To make it safer for older people, the city added four seconds to the time pedestrians are given to cross intersections like Broadway and 72nd Street.

The New York Times, July 28, 2010, by Anemona Hartocollis  —  New York City has given pedestrians more time to cross at more than 400 intersections in an effort to make streets safer for older residents. The city has sent yellow school buses, filled not with children but with elderly people, on dozens of grocery store runs over the past seven months.

Ana Andujar, 84, second from left, and others attended a meeting in East Harlem on how to make the city more age-friendly.

Emily Berl for The New York Times

The city has allowed artists to use space and supplies in 10 senior centers in exchange for giving art lessons. And it is about to create two aging-improvement districts, parts of the city that will become safer and more accessible for older residents.

Happy resident in a NYC Senior Center

People live in New York because it is like no place else — pulsating with life, energy and a wealth of choices — but there is some recognition among city planners that it could be a kinder and gentler place in which to grow old.

The city’s efforts, gaining strength as the baby boomer generation starts reaching retirement age, are born of good intentions as well as an economic strategy.

“New York has become a safer city, and we have such richness of parks and culture that we’re becoming a senior retirement destination,” said Linda I. Gibbs, New York’s deputy mayor for health and human services. “They come not only with their minds and their bodies; they come with their pocketbooks.”

Retired Couple Biking in Central Park, NYC

The round trip back to cities among empty nesters, rejoining those who simply grow old where they were once young, goes on, of course, across the country, and New York is not the only place trying to ease that passage. Cities like Cleveland and Portland, Ore., have taken steps to become more “age-friendly.” But perhaps never has a city as fast-paced and youth-oriented as New York taken on the challenge.

The Department of City Planning predicts that in 20 years, New York’s shares of schoolchildren and older people will be about the same, 15 percent each, a sharp change from 1950, when schoolchildren outnumbered older residents by more than 2 to 1. By 2030, the number of New Yorkers age 65 and over — a result of the baby boomers, diminished fertility and increasing longevity — is expected to reach 1.35 million, up 44 percent from 2000.

Their economic power is significant. About a third of the nation’s population is over 50, and they control half of the country’s discretionary spending, according to a recent report by AARP, a group representing the interests of retirees. In some ways, the city has tackled the toughest challenges of making itself attractive to its older residents and those across the country who might consider retiring to the Upper East Side or Brooklyn Heights.

Crime has been in decline for close to two decades; the city has added more parkland than at any similar period in its history; and the 311 system has made dealing with the bureaucracy of government agencies and social services more manageable.

Now, the city is looking to enhance life here in more modest, but meaningful, ways. The New York Academy of Medicine adopted the idea of creating an age-friendly city from the World Health Organization in 2007, and went to the City Council and the Bloomberg administration for financial and political support. The academy has held more than 30 town hall meetings and focus groups with thousands of older people across the city. This summer, it is holding more intimate focus groups in East Harlem and on the Upper West Side.

What people say they want most of all is to live in a neighborly place where it is safe to cross the street and where the corner drugstore will give them a drink of water and let them use the bathroom. They ask for personal shoppers at Fairway to help them find the good deals on groceries. They want better street drainage, because it is hard to jump over puddles with walkers and wheelchairs.

“No bingo played here” could be Ms. Gibbs’s motto. She is the conceptual artist behind the city’s initiative, working with the Academy of Medicine. She is at the tail end of the boomer generation, having turned 51 on Sunday, her silvery bob a rebuke to fears of aging.

“The whole conversation around aging has, in my mind, gone from one which is kind of disease oriented and tragic, end- of-life oriented,” Ms. Gibbs said, to being “much more about the strength and the fidelity and the energy that an older population contributes to our city.”

Retired woman enjoys the flowers in NYC Central Park

One of her ideas is to hold a contest to design a “perch” to put in stores or on sidewalks where tired older residents doing errands could take a break. When boomers talk, she listens.

On Thursday, Dorian Block, a policy associate at the academy, held a focus group at the Carver Houses, a city housing project at 103rd Street and Madison Avenue in East Harlem. Sixteen people showed up. (Some meetings have drawn hundreds.)

They complained about broken elevators and litter, and some confessed to being lonely. They said that more stores should have public bathrooms. Now, said Dolores Marquez, 72, “I go to McDonald’s and then I take a coffee because I have to go to the bathroom.”

The academy plans to incorporate the results of the focus groups into two pilot aging-improvement districts, one in East Harlem and the other on the Upper West Side, somewhat akin to business-improvement districts.

The exact details of how the districts will function are still being worked out, but the goal is to create a public-private partnership that would encourage businesses to voluntarily adopt amenities for the elderly. Examples could include window stickers that identify businesses as age-friendly; extra benches; adequate lighting; menus with large type; and even happy hour for older residents.

Living on a pension, but exercising at a reasonably priced gym

The new districts will be run by the academy, and eventually handed over to community groups and expanded to other neighborhoods, said Ruth Finkelstein, the academy’s vice president for health policy. Some worry that what the Bloomberg administration is proposing is a menu of quick and dirty solutions for older residents while, in a tough economy, traditional services like senior centers and bus routes are being cut back.

“When we’re talking about age-friendly, it should not only be the boomers who have retired from law firms, as opposed to the people who have worked all their lives and are now living in Brownsville,” said David Jones, president of the Community Service Society, which advocates for poor people and immigrants.

Fredda Vladeck, an expert at the United Hospital Fund in “naturally occurring retirement communities,” said she worried that the city would forget the frail older people. Ms. Gibbs said the point was to build on what is already there, and to make life better for everyone.

The city enlisted students at New York University’s Wagner Graduate School of Public Service to develop a walking survey that, if adopted, will rate the city’s age-friendliness by standards like the frequency of cracked sidewalks and hospitals.

Slowing the pace of life is tough in New York, where every red light is viewed as a challenge. But the city is trying. While most adults average four feet per second when crossing the street, older residents manage only three, transportation experts say. So signals have been retimed at intersections like Broadway and 72nd Street, where pedestrians now have 29 seconds to cross, four more than before.

Even senior centers are being redefined as places with artists in residence, like Judy Hugentobler, a sculptor from Staten Island. Ms. Hugentobler is teaching art classes at the Educational Alliance’s Sirovich Senior Center, on East 12th Street, in exchange for being able to use the kilns, clay and glazes in her projects.

“Senior centers are great, but they have a stigma whether you like it or not,” said Councilwoman Gale A. Brewer of the Upper West Side. “It’s just not for everybody. But what is for everybody is a bench. What is for everybody is discounts at the grocery store when you’re over 65.”

New York Transit is Fairly Easy to Navigate

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The structure of part of a DNA double helix

Deoxyribonucleic acid ( /diːˌɒksɨˌraɪbɵ.n(j)uːˈkleɪ.ɪk ˈæsɪd/ (help·info)) (DNA) is a nucleic acid that

contains the genetic instructions used in the development and functioning of all known living organisms and some viruses. The main role of DNA molecules is the long-term storage of information. DNA is often compared to a set of blueprints, like a recipe or a code, since it contains the instructions needed to construct other components of cells, such as proteins and RNA molecules. The DNA segments that carry this genetic information are called genes, but other DNA sequences have structural purposes, or are involved in regulating the use of this genetic information.

Chemically, DNA consists of two long polymers of simple units called nucleotides, with backbones made of sugars and phosphate groups joined by ester bonds. These two strands run in opposite directions to each other and are therefore anti-parallel. Attached to each sugar is one of four types of molecules called bases. It is the sequence of these four bases along the backbone that encodes information. This information is read using the genetic code, which specifies the sequence of the amino acids within proteins. The code is read by copying stretches of DNA into the related nucleic acid RNA, in a process called transcription.

Within cells, DNA is organized into long structures called chromosomes. These chromosomes are duplicated before cells divide, in a process called DNA replication. Eukaryotic organisms (animals, plants, fungi, and protists) store most of their DNA inside the cell nucleus and some of their DNA in organelles, such as mitochondria or chloroplasts.  In contrast, prokaryotes (bacteria and archaea) store their DNA only in the cytoplasm. Within the chromosomes, chromatin proteins such as histones compact and organize DNA. These compact structures guide the interactions between DNA and other proteins, helping control which parts of the DNA are transcribed.

Genetics is the study of genes, and tries to explain what they are and how they work. Genes are how living organisms inherit features from their ancestors; for example, children usually look like their parents because they have inherited their parents’ genes. Genetics tries to identify which features are inherited, and explain how these features are passed from generation to generation.

In genetics, a feature of a living thing is called a “trait“. Some traits are part of an organism’s physical appearance; such as a person’s eye-color, height or weight. Other sorts of traits are not easily seen and include blood types or resistance to diseases. Some traits are inherited through our genes, so tall and thin people tend to have tall and thin children. Other traits come from interactions between our genes and the environment, so a child might inherit the tendency to be tall, but if they are poorly nourished, they will still be short. The way our genes and environment interact to produce a trait can be complicated. For example, the chances of somebody dying of cancer or heart disease seems to depend on both their genes and their lifestyle.

Genes are made from a long molecule called DNA, which is copied and inherited across generations. DNA is made of simple units that line up in a particular order within this large molecule. The order of these units carries genetic information, similar to how the order of letters on a page carry information. The language used by DNA is called the genetic code, which lets organisms read the information in the genes. This information is the instructions for constructing and operating a living organism.

The information within a particular gene is not always exactly the same between one organism and another, so different copies of a gene do not always give exactly the same instructions. Each unique form of a single gene is called an allele. As an example, one allele for the gene for hair color could instruct the body to produce a lot of pigment, producing black hair, while a different allele of the same gene might give garbled instructions that fail to produce any pigment, giving white hair. Mutations are random changes in genes, and can create new alleles. Mutations can also produce new traits, such as when mutations to an allele for black hair produce a new allele for white hair. This appearance of new traits is important in evolution.

Genes and inheritance

A section of DNA; the sequence of the plate-like units (nucleotides) in the center carries information.

Green eyes are a recessive trait.

Genes are inherited as units, with two parents dividing out copies of their genes to their offspring. You can think of this process like mixing two hands of cards, shuffling them, and then dealing them out again. Humans have two copies of each of their genes (i.e., two alleles) and when people reproduce they make copies of their genes and put them into eggs or sperm, but only put in one copy of each type of gene. When an egg joins with a sperm, this gives a child a complete set of genes. This child will have the same number of genes as its parents, but for any gene one of their two copies will come from their father, and one from their mother.

The effects of this mixing depends on the types (the alleles) of the gene you are interested in. If the father has two alleles for green eyes, and the mother has two alleles for brown eyes, all their children will get two alleles that give different instructions, one for green eyes and one for brown. The eye color of these children depends on how these alleles work together. If one allele overrides the instructions from another, it is called the dominant allele, and the allele that is overridden is called the recessive allele. In the case of a daughter with both green and brown alleles, brown is dominant and she ends up with brown eyes.[2]

Although the green color allele is still there in this brown-eyed girl, it doesn’t show. This is a difference between what you see on the surface (the traits of an organism, called its phenotype) and the genes within the organism (its genotype). In this example you can call the brown allele “B” and the green allele “g”. (It is normal to write dominant alleles with capital letters and recessive ones with lower-case letters.) The brown-eyed daughter has the “brown eye phenotype” but her genotype is Bg, with one copy of the B allele, and one of the g allele.

