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Lecture 4B: Stress & Diathesis

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重性抑郁人群：公共卫生解决方法

约翰霍普金斯大学

4.6（152 個評分） | 13K 名學生已註冊

Public Mental Health is the application of the principles of medicine and social science to prevent the occurrence of mental and behavioral disorders and to promote mental health of the population. This course illustrates the principles of public health applied to depressive disorder, including principles of epidemiology, transcultural psychiatry, health services research, and prevention. It is predicted that by 2020 depressive disorder will be the most important cause of disease burden in the entire world! Every human being suffers from feeling depressed at some point or other, but only about one fifth of the population will experience an episode of depressive disorder over the course of their lives. This course illuminates the public health approach to disease, and the particular complexities of applying this approach to mental disorders, using depression as the exemplar.

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4.6（152 個評分）

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CM

Dec 13, 2018

Great course ! I learned information that i never knew existed.

DW

Apr 06, 2018

Very interesting course. Good structure and presentation, too.

從本節課中

The Search for Etiologic Clues

This week the focus is on possible causes for depressive disorder, including inheritance, stress, social life, work life, and the evolution of modern living.

Lecture 4A: Inheritance9:28

Lecture 4B: Stress & Diathesis7:35

Lecture 4C: Social Supports5:37

Lecture 4D: Work, Family, and Life Stage7:39

Lecture 4E: Recency of Birth20:42

教學方

William Eaton, PhD
Professor, Mental Health
Wietse A. Tol, PhD
Ali & Rose Kawi Assistant Professor, Mental Health
Ramin Mojtabai, MD
Associate Professor, Mental Health

腳本

So I'm going to call this, Stress and Diathesis, and you'll see why.

So we have a case control study that I have already presented to you from George

Brown and Tirril Harris, called, The Social Origins

of Depression, it's a book by Brown and Harris.

And I presented two of the three columns to you

last time, to be clear about the case control study.

I presented the middle and right most column.

But I want to make a little bit of a point

about this.

And that is the, it turns out you'll see, later in the course, in the lectures by

Ramin Mojtabi that many cases of depression are basically never treated.

They do not get into treatment their entire lives.

If we study just patients, that's the

left-hand column, as George Brown did, we worry

that the patients are different from the

general population, who may have depressive disorder also.

So, Brown compared cases from poor patients to controls, from the

survey, he also, in the survey identified cases from the survey.

So you can say, the 68 versus 20 is the figure we looked at before,

but it's not very different from the

patient cases, 61 percent have a severe event.

And so, this again is showing us that life events are associated with onset

of depression and we can remember the story

of Debra who suffered through the Buffalo creek flood

from the first lecture and she more or

less recited the the diagnostic criteria for depressive disorder.

And we do not think that

Deborah's depressive disorder was caused by inheritance.

We imagine it was caused by the Buffalo Creek flood.

Now, let's consider these two things interacting and

this is from Ken Kendler's population based twin registry, and so we have the

twin pairs graded as to the density of their risk for depressive disorder.

So for example if we have a dizygotic twin

we're sharing 50% of the gene with that twin.

And that twin is normal, we have the

lowest risk for depressive disorder in terms of inheritance.

And, likewise, if the monozygotic co-twin is normal,

we have a low risk for depressive disorders.

If the dizygotic twin is a case of depressive disorder, then

we are at higher risk for depressive disorder from our inheritance.

And, likewise, if the monozygotic twin is a case,

we are at even higher risk for a disorder.

So, now consider that grading of a risk through genetics in interaction with

whether there has been a life event prior to the month of onset.

And you can see, if there's

no life event, there's not much depressive disorder.

It's the life event that potentaties the genetic mechanism

and spreads people out according to their genetic risks.

So, this is an example of a gene environment interaction.

And the highest risk, you can see, about 14% of genetically dense or

risky sample who have had a life event have an onset of depressive disorder.

That's a high percentage to have an onset.

Now, let's consider one other possibility.

What's happening is we're getting more and more complex in terms of our methodolgy.

I presented to you the case control, and the cohort study,

and the ecologic study, as in a way kind of pure types.

But we use that language, and that conceptual basis

to study lots of different situations of data collection.

And one of the most important of these situations is simply

a general population survey.

And this is a particular general population survey as it happens, of, of

twins, but I'll show you lots of data below, of general population surveys.

And I'll be using the term incidence

sometimes, and that brings the cohort concept into

play, that's a prospective study, and sometimes

I'll be using the word prevalence, or association.

And that brings the case control logic

into play, which is the retrospective logic.

Here is a personality trait, called

neutroticism, this is a well studied trait,

and neuroticism is the tendency that an

individual has to react strongly to stress.

So, it means people get anxious or moody

or distressed or upset in the context of stress.

Some people do more, we know this, some people are calm in

the face of stress and some people are all anxious and upset in the face of stress.

So we measure that trait, neuroticism, then we look forward in time.

To people who have more neuroticism, or less neuroticism.

And we consider stressful life events in that context.

So if you look on the left hand chart, that's the males, and you can see

that some of those males, the orange triangles,

and the orange bar, have very high neuroticism.

And they are much more likely to have an episode of depression in the future.

In other words the trade is measured at one point in

time and they have incidents of depression after that point in time.

That's the cohort logic.

And so you can see that the orange bar is

higher than the red and, and blue and green bars.

And that means that neuroticism is related to onset of depression.

But you can also see that it's

interacting with stressful life events.

So, people who have a severe life event and a

life event that's rated as severely upsetting to their life

plans and the meaning of their life, those people have

the most likely possibility of having an episode of depressive disorder.

And so as you move from left to right the stress of the

life event gets from none or minor to severe and their risk for depression

goes up and this is true for males and females.

And one final note about males and females.

Again we see females have slightly higher risk for

depressive disorder at any given level of neuroticism, and at

any given level of stressful life events, the females

are more likely to have an episode of depressive disorder.

So, this leads us into, this is a

conceptualization of these data, called the Diathesis Stress Model,

this is a drawing by me, a redrawing of a model that was first drawn by Joe Zuben.

So, many decades ago, this one is in color and it's prettier,

but it's actually showing the way in which genes interact with stress.

This is something I've shown you a couple of times, just now, in the slides.

What we have is, we have some people with very few genes for a depressive disorder.

Or a very low genetic

loading for depressive disorder and those people can tolerate lots of stress.

Even very high levels of stress they will

not have an episode of depressive disorder so we

think of for example and John McCain in

the prison in north Vietnam he was possibly resistant.

To having an episode of depressive

disorder, possibly because of his genetic makeup.

And we have some people who have many

genes for depressive disorder, but they live in a good environment.

Somehow their environment is protected, and so

we can think the even though they're

heavily loaded for the inheritance of depressive

disorder, the environment doesn't produce it in them.

So, this is an additive interaction of genes and stress.

And you can see there, somewhere along the way, there is a boundary of diagnosis.

And as we move up toward

the upper right corner we get more genes, more stress.

Any combination, but more of them are likely to

have a more severe episode of, of depressive disorder.

So in this section we're studying,

basically, the way genes and stress interact.

And those are the two most important aspects of

depression as I told you in the first lecture.

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