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Embracing the Promise of Biological Enhancement
by Ramez Naam
Contents
Introduction: Healing and Enhancing
How medicine is leading to enhancement. The moral and ethical case for
individual and family choice.
Chapter 1: Choosing Our Bodies
Gene therapy from Ashanti DeSilva (the first human patient) to boosting
strength, speed, and stamina.
Chapter 2: Choosing Our Minds
Gene therapy and next gen smart-drugs could soon alter memory, attention, and
personality.
Chapter 3: Created Equal
The intersection of enhancements, economics, and the law. Market mechanisms and
dropping costs. The risks of prohibition and black markets. The value of
investing in human resources.
Chapter 4: Methuselah's Genes
Single genetic changes can double life span in many species. The prospects for
extending human life.
Chapter 5: Choosing Our Life Spans
More on the prospects of genetically and bioechemically slowing, halting, or
reversing human aging.
Chapter 6: Methuselah's World
Impact of slowed aging on population, economics, politics, the workforce, and
civil culture.
Chapter 7: A Child of One's Own
2 million "test tube babies" have been born. Trends in using technology to
control reproduction.
Chapter 8: A Child of Choice
The intersection of genetic engineering with reproductive technology. Myths
and realities of "designer babies" and human cloning. The case for choice as
freedom and prohibition as eugenic.
Chapter 9: The Wired Brain
Brain implants have restored vision to the blind and motion to the paralyzed.
What the future holds.
Chapter 10: World Wide Mind
Neural implants to alter memory, perception, and particularly communication. The
prospects for mind-to-mind communication and an information revolution. The
effect on collective intelligence and culture.
Chapter 11: Life Without Limits
What does it mean to be human? The case that we are defined not by our limits,
but by our constant striving to overcome them. The evolutionary history of
humanity, and speculation on our deep evolutionary future.
Chapter 1
Choosing
Our
Bodies
>In 1989, Raj and Van DeSilva were desperate. Their daughter Ashanti, just
four, was dying. She was born with a crippled immune system, a consequence of a
problem in her genes.
Every human being has around thirty thousand genes. In fact, we have two
copies of each of those genes--one inherited from our mother, the other from our
father. Our genes tell our cells what proteins to make, and when.
Each protein is a tiny molecular machine. Every cell in your body is built out
of millions of these little machines, working together in precise ways. Proteins
break down food, ferry energy to the right places, and form scaffoldings that
maintain cell health and structure. Some proteins synthesize messenger molecules
to pass signals in the brain, and other proteins form receptors to receive those
signals. Even the machines inside each of your cells that build new
proteins—called ribosomes—are themselves made up of other proteins.
Ashanti DeSilva inherited two broken copies of the gene that contains the
instructions for manufacturing a protein called adenoside deaminase (ADA). If
she had had just one broken copy, she would have been fine. The other copy of
the gene would have made up the difference. With two broken copies, her body
didn't have the right instructions to manufacture ADA at all.
ADA plays a crucial role in our resistance to disease. Without it, special
white blood cells called T cells die off. Without T cells, ADA-deficient
children are wide open to the attacks of viruses and bacteria. These children
have what's called severe combined immune deficiency (SCID) disorder, more
commonly known as bubble boy disease.
To a person with a weak immune system, the outside world is threatening.
Everyone you touch, share a glass with, or share the same air with is a
potential source of dangerous pathogens. Lacking the ability to defend herself,
Ashanti was largely confined to her home.
The standard treatment for ADA deficiency is frequent injections of PEG-ADA,
a synthetic form of the ADA enzyme. PEG-ADA can mean the difference between life
and death for an ADA-deficient child. Unfortunately, although it usually
produces a rapid improvement when first used, children tend to respond less and
less to the drug each time they receive a dose. Ashanti DeSilva started
receiving PEG-ADA injections at the age of two, and initially she responded
well. Her T-cell count rose sharply and she developed some resistance to
disease. But by the age of four, she was slipping away, no longer responding
strongly to her injections. If she was to live, she'd need something more than
PEG-ADA. The only other option at the time, a bone-marrow transplant, was ruled
out by the lack of matching donors.
In early 1990, while Ashanti's parents were searching frantically for help,
French Anderson, a geneticist at the National Institutes of Health, was seeking
permission to perform the first gene-therapy trials on humans. Anderson, an
intense fifth-degree blackbelt in tae kwon do and respected researcher in the
field of genetics, wanted to show that he could treat genetic diseases caused by
faulty copies of genes by inserting new, working copies of the same gene.
Scientists had already shown that it was possible to insert new genes into
plants and animals. Genetic engineering got its start in 1972, when geneticists
Stanley Cohen and Herbert Boyer first met at a scientific conference in Hawaii
on plasmids, small circular loops of extra chromosomal DNA in which bacteria
carry their genes. Cohen, then a professor at Stanford, had been working on ways
to insert new plasmids into bacteria. Researchers in Boyer's lab at the
University of California in San Francisco had recently discovered restriction
enzymes, molecular tools that could be used to slice and dice DNA at specific
points.