Now imagine that this woman grows up and has children with a brown-eyed man who also has a Bg genotype. Her eggs will be a mixture of two types, one sort containing the B allele, and one sort the g allele. Similarly, her partner will produce a mix of two types of sperm containing one or the other of these two alleles. Now, when the alleles are mixed up in their offspring, these children have a chance of getting either brown or green eyes, since they could get a genotype of BB = brown eyes, Bg = brown eyes or gg = green eyes. In this generation, there is therefore a chance of the recessive allele showing itself in the phenotype of the children – some of them may have green eyes like their grandfather.

Many traits are inherited in a more complicated way than the example above. This can happen when there are several genes involved, each contributing a small part to the end result. Tall people tend to have tall children because their children get a package of many alleles that each contribute a bit to how much they grow. However, there are not clear groups of “short people” and “tall people”, like there are groups of people with brown or green eyes. This is because of the large number of genes involved; this makes the trait very variable and people are of many different heights.Inheritance can also be complicated when the trait depends on the interaction between genetics and the environment. This is quite common, for example, if a child does not eat enough nutritious food this will not change traits like eye color, but it could stunt their growth.
Inherited diseases
Some diseases are hereditary and run in families; others, such as infectious diseases, are caused by the environment. Other diseases come from a combination of genes and the environment.  Genetic disorders are diseases that are caused by a single allele of a gene and are inherited in families. These include Huntington’s disease, Cystic fibrosis or Duchenne muscular dystrophy. Cystic fibrosis, for example, is caused by mutations in a single gene called CFTR and is inherited as a recessive trait.

Other diseases are influenced by genetics, but the genes a person gets from their parents only change their risk of getting a disease. Most of these diseases are inherited in a complex way, with either multiple genes involved, or coming from both genes and the environment. As an example, the risk of breast cancer is 50 times higher in the families most at risk, compared to the families least at risk. This variation is probably due to a large number of alleles, each changing the risk a little bit.  Several of the genes have been identified, such as BRCA1 and BRCA2, but not all of them. However, although some of the risk is genetic, the risk of this cancer is also increased by being overweight, drinking a lot of alcohol and not exercising.   A woman’s risk of breast cancer therefore comes from a large number of alleles interacting with her environment, so it is very hard to predict.

How genes work

Genes make proteins
The function of genes is to provide the information needed to make molecules called proteins in cells.  Cells are the smallest independent parts of organisms: the human body contains about 100 trillion cells, while very small organisms like bacteria are just one single cell. A cell is like a miniature and very complex factory that can make all the parts needed to produce a copy of itself, which happens when cells divide. There is a simple division of labor in cells – genes give instructions and proteins carry out these instructions, tasks like building a new copy of a cell, or repairing damage.  Each type of protein is a specialist that only does one job, so if a cell needs to do something new, it must make a new protein to do this job. Similarly, if a cell needs to do something faster or slower than before, it makes more or less of the protein responsible. Genes tell cells what to do by telling them which proteins to make and in what amounts.

Genes are expressed by being transcribed into RNA, and this RNA then translated into protein.

Proteins are made of a chain of 20 different types of amino acid molecules. This chain folds up into a compact shape, rather like an untidy ball of string. The shape of the protein is determined by the sequence of amino acids along its chain and it is this shape that, in turn, determines what the protein will do.  For example, some proteins have parts of their surface that perfectly match the shape of another molecule, allowing the protein to bind to this molecule very tightly. Other proteins are enzymes, which are like tiny machines that alter other molecules.

The information in DNA is held in the sequence of the repeating units along the DNA chain.  These units are four types of nucleotides (A,T,G and C) and the sequence of nucleotides stores information in an alphabet called the genetic code. When a gene is read by a cell the DNA sequence is copied into a very similar molecule called RNA (this process is called transcription). Transcription is controlled by other DNA sequences (such as promoters), which show a cell where genes are, and control how often they are copied. The RNA copy made from a gene is then fed through a structure called a ribosome, which translates the sequence of nucleotides in the RNA into the correct sequence of amino acids and joins these amino acids together to make a complete protein chain. The new protein then folds up into its active form. The process of moving information from the language of DNA into the language of amino acids is called translation.

DNA replication. DNA is unwound and nucleotides are matched to make two new strands.

If the sequence of the nucleotides in a gene changes, the sequence of the amino acids in the protein it produces may also change – if part of a gene is deleted, the protein produced will be shorter and may not work any more.  This is the reason why different alleles of a gene can have different effects in an organism. As an example, hair color depends on how much of a dark substance called melanin is put into the hair as it grows. If a person has a normal set of the genes involved in making melanin, they make all the proteins needed and they grow dark hair. However, if the alleles for a particular protein have different sequences and produce proteins that can’t do their jobs, no melanin will be produced and the hair will be white. This condition is called albinism and the person with this condition is called an albino.
Genes are copied
Genes are copied each time a cell divides into two new cells. The process that copies DNA is called DNA replication.  It is through a similar process that a child inherits genes from its parents, when a copy from the mother is mixed with a copy from the father.

DNA can be copied very easily and accurately because each piece of DNA can direct the creation of a new copy of its information. This is because DNA is made of two strands that pair together like the two sides of a zipper. The nucleotides are in the center, like the teeth in the zipper, and pair up to hold the two strands together. Importantly, the four different sorts of nucleotides are different shapes, so in order for the strands to close up properly, an A nucleotide must go opposite a T nucleotide, and a G opposite a C. This exact pairing is called base pairing.

When DNA is copied, the two strands of the old DNA are pulled apart by enzymes which move along each of the two single strands pairing up new nucleotide units and then zipping the strands closed. This produces two new pieces of DNA, each containing one strand from the old DNA and one newly made strand. This process isn’t perfect and sometimes the proteins will make mistakes and put the wrong nucleotide into the strand they are building. This causes a change in the sequence of that gene. These changes in DNA sequence are called mutations  Mutations produce new alleles of genes. Sometimes these changes stop the gene from working properly, like the melanin genes discussed above. In other cases these mutations can change what the gene does or even let it do its job a little better than before. These mutations and their effects on the traits of organisms are one of the causes of evolution.

Genes and evolution

Mice with different coat colors.

A population of organisms evolves when an inherited trait becomes more common or less common over time.  For instance, all the mice living on an island would be a single population of mice. If over a few generations, white mice went from being rare, to being a large part of this population, then the coat color of these mice would be evolving. In terms of genetics, this is called a change in allele frequency—such as an increase in the frequency of the allele for white fur.

Alleles become more or less common either just by chance (in a process called genetic drift), or through natural selection.  In natural selection, if an allele makes it more likely that an organism will survive and reproduce, then over time this allele will become more common. But if an allele is harmful, natural selection will make it less common. For example, if the island was getting colder each year and was covered with snow for much of the time, then the allele for white fur would become useful for the mice, since it would make them harder to see against the snow. Fewer of the white mice would be eaten by predators, so over time white mice would out-compete mice with dark fur. White fur alleles would become more common, and dark fur alleles would become more rare.

Mutations create new alleles. These alleles have new DNA sequences and can produce proteins with new properties. So if an island was populated entirely by black mice, mutations could happen creating alleles for white fur. The combination of mutations creating new alleles at random, and natural selection picking out those which are useful, causes adaptation. This is when organisms change in ways that help them to survive and reproduce.

Genetic engineering

Since traits come from the genes in a cell, putting a new piece of DNA into a cell can produce a new trait. This is how genetic engineering works. For example, crop plants can be given a gene from an Arctic fish, so they produce an antifreeze protein in their leaves.  This can help prevent frost damage. Other genes that can be put into crops include a natural insecticide from the bacteria Bacillus thuringiensis. The insecticide kills insects that eat the plants, but is harmless to people.  In these plants the new genes are put into the plant before it is grown, so the genes will be in every part of the plant, including its seeds. The plant’s offspring will then inherit the new genes, something which has led to concern about the spread of new traits into wild plants.

The kind of technology used in genetic engineering is also being developed to treat people with genetic disorders in an experimental medical technique called gene therapy. However, here the new gene is put in after the person has grown up and become ill, so any new gene will not be inherited by their children. Gene therapy works by trying to replace the allele that causes the disease with an allele that will work properly.

 “It’s tough to make predictions, especially about the future”
            – Yogi Berra

Princeton Longevity Center Medical News, July 27, 2010, by David Fein MD  —  We all want to find a crystal ball that can foretell our future, especially about our health. With the decoding of the human genome in 2003 expectations ran high that within a few years we would be able to pinpoint the genetic cause of many diseases. And it is true that medical research is increasingly finding associations between a wide range of disease and genetic mutations.
The complexity and cost of performing genetic testing has rapidly come down.  Many genetic tests are now widely available at a reasonable cost.  This has led to a number of companies offering genetic screening tests to the general public, often without the need for a physician prescription.

It’s an enticing idea to have a painless test that can potentially tell your health future.  But before you get a genetic test there are some pitfalls to keep in mind.

Genetic “screening tests” are now are offered “direct to the consumer” by a variety of companies such as 23andMe and Navigenics.  Genetic screening tests are not a complete sequencing of your DNA such as was done for the Human Genome Project.  That is still far too costly and time consuming.  Instead, these tests look for Single Nucleotide Polymorphisms (SNPs) which are pinpoint variations in a gene.  These genetic variants can alter how a gene functions. The tests typically involve analyzing hundreds of thousands of SNPs that are believed to be associated with the risk of certain diseases or changes in how you may metabolize specific medications.

23andMe, for example, currently provides information on 162 gene-trait associations, including genes for disease risk, drug response and whether you are a carrier of inheritable diseases such as Tay-Sachs or breast cancer. According to their website, they divide the significance of the associations into “established research” and “preliminary research”. Established research associations are those that have been confirmed in at least two large studies or “have gained widespread scientific acceptance in the scientific community.” Preliminary research associations are those that “still need to be confirmed by the scientific community” and “may not stand the rigors of scientific replication.”

That is an important distinction to keep in mind.  Many of those associations between an SNP and a particular disease may not be as clear-cut as we think. Data that “still need to be confirmed by the scientific community” could be a weak link for making major life decisions.

Even putting aside the concerns about the accuracy of the data interpretation, there is still the issue of what to do with your results.

Genetic testing can’t tell you with any certainty whether you will develop a disease or not.  Your genes load the gun but it is your environment that pulls the trigger.  Simply having a genetic predisposition to a disease, such as Type II Diabetes, does not mean you will actually become diabetic.  That gene will interact with your weight, diet, level of physical activity and many other factors.  Simply finding the presence of a genetic variant can’t tell us whether the gene ends up being expressed as a disease. 
Not having the gene doesn’t mean you are safe, either.  Even if you don’t have a gene for Type II Diabetes, it is likely that a rigorous effort at overeating and avoiding physical activity will get you there anyway.

