Hi everyone and welcome to our last video for module 6.

In our previous video, I

talked about some features of events that make them more likely to be perceived as
stressful. In that video, I highlighted that there are individual differences in how much
weight each particular person places on the different factors.

In this video, I’m going to talk about some more individual differences, but this time
in our particular physiological responses to stress. So remember, first we do our
appraisal, which often happens unconsciously. Then, once we’ve determined that
something is stressful, we then have a stress reaction, or response, to that stimulus.
Our stress responses, while generally following the same course of events, like an
increase in heart rate and blood pressure and release of certain hormones, can still
vary quite a bit between different people in terms of the magnitude of those
responses and how long they last. I’m going to touch on some reasons for differences
in our individual stress responses related to our experience with stress in this video.
But, to start off, I’m going to first touch on some of the effects that stress can have on
our bodies before we’re even born.

Long-Term Effects of
Early Stressful Life Experiences
LO5: What Prenatal Effects:
are the • Offspring are more anxious (animal studies)
sources of
chronic
• Amygdala
stress? • Metabolic imprinting (thrifty metabolism)
• Generational effects
• Quebec ice storm of 1998
• Effects on offspring at 2 and 5.5yo
• Postnatal Effects:
• Romanian orphanages
• “Risky families”
For our first topic for this video, I’m going to talk about some of the long-term effects
that can arise from early exposure to a large and chronic amount of stress. We’ll
start with prenatal effects of stress. These are effects of stress experienced by our
mothers when they are pregnant with us. Because the mother and fetal blood supply
are so closely intertwined, if a mother is stressed during pregnancy, the stress
hormones that flow through her blood stream are also flowing through her fetal
blood supply. Those stress hormones can have significant effects on fetal
development.

One effect that can happen is essentially a programming of the fetal stress response
to be more sensitive, leading to more anxious offspring both at baseline and
offspring that get especially stressed out by stressful events. This phenomenon has
been primarily studied in animals in order to try to separate effects of prenatal stress
from the effects of being raised by a mother that is more anxious. It’s hard to find a
situation where a woman was stressed during pregnancy but was then super calm
while raising her child. But you can more easily set up this situation with animals by
cross fostering off-spring: having the offspring be born by one mother but then raised
by a different, calmer female. Animal studies have shown that when pregnant
animals are significantly stressed during pregnancy, their offspring won’t explore as
much in novel environments, defecate more in new environments, avoid stimuli like
bright lights, and stay around the edges of an environment instead of venturing into
the middle. They also don’t learn as well in novel settings. These are all classic
indicators of anxious behaviour in animals, suggesting that prenatal stress exposure
leads to more anxious offspring.

Stress research on animals also allows us to examine the changes in the brain that
may happen due to prenatal stress exposure. In rats, when a pregnant female is
significantly stressed, her offspring tend to be born with more receptors for stress
hormones in their amygdala, which may help explain some of their increased anxiety-
like behaviour. If there are more receptors for stress hormones in the amygdala, then
it takes a smaller concentration of stress hormones to cause a larger amygdala
response to stressful stimuli.

Another interesting effect that can happen due to prenatal stress exposure highlights
the adaptive nature of our bodies. During gestation, the body of the fetus is learning
about the outside world through the information it gets from its mother’s blood
supply. It is learning what kind of world it will be born into. So things that happen to
that fetal body in the womb can lead that body to make changes during its
development that will determine how that body deals with the world after birth. For
example, is it going to be born into a world with a lot of resources for growth and

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development, so it doesn’t have to worry about hoarding the resources it does get its
hands on? Or perhaps is it being born into a world where resources are scarce, so it
better use the ones it has to the best of its ability? If you’ve seen the Hunger Games,
it would be like learning in the womb that you’re either being born into the Capital
(resource rich) or District 12 (resource poor). People behave very differently in those
two environments.

During the latter part of pregnancy, the fetal body learns about the amount of
nutrients it is receiving. If the pregnant mother isn’t getting enough nutrients, then
the fetus isn’t getting enough either. This can cause the fetus to develop what is
called a thrifty metabolism. Just like a thrifty person likes to hang on to their money,
a thrifty body likes to hang on to its nutrients. So basically, for the rest of their life,
that fetus will be especially good at storing nutrients.

What do you think this could put the child at risk for later in life? That child is now
already more at risk for obesity later in life, and the complications that tend to come
along with obesity, like adult-onset diabetes and cardiovascular disease. So before
the child has even started to eat on their own, and without really having experienced
any psychological stressors of their own, they are already at an increased risk of all
these things. These phenomena, when they were first described, were given the
name FOAD (Fetal Origins of Adult Disease).

