Readers Read

Readers Read


Books Section

Reading Sections

Book Publishing News
Children's Books
General Fiction

Survival of the Sickest
by Dr. Sharon Moalem
HarperCollins, 2007

From Chapter III

Click here
for ordering information.

IF you're of Asian descent and have ever had an alcoholic beverage, there's a fifty-fifty chance your heart rate shot up, your temperature climbed, and your face turned bright red. If you're not Asian but you've ever been in a bar frequented by people with an Asian background, chances are you've seen this reaction. It's called Asian flush or, more formally, alcohol flush response. It happens to as many as half of all people of Asian descent, but it's uncommon in just about every other population group. So what's the story?

When you consume alcohol, your body detoxifies it and then extracts calories from it. It's a complex process that involves many different enzymes and multiple organs, although most of the process takes place in the liver. First, an enzyme called alcohol dehydrogenase converts the alcohol into another chemical called acetaldehyde; another enzyme—cleverly called acetaldehyde dehydrogenase—converts the acetaldehyde into acetate. And a third enzyme converts that into fat, carbon dioxide, and water. (The calories synthesized from alcohol are generally stored as fat—beer bellies really do come from beer.)

Many Asians have a genetic variation (labeled ALDH2*2) that causes them to produce a less powerful form of acetaldehyde dehydrogenase—one that isn't as effective in converting acetaledehyde, that first by-product of alcohol, into acetate. Acetaldehyde is thirty times as toxic as alcohol; even very small amounts can produce nasty reactions. And one of those reactions is the flushing response. That's not all it does, of course. After even one drink by people who have the ALDH2*2 variation, the acetaldehyde buildup causes them to appear drunk; blood rushes to their face, chest, and neck; dizziness and extreme nausea set in—and the drinker is on the road to a nasty hangover. Of course, there's a side benefit to all this—people who have ALDH2*2 are highly resistant to alcoholism. It's just too unpleasant for them to drink!

In fact, the resistance to alcoholism is so strong in people with ALDH2*2 that doctors often prescribe alcoholics with a drug called disulfiram, which essentially mirrors the ALDH2*2 effect. Disulfiram (Antabuse) interferes with the body's own supply of the acetaldehyde dehydrogenase enzyme, so anyone who drinks alcohol while taking it ends up with something that looks an awful lot like Asian flush and feels truly awful to boot.

So why is the ALDH2*2 variation so common among Asians and virtually nonexistent among Europeans? It's all about clean water. As humans began to settle in cities and towns, they got their first taste of the sanitation and waste management problems that still plague cities today—but without even the possibility of modern plumbing. This made clean water a real challenge, and some theories suggest that different civilizations came up with different solutions. In Europe, they used fermentation—and the resulting alcohol killed microbes, even when, as was often the case, it was mixed with water. On the other side of the world, people purified their water by boiling it and making tea. As a result, there was evolutionary pressure in Europe to have the ability to drink, break down, and detoxify alcohol, while the pressure in Asia was a lot less.

From Chapter V

The family of streptococcal bacteria is responsible for a wide range of human disease—from strep throat to scarlet fever, bacterial pneumonia, and rheumatic fever. Many types of streptococcal bacteria exhibit a phenomenon called molecular mimicry in which they display characteristics of human cells in order to trick the immune system. The cells these bacteria mimic include cells found in the heart, the joints, and even the brain. When you have a bacterial infection, your immune system produces antibodies to attack the invaders. When the invaders are partially disguised through molecular mimicry, they can cause an autoimmune disorder. The immune system recognizes the threat posed by bacterial invaders, but the antibodies it produces attack all the cells that resemble the bacteria—including the body's own cells. That's how some children who have rheumatic fever end up with heart problems—antibodies attack the heart valve because the infecting bacteria resembles it in some ways.

Dr. Susan Swedo, a researcher at the National Institute of Mental Health, believes that certain strep infections can trigger an autoimmune disorder that leads to an antibody-led attack on the basal ganglia, the part of the brain believed to control movement. Researchers call this condition PANDAS—pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection. Parents of children with PANDAS describe heartbreaking transformations, often overnight. Shortly after infection, children suddenly display repetitive tics and uncontrolled touching, as well as serious anxiety.

It's not clear that this is actual host manipulation—that depends on whether the change in behavior helps the bacteria to spread. Theoretically, of course, it's not hard to imagine how uncontrolled, repetitive touching of toys, furniture, and other kids would help the virus to spread. It's also possible that there is a relationship between obsessive-compulsive disorder and strep infections that isn't host manipulation itself, but the by-product of the bacteria's effort to fool the immune system.

One thing is clear—we are just beginning to understand the myriad ways our behavior is affected by infectious agents. One very new avenue of research is exploring the striking possibility that sexually transmitted diseases may actually influence sexual behavior. Now, I'm not suggesting that this kind of influence will transform a happily married man into an insatiable cheat. In fact, that wouldn't necessarily be in the virus's (or fungus's or bacteria's) interest. Too much promiscuity on the part of the host could disable it with other, potentially more damaging, diseases. And that would leave the parasite stuck in a host that couldn't get around. From the sexually transmitted parasite’s point of view, it may want you to have more sex—but not too much sex.