You could argue that knowing you have the gene for Type II Diabetes might make you more careful about your lifestyle in hopes of avoiding the disease.  If you are successful in making those changes then perhaps the test is useful.
On the other hand, the test results could lead you to feel that since you are more likely to get Diabetes at some point anyway, there is no point in depriving yourself now.  In that case, the test results may actually increase your risk and become a self-fulfilling prophecy.

Using Type II Diabetes as an example has the advantage of there being the potential for you to do something that may change your outcome.  Many other conditions included in genetic screening tests have no known effective means of prevention or add little to the advice you would get anyway. 

There is likely to be very limited value in a test that tells you that the risk of Alzheimer’s Disease in the general population is 4% but your risk is 30%.  That information will probably cause you significant long-term anxiety even though it is still more likely that you will not get the disease.  And, the test does not tell you when it might strike.  Every little normal moment of distraction or forgetfulness is likely to taken as the first sign of the disease.  You may never develop Alzheimer’s Disease or it might not start until you are in your 80’s, but losing your car keys at 50 will have you shopping for a nursing home.  Knowing you are at higher risk could push you to make decisions about your life that turn out to be unwarranted.

It is important to make a distinction between a genetic test ordered by your physician to look for a evidence of a specific condition versus the genetic screening tests.  There is a growing list of very useful genetic tests for diagnostic and treatment decisions.  Physicians are increasingly shifting to looking at genetic markers to diagnose cancers, metabolic disease, clotting disorders and many other conditions.  Genetic tests can also help to guide decisions about the choice of medications that you are likely to respond to best and to determine the optimum dosage.

Genetic testing will become increasingly important in the coming years.  If properly used it can be a powerful tool.  At this point genetic screening tests appear unlikely to offer enough benefit to warrant widespread use without medical counseling as to the appropriate use and the meaning of the results.

Computer Model of the DNA Helix

Despite what you may have seen in some textbooks, DNA is not built like a twisted ladder. The helix, or spiral, is an inherent feature of the DNA molecule. Notice, for instance, that in the picture below, that the groove on the left side of the picture is much larger than the right side. This is because the paired bases in the center meet each other at an angle.

DNA is a very large molecule; the image here shows only a tiny fraction of the typical molecule. If an entire molecule of DNA from the virus “bacteriophage lambda” were shown at this scale, the image would be 970 meters high. For the bacterium Escherichia coli, the image would be 80 kilometers long. And for a typical piece of DNA from a eukaryote cell, the image would stretch for 1600 kilometers, about as far as it is from Dallas to Washington, D. C.! Obviously such a large molecule is not fully stretched out inside the cell, but is wound around proteins called histones which protect the DNA.

You might also notice in the image that the two halves do not quite come in contact. In fact they are held together by hydrogen bonds, a sort of electrical attraction between partially negative atoms on the base of one side with the partially positive atoms on the other. Both sides have positive and negative charges. A single such pairing would not hold the molecule together well, but several million such bonds are quite effective. This also has the advantage that little effort is required to pull the two halves apart for replication, when the DNA is copied, and for transcription, when the DNA message is read. The message of DNA is the information from which the cell and its components are built.


This model of DNA appears courtesy of the Image Library of Biological Macromolecules based in Jena, Germany, which maintains a large archive of spectacular computer graphics of DNA, RNA, and proteins. The background for this page was made by Jim Angus at the Los Angeles County Museum.

The Bergen Record, July 27, 2010, ny Barbara Williams  —  Michael Stanzione just wants to go home.

The Saddle Brook resident has been stuck in the hospital for three years, away from his wife, Debra, and 7-year-old son, Brian. He faces a lifetime in a pale yellow cubicle of a room at Bergen Regional Medical Center because insurance won’t pay for home health care

Stanzione, 52, is caught in an insurance quagmire — smack between inadequate coverage by Aetna and Medicare and ineligibility for standard Medicaid coverage.

“I’ve been trying to get home since May 2009,” he said. “But I’m not giving up. I have faith and that is keeping me going.”

Stanzione has Pompe disease, a rare and often fatal genetic illness that has left him on a ventilator.

His arms and legs are weakened by the disease and the muscles surrounding his lungs are so seriously compromised that they can’t expand his chest cavity enough so the lungs can take in air.

If he went home, he would need full-time nursing care to make sure the ventilator that helps him breathe is working properly — and to come to his aid if he starts choking.

But Stanzione isn’t bedridden and he believes he is capable of much more than languishing in a hospital room.

At the hospital, he walks short distances with a walker and sits for hours in a wheelchair working on his computer. He tosses a ball to his son when Brian and Debra visit on weekends. Stanzione says he is capable of doing light chores, such as making sandwiches and folding laundry in his Cape Cod house. He says he may even be able to work several hours a day as a computer programmer for his previous employer, Affiliated Computer Services.

Dr. Steven Jacoby, a pulmonologist who oversees Stanzione’s care from The Valley Hospital in Ridgewood, said he thinks Stanzione “would do fine at home.”

“It’s the stupidity of insurance that’s keeping him in the hospital,” Jacoby said.

Paying the price?

His care at Bergen Regional is paid for through Institutional Medicaid, but it does not cover services outside a facility. Standard Medicaid coverage does offer home services, but Stanzione’s disability income disqualifies him for that insurance. Meanwhile, Aetna, which covers the family through Debra’s employer, pays nothing for Stanzione’s hospitalization because the family is covered through Institutional Medicaid.

“Since Aetna isn’t paying anything right now, funding full-time home health care isn’t financially beneficial,” Jacoby said. “But overall for the system, it would be cheaper to have him home.”

If Stanzione went home, Aetna would pay for 60 four-hour visits a year, said Susan Millerick, an Aetna spokeswoman.

Part-time care could also be funded through Medicare, but exactly how many hours couldn’t be determined, said Jeffrey Hall, regional director for external communications for the Centers for Medicare and Medicaid Services. Karyn Ottman, Stanzione’s social worker at Bergen Regional, said she has never seen Medicare approve more than two to four hours on weekdays.

Even if the Aetna and the Medicare coverage were combined, it wouldn’t pay for enough hours for an aide.

Stanzione’s hope lies with a Medicaid waiver. He applied a few weeks ago but fears his $2,600 monthly disability payments, well over the $1,215 maximum allowed by Medicaid, would disqualify him.

“After that, we don’t have a Plan B,” Debra Stanzione said. “We’ve been told keeping him in the hospital is sort of like shopping in bulk — the more you have, the cheaper it is. But we’re not settling for that. We want him home.”

In the last three years, Stanzione has been home only once, for an hour last Christmas. He keeps pictures of the visit on his wall.

Michael Stanzione just wants to go home.

The Saddle Brook resident has been stuck in the hospital for three years, away from his wife, Debra, and 7-year-old son, Brian. He faces a lifetime in a pale yellow cubicle of a room at Bergen Regional Medical Center because insurance won’t pay for home health care.

Stanzione, 52, is caught in an insurance quagmire — smack between inadequate coverage by Aetna and Medicare and ineligibility for standard Medicaid coverage.

“I’ve been trying to get home since May 2009,” he said. “But I’m not giving up. I have faith and that is keeping me going.”

Stanzione has Pompe disease, a rare and often fatal genetic illness that has left him on a ventilator.

His arms and legs are weakened by the disease and the muscles surrounding his lungs are so seriously compromised that they can’t expand his chest cavity enough so the lungs can take in air.

If he went home, he would need full-time nursing care to make sure the ventilator that helps him breathe is working properly — and to come to his aid if he starts choking.

But Stanzione isn’t bedridden and he believes he is capable of much more than languishing in a hospital room.

At the hospital, he walks short distances with a walker and sits for hours in a wheelchair working on his computer. He tosses a ball to his son when Brian and Debra visit on weekends. Stanzione says he is capable of doing light chores, such as making sandwiches and folding laundry in his Cape Cod house. He says he may even be able to work several hours a day as a computer programmer for his previous employer, Affiliated Computer Services.

Dr. Steven Jacoby, a pulmonologist who oversees Stanzione’s care from The Valley Hospital in Ridgewood, said he thinks Stanzione “would do fine at home.”

“It’s the stupidity of insurance that’s keeping him in the hospital,” Jacoby said.

Paying the price?

His care at Bergen Regional is paid for through Institutional Medicaid, but it does not cover services outside a facility. Standard Medicaid coverage does offer home services, but Stanzione’s disability income disqualifies him for that insurance. Meanwhile, Aetna, which covers the family through Debra’s employer, pays nothing for Stanzione’s hospitalization because the family is covered through Institutional Medicaid.

“Since Aetna isn’t paying anything right now, funding full-time home health care isn’t financially beneficial,” Jacoby said. “But overall for the system, it would be cheaper to have him home.”

If Stanzione went home, Aetna would pay for 60 four-hour visits a year, said Susan Millerick, an Aetna spokeswoman.

Part-time care could also be funded through Medicare, but exactly how many hours couldn’t be determined, said Jeffrey Hall, regional director for external communications for the Centers for Medicare and Medicaid Services. Karyn Ottman, Stanzione’s social worker at Bergen Regional, said she has never seen Medicare approve more than two to four hours on weekdays.

Even if the Aetna and the Medicare coverage were combined, it wouldn’t pay for enough hours for an aide.

Stanzione’s hope lies with a Medicaid waiver. He applied a few weeks ago but fears his $2,600 monthly disability payments, well over the $1,215 maximum allowed by Medicaid, would disqualify him.

“After that, we don’t have a Plan B,” Debra Stanzione said. “We’ve been told keeping him in the hospital is sort of like shopping in bulk — the more you have, the cheaper it is. But we’re not settling for that. We want him home.”

In the last three years, Stanzione has been home only once, for an hour last Christmas. He keeps pictures of the visit on his wall.

“It was really nice,” Stanzione said, a smile skipping across his face. “It felt good to be home and the emergency workers who brought me there did it on their own time.”

Having her husband away so long “is a missing link in our family,” Debra Stanzione said.

“I really want him home, but my heart aches for our son,” she said. “He did everything with Mike; he’s such a daddy’s boy. Mike hasn’t been home since Brian was 4.”

While the family struggles to reside under the same roof, friends are joining together to offer support. They have planned a golf event — information is available at golf4mike.com — for Aug 6 to raise money for his home care. They hope to make it an annual event.

“It’s very humbling to have so much stuff done for you,” Stanzione said. “I don’t even know how to begin to thank everyone.”

Meanwhile, he continues his nightly ritual of talking to his family via a webcam, e-mailing friends and watching baseball.

“That’s another reason I have to get home — my wife may be influencing my son,” Stanzione joked. “She likes the Mets and country music and I’m a San Francisco Giants and Beatles fan.”

He worries that his son will lose all memory of him living at home.

“I don’t want him to only remember me being in a hospital,” Stanzione said. “But it’s been so long since I’ve been home, I don’t know if all those memories are gone.”

Disease far from common

Fewer than 10,000 Americans have Pompe disease. They lack an enzyme that breaks down glycogen, a stored form of sugar. This abundance of glycogen accumulates throughout the body, but concentrates in and causes deterioration of the heart and skeletal muscles.