This information helps us explain some of the differences in external factors related
to obesity risk that we explored in module 4. Two different people could both eat the
same amount and type of food, but if one person has a thrifty metabolism, their body
will be more efficient at storing those nutrients in the form of fat compared to
someone that doesn’t have a thrifty metabolism, where it might be easier for them
to burn those calories.

There’s a really interesting real-world case study that highlights this phenomenon of
thrifty metabolism that has to do with the Dutch famine that happened during WWII.
The Nazis had occupied some of the Netherlands during the war. During a particular
winter, the Nazis were being pushed back and the Allies were coming to liberate the
Dutch. The Nazi’s weren’t too pleased about this, so they cut off food transport to the
Dutch. 16,000-22,000 people starved to death that winter due to lack of resources.
There were pregnant women who survived this winter of starvation, but their fetuses
were not unharmed. Follow up research showed that many of the children of women
that were pregnant during the Dutch famine developed thrifty metabolisms and were
at higher risk for obesity and obesity-related diseases later in life.

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Now, if you think that is nuts that stress from lack of resources experienced
prenatally can have such a dramatic effect on the body’s development, it gets more
nuts. There are also generational effects of thrifty metabolism if it is severe in the
first generation, like it was with the Dutch famine cohort. A generational effect
means that the GRANDCHILDREN of the women that were pregnant during the Dutch
famine also had milder versions of thrifty metabolism! Here is how this phenomenon
works: You have this fetus that developed a thrifty metabolism due to lack of
resources during prenatal development. That child grows up and gets pregnant with a
child of their own. When her little fetus is growing away in her womb, the child of the
Dutch famine survivor (the pregnant person) is nice and healthy and has an adequate
supply of nutrients throughout her pregnancy. This is a much better scenario than
she had when she was a fetus. But wait, this pregnant person has a thrifty
metabolism. This means that her body hoards a large portion of those nutrients she
is getting during pregnancy for herself, in case that famine predicted when she was a
fetus ever materializes. This then means that not as many nutrients are getting to
HER fetus, which means the body of that fetus (the grandchild of the Dutch famine
survivor) will be programmed to expect a world with limited resources. That fetus will
then have a milder case of thrifty metabolism. This effect isn’t programmed by genes
directly but rather by the environment of the mother’s metabolism and circulatory
system. Crazy, right? There is evidence showing that grandchildren of Dutch famine
survivors were born with lower than expected birth weights because they weren’t
getting enough nutrients from their mother’s body because their mother’s body was
hoarding them.

I’ll talk about one more study highlighting the lasting effects of prenatal stress. This
study hits closer to home as it involves the Quebec ice storm from January 1998.
Women who were pregnant and living in Quebec during the ice storm were assessed
in June 1998 for both objective (i.e., how much the ice storm impacted them, like
how many days they were out of power, and whether they were able to access food
and water), and subjective (i.e., how stressed did they feel from those circumstances)
measures of stress. The researchers then followed the women for years to assess the
impact of that stress on their children that were in utero when the ice storm
happened. They assessed the children’s cognitive and language skills at two followups
points: when they were 2 and 5.5 years old. After controlling for maternal
personality, the researchers found that the greater the extent to which the mother
was exposed to stress from the ice storm according to objective measures, the
poorer the child’s cognitive and language development were at age two. At 5.5 years
old, these effects persisted. Children who were exposed in utero to a high level of
stress from the ice storm scored lower on IQ and language tests compared to children
who were exposed in utero to moderate or low levels of stress. So here we see that
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prenatal stress leads to not only changes at the biological level, like modifying
metabolism, but changes at the psychological level as well, like affecting cognition
and learning ability.

Now that we’ve touched on some prenatal stressors that can have lasting effects, I
want to touch on a couple post-natal stressors that can be experienced early in life
and also have long-lasting effects on one’s experience of and response to stress. The
first example I want to touch on is a study done of children that were living in
orphanages in Romania. If you’ve ever seen stories about these orphanages, they
were not great places. Babies were left in their cribs all alone all day except when
they needed to be fed or changed. There were no toys for them to play with and no
adults gave them any kind of affection or loving contact. So they spent some of their
earliest days in a very deprived environment, which can be incredibly stressful. The
graph on the slide shows the results of a study looking at children that were adopted
from Romanian orphanages into loving families. The results show that the longer the
children spent in the orphanage before being adopted, the higher their nighttime
resting cortisol levels. They had higher cortisol levels even when they were relaxed.
And these measurements were taken over a year after the children were adopted,
showing the lasting effects of that early environmental stress on these children’s
stress response. Their stress response was now basically overactive because they had
higher levels of stress hormones in their bodies even when they weren’t stressed.

