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.
Lecture 4B: Stress & Diathesis
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來自 Johns Hopkins University 的課程
重性抑郁人群：公共卫生解决方法
110 個評分
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.
與講師見面
William Eaton, PhDProfessor, Mental Health
Bloomberg School of Public Health
Wietse A. Tol, PhDAli & Rose Kawi Assistant Professor, Mental Health
Bloomberg School of Public Health
Ramin Mojtabai, MDAssociate Professor, Mental Health
Bloomberg School of Public Health
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.
