posted July 14, 2000 01:52 AM            

We *civilized* people have the resources, $, (and cameras) to document these problems.
And we individually can sometimes spare the time to look in our family photo albums to see that our immediate relatives and/or neighbors often had these problems like us.

And typically we blame our "genetics".

However we must also have the same DNA as our ancestors. That's how it goes. People who had to get along without liposuction etc. Built log cabins without chainsaws, and pyramids without electricity. Yet we moderns develop a wide range of ills that would hardly seem to serve us well should anybody revisit the pleistocene.

Were our ancestors a bunch of degenerates as well? -just put-up with their defects seeing as nothing could be done to help anyhow? Was half of the population always unable to see properly, chew properly, and the rest? Can anybody prove they weren't?

What's up with this? Such large fractions of the current general population suffer from multiple afflictions, yet seldom has anybody conclusively pointed to any specific set of gene mutations responsible for the particulars. For example: what's responsible for myopia, why do so many adults find they still have little room for wisdom teeth?

Is it because we are not looking hard enough for such mutations? Is it that our current environment prevents the proper expression of existing genes which otherwise would work just fine? Or at least function much better under different conditions than they appear to do for many of us just now?

For example: too little folic acid during pregnancy can render people susceptible to spinal bifida. Leading to a conclusion that if mother's diet were *better*, the child would not be born disabled. And a next child born might just be fine too. Or wearing tight shoes might give some of us bunions that otherwise wouldn't have grown. Whatever. How do we explain the 'biggies' if we don't wish to think our DNA is or has been corrupted somehow? How much should we blame on table sugar (Black Death)? How 'plastic' is our gene expression?

posted July 14, 2000 12:55 PM            

Good rant! Kinda along the same lines as how i've been thinking. Americans are just plain lazy! Don't even get me started on my soapbox-talk about this! It's pathetic how we are so spoiled to not have to do anything the hard way anymore. No wonder the obesity rate is so damn high and health problems run amok. It's ridiculous...

posted July 14, 2000 01:26 PM            

I had wisdom teeth pulled at 16 to "make room", I got contacts at 19 (ironically after I started working with computers) because of poor eyesight...oh and adenoids removed at 8 or so...because I couldn't breathe properly...tubes were put briefly in my ears during this time because my ears were not draining properly....

Now my mom has poor eyesight and also had her wisdom teeth pulled...is that genetics or just the "fix of the day"? I don't know.

I think acne, overfat, weakness are a definite product of our civilization today...its been said before, we drive everywhere, have inactive jobs, stare at the computer all day or the tv...we use power tools to build (or better yet hire a contractor), we eat foods with dyes, preservatives and chemicals we can't even pronounce, we are barraged with "go faster, do more, spend more, eat more" and "unwind, relax, take this pill, drink this drink" messages that are supposed to make our lives better. Hence the need for acne meds, lipo, even "new" diagnosis such as ADD (what a crock THAT is)

I think our 'ancestors' - if they had these similar problems - didn't concern themselves with anything beyond survival. You had to work, and work hard in those days...

I don't really have a point...its just thoughts.

------------------
Patience is a bitter plant, but it has sweet fruit.

posted July 15, 2000 01:29 AM            

The flip side of this is that many of these problems can be prevented with lifestyle modifications. From a genetic point of view we still think of these 'defects' as an increased tendency to develop a certain disease, not a certainty. This is the area where epidemiologists and geneticists are working together to figure out what's the genetic component, and what's the environmental. I will venture to say most of the unsolved genetic diseases are in this category. They consist of lots of different genes working together with lots of different environmental stuff to cause or protect against a certain disease. In spite of all the Hoopla surrounding the Human Genome Project, these diseases may take another few decades to unravel the causes and preventative treatments.

posted July 16, 2000 10:58 AM            

How come Animals never get heart attacks?

How can animals never brush their teeth and live many, many years without loosing one tooth?

To me, the single biggest factor in any persons life is diet.

LAte

posted July 16, 2000 05:10 PM            

Pardoning the genome
(posted July 14, 2000)

posted July 16, 2000 07:14 PM            

There's a lot of attention being focused on genetics right now with Genome in the spotlight. But, I am curious about the study of embryology as an answer to diseases - especially cancer. Those seem to be the only two times when cells multiply so rapidly - birth and cancer. This stem cell stuff has really got my interest, but apparently there morality issues that get in the way. There doesn't seem to be much interest or money put into this area, but I think answers could lie here, too.

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{{-}}

posted July 16, 2000 08:03 PM            

Cancer -- Nature, Nurture, or Both

The relative roles of genetic constitution and environmental exposure in the causation of cancer have been debated
for decades. (1) Geographic differences, trends over time in the risk of cancer, and detailed studies of migrant
populations overwhelmingly implicate environmental exposures as major causal factors and often identify the
responsible carcinogens (e.g., tobacco, alcohol, radiation, occupational toxins, infections, diet, drugs). From this
work has come the widely accepted estimate that 80 to 90 percent of human cancer is due to environmental
factors. (2) Yet in the past 15 years, the explosion of molecular genetics has overshadowed environmental
explanations by revealing genetic mechanisms underlying cancer. This is why the current confusion about
environmental and genetic risk factors for cancer -- on the part of patients, their families, clinicians, researchers,
public policy makers, and the general public -- is not surprising.

The gold standard for distinguishing genetic from environmental traits has been the study of twins. Comparing the
incidence of disease in unrelated people, fraternal twins, and identical twins allows the heritable and environmental
components of risk to be estimated. The study described by Lichtenstein and his colleagues in this issue of the
Journal (3) has several advantages over previous studies of cancer in twins. It is population-based, the outcomes
are derived from complete data on incidence, and the size of the population studied is four times as great as in any
previous effort.

