Happy Birthday, Mom.

Today would have been Mom's 74th birthday. (She's at left in this photo with her mother Lillian)

I figure she'll go for a walk with Frisky, have coffee with Lillian.

Beat Acie at Casino.

Plant a flower.

Do a jitterbug with Nolan Landry.

Eat a few boiled crabs and crawfish.

Sew a blouse.

Dress up in something red (Lucifer be damned).

Sing a Barbra Streisand song.

Flirt with an archangel.

Change a baby who died young's diaper.

Take a nap.

Drink some wine.

And have a good laugh - especially that Emile's still down here.

Jesus was an Independent

It's high time this intellectual argument be put forth about Jesus' preference in politics: He had none. Amen. Period. Enjoy.


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April 9, 2006
Op-Ed Contributor
Christ Among the Partisans
By GARRY WILLS
Chicago

THERE is no such thing as a "Christian politics." If it is a politics, it cannot be Christian. Jesus told Pilate: "My reign is not of this present order. If my reign were of this present order, my supporters would have fought against my being turned over to the Jews. But my reign is not here" (John 18:36). Jesus brought no political message or program.

This is a truth that needs emphasis at a time when some Democrats, fearing that the Republicans have advanced over them by the use of religion, want to respond with a claim that Jesus is really on their side. He is not. He avoided those who would trap him into taking sides for or against the Roman occupation of Judea. He paid his taxes to the occupying power but said only, "Let Caesar have what belongs to him, and God have what belongs to him" (Matthew 22:21). He was the original proponent of a separation of church and state.

Those who want the state to engage in public worship, or even to have prayer in schools, are defying his injunction: "When you pray, be not like the pretenders, who prefer to pray in the synagogues and in the public square, in the sight of others. In truth I tell you, that is all the profit they will have. But you, when you pray, go into your inner chamber and, locking the door, pray there in hiding to your Father, and your Father who sees you in hiding will reward you" (Matthew 6:5-6). He shocked people by his repeated violation of the external holiness code of his time, emphasizing that his religion was an internal matter of the heart.

But doesn't Jesus say to care for the poor? Repeatedly and insistently, but what he says goes far beyond politics and is of a different order. He declares that only one test will determine who will come into his reign: whether one has treated the poor, the hungry, the homeless and the imprisoned as one would Jesus himself. "Whenever you did these things to the lowliest of my brothers, you were doing it to me" (Matthew 25:40). No government can propose that as its program. Theocracy itself never went so far, nor could it.

The state cannot indulge in self-sacrifice. If it is to treat the poor well, it must do so on grounds of justice, appealing to arguments that will convince people who are not followers of Jesus or of any other religion. The norms of justice will fall short of the demands of love that Jesus imposes. A Christian may adopt just political measures from his or her own motive of love, but that is not the argument that will define justice for state purposes.

To claim that the state's burden of justice, which falls short of the supreme test Jesus imposes, is actually what he wills — that would be to substitute some lesser and false religion for what Jesus brought from the Father. Of course, Christians who do not meet the lower standard of state justice to the poor will, a fortiori, fail to pass the higher test.

The Romans did not believe Jesus when he said he had no political ambitions. That is why the soldiers mocked him as a failed king, giving him a robe and scepter and bowing in fake obedience (John 19:1-3). Those who today say that they are creating or following a "Christian politics" continue the work of those soldiers, disregarding the words of Jesus that his reign is not of this order.

Some people want to display and honor the Ten Commandments as a political commitment enjoined by the religion of Jesus. That very act is a violation of the First and Second Commandments. By erecting a false religion — imposing a reign of Jesus in this order — they are worshiping a false god. They commit idolatry. They also take the Lord's name in vain.

Some may think that removing Jesus from politics would mean removing morality from politics. They think we would all be better off if we took up the slogan "What would Jesus do?"

That is not a question his disciples ask in the Gospels. They never knew what Jesus was going to do next. He could round on Peter and call him "Satan." He could refuse to receive his mother when she asked to see him. He might tell his followers that they are unworthy of him if they do not hate their mother and their father. He might kill pigs by the hundreds. He might whip people out of church precincts.

The Jesus of the Gospels is not a great ethical teacher like Socrates, our leading humanitarian. He is an apocalyptic figure who steps outside the boundaries of normal morality to signal that the Father's judgment is breaking into history. His miracles were not acts of charity but eschatological signs — accepting the unclean, promising heavenly rewards, making last things first.

He is more a higher Nietzsche, beyond good and evil, than a higher Socrates. No politician is going to tell the lustful that they must pluck out their right eye. We cannot do what Jesus would do because we are not divine.

It was blasphemous to say, as the deputy under secretary of defense, Lt. Gen. William Boykin, repeatedly did, that God made George Bush president in 2000, when a majority of Americans did not vote for him. It would not remove the blasphemy for Democrats to imply that God wants Bush not to be president. Jesus should not be recruited as a campaign aide. To trivialize the mystery of Jesus is not to serve the Gospels.