This same kind of effect is seen in children that grow up in environments that aren’t
quite as stressful as the Romanian orphanages. There is a lot of research suggesting
that children that grow up in ‘risky families’, families that are high in conflict or
abuse and low in warmth and nurturance, develop problems with their
stressregulatory systems. They tend to have heightened sympathetic reactivity to
stressors and exaggerated cortisol responses. So we again see this pattern of early
life exposure to excessive stress resulting in a stress response that becomes more
sensitive and over-active. Because these children now have more sensitive stress
responses, and aren’t as able to regulate them (meaning that they have a stronger
stress response and it’s harder to turn it off), they are at a much higher risk for
stressrelated disease throughout their lives due to their early exposure to excessive
stress.

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 Individual Differences
in Stress Reactivity

LO2: What
theories and
models are
used to
study
stress?

 Stress Reactivity: Degree of change that occurs in autonomic,

neuroendocrine, and immune responses as a result of stress.
 Genetic, prenatal, early life, situational
 High vs. low reactivity can contribute to differential risk for stress-relat
disease ed

 Prenatal effects: Learn how stressful the world is

• High stress: Excessive glucocorticoid secretion
• Fewer glucocorticoid receptors in the hippocampus
• Elevated basal levels, larger stress-response, sluggish recovery

On the previous slide, I described some ways that early stress exposure can lead to
changes in how the stress response functions. Namely, typically making it more
sensitive. Now I’m going to delve a little deeper into the suspected mechanisms for
how this change actually happens.

When we talk about stress reactivity, we’re talking about the changes that happen in
the body in response to stress. Those changes are all the physical things we’ve talked
about in earlier videos, such as the activation of the sympathetic nervous system and
the release of a variety of stress-related neurotransmitters and hormones, like
adrenaline and cortisol. We know these changes happen to mobilize our bodies to
deal with whatever the stressful emergency is.

When we talk about differences in stress reactivity, or differences in how the stress
response functions, that just means that there’s a difference in how strong this
physical reaction to stress is in different people. Some people show very small
responses to stressful circumstances, whereas others show large responses. There
are a variety of reasons for these differences. Some of the difference can be
attributed to genetics. Our genes contribute a lot of the variability in terms of the way

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our bodies and brains develop. Other reasons are environmental, related to things
like prenatal and early life exposure to stress that I talked about on the previous slide.
Other environmental factors can include things that happen later in life, like exposure
to traumatic levels of stress, which we’ll talk about more on the next slide.

And then there are also some more subtle factors that can affect the strength of our
stress response at any given time. For example, some subtle situational factors, like
what you’ve recently eaten, can impact how strongly your body reacts to a stressor.
Your text describes research suggesting that in healthy young adults, those who ate a
high-fat meal rather than a low-fat meal showed greater cardiovascular reactivity in
response to a stressor. Findings like these again highlight the interconnectedness of
all our body systems. Something that happens in your digestive system can influence
your stress response system, and we know the stress response system can influence
the digestive system.

So, there are many factors that can contribute to variability in stress reactivity of the
body. And then those feelings in the body can contribute to how stressful we
subjectively rate certain stressors to be. Here we also have a two-way street between
the mind and the body. Our mind can cause a stress response in our body, but then
often we look to our body to determine how we feel about something. If our body is
having a strong stress reaction, that must mean this event is pretty bad, right? So that
can cause our mind to interpret that maybe this event is even worse than we
originally thought. This is what I often call the spiral of stress. First we start by getting
psychologically stressed out, then our body has a response, then we recognize that
response in our body as a response to danger, and essentially get even more stressed
out by our body’s own stress response. And as I mentioned earlier in this video,
having a stronger physical stress response can put someone at a higher risk for
stressrelated disease because it puts more wear and tear on the body each time you
have a stress response.

Ok, now let’s get into that mechanism that I mentioned earlier. In addition to learning
about whether there is food available in the world, like I talked about with thrifty
metabolism on the previous slide, the developing fetus is also learning about how
stressful the world is. How can they do this without yet being independently present
in the world? They do it through the information they get from their mother’s
circulatory system, because stress hormones like cortisol readily pass from the
mother to the fetus. If there are a lot of stress hormones entering the fetus’
circulatory system, then the fetus learns that it is indeed a stressful world out there.
(Not in a sentient – “man it’s going to suck being born into this place” kind of way,
but in a physical “body being prepared to always have a lot of stress hormones
flowing through it” kind of way.) To prepare for that world, the fetus’ body is then

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programmed to secrete a lot of stress hormones. This can happen in a few different
ways.

