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Lecture 6

Lecture 6.docx

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William Magee

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Lecture 6: SOC243: Feb 14 I. Childhood Adversity and Susceptibility to Chronic Diseases Later in Life II. Placing Childhood Adversity I n the context of the Political Economy of Family and Work Stress and Social Policy III. The Historical Context of work Stress and Health I. Childhood Adversity and Susceptibility to Chronic Diseases Later in Life  A lot of research on childhood and adult health, have followed children until later in life and watched their heart attack rates,  Correlational evidence: correlations of adult illnesses with retrospective reports of childhood stress—what are the issues?  Probably greater problems with information on when things happened than whether or not they occurred *can collect data on adults and ask if they’ve been emotionally abused during childhood  Shows that childhood stressors have an impact on health  Another issue: ex. Being born Jewish during the Nazi era o Among Jews arriving as children to Israel post WWII (and born during the war), later adult cancer rate was 3.5 times as high than for same- aged immigrants who arrived pre-war.  Being exposed to the war itself increases the risk of cancer (3 ½ times as likely to get cancer) but it’s not clear if the stress of hiding, childhood trauma, leads to cancer. Need alternative studies to see other areas ie. Lack of nutrition at that time, maybe it’s not psychological stress, could be other stresses Does-response evidence  If you just study trauma stresses, just having trauma is big, having another thing and another thing isn’t going to amount to that trauma  But if you study smaller stresses, you’re going to find that it adds up  Research reviewed in Miller, Chen and Parker suggests that each additional kind of early adversity experienced led to a 20% increase in CHD incidence. They report similar findings for CVD (stroke), hospitalization for autoimmune diseases, mortality due to violence, accidents, and drug/alcohol related mortality  Latent (or lagged effects) suggests there may be ‘windows of vulnerability’ to ‘biological embedding’ of adversity o Example of children are vulnerable, and susceptible so children can become scarred (biological embedding) refers to how does experience get into the biology (under the skin) o Compliment the kinds of interpersonal processes, one stress leads to another Thinking around control variables  Effects of low SES/poverty on all cause mortality also observed after adult SES controlled Childhood SES --------------------- Adult mortality Adult SES In this case adult SES is a mediator of the effect of childhood SES (ie. Comes between childhood SES and adult mortality) Usually the adult ses is a mediator (this is the line that usually happens) Ex. Why does children who are poor, become poor in adulthood, and poor when they die? -There’s also the question about the nature of scars. If there is a scarring process, what is the nature of that scarring process Controlling traditional risk factors and ‘third variables’ I.e. traditional CHD risk factors, including demographics, smoking, exercise, adiposity, diabetes and hypertension Childhood stress ------- CHD incidence Traditional risk factors Third variables and spurious effects i.e. genetic effects The only way of dealing with third variables is to conduct experiments, but can’t because you can’t say you be poor, you be rich, so only stuck looking at correlation and statistics Epigenetic and Related Processes  Epigenetic describes stable changes in the activity of a gene that arise without changes to its DNA sequence – i.e. gene expression  Epigenetic alterations occur in two main ways: methylation – which controls whetehr the gnee is ‘switched’ on or off.  Chromatin remodelling involves how easily transcription occurs (RNA_DNA processes)  Related: telomere shortening (telomeres cover ends of chromosomes)— related to aging o Get shorted with age and also get shorter with stress o  stress makes you get old faster Changes represent predictive adaptive responses  Inclusive fitness, Darwinism, adaptive in terms of evolution  Increased stress reactivity can be adaptive in the context of risk/threats of physical harm. Organisms that possess the proinflammatory tendencies might enjoy a survival advantage because the response can accelerate the healing of wounds, and the clearing of secondary infections Fetal Origins Hypothesis  A version of the fetal programming hypothesis – nutritional deficits in childhood compensated for in development in a way that protects heart, brain, and pancreas. The result small body sizes, low skeletal muscle, and high visceral fat—leading to later obesity when food is not scarce  Dutch Famine (‘Dutch Hunger Winter’ 1944-1945): average cal/person – 400-800/day) o Saw the effects on children who went through the period (saw lots of biological effects, heart disease, and obesity  idea that you’re programmed now to store as much fat as possible, because you’re exposed to that environment when you were young) Stress response propensities in social context  Vigilance is relatively high among children raised in low SES households. They more likely than others to attend to angry faces, presumably reflecting heightened sensitivity to threatening emotional information. Amygdala activity support this connection  Physically abused children have selective attention for angry facial displays and are slower to turn away from them than unexposed controls. They are also more readily identifying anger in faces with ambiguous expressions. They orient their attention toward others’ conflictual interactions more than controls. In general they seem to come to view the world as a threat-laden place that requires high levels of vigilance
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