The Gospels are scary, dark and demanding. It is not surprising that people want to tame them, dilute them, make them into generic encouragements to be loving and peaceful and fair. If that is all they are, then we may as well make Socrates our redeemer.

It is true that the tamed Gospels can be put to humanitarian purposes, and religious institutions have long done this, in defiance of what Jesus said in the Gospels.

Jesus was the victim of every institutional authority in his life and death. He said: "Do not be called Rabbi, since you have only one teacher, and you are all brothers. And call no one on earth your father, since you have only one Father, the one in heaven. And do not be called leaders, since you have only one leader, the Messiah" (Matthew 23:8-10).

If Democrats want to fight Republicans for the support of an institutional Jesus, they will have to give up the person who said those words. They will have to turn away from what Flannery O'Connor described as "the bleeding stinking mad shadow of Jesus" and "a wild ragged figure" who flits "from tree to tree in the back" of the mind.

He was never that thing that all politicians wish to be esteemed — respectable. At various times in the Gospels, Jesus is called a devil, the devil's agent, irreligious, unclean, a mocker of Jewish law, a drunkard, a glutton, a promoter of immorality.

The institutional Jesus of the Republicans has no similarity to the Gospel figure. Neither will any institutional Jesus of the Democrats.

Garry Wills is professor emeritus of history at Northwestern University and the author, most recently, of "What Jesus Meant."
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Loving Life vs Long Life

I could not possibly agree more with the thrust of this article's argument : it's far far better to enjoy your life than to scheme about living longer. "It's not the years in your life that matter - it's the life in your years!"

The New York Times
April 9, 2006
Critic's Notebook
Be Merry, Not Ancient
By FRANK BRUNI

BECAUSE we all needed yet another set of rules to follow, because we had not yet been sufficiently bombarded with dictates about the colors of the fruits and vegetables we should eat and the ideal intake of alcohol and the optimal frequency of low-impact exercise, the Journal of the American Medical Association came along last week to tell us that serious calorie restriction might best serve the quest for a long, disease-free life.

The number of calories in the daily diets of some participants in this latest study was — gulp — 890. Which, by my nonscientific research, is less than the average teenage or adult American who lives within a half mile of a Burger King and has not had gastric bypass surgery consumes for dinner. That might be considered a helpful target, except that it's so ludicrously unattainable, in professions other than modeling and zip codes other than 90210, that there isn't anything helpful about it.

It's also hard to see the point of it. If living to 99 means forever cutting the porterhouse into eighths, swearing off the baked potato and putting the martini shaker into storage, then 85 sounds a whole lot better, and I'd ratchet that down to 79 to hold onto the Häagen-Dazs, along with a few shreds of spontaneity. It's a matter of priorities.

Do we really want as many years as we can get, no matter how we get them? At what point does the pursuit of an extended life — a pursuit that pivots on the debatable assumption that habit can outwit heredity, not to mention chance— become the entire business of a life? Is longevity all it's cracked up to be?

Scientists and medical doctors are certainly obsessed with it, charting a tedious path of pleasures assiduously portioned and rituals steadfastly maintained. Cut back on caffeine. Stop after a glass and a half of red wine. Make an enemy of red meat. Make friends with flossing — which, it turns out, may have benefits that go beyond admirable dental hygiene to the prevention of heart disease and diabetes.

Month after month brings study after study, and the only thing more addling than keeping track of all the information is resolving the contradictions it seems to contain.

Take the matter of weight. If memory serves me (it may not, given my failure to toe the line on wine) and a Nexis search isn't failing me, we received a different set of instructions just a year ago.

Last April, a study also published in the Journal of the American Medical Association, more commonly known as the Journal of Utterly Mixed Signals, demonstrated a correlation between being very thin and an increased risk of death. The study indicated that people who are overweight but not obese might be better off, at least in terms of attaining the coveted status and Pensacola retirement home of the nonagenarian.

I'm no expert on metabolism, but I bet that the 890-calorie-a-day diet followed by some participants in the new study would lead, over time, to a condition that looks an awful lot like extreme thinness. So what should I have for breakfast? A cup of low-fat yogurt or a salt bagel with a schmear?

Yes, I'm painting with a broad brush; the studies in question are more nuanced and less definitive than I'm making them out to be. The cap of 890 calories a day was a short-term fix, not a long-term prison. There might be allowances, down the road, for a Whopper with cheese. Followed, of course, by some vigorous flossing and a brisk 40-minute walk.

But the larger point remains. We are awash in behavioral strictures, many of them conflicting.

After years of being schooled in the transcendent virtues of low-fat diets, we were informed two months ago — in, you guessed it, the Journal of the American Medical Association — that this education might be flawed. An eight-year, $415 million federal study of nearly 49,000 women found that those who maintained low-fat diets had the same rates of breast cancer, colon cancer and heart attacks as those who ate what they wanted.

