Professional Documents
Culture Documents
( )
, 2014
26/01 03/02 3.2
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. 10
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STRESS
STRESS
Eustress
Distress
Positiv
e
Reaction to
Stress
Negative
Very
Low
Stress
Level
Very
High
BURN
OUT
()
(Distress)
EUSTRESS
( )
H
STRESS
Appraisal
Stressor
Stress
Coping
Outcome
EKKIN
Miller, A., Maletic, V. & Raison, C.L. (2009). Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Biological Psychiatry, 65, 732-741.
STRESS
STRESS
GRAY
BLUE .
KAI -
STRESS: work
related stress,
including role
conflict &
burnout
Summary:
Scientists have shown that anger, anxiety, and depression not only affect the functioning of the heart,
but also increase the risk for heart disease. Stroke and heart attacks are the end products of
progressive damage to blood vessels supplying the heart and brain, a process called atherosclerosis.
Atherosclerosis progresses when there are high levels of chemicals in the body called proinflammatory cytokines. It is thought that persisting stress increases the risk for atherosclerosis and
cardiovascular disease by evoking negative emotions that, in turn, raise the levels of proinflammatory chemicals in the body.
Atherosclerosis progresses when there are high levels of chemicals in the body called proinflammatory cytokines.
It is thought that persisting stress increases the risk for atherosclerosis and cardiovascular disease by
evoking negative emotions that, in turn, raise the levels of pro-inflammatory chemicals in the body.
Researchers have now investigated the underlying neural circuitry of this process, and report their
findings in the current issue ofBiological Psychiatry.
"Drawing upon the observation that many of the same brain areas involved in emotion are also
involved in sensing and regulating levels of inflammation in the body, we hypothesized that brain
activity linked to negative emotions -- specifically efforts to regulate negative emotions -- would
relate to physical signs of risk for heart disease," explained Dr. Peter Gianaros, Associate Professor at
the University of Pittsburgh and first author on the study.
Summary
In preclinical studies, the combination of chronic stress and a high sugar/fat diet is a
more potent driver of visceral adiposity than diet alone, a process mediated by
peripheral neuropeptide Y (NPY).
Methods
In a human model of chronic stress, we investigated whether thesynergistic
combinationof highly palatable foods (HPF; high sugar/fat) and stress was associated
with elevated metabolic risk. Using a case-control design, we compared 33 postmenopausal caregivers (the chronic stress group) to 28 age-matched low-stress
control women on reported HPF consumption (modified Block Food Frequency
Questionnaire), waistline circumference, truncal fat ultrasound, and insulin sensitivity
using a 3-h oral glucose tolerance test. A fasting blood draw was assayed for plasma
NPY and oxidative stress markers (8-hydroxyguanosine and F2-Isoprostanes).
Results
Among chronically stressed women only, greater HPF consumption was associated
with greater abdominal adiposity, oxidative stress, and insulin resistance at baseline
(allp's.01). Furthermore, plasma NPY was significantly elevated in chronically
stressed women (p<.01), and the association of HPF with abdominal adiposity was
stronger among women with high versus low NPY. There were no significant
predictions of change over 1-year, likely due to high stability (little change) in the
primary outcomes over this period.
Discussion
Chronic stress is associated with enhanced vulnerability to diet-related metabolic risk
(abdominal adiposity, insulin resistance, and oxidative stress). Stress-induced
peripheral NPY may play a mechanistic role.
STRESS,
:
50
Thompson, R. A., & Nelson, C. A. (2001). Developmental science and the media: Early
brain development. American Psychologist, 56(1), 5-15.
, S
Indulgent lifestyle
Energy imbalance
Stress
Aging
Epigenetics
CH3
CH3CH3
Previous
generations
experiences
behavior, Genotype
nutrition
Oscillatory,
circadian, seasonal
rhythms perturbation
Metabolic,
neuronal
malprogrammin
g
Mitochondrial
dysfunction
Chromosome/
DNA
damage/telom
eres
STRESS
.D
etS
TY A
Stressed, hurried,
angry, hostile,
organized, on time.
Body produces an
extra amount of stress
hormones.
Take the positive
qualities and reduce
anger and hostility.
T B
Procrastinate, weight
gain, creative, laid
back, no worries.
Take the good and
reduce putting off
responsibilities.
48
(hostility),
(anger) (cynicism)
.
,
.
, Suarez Richards
LDL-
,
.
,
,
T D
Distressed
personality with
negative emotions.
Tends to be
depressed, anxious,
and insecure.
Exercise, relaxation
and a healthy diet
can help.
Produce a large amount
of harmful
catecholamines when
stressed that damage
the heart and increase
risk for sudden heart
attack.
Faulty perceptions of
stressor perceive
nearly every stressor as
life and death.
Could be any personality
type.
Reframing, thought
stopping, and relaxation
are important.
51
1 -
.
2
.
PTSD
PTSD
-
< 10%
AFFECTIVE DISORDERS
1.02.2015
STRESS
( :
80% IGs..)
ANO ..
STRESS
HRV
STRESS
VitruvianMan
LeonardoDaVinci
O,
DNA repair
Immune competence
Neurologic acuity
Neuromuscular activity
Better memory
Resistance/ adaptation
to stress
1. Relax neck and shoulders
2. Take a stretch
3. Get a massage
4. Exercise
5. Count to 10
6. Control your thoughts
7. Fantasize
8. Congratulate yourself
9. Ignore the problem if appropriate, after evaluation
10. Perform self maintenance
11. Talk to a counselor
12. Meditate
13. Pray
14. Remember your purpose
-
15. Take a break
16. Try progressive relaxation
17. Try yoga
18. Try aroma therapy
19. Laugh
20. Prioritize daily tasks
21. Learn something
22. Practice a hobby
.
.
?
Newsweek
March 26, 2007
STRESS
STRESS ,
EIA
DISTRESS
.
.