Over hot pastrami and corned-beef sandwiches, the two Californian researchers
concluded that their technologies complemented one another. Boyer's restriction
enzymes could isolate specific genes, and Cohen's techniques could then deliver
them to bacteria. Using both techniques researchers could alter the genes of
bacteria. In 1973, just four months after meeting each other, Cohen and Boyer
inserted a new gene into the Escherichia coli bacterium (a regular resident of
the human intestine).
For the first time, humans were tinkering directly with the genes of another
species. The field of genetic engineering was born. Boyer would go on to found
Genentech, the world's first biotechnology company. Cohen would go on to win the
Nobel Prize in 1986 for his work on cell growth factors.
Building on Cohen and Boyer's work with bacteria, hundreds of scientists went
on to find ways to insert new genes into plants and animals. The hard work of
genetically engineering these higher organisms lies in getting the new gene into
the cells. To do this, one needs a gene vector—a way to get the gene to the
right place. Most researchers use gene vectors provided by nature: viruses. In
some ways, viruses are an ideal tool for ferrying genes into a cell, because
penetrating cell walls is already one of their main abilities. Viruses are
cellular parasites. Unlike plant or animal cells, or even bacteria, viruses
can't reproduce themselves. Instead, they penetrate cells and implant their
viral genes; these genes then instruct the cell to make more of the virus, one
protein at a time.
Early genetic engineers realized that they could use viruses to deliver
whatever genes they wanted. Instead of delivering the genes to create more
virus, a virus could be modified to deliver a different gene chosen by a
scientist. Modified viruses were pressed into service as genetic "trucks,"
carrying a payload of genes loaded onto them by researchers; these viruses don't
spread from cell to cell, because they don't carry the genes necessary for the
cell to make new copies of the virus.
By the late 1980s, researchers had used this technique to alter the genes of
dozens of species of plants and animals—tobacco plants that glow, tomatoes that
could survive freezing, corn resistant to pesticides. French Anderson and his
colleagues reasoned that one could do the same in a human being. Given a patient
who lacked a gene crucial to health, one ought to be able to give that person
copies of the missing gene. This is what Anderson proposed to do for Ashanti.
Starting in June of 1988, Anderson's proposed clinical protocols, or
treatment plans, went through intense scrutiny and generated more than a little
hostility. His first protocol was reviewed by both the National Institutes of
Health (NIH) and the Food and Drug Administration (FDA). Over a period of seven
months, seven regulatory committees conducted fifteen meetings and twenty hours
of public hearings to assess the proposal.
In early 1990, Anderson and his collaborators received the final approval
from the NIH's Recombinant DNA Advisory Committee and had cleared all legal
hurdles. By spring, they had identified Ashanti as a potential patient. Would
her parents consent to an experimental treatment? Of course there were risks to
the therapy, yet without it Ashanti would face a life of seclusion and probably
death in the next few years. Given these odds, her parents opted to try the
therapy. As Raj DeSilva told the Houston Chronicle, "What choice did we have?"
Ashanti and her parents flew to the NIH Clinical Center at Bethesda,
Maryland. There, over the course of twelve days, Anderson and his colleagues
Michael Blaese and Kenneth Culver slowly extracted some of Ashanti's blood
cells. Safely outside the body, the cells had new, working copies of the ADA
gene inserted into them by a hollowed-out virus. Finally, starting on the
afternoon of September 14, Culver injected the cells back into Ashanti's body.
The gene therapy had roughly the same goal as a bone-marrow transplant—to
give Ashanti a supply of her own cells that could produce ADA. Unlike a
bone-marrow transplant, gene therapy carries no risk of rejection. The cells
Culver injected back into Ashanti's bloodstream were her own, so her body
recognized them as such.
The impact of the gene therapy on Ashanti was striking. Within six months,
her T-cell count rose to normal levels. Over the next two years, her health
continued to improve, allowing her to enroll in school, venture out of the
house, and lead a fairly normal childhood.
Ashanti is not completely cured—she still takes a low dose of PEG-ADA.
Normally the dose size would increase with the patient's age, but her doses have
remained fixed at her four-year-old level. It's possible that she could be taken
off the PEG-ADA therapy entirely, but her doctors don't think it's yet worth the
risk. The fact that she's alive today—let alone healthy and active—is due to her
gene therapy, and also helps prove a crucial point: genes can be inserted into
humans to cure genetic diseases.
From Healing to Enhancing
After Ashanti's treatment, the field of gene therapy blossomed. Since 1990,
hundreds of labs have begun experimenting with gene therapy as a technique to
cure disease, and more than five hundred human trials involving over four
thousand patients have been launched. Researchers have shown that it may be
possible to use gene therapy to cure diabetes, sickle-cell anemia, several kinds
of cancer, Huntington's disease and even to open blocked arteries.