So, I'll have that bagel with a schmear, but not simply because one study among many gave me a green light, at least for the moment. I'll have it because it makes me happy, which has to count for something.

And even if the new study is wrong and the old studies were right and the schmear robs me of some time on the tail end of my days, I may not have enough money in my 401(k) to go the full distance, and I'm definitely not counting on Social Security to pick up the slack.

Which raises additional concerns. What happens to all of us, as a society, if 100 becomes the new 80? Plastic surgeons may get even richer and the populations of Florida and Arizona may swell, but will pension funds still be there for us? Will prescription drug benefits?

Each of us can individually hunker down for the long haul, squirreling away our money instead of spending it on hedonistic vacations, exercising faithfully so that our limbs stay as limber as our nipped-and-tucked faces are taut. But doesn't the quality of our days matter as much as the quantity of them?

Pondering this question, I riffled through some obituaries.

Richard Burton died at 58 — no doubt fewer years than he or anyone else would want — but wasn't his a swashbuckling, gallivanting life that was in many ways worth envying, Liz or no Liz?

Strom Thurmond died at 100. "In those last years," according to the obituary by Adam Clymer in The New York Times, "he had to be helped onto the Senate floor by aides, who also told him, in voices audible in the Senate gallery, how to vote."

Of course neither man planned it that way, and that may be the most important lesson of all.

We can't really predict tomorrow. We can't guarantee its arrival with a specified number of calories or a given allotment of sleep, with milligrams of dark chocolate or ounces of fiber. But we can often determine the measure of joy we wring out of today.

I also riffled through a book of quotations and immediately found this proverb: "He lives long who lives well." I don't think those last two words are really about blueberries, broccoli and green tea. And I'm not sure the first three are about anything as literal and prosaic as a tally of years.
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Littoral Evolution

Is this not a marvellous story or WHAT? How can we not be moved by such stuff? Creationism Foomationism - evolution is SOOOOOOOO obvious ! Viva las Science teachers ! Enjoy.

The New York Times
April 6, 2006
Fossil Called Missing Link From Sea to Land Animals
By JOHN NOBLE WILFORD

Scientists have discovered fossils of a 375-million-year-old fish, a large scaly creature not seen before, that they say is a long-sought missing link in the evolution of some fishes from water to a life walking on four limbs on land.

In two reports today in the journal Nature, a team of scientists led by Neil H. Shubin of the University of Chicago say they have uncovered several well-preserved skeletons of the fossil fish in sediments of former streambeds in the Canadian Arctic, 600 miles from the North Pole.

The skeletons have the fins, scales and other attributes of a giant fish, four to nine feet long. But on closer examination, the scientists found telling anatomical traits of a transitional creature, a fish that is still a fish but has changes that anticipate the emergence of land animals — and is thus a predecessor of amphibians, reptiles and dinosaurs, mammals and eventually humans.

In the fishes' forward fins, the scientists found evidence of limbs in the making. There are the beginnings of digits, proto-wrists, elbows and shoulders. The fish also had a flat skull resembling a crocodile's, a neck, ribs and other parts that were similar to four-legged land animals known as tetrapods.

Other scientists said that in addition to confirming elements of a major transition in evolution, the fossils were a powerful rebuttal to religious creationists, who have long argued that the absence of such transitional creatures are a serious weakness in Darwin's theory.

The discovery team called the fossils the most compelling examples yet of an animal that was at the cusp of the fish-tetrapod transition. The fish has been named Tiktaalik roseae, at the suggestion of elders of Canada's Nunavut Territory. Tiktaalik (pronounced tic-TAH-lick) means "large shallow water fish."

"The origin of limbs," Dr. Shubin's team wrote, "probably involved the elaboration and proliferation of features already present in the fins of fish such as Tiktaalik."

In an interview, Dr. Shubin, an evolutionary biologist, let himself go. "It's a really amazing, remarkable intermediate fossil," he said. "It's like, holy cow."

Two other paleontologists, commenting on the find in a separate article in the journal, said that a few other transitional fish had been previously discovered from approximately the same Late Devonian time period, 385 million to 359 million years ago. But Tiktaalik is so clearly an intermediate "link between fishes and land vertebrates," they said, that it "might in time become as much an evolutionary icon as the proto-bird Archaeopteryx," which bridged the gap between reptiles (probably dinosaurs) and today's birds.

The writers, Erik Ahlberg of Uppsala University in Sweden and Jennifer A. Clack of the University of Cambridge in England, are often viewed as rivals to Dr. Shubin's team in the search for intermediate species in the evolution from fish to the first animals to colonize land.

H. Richard Lane, director of paleobiology at the National Science Foundation, said in a statement, "These exciting discoveries are providing fossil 'Rosetta Stones' for a deeper understanding of this evolutionary milestone — fish to land-roaming tetrapods."

