September 02, 2006
Small Genetic Role For Determining Longevity

The New York Times has an excellent article surveying what is known about the role genetic inheritence in determining life expectancy and mortality. Recent studies on twins point toward a much smaller than expected role for genetics in determing life expectancy.

His solution, a classic one in science, was to study twins. The idea was to compare identical twins, who share all their genes, with fraternal twins, who share some of them. To do this, Dr. Christensen and his colleagues took advantage of detailed registries that included all the twins in Denmark, Finland and Switzerland born from 1870 to 1910. That study followed the twins until 2004 to 2005, when nearly all had died.

Now, Dr. Christensen and his colleagues have analyzed the data. They restricted themselves to twins of the same sex, which obviated the problem that women tend to live longer than men. That left them with 10,251 pairs of same-sex twins, identical or fraternal. And that was enough for meaningful analyses even at the highest ages. “We were able to disentangle the genetic component,” Dr. Christensen said.

But the genetic influence was much smaller than most people, even most scientists, had assumed. The researchers reported their findings in a recent paper published in Human Genetics. Identical twins were slightly closer in age when they died than were fraternal twins.

But, Dr. Christensen said, even with identical twins, “the vast majority die years apart.”

On average identical twins die over 10 years apart. I would not have expected that result.

Even the role for genetic inheritance for cancer risk differences is seen as fairly small.

In a paper in The New England Journal of Medicine in 2000, Dr. Paul Lichtenstein of the Karolinska Institute in Stockholm and his colleagues analyzed cancer rates in 44,788 pairs of Nordic twins. They found that only a few cancers — breast, prostate and colorectal — had a noticeable genetic component. And it was not much. If one identical twin got one of those cancers, the chance that the other twin would get it was generally less than 15 percent, about five times the risk for the average person but not a very big risk over all.

Of course there are people who have genetic variations which put them at very high risk of cancer.

Alzheimer's risk has a larger genetic component.

Dr. Gatz and Dr. Pedersen analyzed data from a study of identical and fraternal Swedish twins 65 and older. If one of a pair of identical twins developed Alzheimer’s disease, the other had a 60 percent chance of getting it. If one of a pair of fraternal twins, who are related like other brothers and sisters, got Alzheimer’s, the other had a 30 percent chance of getting it.

But, Dr. Pedersen noted, Alzheimer’s is so common in the elderly that it occurs in 35 percent of people age 80 and older.

Note there are some complicating factors here. Most notably, some genetic variations put you at risk for some disease only if you do or do not do some certain thing. For example, a genetic variation for apolipoprotein E increases risk of Alzheimer's but if you have that apoliprotein E allele then diet can greatly reduce the risk. So if you live in a culture where the customary foods cancel out the genetic risk you aren't going to be at much greater risk from that genetic allele. But if you live in a culture where you eat customary foods which do not provide compensating protections then carrying that genetic allele will put you at much greater risk of Alzheimer's.

One theory of aging and longevity is that we randomly collect defects and damage during development and also during aging. Given that the process of collecting those defects is random their distribution is random. If you are lucky your defects will accumulate with a fairly even distribution throughout the body. That way it will take longer for one organ to collect enough defects to fail entirely. But if you are unlucky then by chance many of your defects will accumulate in one organ or one part of an organ (e.g. in a heart valve) or in one cell (e.g. a set of mutations that make the cell become cancerous) to the point of failure and then you'll die sooner. Twins won't live the same amount of time because they each will accumulate defects in a different random distribution.

So what's the take-away lesson from this article? There's no reason for complacency about your life expectancy. Say your parents or grandparents lived a long time. So what. That's no guarantee you won't get cancer tomorrow or have a heart attack next week. Your defects are accumulating randomly. You might be accumulating a cluster somewhere that is going to kill you years before other family members die. If you want to live a very long time then support SENS research. Anything short of SENS technologies can't save you from the damage building up within.

The whole article is worth reading.

Share |      Randall Parker, 2006 September 02 12:17 PM  Aging Genetics


Comments
Doug said at September 7, 2006 11:40 AM:

It seems that a statistical artifact called "central tendency" ought to be considered in evaluating the contribution of genetics to longevity. Central tendency is, well, the tendency for measures that involve a summation over the values from a large number of independent events to fall largely within a small portion of the entire range of sums that is mathematically possible. As a pertinent example, let the number of genes in the human genome be 40,000. Let each gene have two alleles, with frequencies in the population of .99 and .01, respectively. Let each allele with frequency .01 be an allele that impairs longevity. Let the occurrence of each allele of each gene be completely unconditional on the occurrence of any allele of any other gene in the genome of an individual. Lastly, let me ignore the complicating factor that each of us routinely has two copies of each gene in our genome. Under this simplified, illustrative set of circumstances, 99% of people will have between 350 and 452 alleles that impair longevity. (I used this binomial calculator to work out the endpoints.) The chance that a given individual would have none of the alleles that impair longevity is vanishingly small. Indeed, only 1 person out of 100,000 would have fewer than 316 alleles that impair longevity; only 1 person out of 100,000 would have more than 490 such alleles.

If our actual circumstances at all resemble my contrived case, then we're very far from knowing how much of an improvement in longevity could be obtained by selecting each allele of each gene solely on the basis of its statistical effect on longevity. Meanwhile, under such circumstances, the vast majority of us occupy positions in a muddled, middle ground.

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