pathological consequence of this stress response under chronic conditions?
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What is the cardiovascular response to acute stress?
What is the pathological consequence of this stress response under chronic conditions?
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What is the gastrointestinal response to acute stress?
What is the pathological consequence of this stress response under chronic conditions?
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What is the gut microbiome?
How might stress influence the microbiome to influence stress-related outcomes in the brain and behavior?
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What is the effect of acute stress on the reproductive system?
What is the pathological consequence of this stress response under chronic conditions?
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What is the effect of acute stress on growth?
What is the pathological consequence of this stress response under chronic conditions?
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What is the effect of acute stress on analgesia?
What is the pathological consequence of this stress response under chronic conditions?
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What is the effect of acute stress on the immune system and inflammatory response?
What is the pathological consequence of this stress response under chronic conditions?
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How does the hippocampus regulate the stress response, mechanistically?
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How does acute versus chronic stress impact memory/LTP, dendritic structure and neurogenesis on the hippocampus?
Which hormones are responsible?
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How does chronic stress influence the anatomy of the amygdala?
What are the pathological consequences of this?
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How does stress during pregnancy in rodents influence the development of the HPA axis in offspring?
How does this happen mechanistically?
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What are some outcomes of prenatal stress on human offspring?
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What are the different effects of mild versus severe stressors in young animals/humans on programming later responses to stress?
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What is the ACE study?
What does a higher ACE score predict for adult health/illness?
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What is the role of epigenetics in programming early life stress effects on offspring stress response?
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Which genes does low maternal care or early life stress change epigenetically?
How are these changes in gene methylation lead to changes in the hormonal stress response?
(Know both effects on glucocorticoid receptor and vasopressin)
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What epigenetic changes are seen in brains of individuals who committed suicide that either did or did not experience childhood abuse?
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