The science foundation and the National Geographic Society were among the financial supporters of the research. Besides Dr. Shubin, the principal discoverers were Edward B. Daeschler of the Academy of Natural Sciences in Philadelphia and Farish A. Jenkins Jr., a Harvard evolutionary biologist. Casts of the fossils will be on view at the Science Museum of London.

Michael J. Novacek, a paleontologist at the American Museum of Natural History in Manhattan, who was not involved in the research, said: "Based on what we already know, we have a very strong reason to think tetrapods evolved from lineages of fishes. This may be a critical phase in that transition that we haven't had before. A good fossil cuts through a lot of scientific argument."

Dr. Shubin's team played down the fossil's significance in the raging debate over Darwinian theory, which is opposed mainly by some conservative Christians in this country, but other scientists were not so reticent. They said this should undercut the argument that there is no evidence in the fossil record of one kind of creature becoming another kind.

One creationist site on the Web (emporium.turnpike.net/C/cs /evid1.htm) declares that "there are no transitional forms," adding: "For example, not a single fossil with part fins, part feet has been found. And this is true between every major plant and animal kind."

Dr. Novacek responded: "We've got Archaeopteryx, an early whale that lived on land, and now this animal showing the transition from fish to tetrapod. What more do we need from the fossil record to show that the creationists are flatly wrong?"

Duane T. Gish, a retired official of the Institute for Creation Research in San Diego, said, "This alleged transitional fish will have to be evaluated carefully." But he added that he still found evolution "questionable because paleontologists have yet to discover any transitional fossils between complex invertebrates and fish, and this destroys the whole evolutionary story."

Dr. Shubin and Dr. Daeschler began their search on Ellesmere Island in 1999. They were attracted by a map in a geology textbook showing an abundance of Devonian rocks exposed and relatively easy to explore. At that time, the land had a warm climate: it was part of a supercontinent straddling the Equator.

It was not until July 2004, Dr. Shubin said, that "we hit the jackpot." They found several of the fishes in a quarry, their skeletons largely intact and in three dimensions. The large skull had the sharp teeth of a predator. It was attached to a neck, which allowed the fish the unfishlike ability to swivel its head.

If the animal spent any time out of water, said Dr. Jenkins, of Harvard, it needed a true neck that allowed the head to move independently on the body.

Embedded in the pectoral fins were bones that compare to the upper arm, forearm and primitive parts of the hand of land-living animals. The joints of the fins appeared to be capable of functioning for movement on land, a case of a fish improvising with its evolved anatomy. In all likelihood, the scientists said, Tiktaalik flexed its proto-limbs mainly on the floor of streams and might have pulled itself up on the shore for brief stretches.

In their report, the scientists concluded that Tiktaalik was an intermediate between the fishes Eusthenopteron and Panderichthys, which lived 385 million years ago, and early tetrapods. The known early tetrapods are Acanthostega and Ichthyostega, about 365 million years ago.

Tiktaalik, Dr. Shubin said, is "both fish and tetrapod, which we sometimes call a fishapod."
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April 7, 2006
Study, in a First, Explains Evolution's Molecular Advance
By KENNETH CHANG
By reconstructing ancient genes from long-extinct animals, scientists have for the first time demonstrated the step-by-step progression of how evolution created a new piece of molecular machinery by reusing and modifying existing parts.

The researchers say the findings, published today in the journal Science, offer a counterargument to doubters of evolution who question how a progression of small changes could produce the intricate mechanisms found in living cells.

"The evolution of complexity is a longstanding issue in evolutionary biology," said Joseph W. Thornton, professor of biology at the University of Oregon and lead author of the paper. "We wanted to understand how this system evolved at the molecular level. There's no scientific controversy over whether this system evolved. The question for scientists is how it evolved, and that's what our study showed."

Charles Darwin wrote in The Origin of Species, "If it would be demonstrated that any complex organ existed which could not possibly have formed by numerous, successive, slight modifications, my theory would absolutely break down."

Discoveries like that announced this week of a fish with limblike fins have filled in the transitions between species. New molecular biology techniques let scientists begin to reconstruct how the processes inside a cell evolved over millions of years.

Dr. Thornton's experiments focused on two hormone receptors. One is a component of stress response systems. The other, while similar in shape, takes part in different biological processes, including kidney function in higher animals.

Hormones and hormone receptors are protein molecules that act like pairs of keys and locks. Hormones fit into specific receptors, and that attachment sends a signal to turn on — or turn off — cell functions. The matching of hormones and receptors led to the question of how new hormone-and-receptor pairs evolved, as one without the other would appear to be useless.

The researchers found the modern equivalent of the stress hormone receptor in lampreys and hagfish, two surviving jawless primitive species. The team also found two modern equivalents of the receptor in skate, a fish related to sharks.

After looking at the genes that produced them, and comparing the genes' similarities and differences among the genes, the scientists concluded that all descended from a single common gene 450 million years ago, before animals emerged from oceans onto land, before the evolution of bones.