Research suggests that when a fetus is exposed to high levels of stress hormones in
utero, there is a permanent decrease in the number of glucocorticoid stress
hormone receptors in the developing brain, specifically in the hippocampus. This is
similar to the idea we talked about with dopamine receptors down regulating if a
person eats too much sugar that causes too much dopamine to be released. Now,
you might ask, why would having fewer receptors for stress hormones lead to more
stress hormones in the body? When glucocorticoids bind to these receptors in the
hippocampus, they tell the brain there are enough glucocorticoids in the system. This
is our negative feedback loop to turn off our stress response when we no longer
need it. So when the system functions normally, stress hormones build up to a
certain level, then when enough stress hormones bind to receptors in the
hippocampus, negative feedback is initiated and a signal is sent to the hypothalamus
to STOP releasing CRH to stop the hormonal stress response of the HPA axis. But, if
there aren’t that many receptors in the hippocampus, then you need an increased
concentration of glucocorticoids in your system before enough of those receptors
become bound to tell the CRH signal to stop… So now the fetus’s brain is essentially
less sensitive to glucocorticoids, so it needs more of them in its system before the
negative feedback cycle is initiated.

This impairment of negative feedback leads to some detrimental consequences.

Much of this research comes from rat studies. The general findings show that
mothers stressed out during pregnancy have offspring that have elevated stress
hormone levels at baseline (similar to the children that lived in the Romanian
orphanages that I talked about on the last slide), they have larger stress responses to
stressful stimuli (so they have higher stress reactivity), and it takes them longer to
shut off their stress response when it is no longer needed. All of these effects
contribute to more stress hormones present in the body all the time, and a higher
risk for ultimately developing diseases related to high stress, like cardiovascular
disease.

Further support for these ideas comes from rat studies in which they injected
pregnant female rats with glucocorticoids instead of actually stressing them out. They
find these same effects in the offspring, which lends weight to the idea that these
effects are brought about by increased levels of glucocorticoids circulating in the
pregnant mother’s bloodstream.

I hope explaining this mechanism helps you connect some of the dots between
prenatal exposure to stress and how that exposure can alter the stress response

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system for the rest of that organism’s life, thus increasing their risk for stress-related
diseases before they ever even encounter any stressors.

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 PTSD and the Hippocampus

LO5: What
are the
Post-Traumatic Stress Disorder (PTSD)
sources of Anxiety disorder associated with serious traumatic events. Symptoms
chronic
stress? can include recurrent thoughts and images of the trauma.
PTSD fromrepeated trauma= smallerhippocampi

Now that we’ve covered a variety of ways that early life exposure can alter our stress
response, I want to touch on a way that exposure to stress later in life can also alter
our stress response. In this case, we’re going to focus on traumatic exposure to
stress.

I’m sure you’ve all covered PTSD in a variety of Psychology courses. It’s also touched
on in Intro Psych. As a brief recap, PTSD is an anxiety disorder associated with serious
traumatic events. One doesn’t have to have experienced the event themselves to
develop PTSD, but they could know someone or in some other way have been
affected by the event, such as people living in New York when 9/11 happened even if
they weren’t anywhere close to the World Trade Centre.

I’ve included on this slide some of the types of traumatic exposure to stress that can
lead to the development of PTSD. You see that some people can be exposed to
traumatic stress through their job, something they had some choice over, such as
police, firefighters, or people in the military, and other people are exposed to
traumatic stressors through no choice of their own, such as people that have been
assaulted or suffered abuse in various forms. PTSD undoubtedly causes great
suffering in people. It’s essentially a stress that stays with them long after the actual
stressful event is over, continually activating their stress response, which we know is
harmful to health.

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I’m going to focus on a pretty specific negative health outcome related to PTSD that
connects back to the mechanism we talked about on the previous slide. Research has
shown that people that suffer from PTSD generally have a smaller volume of the
hippocampus compared to control individuals matched for things like gender, age,
and size, that do not suffer from PTSD. You can see this result in the graph on the
slide. While the hippocampi in both hemispheres appear to be smaller in people with
PTSD, the right hemisphere appears to be particularly affected. (There is evidence on
lateralization of brain function that suggests that the right hemisphere is particularly
involved in negative emotional responses.) This volume loss does not extend to the
rest of the brain but rather appears to be specific to just the hippocampus. Other
evidence suggests that if the PTSD is a result of repeated traumatic stress exposure,
the volume of the hippocampus is even smaller. Researchers have taken these
finding to suggest that the experience of constant stress as a result of severe and
chronic PTSD may ultimately damage the hippocampus, making it smaller.

