It is well known that adults with psychological problems
and dementia often have a history of childhood psychological trauma. Some of
these individuals exhibit very real, physical alterations in a part of the
brain called the orbitofrontal cortex. Yet a direct link between such early
trauma and neurological changes has been difficult to find so far.
Research on Alzheimer’s disease has taught us that the
disease is complex. There is little overall understanding of how Alzheimer’s
disease starts and then develops. Despite this lack of understanding, once we
observe the decline in cognitive capacity there seems to be a fast and
unrelenting pattern of diminished capacity in the patient. The symptoms are
real regardless of our lack of knowledge of its causes and development. Very
slowly we are moving away from the shock and awe of the disease to looking at patterns
and associations.
Although there is closer correlation of Alzheimer’s
disease among twins that share the same genetic makeup—monozygotic/identical in
contrast to dizygotic twins—there is nevertheless still a difference among
identical twins. This variance indicates that non-genetic factors are playing a
role in the expression of Alzheimer’s disease. Aging by itself is associated
with epigenetic influences, with younger twins being more epigenetically
similar than older twins. Such non-genetic factors might also explain why women
are more prone to Alzheimer’s disease then men suggesting an important role for
external factors.
The interconnections that are being made today across
diseases—e.g. amyloidosis—and the connection between genes and geography—e.g.
epigenetics—all point towards the need for a unified theory of Alzheimer’s
disease. There are emerging attempts to do this through a public health
approach. But this needs to be broadened further and some of the processes
involved in promoting the disease need to be further elucidated. The main theme emerging from the periphery of
research is a renewed interest in the importance of emotions in the maintenance
of diseases. Although the main reason for this interest might be the
observation that emotions have biological repercussions, nevertheless this
points to a pivotal change in perception of how we view diseases. We are
looking at diseases as involving broader facets—e.g. emotions—as well as longer
periods—e.g. development.
The “Barker Hypothesis” complements this view, that early
childhood trauma--initial focusing on low birth weight—starts a cascade of
negative events that are only expressed in adulthood or late adulthood. The
realization that chronic diseases, including Alzheimer’s disease, have
developmental origins, has started to attract a life-course approach. Diane
Miller and James O'Callaghan with the CDC-National Institute for Occupational
Safety and Health explored this hypothesis for Alzheimer’s disease identifying
certain childhood conditions that can contribute to Alzheimer’s disease. Some
researchers are also examining specific mechanisms for this chronic disease
process. Debomoy K. Lahiri with Indiana University School of Medicine and his
colleagues have proposed an epigenetic model of chronic disease. In this model,
environmental agents (e.g., heavy metals), intrinsic factors (e.g.,
inflammatory cytokines), and dietary factors (e.g., folate and cholesterol)
could alter gene expression through epigenetic influences. These changes that
occur during childhood will not be expressed until significantly later in life.
There are other factors that change epigenetics. Adverse
childhood experiences—economic hardship, sexual and physical abuse, divorce,
homelessness, hunger—initiate a cascade of risk behaviors that are associated
with enduring changes in the body and brain—nervous, endocrine, and immune
systems. And adverse childhood experiences are common, with rates between 5–35%
for physical abuse, 4–9% for severe emotional abuse,15–30% for sexual abuse in
girls and 5–15% in boys, and 6–12% for neglect.
In a 1997 study of over a thousand Californian elderly community
residents the Australian epidemiologist John Lynch with Adelaide University and
his colleagues found that self-reported cognitive function was lower than
expected for those who had experienced sustained economic hardship, even after
adjusting for age, sex, and co-morbidity. Poverty, larger family size and urban
residence are also associated with increased Alzheimer’s disease risk.
Conservative estimates suggest that every year in the
United States more than 1 million children are exposed to sexual or physical
abuse or severe neglect. Unfortunately, this is only the tip of the iceberg.
Emotional abuse is by definition comorbid with sexual and physical abuse and
may occur alone at even higher rates.
Developmental considerations are important since the
brain is an evolving structure and is more vulnerable at certain times than
others. In brain development for example, we start to see grey matter loss at
age seven which continues throughout older age.
In contrast, glial cells in the white matter increase until
approximately the mid-40 and peaking at around age 50. Emotional trauma at
these vulnerable stages have been shown to have long term effects on the
developing brain. There is some support for this view from studies that report
that people who engage in mentally stimulating activities at both younger and
older ages are less likely to develop Alzheimer's disease.
These epigenetic changes can also be transmitted to the
next generation. Some adverse childhood events continue to have a negative
effect on later-life cognitive performance on some people. In contrast there
are others who seem resilient to this negative effect. Such variance underlie
the necessity to consider events individually and not as global test scores. We
are still a long way from undertaking experiments that exposes the true nature
of Alzheimer’s disease, but at least we are starting to define the horizon. A
horizon outside of the research cul de sac that has been defined by the federal
government’s Alzheimer’s disease research guidelines.
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