The team recreated the ancestral receptor in the laboratory and found that it could bind to the kidney regulating hormone, aldosterone and the stress hormone, cortisol.

Thus, it turned out that the receptor for aldosterone existed before aldosterone. Aldosterone is found just in land animals, which appeared tens of millions of years later.

"It had a different function and was exploited to take part in a new complex system when the hormone came on the scene," Dr. Thornton said.

What happened was that a glitch produced two copies of the receptor gene in the animal's DNA, a not-uncommon occurrence in evolution. Then, for reasons not understood, two major mutations made one receptor sensitive just to cortisol, leading to the modern version of the stress hormone receptor. The other receptor became specialized for kidney regulation.

Dr. Thornton said the experiments showed how evolution could and did innovate functions over time. "I think this is likely to be a very common theme in how complex molecular systems evolved," he said.

Christoph Adami, a professor of life sciences at the Keck Graduate Institute in Claremont, Calif. who wrote an accompanying commentary in Science, said the research showed how evolution "takes advantage of lucky circumstances and builds upon them."

Dr. Thornton said the experiment refutes the notion of "irreducible complexity" put forward by Michael J. Behe, a professor of biochemistry at Lehigh University.

Dr. Behe, a main advocate of intelligent design, the theory that life is so complicated that the best explanation is that it was designed by an intelligent being, has compared an irreducibly complex system to a mousetrap. Take away any piece, and the mousetrap fails to catch mice. Such all-or-none systems could not have arisen with incremental changes, Dr. Behe has argued.

Dr. Thornton said the key-and-lock mechanism of a hormone-receptor pair was "an elegant exemplar of a system that has been called irreducibly complex."

"Of course," he added, "our findings show that it is not irreducibly complex."

Dr. Behe described the results as "piddling." He wondered whether the receptors with the intermediate mutations would be harmful to the survival of the organisms and said a two-component hormone-receptor pair was too simple to be considered irreducibly complex. He said such a system would require at least three pieces and perform some specific function to fit his notion of irreducibly complex.

What Dr. Thornton has shown, Dr. Behe said, falls within with incremental changes that he allows evolutionary processes can cause.

"Even if this works, and they haven't shown that it does," Dr. Behe said, "I wouldn't have a problem with that. It doesn't really show that much."
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Gandhi's Seven Sins

No silly, this isn't a list of the only 7 sins Gandhi committed - it's a list of the seven things he considered the most grievous sins. Read it and weep.




Wealth without Work


Pleasure without Conscience


Knowledge without Character


Commerce without Morality


Science without Humanity


Worship without Sacrifice


Politics without Principle.

The edge of lite.

The New York Times
Printer Friendly Format Sponsored By

April 5, 2006
Low-Calorie Diet May Lead to Longer Life
By DENISE GRADY

A low-calorie diet, even in people who are not obese, can lead to changes in metabolism and body chemistry that have been linked to better health and longer life, researchers are reporting.

The findings lend support to the theory that eating less, long known to prolong life in rats and mice, may do the same for people, by preventing heart disease, cancer, diabetes and other diseases, and by slowing aging.

The notion that going hungry could be the fountain of youth has captivated scientists and the public. Calorie restriction, the scientific name for a regimen high in nutrients but low in calories, is the subject of intense research, and some people have already begun trying it on their own.

There is a Calorie Restriction Society with members all over the world, and its president, Brian M. Delaney, estimates that the people experimenting on themselves number in the thousands.

But there is no proof that calorie restriction works in people, largely because it is difficult and expensive to study; it can also take decades to measure an effect on life span.

"There is no data on non-obese humans," said Eric Ravussin, chief of health and performance enhancement at the Pennington Biomedical Research Center at Louisiana State University. Earlier studies had proved that low-calorie diets could reduce weight and alter metabolism in obese people.

A six-month study in 48 people directed by Dr. Ravussin, being published today in The Journal of the American Medical Association, is the first rigorous test of calorie restriction in people who are overweight but not obese. Most participants reduced calories by 25 percent, but some cut back more and ate only 890 calories a day for several months.

"There's never been a study like this one," said Dr. Evan Hadley, director of geriatrics and clinical gerontology at the National Institute on Aging, which paid for the study. He called the results "striking," even though the experiment was only a pilot study for a two-year trial of calorie restriction due to begin in the fall.

Among the main findings of Dr. Ravussin's study was that calorie restriction led to decreases in insulin levels and body temperature. Both are considered signs of longevity, partly because an earlier study by other researchers found both traits in long-lived people. The diet also led to a drop in thyroid hormones and declines in DNA damage.

But Dr. Ravussin and Dr. Hadley cautioned that the study was preliminary, and that it did not prove that calorie restriction could make people healthier or add years to their lives.

"It's an important step along the way," Dr. Hadley said.