Every two weeks, Stanzione goes to Valley for enzyme replacement therapy, an intravenous drip with a drug called lumizyme that prompts cells to process the poisonous buildup and allows muscles to regain strength. The development of its older sister drug, myozyme, was the focus of the movie, “Extraordinary Measures,” starring Harrison Ford. The film was adapted from former Englewood resident John Crowley’s book, “Chasing Miracles,” which chronicled his efforts to make the drug available to two of his children afflicted with Pompe.

Stanzione was 35 when he first noticed symptoms — some leg pains and a sore back. A weekend baseball player, he thought he just had a bad back and didn’t seek treatment until he was 40. By then his gait was off, and he had difficulty navigating stairs. In 1998, his New Year’s resolution was to find out what was wrong.

A slew of doctor visits and tests left him misdiagnosed for almost a decade with polymyositis, a painful autoimmune inflammation of muscle tissue. His pain and weakness continued to worsen until March 2007, when he landed in Valley’s emergency room barely able to breathe, walk or swallow. His weakened muscles prevented his lungs from expelling carbon dioxide fast enough and doctors said that without care he would have been in a coma or dead within 24 hours.

Doctors at Valley correctly diagnosed his condition as Pompe, but he contracted infections that further weakened him and he needed a gastric tube inserted because he couldn’t swallow.

For two years, he was unable to eat or drink. He didn’t walk for eight months. In addition to the ventilator, he has a tracheotomy and an inflatable cuff around his throat that allows him to breathe and speak. He’s made the rounds of area hospitals, including Meadowlands Hospital in Secaucus and the University of Medicine and Dentistry in Newark, for treatments.

But Stanzione has slowly rallied, surprising even his doctors. Although he still has the gastric tube for liquids, his throat muscles have strengthened enough for him to eat chicken and pasta.

One day soon, he hopes to be sipping coffee while his son gets ready for school.

“I miss coffee,” he said. “But I really miss my wife and son. I want to watch him leave for school, help him with his homework and kiss him goodnight every night.”

E-mail: williamsb@northjersey.com

“It was really nice,” Stanzione said, a smile skipping across his face. “It felt good to be home and the emergency workers who brought me there did it on their own time.”

Having her husband away so long “is a missing link in our family,” Debra Stanzione said.

“I really want him home, but my heart aches for our son,” she said. “He did everything with Mike; he’s such a daddy’s boy. Mike hasn’t been home since Brian was 4.”

While the family struggles to reside under the same roof, friends are joining together to offer support. They have planned a golf event — information is available at golf4mike.com — for Aug 6 to raise money for his home care. They hope to make it an annual event.

“It’s very humbling to have so much stuff done for you,” Stanzione said. “I don’t even know how to begin to thank everyone.”

Meanwhile, he continues his nightly ritual of talking to his family via a webcam, e-mailing friends and watching baseball.

“That’s another reason I have to get home — my wife may be influencing my son,” Stanzione joked. “She likes the Mets and country music and I’m a San Francisco Giants and Beatles fan.”

He worries that his son will lose all memory of him living at home.

“I don’t want him to only remember me being in a hospital,” Stanzione said. “But it’s been so long since I’ve been home, I don’t know if all those memories are gone.”

Disease far from common

Fewer than 10,000 Americans have Pompe disease. They lack an enzyme that breaks down glycogen, a stored form of sugar. This abundance of glycogen accumulates throughout the body, but concentrates in and causes deterioration of the heart and skeletal muscles.

Every two weeks, Stanzione goes to Valley for enzyme replacement therapy, an intravenous drip with a drug called lumizyme that prompts cells to process the poisonous buildup and allows muscles to regain strength. The development of its older sister drug, myozyme, was the focus of the movie, “Extraordinary Measures,” starring Harrison Ford. The film was adapted from former Englewood resident John Crowley’s book, “Chasing Miracles,” which chronicled his efforts to make the drug available to two of his children afflicted with Pompe.

Stanzione was 35 when he first noticed symptoms — some leg pains and a sore back. A weekend baseball player, he thought he just had a bad back and didn’t seek treatment until he was 40. By then his gait was off, and he had difficulty navigating stairs. In 1998, his New Year’s resolution was to find out what was wrong.

A slew of doctor visits and tests left him misdiagnosed for almost a decade with polymyositis, a painful autoimmune inflammation of muscle tissue. His pain and weakness continued to worsen until March 2007, when he landed in Valley’s emergency room barely able to breathe, walk or swallow. His weakened muscles prevented his lungs from expelling carbon dioxide fast enough and doctors said that without care he would have been in a coma or dead within 24 hours.

Doctors at Valley correctly diagnosed his condition as Pompe, but he contracted infections that further weakened him and he needed a gastric tube inserted because he couldn’t swallow.

For two years, he was unable to eat or drink. He didn’t walk for eight months. In addition to the ventilator, he has a tracheotomy and an inflatable cuff around his throat that allows him to breathe and speak. He’s made the rounds of area hospitals, including Meadowlands Hospital in Secaucus and the University of Medicine and Dentistry in Newark, for treatments.

But Stanzione has slowly rallied, surprising even his doctors. Although he still has the gastric tube for liquids, his throat muscles have strengthened enough for him to eat chicken and pasta.

One day soon, he hopes to be sipping coffee while his son gets ready for school.

“I miss coffee,” he said. “But I really miss my wife and son. I want to watch him leave for school, help him with his homework and kiss him goodnight every night.”

A new form of paper made of super-thin sheets of carbon could help fight disease-causing bacteria in applications ranging from anti-bacterial bandages to food packaging. (Credit: ACS Nano)

 

 

American Chemical Society, July 26, 2010  —  A new form of paper with the built-in ability to fight disease-causing bacteria could have applications that range from anti-bacterial bandages to food packaging that keeps food fresher longer to shoes that ward off foot odor. A report about the new material, which consists of the thinnest possible sheets of carbon, appears in ACS Nano, a monthly journal.

Chunhai Fan, Qing Huang, and colleagues explained that scientists in the United Kingdom first discovered the material, known as graphene, in 2004. Since then, the race has been on to find commercial and industrial uses for graphene. Scientists have tried to use graphene in solar cells, computer chips, and sensors. Fan and Huang decided to see how graphene affects living cells.

So they made sheets of paper from graphene oxide, and then tried to grow bacteria and human cells on top. Bacteria were unable to grow on the paper, and it had little adverse effect on human cells.

“Given the superior antibacterial effect of graphene oxide and the fact that it can be mass-produced and easily processed to make freestanding and flexible paper with low-cost, we expect this new carbon nanomaterial may find important environmental and clinical applications,” the reports states.

Journal Reference:

  1. 1.                        Wenbing Hu, Cheng Peng, Weijie Luo, Min Lv, Xiaoming Li, Di Li, Qing Huang, Chunhai Fan. Graphene-Based Antibacterial Paper. ACS Nano, 2010; : 100701135317095 DOI: 10.1021/nn101097v

Top of Form

American Chemical Society (2010, July 26). New antibacterial material for bandages, food packaging, shoes. ScienceDaily. Retrieved July 26, 2010, from http://www.sciencedaily.com­ /releases/2010/07/100721133219.htm

No needle: Microneedles made of a polymer that dissolves in body tissues can be used to deliver vaccines directly and painlessly into the skin. The microneedles shown here, inserted into pig skin, dissolve in a matter of minutes.  Credit: Sean Sullivan, Georgia Institute of Technology

 

 

A new technology delivers a vaccine in a painless, biodegradable skin patch.

 

MIT Technology Review, July 26, 2010, by Courtney Humphries  —  Getting vaccinated for the flu or other infections could become as easy as pressing a patch onto the skin–no shot in the arm required

A new paper published in Nature Medicine describes a patch that holds an array of microneedles that administer a vaccine and dissolve painlessly. That could make it possible for people to get inoculated more easily and even administer their own vaccines.

Most vaccines are delivered by an injection into muscle. But Mark Prausnitz, lead author of the paper and a chemical and biological engineer at Georgia Institute of Technology, says that the surface of the skin could be a better entry point. Because the body expects to encounter harmful invaders on its surfaces, the skin is loaded with cells that can launch an immune response–a key step for a vaccine to work.

Researchers have investigated other microneedle patches as a way to deliver drugs. This version, a collaboration between the labs of Prausnitz and Richard Compans, a microbiologist at Emory, adds an innovation: The needles are constructed out of a polymer that dissolves in bodily fluids. Just several hundred micrometers in length, the needles can penetrate the outer layers of the skin before melting away in a few minutes. As they do so, a vaccine encapsulated in the needles travels into the skin. Only a thin biodegradable backing is left behind, and it washes away in water.

Researchers tested the patches on mice and found that the animals that received the flu vaccine by skin patch could fight off an infection 30 days later just as well as mice that had received an injection. Furthermore, mice vaccinated through the skin had a much lower level of virus in their lungs, suggesting that the patch could provoke a more effective immune response.

Prausnitz and his collaborators are seeking funding for a clinical trial of the influenza vaccine patch in humans. They are also investigating the possibility of using a similar system for other types of infectious diseases.

Samir Mitragotri, a chemical engineer at the University of California, Santa Barbara, says that the work is “highly innovative,” and that the dissolving microneedles solve two important problems in immunization: They are painless, and they avoid the need to dispose of medical waste.

Bruce Weniger, a flu vaccine researcher at the Centers for Disease Control and Prevention, adds that the patches would be less invasive for patients and easier to deliver to remote populations. As such, they could help make vaccination campaigns easier in developing countries. But Weniger adds that economics may get in the way of replacing existing vaccine shots with patches.

 

Making bone: Stem cells derived from skin are better at forming bone cells (right) than stem cells derived from blood (left) are, because skin is more closely related to bone. Colonies of bone cells are shown in red.   Credit: Kitai Kim, Children’s Hospital

Engineered stem cells carry markers of their former identities–a trait that could hinder research into diseases.

MIT Technology Review, July 26, 2010, by Lauren Gravitz  —  While reprogrammed stem cells–those derived from fully differentiated adult cells–can be transformed into any type of tissue, scientists have now discovered that they preserve a memory of where they came from. That memory appears to influence the cells’ development; reprogrammed stem cells are more easily converted back to their original identity, according to a study released online today in Nature. The findings could affect research into the two main uses for reprogrammed stem cells; growing efforts to study disease in cells derived from patients with those diseases, and the development of replacement cell therapies.

A few years ago, researchers developed a way to reprogram adult cells into stem cells using a simple combination of genetic or chemical factors, no embryo required. Like embryonic stem cells, these induced pluripotent stem (iPS) cells can both reproduce themselves and differentiate into just about any type of tissue in the body. The technology spread rapidly around the globe, providing a way to study stem cells and their potential therapeutic benefits without the technical and ethical hurdles of using cells derived from embryos. But three years later, complications continue to crop up.

While iPS cells have passed all the traditional tests of so-called pluripotency–the ability to differentiate into any type of tissue–and appear genetically identical to embryonic stem cells, they do have limitations. George Daley and his colleagues have found, by studying stem cells from mice, that cells derived from blood are better able to differentiate back into blood cells than into bone; those derived from bone make poor blood cells and even poorer neurons.

