prevents LDL from binding with receptors on the surface of cells.
As a result, fewer LDLs are removed from the blood, and cholesterol carried by LDL is at a much higher level than normal. This
promotes atherosclerosis. Other APOB gene variations cause too
low a level of LDL in the blood, reducing the amount of cholesterol
below the level needed for normal growth and development. Cholesterol is, as noted, necessary for human life. Studies have shown
that there are other genes (LDLR, APOE, and PCSK9) that play a
critical role in LDL synthesis or transportation, affecting not only
LDL levels but also the risk of coronary heart disease and mortality.
Knowledge Is power
While it appears that we know exactly how bodily functions work,
the truth is that the human body is a complex organism. What we
currently know about disease-gene links is, in many cases, merely
probabilistic. How a gene actually functions to cause, stop, or control disease often is unknown—and the study of the link between
disease and genes is more statistical than medical. These relationships are useful primarily in creating probabilistic relationships
between the presence of certain alleles, either alone or in combination with others, and the likelihood that disease will develop.
Since virtually every human condition (other than, perhaps, in-
jury) has, in addition to diet, lifestyle, and environmental exposure,
a basis in our genes, knowing the good and bad genetic links for
conditions such as coronary heart disease would be helpful both in
medicine and in insurance rating. Timely discovery of any disease
that develops without early symptoms allows for treatment that
could prevent or moderate future adverse outcomes. Knowledge
of genes that either encourage or discourage the development of
coronary heart disease and other conditions clearly would be use-
ful in better underwriting and classification of risk.
tom BAKos, a fellow of the Society of Actuaries and a member
of the Academy, is a consulting actuary with Tom bakos Consulting
Inc., and can be reached at tbakos@bakosenterprises.com.
cHiAnG-cHinG HuAnG is an assistant professor of
preventive medicine and genetic medicine at northwestern
University in Chicago, and can be reached at huangcc@
northwestern.edu.
mArc KLiBAnow is chief executive officer of Genowledge
LLC, a genomics and biostatistics concern, and can be reached at
marc@genowledge.org.
This article is solely the opinion of its authors. It does not express the official
policy of the American Academy of Actuaries; nor does it necessarily reflect
the opinions of the Academy’s individual officers, members, or staff.
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CAS 2011
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