Scientists have known for years that when people cut calories and lose weight, the body tries to compensate by slowing its metabolic rate. The slowing is a defensive mechanism to fight weight loss. It was probably preserved by evolution because it saved people from starving to death when food was scarce, but it is the bane of dieters because it means that the more weight they lose, the harder it is to keep reducing.

Several explanations exist for why a strict diet, low in calories but high in nutrients, may slow aging. Many scientists think that an important factor in aging is DNA damage caused by free radicals, highly reactive oxygen-containing molecules formed during normal metabolism. Eating less leads to a slower metabolism and fewer free radicals.

Another possibility is that being deficient in calories turns certain genes on and off, with a net effect of slowing the clock.

In rhesus monkeys, calorie restriction has had pronounced effects. A University of Wisconsin team led by Richard Weindruch has been studying 76 monkeys for more than a decade, half on low-calorie diets and half in a control group that eats normally.

The low-calorie animals weigh about 30 percent less and have 70 percent less body fat than the controls, as well as lower insulin levels. The calorie-restricted monkeys have had two cases of cancer, compared with five in the controls. The controls have had twice the death rate from aging-related diseases like heart failure and diabetes. About 90 percent of the monkeys on low-calorie diets are still alive, compared with only about 70 percent of the controls.

Dr. Ravussin's study included men and women, ages 27 to 49, who were overweight but not obese. Some were just a bit heavy, but others were 30 pounds overweight.

For six months, a control group ate a diet created to maintain members' weights. Another group ate 75 percent of what members needed to keep their weight steady. A third group had members' calories cut 12.5 percent and their exercise increased to burn off 12.5 percent.

The final group went on an extreme diet of 890 calories a day — less than half of what most adults need — for two or three months, until members lost about 15 percent of their body weight. They then switched to a diet meant to keep them at their new lower weight.

Part of the reason for the study, Dr. Ravussin said, was to find out whether people could stand calorie restriction. The participants, who were paid, turned out to be highly motivated, he said. Some were concerned about their weight and health. They had to take time off work for metabolism tests and also ate many meals at the clinic.

Jerelyn Key, 44, a Social Security claims representative, joined because she wanted to learn better eating habits for herself and her family. Ms. Key was assigned to the very-low-calorie group. For two months, she ate four or five shakes a day and a specially formulated "brownie," adding up to just 890 calories a day. She is 5-foot-7, and her starting weight was 165 to 170; after two months she had lost about 28 pounds.

"I look back now wondering how I managed to do it," Ms. Key said. She has regained a bit and now weighs 140 to 145 pounds.

Another participant, Oscar Couvillion, 45, an insurance database administrator, said he was lured by a radio advertisement offering participants $7,000. There was heart disease in Mr. Couvillion's family, and at 5-foot-9, he weighed 192 pounds, about 30 pounds too much.

He wound up in the group assigned to cut calories by 25 percent. At first, he said, "I was starving to death, I had headaches, I was grouchy." But cheered on by therapists in the study, he stuck with it and lost 30 pounds. He said joining the study was one of the best decisions he had ever made.

"You're not going to ask me what I weigh now, are you?" he said, adding that he weighed 176. "I have to repent. Now I know what to do."

Escape from Hell

This may be one of the most important articles I have ever published on any of my blogs. Please, read it carefully and use the information to help someone you know and love. Enjoy.


The New York Times
April 2, 2006
A Depression Switch?
By DAVID DOBBS

Deanna Cole-Benjamin never figured to be a test case for a radical new brain surgery for depression. Her youth contained no traumas; her adult life, as she describes it, was blessed. At 22 she joined Gary Benjamin, a career financial officer in the Canadian Army, in a marriage that brought her happiness and, in the 1990's, three children. They lived in a comfortable house in Kingston, a pleasant university town on Lake Ontario's north shore, and Deanna, a public-health nurse, loved her work. But in the last months of 2000, apropos of nothing — no life changes, no losses — she slid into a depression of extraordinary depth and duration.

"It began with a feeling of not really feeling as connected to things as usual," she told me one evening at the family's dining-room table. "Then it was like this wall fell around me. I felt sadder and sadder and then just numb."

Her doctor prescribed progressively stronger antidepressants, but they scarcely touched her. A couple of weeks before Christmas, she stopped going to work. The simplest acts — deciding what to wear, making breakfast — required immense will. Then one day, alone in the house after Gary had taken the kids to school and gone to work, she felt so desperate to escape her pain that she drove to her doctor's office and told him she didn't think she could go on anymore.

"He took one look," she told me later, "and said that he wanted me to stay right there in the office. Then he called Gary, and Gary came to the office, and he told us he wanted Gary to take me straight to the hospital."

