Psychosomatic Medicine
71, no. 2 (February 2009), 243–50. For more on the relationship
between ACE Scores and disease, see
http://www.cdc.gov/ace/outcomes.htm
(accessed February 20,
2015).
The more categories of Adverse Childhood Experiences:
M. Dong, W. H. Giles, V. J. Felitti, et al.,
“Insights into Causal Pathways for Ischemic Heart Disease: Adverse Childhood Experiences Study,”
Circulation
110, no. 13 (September 28, 2004), 1761–66.
In other words, when a child is young and his brain:
I’ve based this description of Michael Meaney’s
gene methylation theory on that provided in an article by Paul Tough, “The Poverty Clinic,”
The New
Yorker
(March 21, 2011), 25–30. For more on how childhood adversity is associated with epigenetic
alterations in the promoters of several genes in hippocampal neurons, see B. Labonté, M. Suderman,
G. Maussion, et al., “Genome-Wide Epigenetic Regulation by Early Life Trauma,”
Archives of
General Psychiatry
69, no. 7 (July 2012), 722–31.
Kaufman found significant differences in epigenetic markers:
N. Weder. H. Zhang, K. Jensen, et al.,
“Child Abuse, Depression, and Methylation in Genes Involved with Stress, Neural Plasticity, and
Brain Circuitry,”
Journal of the American Academy of Child and Adolescent Psychiatry
53, no. 4
(April 2014), 417–24.e5.
Seth Pollak, PhD, professor of psychology and director:
S. E. Romens, J. McDonald, J. Svaren, et
al., “Associations Between Early Life Stress and Gene Methylation in Children,”
Child Development
(July 24, 2014). You can read more about Seth Pollak’s recent work in the web article “Abuse Casts
a
Long
Shadow
by
Changing
Children’s
Genes,”
by
Eleanor
Nelsen,
http://www.pbs.org/wgbh/nova/next/body/epigenetics-abuse
(accessed February 15, 2015). Prior to
Seth Pollak’s work, Moshe Szyf and Michael Meaney at McGill University found in 2005 that rat
pups raised by abusive mothers demonstrated epigenetic changes. M. J. Meaney and M. Szyf,
“Environmental Programming of Stress Responses Through DNA Methylation: Life at the Interface
Between a Dynamic Environment and a Fixed Genome,”
Dialogues
,
Clinical Neuroscience
7, no. 2
(2005), 103–23.
“A crucial set of brakes are off”:
According to Seth Pollak, PhD, it is important to note that in
human epigenetic studies, “We can’t really know for sure that what we have observed in children
reflects this problem in the stress response system. Nonhuman animal studies measure the gene right
from the brain (using the animal brain tissue). We can’t do that with children, of course, so we take
the genes from blood. But blood is far away from the brain. If the gene we find in the blood is
working the same as the gene in the brain, then we know our theory is true. However, if the gene
functions differently in the blood than in the brain, we can’t say the brake on the stress response
system is broken. But we can say that the stress response system will affect the child’s immune
system. This means that stress-exposed children will be less able to fight off pathogens and will be
more susceptible to illness. In fact, we have found this to be the case.” For more on this, see E. A.
Shirtcliff, C. L. Coe, and S. D. Pollak, “Early Childhood Stress Is Associated with Elevated Antibody
Levels to Herpes Simplex Virus Type 1,”
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