Although the current study has many strengths, its weaknesses illustrate the difficulties of using data on twins in
studies of cancer. The study included more than 10,000 cancers in a total population of nearly 90,000 twins in
Scandinavia, but the data effectively address cancer at only the four or five most common anatomical sites -- and
even for some of these, without much precision. The confidence intervals for the heritable proportion of
susceptibility to stomach, colorectal, breast, and lung cancer all extend roughly from 5 percent to 50 percent, a
fairly large range. The study lacks information on screening practices, which is quite possibly an issue in studies of
twins. It also lacks data on specific types of exposure (e.g., tobacco use), so issues of interactions between genes
and environment cannot be addressed. Indeed, the statistical model used specifically assumes no such interactions,
ensuring that if any do exist, they will probably show up partly in the estimated environmental component of risk
and partly in the heritable component. These practical limitations are inherent in studies of cancer in twins, and
they indicate that delineation of the specific environmental and genetic components of the risk of cancer is likely to
depend on the emerging new generation of large molecular epidemiologic studies -- both population-based and
family-based -- rather than on studies of twins.

Despite its limitations, the study by Lichtenstein et al. provides new and valuable information for the
nature-versus-nurture debate. In general, environmental factors were the dominant determinants of the
site-specific risk of cancer. For cancer at four of the five common anatomical sites, estimates of the proportion of
risk due to environmental effects were all 65 percent or greater. Though considerably less precise, estimates of the
proportion of susceptibility that was due to environmental factors were generally even higher for cancer at the six
next most frequent sites studied. These findings are consistent with the conclusions of studies of migrant groups.
For example, rates of breast cancer among women who have recently immigrated to the United States from rural
Asia are similar to those in their homelands and about 80 percent lower than the rates among third-generation
Asian-American women, who have rates similar to or higher than those among white women in the United States.
(4) This pattern is entirely consistent with the estimates by Lichtenstein et al. in this study that 73 percent of the
causation of breast cancer is environmental and 27 percent heritable, particularly if a portion of the effect of
heritable factors relates to genetic modification of environmental risk factors.

Although environmental effects may predominate, the findings with regard to heritability are noteworthy. Rates of
concordance were generally higher in monozygotic pairs of twins than in dizygotic pairs, and the estimates of the
proportion of susceptibility to cancer that was due to heritable effects ranged from 26 percent to 42 percent for
cancer at the five common sites. These are substantial burdens of cancer risk, and substantially higher than
estimates of risk based on a family history of a particular cancer. This degree of influence is also what would be
expected if genetic effects are not limited to the rare, highly penetrant mutations that can result in familial cancer,
but are also the result of polymorphisms that carry a much lower level of risk, do not result in an excess of cancer
in families, and are much more prevalent than highly penetrant mutations in the general population. The most
noteworthy effect of heritable factors is clearly that identified for prostate cancer (42 percent of risk). Like the
other common cancers, prostate cancer shows marked international variation, and the risk among migrant groups
tends to rise toward the level in the adopted country over several generations, indicating a substantial
environmental component of the risk of this cancer. (5) Nonetheless, a number of large-scale studies have
searched for risk factors for prostate cancer and have found few. This lack of evidence stands in stark contrast to
the situation with respect to breast, lung, and stomach cancer, for example, for which such studies have identified
a variety of lifestyle-related, infectious, reproductive, and other environmental factors that are associated with
moderate-to-high levels of risk. Perhaps prostate cancer does have a greater heritable component than cancer at
these other sites. If some of the inherited factors are involved in modifying the risk associated with environmental
factors, then success in identifying these two kinds of influences may depend on direct exploration of interactions
between genes and environment.

The estimates of absolute concordance are telling. For cancer at the common sites in monozygotic twins, the rate
of concordance is generally less than 15 percent. Thus, the fatalism of the general public about the inevitability of
genetic effects should be easily dispelled. There is a low absolute probability that a cancer will develop in a person
whose identical twin -- a person with an identical genome and many similar exposures -- has the same type of
cancer. This should also be instructive to some scientists and others interested in individual risk assessment who
believe that, with enough information, it will be possible to predict accurately who will contract a disease and who
will not. With a few rare exceptions, any such deterministic approach to a disease as multifactorial as cancer
seems doomed, and the data on twins seem to confirm that. This lack of absolute predictability, too, should not be
surprising, given what we know about the risk of second primary cancers in paired organs. (6) For example, a
woman's average annual risk of a contralateral breast cancer after the diagnosis of a first primary breast cancer is
about 0.8 percent (7,8) -- and this risk is for a person with, obviously, not only the identical genome, but also the
identical complex of exposures.

Several things seem clear with respect to the importance of genetic and environmental factors in the causation and
control of cancer. First, knowledge of one should expand our knowledge of the other. Information about types of
environmental exposure that affect the risk of cancer should point to genes that might modify this risk, and the
identification of genes associated with risk could help to indict previously unrecognized environmental risk factors.
(9) Second, when genes and environment interact to produce a risk greater than the sum of their independent
effects, this interactive component can be eliminated by removing either the genetic or the environmental factor.
Finally, for cancer at many sites there are limited effective options for prevention. For this reason, unique
opportunities to expand our knowledge of risk factors should be exploited regardless of their source. Perhaps it is
time to drop the competition implied by talking about a debate over nature versus nurture in favor of efforts to
exploit every opportunity to identify and manipulate both environmental and genetic risk factors to improve the
control of cancer.