They drove to the Providence Continuing Care Center's mental-health hospital, still known locally as the Kingston Psychiatric Hospital, or K.P.H., its name when it was built in the 1950's. "It's a dingy, archaic place," Deanna said, "typical of older mental hospitals." There, in the locked ward that also contained psychotic patients, she would spend the next 10 months straight and about 85 percent of the three years after that. Her depression would prove resistant to every class of antidepressant, numerous combinations of antidepressants and anti-anxiety drugs, intensive psychotherapy and about a hundred sessions of electroconvulsive therapy. Patients who have failed that many treatments usually don't emerge from their depressions.

Finally, in the spring of 2004, Deanna's psychiatrist at the hospital, Dr. Gebrehiwot Abraham, received a fax from a University of Toronto research team asking if he had an appropriate candidate for a clinical trial of a new, experimental surgery for treatment-resistant depression. The operation borrowed a procedure called deep brain stimulation, or D.B.S., which is used to treat Parkinson's. It involves planting electrodes in a region near the center of the brain called Area 25 and sending in a steady stream of low voltage from a pacemaker in the chest. One of the study's leaders, Dr. Helen Mayberg, a neurologist, had detected in depressed patients what she suspected was a crucial dysfunction in Area 25's activity. She hypothesized that the electrodes might modulate the area and ease the depression.

The procedure, Dr. Abraham told Deanna and Gary, had worked safely in thousands of Parkinson's patients. But it would carry some risk of neural complications (it was, after all, brain surgery), it would be uncomfortable and it might not work.

"We were in tears," said Deanna, who is now 41. "We felt we'd tried everything and nothing worked. But we talked about it and decided, 'Well, what have we got to lose?"'

What she hoped to lose, of course, was her depression. But depression, which 5 to 10 percent of Americans suffer in any given year and about 15 percent will suffer in their lifetimes, can be hard to lose. Drugs, as shown in a comprehensive study released last month by the National Institute of Mental Health, are effective in only half of patients with major depression. Psychotherapy does no better. For those people who are not helped by therapy or drugs, electroconvulsive therapy, or ECT, can bring relief. But few of those cures are complete. These therapies usually ease rather than cure depression while sometimes bringing side effects like insomnia or memory loss, and their potency often proves fleeting; as many as half to two-thirds of those successfully treated relapse within two years. Neither neuroscientists nor psychiatrists can say exactly what depression is. Neurologically and psychologically, what Hippocrates called the "black bile" and Susan Sontag "melancholy minus its charms" presents an almost impossibly complicated puzzle.

The expectations for the Toronto team's D.B.S. study were accordingly modest. When I later asked Mayberg's collaborator Dr. Andres Lozano, the neurosurgeon who performed the operations, what he had expected, he replied, "Nothing."

As it turned out, 8 of the 12 patients he operated on, including Deanna, felt their depressions lift while suffering minimal side effects — an incredible rate of effectiveness in patients so immovably depressed. Nor did they just vaguely recover. Their scores on the Hamilton depression scale, a standard used to measure the severity of depression, fell from the soul-deadening high 20's to the single digits — essentially normal. They've re-engaged their families, resumed jobs and friendships, started businesses, taken up hobbies old and new, replanted dying gardens. They've regained the resilience that distinguishes the healthy from the depressed.

These results brought a marvelous surprise to both the patients and the doctors involved — and nervous anticipation about whether their luck will hold. Though a few of the patients are more than two years out from the surgery, none completely trust their cure. No one can tell them for sure that it will last, and they worry. The study doctors and the wider medical community, meanwhile, are guarded about whether D.B.S. will prove so effective in larger trials. "I can't emphasize enough that we need a large, randomized study to confirm this as a treatment," says Valerie Voon, a University of Toronto psychiatrist who was with the team for the first six patients and who is now a research fellow at the National Institutes of Health.

Those caveats notwithstanding, many scientists following the trial say they believe it will change how psychiatrists define and treat mood disorders. Mayberg, who speaks of a "paradigm shift," notes that she developed the trial to evaluate not a treatment but a hypothesis. In that sense the trial succeeded. Mayberg's focus on Area 25 tests the emerging "network" model of mood disorders, a new way of looking at psychiatric conditions that isn't restricted by the neurochemical model of mood that has dominated over the past quarter century or so. Rather, it incorporates neurochemistry into the concept of the brain as a circuit board or wiring diagram. The network model carries profound implications for research and, ultimately, treatment. The Prozac revolution showed everyone that tweaking neurochemistry can dampen and sometimes extinguish depression — but only through a generalized approach, hitting the entire brain. ("Carpet-bombing," one neuroscientist calls it.) And the 50 percent success rate of antidepressant drugs suggests that they aren't hitting depression's central mechanism. The network approach, on the other hand, focuses on specific nodes, pathways and gateways that might be approached with various treatments — electrical, surgical or pharmacological. This small trial appears to confirm this model so emphatically that it's already changing the neuropsychiatric view of the brain and the direction of research.