Daley’s team also compared mouse iPS cells to those that had undergone nuclear transfer, the technique used to clone Dolly the sheep. The two methods trigger different mechanisms to push a cell back to a stem-cell state, and the chemical methods of iPS cell reprogramming appear to be less thorough. The iPS cells maintain chemical modifications on their DNA indicative of their previous identity, while nuclear transfer wipes the slate clean. (It wasn’t possible to do similar experiments with human cells, because no one has yet cloned human cells.)

The findings create a snag for the use of iPS cells for basic disease research. Many scientists have been collecting skin samples from patients with various diseases, reprogramming them back to iPS cells, and then prompting them to differentiate into tissues affected by the disease. This allows them to examine how the disease unfolds at a molecular level. But if the disease is a neurologic one, such as Parkinson’s, or anything not related to skin tissue, the variation that occurs due to the originating tissue could mask effects of the disease.

In terms of developing replacement cell therapies from iPS cells, the finding may be a boon. “It’s a double-edged sword,” says Daley. “It’s been very challenging to make and direct differentiation of iPS cells into specific tissues.” Starting off with the tissue of interest may make that easier, he says. To grow new bone cells, for example, scientists would be better off taking a bone biopsy from the patient as starting material, rather than beginning with blood or skin cells.

A second study released online today in Nature Biotechnology shows that these cellular memories fade after the cells have been grown for successive generations. “When the cells undergo hundreds of thousands of cell divisions, this memory seems to disappear,” says Harvard stem cell biologist Konrad Hochedlinger, who led the second study. “The cells become indistinguishable from each other, and the differences we observe early on seem to vanish.” But because extensive culturing can also introduce genetic mutations in the cells, this may not be a viable solution to wiping cellular memory.

Collectively, the studies make clear that researchers still have a lot to understand about iPS cells. “If for no other reason, we should still be studying nuclear transfer in order to study how nature does its own programming,” says Evan Snyder, who directs the stem cell and regenerative biology program at the Sanford-Burnham Medical Research Institute in La Jolla, CA. Snyder was not involved with the research. Nuclear transfer is a tricky process, never successfully performed in human cells and not a likely candidate for therapeutic use. But even as a research tool, it’s largely disappeared, and few labs continue to study it now that they can create their own iPS cells

Richard Baxter, MD, talks about the benefits of wine for your health and appearance.

Reviewed by Laura J. Martin, MD

WebMD.com, July/August 2010, by Denise Mann  —  The latest antiaging weapon is not an injection or a wonder cream, and it doesn’t involve any nipping or tucking either.

It’s a glass of red wine a day for women and two for men, according to Richard A. Baxter, MD, a plastic surgeon in Seattle and the author of Age Gets Better with Wine. Baxter gave a talk on wine and beauty at the annual meeting of the American Society for Aesthetic Plastic Surgery in Washington, D.C.  WebMD sat down with him to discuss exactly how age gets better with wine.  Here’s what he had to say:

Q  –  Wine and beauty, really?

A  –  There is quite a lot of data on the wine and beauty connection. I was surprised at how extensive the data is on wine as an anti-aging intervention.

Q  –  What is it about wine that can help us age and look better?

A  –  The mechanism is the antioxidants in red wine. Antioxidants sop up damaging free radicals that play a role in aging and age-related diseases. There is a much higher concentration of antioxidants called polyphenols, including resveratrol, in wine compared to grape juice. In wine, the skin and seeds are part of the fermenting process, but both are removed when making grape juice. 

I think stress has something to do with it, too. It is difficult to sort out how much of the benefits are from the chemical properties of wine vs. the types of behaviors that wine drinkers tend to have such as less stress in their lives. Wine is part of the Mediterranean diet, which is also rich in fresh fruits and vegetables, whole grains, nuts and seeds, legumes, seafood, yogurt, and olive oil. This diet is more of a lifestyle that includes drinking wine with dinner. Studies show that the Mediterranean diet is associated with longer, healthier lives.

Q  –  Any caveats?

A  –  Drinking a glass of red wine a day is the single most important thing that you can do other than nonsmoking, from an anti-aging point of view, but you can have too much of a good thing. Drinking more than recommended can have the opposite effect on your appearance and health.

Q  –  What is your wine prescription for WebMD readers?

A  –  A glass a day and your skin will glow. As anti-aging advice, this is as good as it gets.

Q  –  Specifically, what benefits can a person expect if they follow your advice?

A  –  You will look better, your skin will glow, and you will live five years longer than a teetotaler. There are also good studies that show people who drink red wine on a regular basis have fewer actinic keratoses [precancerous skin lesions]. You will have a significantly lower risk of Alzheimer’s disease, cancer, diabetes, and all of the things that go along with aging. People assume that drinking would decrease brainpower as you get old, but the most amazing thing is that regular wine drinkers have an 80% lower risk of developing Alzheimer’s disease.

Q  –  What about people who can’t consume alcohol?

A  –  People who can’t drink wine should just look to other whole foods with polyphenols and antioxidants, like pomegranates and blueberries. Or go for dark chocolate. It does a lot of the same things as wine. Both dark chocolate and red wine have been shown to protect the skin from sun damage.

Q  –  Will winemakers put plastic surgeons out of business?

A  –  No. It’s an adjunctive thing.

Q  –  There are some supplements out there that say they have the ingredients — namely resveratrol — that make red wine so healthy. Do they work?

A  –  The data is really minimal in terms of the effectiveness of resveratrol supplements. The jury is out about whether you get same benefits in a pill that you get with a glass of red wine.

Q  –  What about skin creams with resveratrol?

A  –  This will be the next big thing in skin care. Stay tuned.

Q  –  Are any wines better than others?

A  –  White wines do not have as many antioxidants as red wines. In terms of reds, it has more to do with the way the grapes are grown than the varieties of wine. Oregon pinot noirs tend to have higher levels of polyphenols and European wines tend to have more polyphenols than American wines, in general.

Q  –  What type of wine do you drink?

A  –  I like all red wines, but I am really partial to Australian shiraz.

SOURCE:  Richard A. Baxter, MD, plastic surgeon; author, Age Gets Better with Wine.

BP’s Horizon Deepwater oil rig collapsed into the sea and spewed oil into the only bluefin spawning ground in the Americas just as the few remaining North American stock giant bluefin were preparing to mate in the Gulf of Mexico.

 

For bluefin tuna and all species of tuna are the living representation of the very limits of the ocean. Their global decline is a warning that we just might destroy our last wild food.

 

By PAUL GREENBERG

In the international waters south of Malta, the Greenpeace vessels Rainbow Warrior and Arctic Sunrise deployed eight inflatable Zodiacs and skiffs into the azure surface of the Mediterranean. Protesters aboard donned helmets and took up DayGlo flags and plywood shields. With the organization’s observation helicopter hovering above, the pilots of the tiny boats hit their throttles, hurtling the fleet forward to stop what they viewed as an egregious environmental crime. It was a high-octane updating of a familiar tableau, one that anyone who has followed Greenpeace’s Save the Whales adventures of the last 35 years would have recognized. But in the waters off Malta there was not a whale to be seen.

What was in the water that day was a congregation of Atlantic bluefin tuna, a fish that when prepared as sushi is one of the most valuable forms of seafood in the world. It’s also a fish that regularly journeys between America and Europe and whose two populations, or “stocks,” have both been catastrophically overexploited. The BP oil spill in the Gulf of Mexico, one of only two known Atlantic bluefin spawning grounds, has only intensified the crisis. By some estimates, there may be only 9,000 of the most ecologically vital megabreeders left in the fish’s North American stock, enough for the entire population of New York to have a final bite (or two) of high-grade otoro sushi. The Mediterranean stock of bluefin, historically a larger population than the North American one, has declined drastically as well. Indeed, most Mediterranean bluefin fishing consists of netting or “seining” young wild fish for “outgrowing” on tuna “ranches.” Which was why the Greenpeace craft had just deployed off Malta: a French fishing boat was about to legally catch an entire school of tuna, many of them undoubtedly juveniles.

Oliver Knowles, a 34-year-old Briton who was coordinating the intervention, had told me a few days earlier via telephone what the strategy was going to be. “These fishing operations consist of a huge purse-seining vessel and a small skiff that’s quite fast,” Knowles said. A “purse seine” is a type of net used by industrial fishing fleets, called this because of the way it draws closed around a school of fish in the manner of an old-fashioned purse cinching up around a pile of coins. “The skiff takes one end of the net around the tuna and sort of closes the circle on them,” Knowles explained. “That’s the key intervention point. That’s where we have the strong moral mandate.”

But as the Zodiacs approached the French tuna-fishing boat Jean-Marie Christian VI, confusion engulfed the scene. As anticipated, the French seiner launched its skiffs and started to draw a net closed around the tuna school. Upon seeing the Greenpeace Zodiacs zooming in, the captain of the Jean-Marie Christian VI issued a call. “Mayday!” he shouted over the radio. “Pirate attack!” Other tuna boats responded to the alert and arrived to help. The Greenpeace activists identified themselves over the VHF, announcing they were staging a “peaceful action.”

Aboard one Zodiac, Frank Hewetson, a 20-year Greenpeace veteran who in his salad days as a protester scaled the first BP deepwater oil rigs off Scotland, tried to direct his pilot toward the net so that he could throw a daisy chain of sandbags over its floating edge and allow the bluefin to escape. But before Hewetson could deploy his gear, a French fishing skiff rammed his Zodiac. A moment later Hewetson was dragged by the leg toward the bow. “At first I thought I’d been lassoed,” Hewetson later told me from his hospital bed in London. “But then I looked down. ” A fisherman trying to puncture the Zodiac had swung a three-pronged grappling hook attached to a rope into the boat and snagged Hewetson clean through his leg between the bone and the calf muscle. (Using the old language of whale protests, Greenpeace would later report to Agence France-Presse that Hewetson had been “harpooned.”)

Ma jambe! Ma jambe!” Hewetson cried out in French, trying to signal to the fisherman to slack off on the rope. The fisherman, according to Hewetson, first loosened it and then reconsidered and pulled it tight again. Eventually Hewetson was able to get enough give in the rope to yank the hook free. Elsewhere, fishermen armed with gaffs and sticks sank another Zodiac and, according to Greenpeace’s Knowles, fired a flare at the observation helicopter. At a certain point, the protesters made the decision to break off the engagement. “We have currently pulled back from the seining fleet,” Knowles e-mailed me shortly afterward, “to regroup and develop next steps.” Bertrand Wendling, the executive director of the tuna-fishing cooperative of which the Jean-Marie Christian VI was a part, called the Greenpeace protest “without doubt an act of provocation” in which “valuable work tools” were damaged.

Metaphorically they are the terminus of an idea: that the ocean is an endless resource where new fish can always be found. In the years to come we can treat tuna as a mile marker to zoom past on our way toward annihilating the wild ocean or as a stop sign that compels us to turn back and radically reconsider.

But the main damage that took place that day was indisputably to the bluefin. After the encounter, the fishermen aboard the Jean-Marie Christian VI transferred the fish alive into a holding cage and slowly towed them away. Soon those tuna would be brought to feeding pens where they will spend at least several months putting on weight. Afterward, they will be slaughtered and sent to Japan, where 80 percent of the world’s Atlantic bluefin tuna are eaten with oblivion.