As far as diseases influencing human sexual behavior, some researchers are examining the possibility that genital herpes may affect human sexual feeling in a way that could influence behavior. Two researchers at the Department of Anatomy and Neurobiology at the University of California at Irvine, Carolyn G. Hatalski and W. Ian Lipkin, have speculated that the herpes virus may heighten sexual feeling because it is so intertwined with the nerves that carry those feelings. They wrote:

It is intriguing to speculate that the ganglion infection may modulate sensory input to sex organs leading to increased sexual activity and enhanced probability of virus transmission.

In other words, sometimes the herpes virus may want you to get some action.

From Chapter VIII

Seth Cook is the oldest living American with a particularly rare genetic disorder. He's lost all his hair. His skin is covered in wrinkles. His arteries are hardened. His joints hurt from arthritis. He takes an aspirin and a blood thinner every day.

He is twelve years old.

Seth has Hutchinson-Gilford progeria syndrome, often just called progeria. Progeria is very rare—thought to occur in just 1 of every 4 to 8 million births. It's also very unfair; the word comes from the Greek for prematurely old, and that's the difficult fate in store for people born with it. Children who have progeria age at up to ten times the speed of people without it. By the time a baby who has progeria is about a year and a half old, his or her skin starts to wrinkle and their hair starts to fall out. Cardiovascular problems, like hardening of the arteries, and degenerative diseases, like arthritis, soon follow. Most people who have progeria die in their teens of a heart attack or a stroke; nobody is known to have lived past thirty.

Hutchinson-Gilford progeria isn't the only disease that causes accelerated aging—it's just the most heartbreaking, because it's the fastest, and it starts at birth. Another aging disorder, Werner syndrome, does'’t manifest itself until someone carrying the mutation that causes it reaches puberty; it's sometimes called adult-onset progeria. After puberty, rapid aging sets in, and people who have Werner syndrome usually die of age- related disease by their early fifties. Werner syndrome, although more common than Hutchinson-Gilford progeria, is still very rare, affecting just one in a million.

Because these rapid-aging diseases are so uncommon, they haven't been the focus of much research (and they're called orphan diseases for that reason). But that's starting to change, as scientists have realized that they hold clues about the normal aging process. In April 2003, researchers announced that they had isolated the genetic mutation that causes progeria. The mutation occurs in a gene that is responsible for the production of a protein called lamin A. Normally, lamin A provides structural support for the nuclear membrane, the package that houses your genes at the core of every cell. Lamin A is like the rods that hold up a tent—the nuclear membrane is organized around it and supported by it. In people who have progeria, lamin A is defective and cells deteriorate much more rapidly.

In 2006, a different team of researchers established a link between lamin A deterioration and normal human aging. Tom Misteli and Paola Scaffidi, researchers at the National Institutes of Health, reported in Science that the cells of normal elderly people show the same kinds of defects that are found in the cells of people who have progeria. That's very significant—it's the first confirmation that the accelerated aging that characterizes progeria is related to normal human aging on a genetic level.

The implications are far-reaching. More or less since Darwin described adaptation, natural selection, and evolution, scientists have been debating where aging fits into the picture. Is it just wear and tear, the way your favorite shirt picks up little stains and rips and marks over the years, eventually fraying and wearing out? Or is it the product of evolution? In other words, is aging accidental or intentional?

Progeria and the other accelerated-aging diseases suggest that aging is preprogrammed, that it's part of the design. Think about it—if a single genetic error can trigger accelerated aging in a baby or an adolescent, then aging can't only be caused by a lifetime of wear and tear. The very existence of the progeria gene demonstrates that there could be genetic controls for aging. That, of course, raises a question you've no doubt come to expect. Are we programmed to die?

Leonard Hayflick is one of the fathers of modern aging research. During the 1960s he discovered that (with one special exception) cells only divide a fixed number of times before they up and quit. This limit on cellular reproduction is appropriately called the Hayflick limit; in humans the limit is around fifty-two to sixty.

The Hayflick limit is related to the loss of a genetic buffer at the end of chromosomes called telomeres. Every time a cell reproduces it loses a little bit of DNA. In order to prevent that information loss from making a difference, your chromosomes have what amounts to extra information at their tips; those bits of information are telomeres.

Imagine you have a manuscript and need to make fifty copies but Kinko's has just thrown you a curveball. Instead of charging you money, they're just going to take one page off the end of your manuscript after every copy. That's a problem—your manuscript is two hundred pages long; if you give them a page after every copy, the last copy is only going to have one hundred fifty pages and whoever gets it is going to miss a quarter of the story. So, being a highly evolved organism with a gift for clever solutions, you add fifty blank pages to the end of your manuscript and present Kinko's with a two-hundred-fifty-page manuscript. Now, all fifty copies will have the complete story; you won’t lose a page of precious information until you decide to make copy fifty-one. Telomeres are like blank pages; as cells reproduce, telomeres are shortened, and the truly valuable DNA is protected. But once a cell replicates between fifty and sixty times, the telomeres are essentially gone and the good stuff is in jeopardy.

Now, why would we evolve a limit against cellular reproduction?

In a word? Cancer.

Excerpted from Survival of the Sickest by Dr. Sharon Moalem. Copyright © 2007 by Dr. Sharon Moalem. All rights reserved. Posted with permission of the publisher. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.

Copyright © 1997-2015 by Writers Write, Inc. All Rights Reserved.