This idea relates to the mechanism for control of the stress response that we talked
about on the previous slide. So there is the possibility that perhaps traumatic stress
exposure may damage the hippocampus, and because the hippocampus is such an
important area for regulation of the stress response, maybe that helps to explain why
PTSD is essentially a dysregulation of the stress response, with the stress response
now hypersensitive to a variety of stimuli related to the initial trauma.

Now, going back to our PTSD occurrence graph, an important thing to notice from
this graph is that not everyone that experiences traumatic stress will develop PTSD.
Even people that have experienced the same event, such as firefighters that
responded to the same traumatic event, or people in the military that were in the
same active combat, will not necessarily all develop PTSD, or develop it to the same
degree. So an important question is what makes some people more susceptible to
developing PTSD from traumatic stress exposure?

Well, perhaps there is another way to interpret the findings of smaller hippocampi
and PTSD. Maybe the hippocampus actually plays a role in determining who is at risk
for developing PTSD. Specifically, it is possible that having a smaller hippocampus in
the first place may be a risk factor for developing a severe case of PTSD following
the experience of a traumatic event. Some people may be born with a smaller
hippocampus, which could interfere with their ability to recover from a traumatic
experience through disrupted feedback of their stress response system, thus putting
them at risk for developing PTSD.

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To examine this idea, one study looked at monozygotic (identical) twins where one
twin had been exposed to a traumatic event (combat) and the other had not. Since
the twins share the same genes, studying them can tell us about the influence of
genetics on the development of certain conditions. For example, in this case, if the
person who developed PTSD has a smaller-than-average hippocampus, and also has a
non-trauma exposed twin who has a smaller-than-average hippocampus, it would
suggest that a smaller hippocampus may be a sign of a genetic vulnerability for the
development of PTSD following a traumatic experience. In fact, this is exactly what
the researchers found. Twins in the study with severe PTSD had a smaller
hippocampus than people without PTSD, and they also had a non-trauma exposed
twin with a smaller than typical hippocampus. Consequently, a smaller hippocampus
may be a risk factor for developing PTSD after a traumatic experience.

But further, it seems that the effect may actually go both ways, because the
traumaexposed twins also tended to have a smaller hippocampus than their non-
trauma exposed twin, suggesting that the trauma, and the associated stress from the
trauma, contributed to additional shrinkage of the hippocampus.

So, we have now seen evidence that excess exposure to stress at any point in life can
have lasting effects on our stress response system, then impacting how we respond
to future stressors, and ultimately impacting our risk for stress-related disease.

This brings me to the end of my video content for module 6. As always, I encourage
you to check out the videos done by your peers for this module to learn more about
those topics.

Now, I never like to leave off just having talked about stress, because it can be pretty
distressing to know that stress has such a dramatic effect on our bodies and that
severe stress exposure can actually impact how we respond to future stressors. But,
in our next module, we will address these topics and what we can do to help combat
the effects that stress has on our bodies and minds when we talk about ways to
moderate our stress experience, or basically, ways to cope with stress. I really look
forward to seeing you there! For now, I have included some resources at the end of
this transcript that you can access if you are finding yourself suffering from a lot of
stress. Please know that you don’t have to suffer alone and there are supports out
there for you. We are all dealing with a lot more stressors on our plates in the crazy
times we’re currently living through. Please do reach out for help and support if you
are struggling. I’ll see you back here for module 7, where I hope you will learn some
useful strategies for helping to manage your stress both in the moment and in the
longer term. Take care of yourselves. Bye for now.

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If you find yourself experiencing stress, MacEwan University offers services to help
manage and cope with stress and anxiety.

Wellness and Psychological Services

Telephone and video counselling options are available: 780-497-
5063 | WPS@macewan.ca
7-103A, City Centre Campus, 10700 – 104 Avenue
Business hours
Monday - Friday
8:30am – 4:30pm

Peer Support
If you need a safe and confidential space to discuss life’s stresses and tough
situations, they have trained listeners waiting to meet with you. Their
online chat service is available Monday to Friday from 9am to 5pm. Phone:
780-497-4776 peersupport@samu.ca

Distress Line
The distress line is available to provide confidential, non-judgmental and shortterm
crisis intervention, emotional support, and resources to people in crisis or distress.
Dial 780-482-4357 to be connected to a listener.