THERE ARE TWO  reasons that a mere fish should have inspired such a high-strung confrontation reminiscent of Greenpeace’s early days as a defender of whales. The first stems from fish enthusiasts who have for many years recognized the particular qualities of bluefin tuna — qualities that were they land-based creatures would establish them indisputably as “wildlife” and not just another “seafood” we eat without remorse. Not only is the bluefin’s dense, distinctly beefy musculature supremely appropriate for traversing the ocean’s breadth, but the animal also has attributes that make its evolutionary appearance seem almost deus ex machina, or rather machina ex deo — a machine from God. How else could a fish develop a sextantlike “pineal window” in the top of its head that scientists say enables it to navigate over thousands of miles? How else could a fish develop a propulsion system whereby a whip-thin crescent tail vibrates at fantastic speeds, shooting the bluefin forward at speeds that can reach 40 miles an hour? And how else would a fish appear within a mostly coldblooded phylum that can use its metabolic heat to raise its body temperature far above that of the surrounding water, allowing it to traverse the frigid seas of the subarctic?

Yes, bluefin tuna are warmblooded.

That bluefin can be huge — 10 feet and more than a thousand pounds — is a side note. For those of us who have seen their football silhouettes arise and vanish in less than a blink of an eye or held them alive, their hard-shell skins barely containing the surging muscle tissue within, they are something bigger than the space they occupy. All fish change color when they die. But with tuna the death shift feels more profound. Fresh from the water, their backs pulsing neon blue, their bellies gleaming silver-pink iridescence, they seem like the ocean itself.

And in a way they are, which explains the second reason bluefin have come to possess such totemic power. For bluefin tuna and all species of tuna are the living representation of the very limits of the ocean. Their global decline is a warning that we just might destroy our last wild food.

In prehistoric times, the hunting of fish began close by, in freshwater rivers and lakes and coastal ocean waters. But as human populations grew, easily accessed grounds fell short of demand. By the late Middle Ages, European stocks of freshwater fish and near-shore ocean species proved insufficient. By then, Basque and Viking fisherman had already moved on to the continental shelves off Canada, ushering in the Age of Cod — an age that escalated until the late 20th century, when some of the largest fishing vessels ever built devastated the once-two-billion-strong stock of cod on the Canadian Grand Banks. But there were still new places to fish. In the 1980s and ’90s, virgin fishing grounds were found in the Southern Hemisphere, and supplies of replacement fish like New Zealand hoki and Chilean sea bass helped seafood supplies keep pace with demand.

But appetites continued to outstrip supply. Global seafood consumption has increased consistently to the point where we now remove more wild fish and shellfish from the oceans every year than the weight of the human population of China. This latest surge has taken us past the Age of Cod and landed us squarely in the Age of Tuna. Fishing has expanded over the continental shelves into the international no-man’s territory known as the high seas — the ocean territory that begins outside of national “exclusive economic zones,” or E.E.Z.’s, usually 200 nautical miles out from a country’s coast, and continues until it hits the E.E.Z. of another country. The high seas are owned by no one and governed by largely feeble multinational agreements. According to the Sea Around Us project of the University of British Columbia’s Fisheries Center, catches from the high seas have risen by 700 percent in the last half-century, and much of that increase is tuna. Moreover, because tuna cross so many boundaries, even when tuna do leave the high seas and tarry in any one nation’s territorial waters (as Atlantic bluefin usually do), they remain under the foggy international jurisdiction of poorly enforced tuna treaties.

The essentially ownerless nature of tuna has led to the last great wild-fish gold rush the world may ever see. The most noticeable result of this has been the decline of the giant Atlantic bluefin tuna. But the Atlantic bluefin is just a symptom of a metastasizing tuna disease. The United Nations’ Food and Agriculture Organization reports that 7 of the 23 commercially fished tuna stocksare overfished or depleted. An additional nine stocks are also threatened. The Pew Environment Group’s tuna campaign asserts that “the boats seeking these tuna are responsible for more hooks and nets in the water than any other fishery.”

Tuna then are both a real thing and a metaphor. Literally they are one of the last big public supplies of wild fish left in the world. Metaphorically they are the terminus of an idea: that the ocean is an endless resource where new fish can always be found. In the years to come we can treat tuna as a mile marker to zoom past on our way toward annihilating the wild ocean or as a stop sign that compels us to turn back and radically reconsider.

“WE FIND OURSELVES  in a precarious situation.” So wrote Ritchie Notar, a co-owner of the internationally acclaimed Nobu restaurant chain, to Greenpeace U.K. back in 2008 after Greenpeace intensified its tuna-defense efforts and put forward the idea that bluefin should no longer be served at Nobu’s establishments. “We are dealing with thousands of years of cultural customs,” Notar continued in correspondence Greenpeace forwarded to me. “The Japanese have relied on tuna and the bounties of the sea as part of their culture and history for centuries. We are absolutely appreciative of your goals and efforts within your cause, but it goes far beyond just saying that we can just take what has now all of a sudden been declared an ‘endangered’ species off the menu. It has to do with custom, heritage and behavior.”

Many nations have contributed to the Atlantic bluefin’s destruction. Europeans and North Africans do most of the catching and ranching of the fish in the world today. The United States continues to allow bluefin fishing in its waters even though the Gulf of Mexico-spawned stock is considered by many scientists to have entered into full-scale collapse. But it is Japan, the world’s largest bluefin importer, that has taken perhaps the most aggressive pro-tuna-fishing position, sometimes assisted by Westerners like Ritchie Notar, who declaim the country’s long tuna-eating tradition. But history shows that Japan’s stake in tuna fishing is recent and, more important, part of the same endgame that has dragged all of humanity into the Age of Tuna. Before 1800, Japanese tuna sushi didn’t even exist.

Trevor Corson is an East Asia scholar turned popular nonfiction writer and author of the 2007 book “The Story of Sushi,” and for select groups he will act as a “sushi concierge,” hosting dinners often at the Jewel Bako Japanese restaurant in Manhattan’s East Village, one of which I attended this past winter. A Corson-guided meal aims to reveal the historical truth of tuna and to represent the very different fish that were the staples of sushi in earlier times. Plate by plate I watched as Corson walked a group of Manhattan professionals through a traditional Edo-period meal of snappers, jacks and other white-fleshed, smaller fish that most definitely did not include “red” tuna. Afterward, Corson sent me an excerpt from a 1999 Japanese anthology titled “Fish Experts Teach the Secrets of the Deliciousness of Fish” to further underline his point. “Originally, fish with red flesh were looked down on in Japan as a low-class food, and white fish were much preferred,” one of the book’s contributors, Michiyo Murata, writes. “Fish with red flesh tended to spoil quickly and develop a noticeable stench, so in the days before refrigeration the Japanese aristocracy despised them, and this attitude was adopted by the citizens of Edo [old Tokyo].” Other Japanese scholars like the sushi historian Masuo Yoshino confirm this. Murata, meanwhile, goes on to note that tuna were introduced into sushi only 170 years ago, when a large catch came into Edo one season. On that day a local sushi chef marinated a few pieces of tuna in soy sauce and served it as “nigiri sushi.” The practice caught on. Occasionally a big bluefin became sushi, but Corson notes these fish were nicknamed shibi — “four days” — because chefs would bury them for four days to mellow their bloody taste.

By the 1930s, tuna sushi was commonplace in Japan, but demand could be met by local supplies of tuna, including the Pacific bluefin species, which dwells in Japan’s coastal waters. It was World War II that took tuna fishing to the next level. “To recover from the devastation of the war,” Ziro Suzuki, formerly of the Japanese Far Seas Research Laboratory, wrote me, “Japanese fishermen needed more tunas to secure food for domestic demand and also to earn more money by exporting tunas for canning industries in Europe and the U.S. Those needs urged the expansion of fishing grounds outside of the historic grounds of the western Pacific.” But this next fishing expansion was technological as well as territorial. Throughout the postwar period, the Japanese perfected industrial long-lining, a practice that employs thousands of baited hooks. In the 1970s Japanese manufacturers developed lightweight, high-strength polymers that were in turn spun into extensive drift nets that could be many miles long. Though drift nets were banned in the high seas by the early ’90s, in the 1970s hundreds of miles of them were often deployed in a single night. When drift nets and long lines were coupled with at-sea freezing technology invented around the same time, Japanese fishermen were able to fish the farthest reaches of the oceans while keeping their frozen tuna sushi-ready for as long as a year.

Kenji Aoki for The New York Times

A major yield of all of this Japanese fishing effort was yellowfin tuna. Though they ate bluefin, Japanese did not hold them in high regard before the 1960s, and it took a confluence of socioeconomic factors in both Japan and the West to bring bluefin to the fore. By the late 1960s, sportfishing for giant bluefin tuna was starting in earnest off Nova Scotia, New England and Long Island. Like the Japanese at the time, North Americans had little regard for bluefin on the plate, usually discarding them after capture.

Bluefin sportfishing’s rise, however, coincided with Japan’s export boom. In the 1960s and ’70s, Japanese planes stuffed with electronics unloaded in the U.S. and returned empty — a huge waste of fuel. But when a Japanese entrepreneur realized he could buy New England and Canadian bluefin for a song, he started filling up all those empty cargo holds with tuna. Exposure to beef and other fatty meats during the U.S. occupation had already drawn the Japanese to appreciate bluefin’s fatty belly (otoro, in sushi terms). The Atlantic bluefin, the biggest bluefin, became the most favored of all. This appreciation boomeranged stateside when Americans started to develop their own raw-fish habit in the late 1970s.

Added to the already significant fishing pressure from the tuna canning industry, Japan’s and now the West’s sushi jones has come to stress populations of large tuna around the world, starting with the most environmentally sensitive Atlantic bluefin but with the risk of spreading to other species. In fact, one subpopulation of Atlantic bluefin has already vanished after heavy fishing by Japanese long-liners: The bluefin that used to congregate off Brazil disappeared in the early bluefin boom of the 1970s. The remaining Atlantic bluefin stocks are trending similarly, and the two other species of bluefin — the Pacific, which ranges between California and Japan, and the southern bluefin, which plies the waters around Australia — are not far behind. In the United States, the direct fishing pressure on bluefin continues — but perhaps a larger problem is that a large quantity of North American bluefin are caught accidentally as “by-catch” when industrial long-liners deploy their legions of hooks in search of yellowfin tuna over the bluefin’s spawning grounds in the Gulf of Mexico. By law, nearly all bluefin caught as by-catch must be dumped back into the sea. Usually by that point they are already dead.

All of this has led the bluefin to become a cause célèbre among conservation groups and the target of several organized “save the bluefin” campaigns. None of them have influenced Japanese consumers. In the case of Nobu, after numerous exchanges with Greenpeace, the sushi restaurant’s owners remained unpersuaded of the need to stop serving the fish. Their only concession was a haiku-esque warning on the menus of its London eateries:

“Bluefin tuna

Is an environmentally threatened species

Please ask your server for an alternative.”