While the goal of gene therapy researchers is to cure disease, gene therapy
could also be used to boost human athletic performance. In many cases, the same
research that is focused on saving lives has also shown that it can enhance the
abilities of animals, with the suggestion that it could enhance men and women as
well.
Consider the use of gene therapy to combat anemia. Circulating through your
veins are trillions of red blood cells. Pumped by your heart, they serve to
deliver oxygen from the lungs to the rest of your tissues, and carry carbon
dioxide from the tissues back out to the lungs and out of the body. Without
enough red blood cells, you can't function. Your muscles can't get enough oxygen
to produce force, and your brain can't get enough oxygen to think clearly.
Anemia is the name of the condition of insufficient red blood cells. Hundreds of
thousands of people worldwide live with anemia, and with the lethargy and
weakness that are its symptoms. In the United States, at least eighty-five
thousand patients are severely anemic as a result of kidney failure. Another
fifty thousand AIDS patients are anemic due to side effects of the HIV drug AZT.
What if there was another way? What if the body could be instructed to
produce more EPO on its own, to make up for that lost to kidney failure or AZT?
That's the question University of Chicago professor Jeffrey Leiden asked himself
in the mid-1990s. In 1997, Leiden and his colleagues performed the first animal
study of EPO gene therapy, injecting lab monkeys and mice with a virus carrying
an extra copy of the EPO gene. The virus penetrated a tiny proportion of the
cells in the mice and monkeys and unloaded the gene copies in them. The cells
began to produce extra EPO, causing the animals' bodies to create more red blood
cells. In principle, this was no different from injecting extra copies of the
ADA gene into Ashanti, except in this case the animals already had two working
copies of the EPO gene. The one being inserted into some of their cells was a
third copy; if the experiment worked, the animals' levels of EPO production
would be boosted beyond the norm for their species.
That's just what happened. After just a single injection, the animals began
producing more EPO, and their red-blood-cell counts soared. The mice went from a
hematocrit of 49 percent (meaning that 49 percent of their blood volume was red
blood cells) to 81 percent. The monkeys went from 40 percent to 70 percent. At
least two other biotech companies, Chiron and Ariad Gene Therapies, have
produced similar results in baboons and monkeys, respectively.
The increase in red-blood-cell count is impressive, but the real advantage of
gene therapy is in the long-lasting effects. Doctors can produce an increase in
red-blood-cell production in patients with injections of EPO itself—but the EPO
injections have to be repeated three times a week. EPO gene therapy, on the
other hand, could be administered just every few months, or even just once for
the patient's entire lifetime.
The research bears this out. In Leiden's original experiment, the mice each
received just one shot, but showed higher red-blood-cell counts for a year. In
the monkeys, the effects lasted for twelve weeks. The monkeys in the Ariad
trial, which went through gene therapy more than four years ago, still show
higher red-blood-cell counts today.
This is a key difference between drug therapy and gene therapy. Drugs sent
into the body have an effect for a while, but eventually are broken up or passed
out. Gene therapy, on the other hand, gives the body the ability to manufacture
the needed protein or enzyme or other chemical itself. The new genes can last
for a few weeks or can become a permanent part of the patient's genome.
Insertional gene vectors penetrate all the way into the nucleus of the cell
and splice the genes they carry into the chromosomes. From that point on, the
new genes get all the benefits your other genes enjoy. The new genes are
shielded from most of the damage that can happen inside your cells. If the cell
divides, the new genes get copied to the daughter cells, just like the rest of
your DNA. Insertional vectors make more or less permanent changes to your
genome.
Noninsertional vectors, on the other hand, don't make it into the nucleus of
your cells. They don't splice the new genes they carry into your chromosomes.
Instead, they deliver their payload of DNA and leave it floating around inside
your cells. The new DNA still gets read by the cell. It still instructs the cell
to make new proteins. But it doesn't get copied when the cell divides. Over
time, it suffers from wear and tear, until eventually it breaks up, and its
effects end.
The difference in durations among drugs, noninsertional vectors and
insertional vectors gives us choices. We can choose to make a temporary change
with a drug, which will wear off in a few hours or days; a semipermanent change
with noninsertional gene therapy, whose effects will last for weeks or months
depending on the genes and type of cell infected; or a permanent change by
inserting new genes directly into your genome. Each of these three options is
appropriate in certain situations. In the context of EPO, the idea of
semipermanent or permanent change by means of gene therapy has definite
advantages. It cuts down on the need for frequent injections, which means that
the gene therapy approach can end up being much cheaper than the drug therapy
approach.
Excerpted from More Than Human by Ramez Naam Copyright © 2005 by Ramez Naam. Excerpted by permission of Broadway, a division of Random House, Inc. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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