Willie Mackenzie of Greenpeace U.K. responded angrily in a note to Ritchie Notar: “Despite the assurances that you take these issues seriously and that you want Nobu to be a leader in this field, you have essentially tried to abdicate responsibility by suggesting that it is down to your customers to decide if they want to eat an endangered species.”

AWAY FROM RESTAURANT menus and the entree preferences of individual consumers, more far-ranging choices are presenting themselves to humanity than picking a California roll or a sliver of otoro. These are choices that will shape the fate of not just Atlantic bluefin tuna, not just all tunas, but all the great sea creatures — sharks, swordfish, marlin, even whales. For every one of these animals is highly migratory and roams the high seas, the vast, ownerless seascape that makes up some 60 percent of the oceans.

Until the 1970s, fishing in the high seas tended to be based on the principles of Hugo Grotius’s 1609 treatise “Mare Liberum” — a document that advocated free use of the oceans by all. But in the last 40 years, Grotius’s “free sea” has grown progressively more circumscribed. Today, high-seas and highly migratory fish are overseen by 18 regional fisheries-management organizations. These “consensus-oriented” institutions, in which each member nation has equal status, can be guided more by political horse-trading than by sound science. A former chairman of the scientific committee of the International Commission for the Conservation of Atlantic Tunas (or Iccat), the body responsible for Atlantic bluefin, told me, “Even though scientific advice says you should stick to a specific catch number, in order to negotiate a deal they tend to nudge that number over a little bit.” That little nudge can be enough to put a population of tuna in jeopardy.

In 2008 Iccat set Atlantic bluefin catch limits that were nearly double what its own scientists recommended. Conservationists howled, and the quotas were reduced sharply. But by the time Iccat met again, in November 2009, environmentalists had come to home in on the historic mismanagement of Atlantic bluefin, many of them arguing that a simple reduction in catch quotas for the coming fishing season was not enough — that in fact a zero-catch quota was the only thing that would stave off the fish’s extinction. Iccat rejected the zero-quota idea. This in turn forced a much more high-pitched confrontation this spring between parties like Japan, which seems to feel that fishery-management problems can be resolved within the status quo, and those who are looking to take the high seas in a profoundly different direction.

The debate was joined when delegates gathered this past March in Doha, Qatar, for a meeting of the United Nations Convention on the International Trade in Endangered Species of Flora and Fauna, or Cites (pronounced SY-tees). It was a meeting that, for fish, could have been as important as the 1982 meeting of the International Whaling Commission that voted to establish a moratorium on commercial whaling worldwide. For if conservationists got their way, Atlantic bluefin would be included in the Cites treaty’s Appendix One — a result that would ban the international trade of the tuna and put them under the jurisdiction of the same U.N. body that oversees tigers, white rhinos and giant pandas. It would be the beginning of a process that would transition Atlantic bluefin tuna from seafood to wildlife.

It is precisely this kind of recasting that happened with whales in the 1980s, and Japan was intent on avoiding a similar recategorization with Atlantic bluefin tuna. As Masanori Miyahara, the director of the Fisheries Agency of Japan, put it to me: “Cites Appendix One is too inflexible . . . once a species is listed in a Cites appendix, it will never be delisted or down-listed as the history of Cites clearly shows.” In other words, once a fish becomes wildlife, it will stay wildlife. A Cites treaty would also allow those countries that happen to have bluefin in their territorial waters to continue to catch them for their own market while excluding all the other treaty member nations — a result that Masanori would surely find not only unfair but also capable of leading to further overfishing. (The European Union has indicated it will continue to catch its allowable quota even if a Cites resolution is passed.)

Japan’s touchiness about fairness on the high seas is understandable given its dependence on seafood. Its per capita seafood consumption is among the highest of any industrialized country. And Japan has not been blind to the problems that come with overfishing and excessively large fishing fleets. Indeed, in the last few years it has tried to rein in its industrial fishing effort, decommissioning vessels, literally pulling hooks out of the water. But this has failed to resolve another problem of the Age of Tuna. Just as the industrialized countries are starting to realize the need for more sensible management of the high seas, developing countries are heading in the opposite direction. “Developing countries firmly believe they have a right to expand their fisheries and that developed countries should reduce their fishing effort to compensate,” Ziro Suzuki wrote me. “In the process of trying to resolve the conflict of interest, the stocks become overfished, and overall fishing effort grows to an unacceptable level. . . . It’s really just another example of the North-South problem, just like CO2 emissions.”

The conflict between the developing and developed world plays an increasingly greater role in tuna negotiations, and at a certain point it is hard to figure out who is manipulating whom in an intrigue involving 175 countries, each trying to game the system. Representatives from both the WWF and the Pew Environment Group told me of a curious imbroglio as the Qatar Cites meeting neared its vote on bluefin. Japanese delegation members supposedly told African representatives that European bluefin fleets would relocate to the coast of Africa and catch African yellowfin tuna if the Cites bluefin motion passed. This despite the fact that European vessels are geared up specifically for bluefin fishing and lack the capacity to pursue yellowfin. Masanori Miyahara of the Fisheries Agency of Japan dismissed this claim as “completely wrong and unfounded. We never told such a thing to anybody. We even haven’t thought such an idea, ever.”

True or not, African nations lined up with Japan. After Libya and Sudan forced a vote, the Atlantic bluefin’s Cites Appendix One listing was rejected by a large majority.

Delegates flew away from Qatar with the status quo in place. The monthlong bluefin purse-seining season set earlier by Iccat for the Mediterranean would stand as it was with quotas above what many scientists had recommended. A month after the Cites meeting, BP’s Horizon Deepwater oil rig collapsed into the sea and spewed oil into the only bluefin spawning ground in the Americas just as the few remaining North American stock giant bluefin were preparing to mate in the Gulf of Mexico. Though the U.S. National Marine Fisheries Service has been deeply critical of the Mediterranean bluefin catch — in 2007, it went so far as to call for a moratorium — it has been noncommittal about the American fishery. When I asked the Fisheries Service if it would consider closing the bluefin season on the heels of the BP spill, I was offered a statement, part of which, recast in verse form, has an almost Nobu-type haiku quality:

“N.O.A.A. Fisheries is carefully monitoring

The spawning of bluefin tuna in the Gulf of Mexico

By collecting larval samples and analyzing reports from scientific observers.”

It seems then that no single nation is ready to commit to a sustainable future for the fish. Some would argue that extirpation might just have to be the bluefin’s fate. Other, smaller tuna might be better suited to industrial exploitation. The bigeye and yellowfin tuna generally grow faster and spawn earlier. And indeed these lesser tuna are already starting to fill in for the bluefin’s absence. In the United States most Americans usuallyend up eating bigeye when they order otoro — the fatty zebra-striped flesh that fetches the highest price on most sushi menus nowadays. But major populations of bigeye tuna are also declining. Should they go away, it’s hard to say what would come next.

we get ourselves out of the Age of Tuna with our moral center and our food supply intact? Can we develop a civilized hunter-gatherer relationship with tuna and indeed with all other fish and reach a point of equilibrium with our last wild food? Can the management bodies that have overseen the collapse of the most magnificent food fish we’ve ever known be trusted to manage what is left in its wake?

The answer depends on where you fall on the fairly broad political spectrum of the world’s different tuna watchers. The Fisheries Agency of Japan maintains that “Japan is committed to ensure the recovery” of the Atlantic bluefin and has stipulated it will support a complete shutdown of the bluefin fishery at next fall’s Iccat meeting, should the scientific committee recommend it. Greenpeace meanwhile has punted on the bluefin political process. “Others have failed our oceans,” Oliver Knowles told the press as he prepared his mini armada off Malta, “so Greenpeace will act.” Greenpeace is calling for a radical realignment of the high seas, to take stewardship away from regional fisheries-management organizations and establish 40 percent of the world’s ocean territory as a marine reserve, a kind of Antarctica-style agreement with shades of whale, where nations, instead of bargaining over quotas, would simply not be able to do any fishing at all in large areas of the oceans. Most other environmental organizations are behind the marine-reserve idea, but they vary in opinion on how big those reserves should be. The Blue Ocean Institute calls for a five-year moratorium on Atlantic bluefin fishing everywhere. TheWWF further advocates that the industrial fishing methods that spread during the Age of Tuna — the drift nets, long lines, purse seines and spotter planes — be done away with. In their view, the “artisanal” single-hook-and-line fishing practices of old are the only way to sustainably hunt big and naturally scarce predators like bluefin.

But if we are to embark on a global project of ramping down tuna fishing, what are we to eat?

Until the modern era, the response to wild-game decline has been a primitive one: widespread destruction of the animals that can’t stand up to our hunting followed by the selection of a handful of ones that we can tame. Out of the many mammals that our forebears ate before the last ice age, humans selected four — cows, pigs, sheep and goats — to be their principal meats. Out of all the many birds that darkened the primeval skies, humans chose four — chickens, turkeys, ducks and geese — to be their poultry.

And indeed, this is a process that is taking shape rapidly with fish. Atlantic salmon are now commercially extinct throughout almost the entirety of their range but have become one of the most widely farmed fish in the world.

But while leaps have been made in taming marine fish, tuna, particularly bluefin tuna, may not make very much sense for the farm. Bluefin ranching as it is practiced in the Mediterranean, and with the Pacific bluefin in Japan and the southern bluefin in Australia, rightly faces strong environmental criticisms since it relies on catching juveniles from the wild and denies those baby bluefin a chance to reach adulthood and breed. Now, however, the final steps of fully taming or “closing the life cycle” of bluefin tuna are under way, which will make it possible for bluefin to be grown from an egg in a laboratory to a full-size adult. In such a system, an isolated “domestic” family of bluefin can be established that need not have any interaction with the wild at all. For several years Japan has been producing small amounts of closed-life-cycle Pacific bluefin (known as Kindai tuna in the market). In Europe and Australia, scientists have used light-manipulation technology as well as time-release hormone implants invented by the Israeli endocrinologist Yonathan Zohar to bring about the first large-scale captive spawning of Atlantic and southern bluefin.

But there are considerable complications ahead. As Richard Smullen, an Australia-based feed-company specialist working to come up with a suitable diet for farmed bluefin, explained: “The thing is the metabolic rate of these fish is very high compared to other fish; they swim fast, they heat their brains and vital organs and are warmer than the surrounding water, so this is energetically expensive. An analogy is like trying to feed an ultramarathon runner — they have the potential to eat a lot and not put on any weight.” Though Smullen says that it is possible to bring feed-conversion ratios for bluefin down, currently it may take 15 pounds of feed to produce a single pound of tuna, roughly 10 times as much as is needed for farmed salmon.

As fisheries decline globally, more and more countries are trying to replace their wild fish with farmed ones. Today 30 million tons of small forage fish are removed from the oceans yearly, with the majority of it going to feed farmed fish. If we end up farming bluefin on the same scale as we now farm salmon, the tuna, with its poor feed-conversion rate, may end up taking the food of the remaining wild fish that we haven’t yet got around to catching.

In addition there is little evidence to suggest that taming a species saves its wild forebear. Tiger farms in China have not halted tiger declines in the wild. Hundreds of millions of farmed Atlantic salmon have not stanched wild Atlantic salmon’s continued decline. Just because we can tame something doesn’t mean we should. The example of whales again rises. As the science historian D. Graham Burnett points out in a coming book on the Save the Whales movement, collaborations between American nuclear scientists and marine biologists were once proposed in the 1960s whereby tropical atolls, leveled by nuclear testing, could be used as giant corrals for the commercial farming of cetaceans. But fortunately for the whale — and I think for us too — we have come to see the whale not as something we fish for, not as something we farm, but as something we appreciate and maybe empathize with. Instead of expanding our stomachs or our wallets, whales have expanded our consciousness, our very humanity. So we have to ask ourselves, is there any rational argument for humans to eat bluefin tuna, wild, ranched or farmed? Is the fish really so special that no substitute will do? If the Japanese adapted to a higher-fat diet in half a century, could they and all sushi lovers not shift gears again and adapt to a sustainable diet?

It was in answer to these questions that I went looking for a farmed fish that could satisfy tuna-eaters at the sushi bar. A fish that had the dense “bite” of tuna but with a smaller ecological footprint — a Volkswagen instead of a Hummer.

My search led me to the coast of the Big Island of Hawaii, where I motored with a tall, optimistic Australian named Neil Anthony Sims. As we donned wetsuits, fins and scuba tanks, Sims rejoiced in telling me tales of his adopted land. Eventually we spat in our masks, adjusted our regulators and dived into the water above Sims’s farm — a huge underwater ziggurat that is the center of his company, Kona Blue Water Farms.

Until recently, most of the fish we’ve chosen to domesticate have been accidents. Salmon, striped bass, trout — we have chosen those species because we knew them as wild game. We seldom considered their biological profiles or whether they jibed well with the ecological limitations of a crowded planet.

But Neil Sims was a fisheries biologist before he was a fish farmer. And it was his direct personal experience with the limitations of fisheries management that persuaded him that fish farming, done right, was a better choice than fish catching.

Sims began his career in the remote Cook Islands of the South Pacific. There he was responsible for managing a giant snail called a trochus that produces an attractive pearly shell, valuable to native jewelers. Over half a decade, he implemented numerous management strategies. Nothing worked — not even shortening the harvest season drastically. The day after one season ended, he came across a bare-chested Polynesian elder who had pulled his dugout canoe onto the beach. Sims looked inside the boat and saw it filled with trochus.

“I yelled at him,” Sims remembers. “Then he yelled at me. He started to cry. Then I started to cry, and then the old bugger finally says: ‘Why? Why did you close the season? There are still some left!’ ” This moment prompted him to look beyond fishing, to an entirely different approach.

Sims was drawn to Hawaii, with its deep near-shore waters and strong currents — attributes favorable to aquaculture that he believed could make ocean farming sustainable. But the fish farming he found on arrival in Hawaii didn’t impress him. “People were trying milkfish and mullet,” Sims recalled. “They start with the letter ‘m’ and they’re all really kind of hmmmmm in the mouth, if you know what I mean.” Sims found the fish too bony and small, with loose, mushy flesh. This was important. Sims’s long-standing beat in the South Pacific had persuaded him that “there was an opportunity for a high-value, sushi-quality fish,” a fish that could fit into the dense-flesh category that the Age of Tuna had cultivated in Japan and indeed throughout the developed world.

After parsing many species he came across Seriola rivoliana. Known in Hawaiias kahala, it is a speedy, firm-fleshed animal of the same family as yellowtail and amberjack. They are only very distantly related to tuna and do not have tuna’s ruby red color, but they still have dense flesh and could easily pass for white albacore sushi. The fat content in Sims’s farmed kahala is around 30 percent, and indeed it is the presence of fat that accounts for much of a sushi fish’s tunalike flavor.

Sims was further intrigued when he found that kahala had barely been fished commercially. In their wild form kahala can carry ciguatera poison — a toxin sometimes deadly to humans that kahala ingest when they feed around coral reefs. But when kahala are isolated away from reefs and fed a traditional aquaculture diet of soy and fishmeal, they are ciguatera-free. (Sims asserts that ciguatera has never been detected in the flesh of his fish.) Since they have not been fished commercially, wild kahala populations are large and unlikely to be severely damaged through interaction with farmed fish. Moreover, kahala are much more “feed efficient” than tuna. The amount of fish required to produce a pound of kahala ranges from 1.6 pounds to 2 pounds, an order of magnitude better than bluefin. And Sims recently began feed trials using diets that contain no directly harvested forage fish. Lastly, unlike tuna, which require a tremendous investment in spawning technology, kahala are naturally fecund: they breed frequently, at least weekly, throughout the year.

THERE ARE, OF COURSE, those who would disagree with Sims’s approach. When I asked Casson Trenor, author of the 2009 book “Sustainable Sushi,” for his impression of the kahala as a farmed fish, he responded that the farming of any carnivore is “fighting the current.” “You may have a farm that has a more efficient protein ratio,” Trenor wrote me, “but produces more waste streams. Perhaps you have a feed pellet that knocks your feed conversion ratio down to 1 to 1, but you continue to host a rampant parasite infestation. . . . We need to identify fish that through their physiology and life history actually lend themselves to clean farming operations.” Trenor’s own compromise is to serve wild “small format” tuna like skipjack or albacore, fish that he feels can embrace the “principles of seasonality, local awareness and sustainability” that sushi originally expressed before it was “transformed through cultural misinterpretation and overzealous globalization into exactly the opposite.”

But as I plunged into the calm blue waters off Kona and inflated my diving vest to gain equilibrium in the water column, I couldn’t help thinking that in a world of environmental evils prosecuted against fish, the farming of a more efficient carnivore than a bluefin under the stewardship of a knowledgeable, environmentally conscious biologist was a good deal better than the rapacious industrial harvesting of “large format” tuna. Looking down at this “cathedral” of fish, as Sims called it, the possibility of a certain balance presented itself. Using technology developed over the last 10 years, Kona Blue has constructed diamond-shape cages that can be moored in the open ocean away from sensitive coastal areas. As I glided down, past the fish swimming in unison in their net pen, I felt a cautious optimism. The site of these pens had been carefully chosen; the swift currents meant that nutrientsdid not accumulate below the pens. And regular monitoring has found the fish to have no internal parasites, unlike the wild kahala. Sims’s commitment to transparency is also encouraging. He regularly posts water-quality reports on his Web site and presumably will do the same as the operation expands.

Sims waved me over to the side of the net pen. I floated above him, close enough to see that the fish actually seemed to recognize him. In what he would later describe to me as the “rock-star effect,” the fish crowded to be close to him. Sims spread his arms out wide and seemed to take in their adulation.

Sims has trademarked his kahala with the name Kona Kampachi — “Kona” for its point of origin, “Kampachi” for the similaranimal in Japan. They retail for $18 to $20 a pound in fillet form and to date have a tenuous foot in the market. Production reached more than a million pounds in 2008, about a third of the amount of bluefin caught in American waters that year. After a hiatus during most of 2009 and the first part of 2010 while Sims reconfigured his cages, the product will be reintroduced this July with even more capacity. Kona Kampachi may not have the rich ruby color of tuna (a color that is often enhanced artificially by “gassing” with carbon monoxide), but it is an extremely pleasant sushi experience. It satisfies the sashimi yen that has been created over the last 30 years — the yen for the firm, energy-rich musculature of a fast-swimming open-ocean fish.

Can we embrace a new set of species that we don’t know intimately in their wild form? Can we come to an understanding of which fish work for us as “seafood” and which fish don’t? I would hope so. The survival of the wild ocean could very well depend on it. I took one more look at Neil Sims floating with arms outstretched, his kahala finning in the current, each one mutely appraising this conductor of a silent concert. The only sound was the whir of bubbles rising by my ears.

SEAFOOD. HOW MANY species suffer those two mean English syllables? Other languages are no kinder. Romance European cultures use the expression “sea fruit,” while Slavs say “sea gifts.” So-called vegetarians rue the killing of farmed terrestrial animals but regularly eat wild fish. Kosher laws mandating merciful animal slaughter don’t apply to fish.

These thoughts were in my head recently when I got perhaps my last look at a wild bluefin tuna, just a month before the Deepwater Horizon rig exploded and collapsed into the Gulf of Mexico. I was 20-odd miles off the coast of Cape Hatteras, N.C., aboard the Sensation, a vessel chartered by the Tag-a-Giant Foundation, a nonprofit organization trying to decode the complex migration patterns of the bluefin and help lay the scientific foundation for the fish’s protection. Tag-a-Giant had been fishing for a couple days, and many people had sat in the fighting chair I now occupied, reeling in tuna after tuna. But for me this was a first. I had never caught a bluefin before.

In the past I would have wanted to savor the fight, to do battle with the fish with lighter, more “sporting” tackle. But considering everything I’d learned about tuna, humans and the chances of the great fish’s survival, it suddenly seemed infinitely more appropriate to fight this tuna with the full expression of humanity’s power. For in the end tuna are no match for us. We have in this final phase of exploitation achieved dominion over the entirety of the watery world, from inland lakes and rivers to the littoral zone to the continental shelf out to the abyssof the high seas. Sitting in the huge fighting chair with the huge rod and reel, in the well of the huge sportfishing vessel, it was inescapably apparent who had the edge.

As my bluefin breached, one of the scientists opened a door at the stern of the boat. A blue vinyl mat was laid down on the deck. The fish came through the door, still “hot,” banging its tail excitedly. But in an instant a biologist named Andre Boustany placed a moist cover over the tuna’s giant eye and a hydration hose in its mouth. The tuna motor mellowed, and at last the fish was beatifically still.

“Do you want to tag him?” Boustany asked me.

I took the sharp four-inch needle from his hand and positioned it just behind the fish’s dorsal fin. Pricking the skin slightly I started to pull my hand away.

“No,” Boustany said, “you gotta really stick it in there.”

Applying more pressure, I felt the needle slide into the flank, felt the resistance of the dense sushi flesh, raw and red and most certainly delicious. But for the first time in my life I felt tuna flesh for what it was: a living, perfect expression of a miraculous adaptation. An adaptation that allows bluefin to cross oceans at the speed of a battleship. An adaptation that should be savored in its own right as the most miraculous engine of a most miraculous animal, not as food.

Perhaps people will never come to feel about a tuna the way they have come to feel about whales. Whales are, after all, mammals: they have large brains; they nurse their young and breed slowly. All of that ensconces them in a kind of empathic cocoon, the warmth of which even the warmest-blooded tuna may never occupy. But what we can perhaps be persuaded to feel, viscerally, is that industrial fishing as it is practiced today against the bluefin and indeed against all the world’s great fish, the very tigers and lions of our era, is an act unbefitting our sentience. An act as pointless, small-minded and shortsighted as launching a harpoon into the flank of a whale.

Paul Greenberg is a frequent contributor to the NYTimes  magazine. This article is adapted from his book “Four Fish: The Future of the Last Wild Food,” which will be published next month by Penguin Press.

Science Weekly: Why you should distrust your senses

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Our fallible senses; newly reunited footage and audio of Apollo 11 mission control; plus, how comics are being used in medicine

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