"People often ask me about the significance of small first studies like this," says Dr. Thomas Insel, who as director of the National Institute of Mental Health enjoys an unparalleled view of the discipline. "I usually tell them: 'Don't bother. We don't know enough.' But this is different. Here we know enough to say this is something significant. I really do believe this is the beginning of a new way of understanding depression."

When she started her research in the late 1980's, Helen Mayberg, too, looked at neurochemistry. "That's where biological psychiatry was then," she told me. "It was about the brain as a bowl of soup. You whip up a chemical, add it and stir. An alchemist point of view. But I soon realized I wanted to find out where things were changing."

Lively, smart and quick-witted, Mayberg talks of brain science with contagious excitement. She possesses just the kind of presence someone having a hole drilled in his head would welcome — authoritative but warm. Mayberg originally considered becoming a psychiatrist, but she didn't like the discipline's resistance at the time (it was the 1970's) to neurological explanations of mood. So she became a behavioral neurologist, doing a residency at Columbia University and then moving to Johns Hopkins.

Setting aside the bowl-of-soup model did not mean deciding that neurochemicals weren't important. Rather it meant deciding that neurochemistry, and particularly the chemistry dictating how individual neurons communicate with one another, was probably driven by traffic between different brain areas, and that identifying the patterns in that traffic might yield new understanding. (Or, using another metaphor, if the brain is an orchestra, then the neurochemical approach focuses on how well individual players listen and respond to the players adjacent to them; the network approach, like a conductor, focuses on how the orchestra's sections — strings, winds, brass, etc. — coordinate and balance volume and tone. When both are working well, you've got music.)

Imaging tools for tracking these relationships, like PET scans and later functional magnetic resonance imagery, were just maturing as Mayberg pursued her work. Neuroscientists were soon using these tools to help identify networks involved in mental processes ranging from distinguishing facial expressions to experiencing alarm or pleasure. Each of these networks engages different brain areas in different combinations. The areas active in recognizing a fearful expression, for instance, won't match those for recalling old memories, though some areas might overlap. Defining the network involved in any given process requires figuring out not just which parts are involved but also which parts are most vital and how one affects another.

By the 1990's, Mayberg was trying to define the network that goes awry in depression. She and other researchers soon established that depression involved abnormal patterns of activity in a network that includes limbic areas (a cluster of evolutionarily older brain areas around the top of the brain stem), which control basic emotions and drives like fear, lust and hunger, and the newer cortex and subcortex responsible for thought, memory, motivation and reward.

Several researchers were working on this. But Mayberg, and, separately, Dr. Wayne Drevets, then at Washington University and now at the N.I.M.H., increasingly homed in on Area 25, which seemed crucial in both its behavior and its position in this network. They found that Area 25 was smaller in most depressed patients; that it lighted up in every form of depression and also in nondepressed people who intentionally pondered sad things; that it dimmed when depression was successfully treated; and that it was heavily wired to brain areas modulating fear, learning, memory, sleep, libido, motivation, reward and other functions that went fritzy in the depressed. It seemed to be a sort of junction box, in short, whose malfunction might be "necessary and sufficient," as Mayberg put it, to turn the world dim. Maybe it could provide a switch that would brighten the dark.

To work the switch, Mayberg needed a knife. In 1999 she moved from the University of Texas at San Antonio to the University of Toronto, where she met Lozano, who had become expert at using deep brain stimulation for treating Parkinson's, the neurological affliction that causes tremors and rigidity as well as cognitive and emotional declines. By the time he and Mayberg met, he'd slipped electrodes into the brains of almost 300 patients.

Depression is more elusive than Parkinson's. But approaching Area 25 with D.B.S. allowed the researchers to use a known tool. Neurosurgeons found as early as the 1950's that they could treat Parkinson's by destroying a small portion of the hyperactive globus pallidus, a brain area that is crucial to movement. The treatment illustrated one of the brain's many oddities: some areas can cause more trouble when they are excessively active than when they have no activity at all. In the early 1990's, surgeons increasingly began to use D.B.S. to quiet the globus pallidus by sending it steady, rapid pulses of low voltage. Patients' tremors would instantly ease or cease; their rigidity and uncontrollable body movements would fade over a week or two. Killing the current revived the symptoms. Surgeons have now implanted D.B.S. electrodes in some 30,000 Parkinson's patients worldwide. The procedure is not a cure-all. It helps some patients less than others, does little to alleviate Parkinson's cognitive and emotional decay and occasionally creates complications including infection, bleeding and memory loss. Its biggest problem may be its success. So many medical centers now do it that some do it badly or on poorly qualified patients. But done well, it usually works.

Mayberg knew all this from the literature and learned more in conversations with Lozano. She grew increasingly convinced that applying D.B.S. to Area 25 might control depression.

"So one day," she told me, "I went to Lozano and said: 'I want to turn off Area 25. Can we put a stimulator there and see if that does it?' And he goes, 'Why not?' "

Occasionally, Deanna felt good enough to go home. This feeling seldom lasted more than a few days. "You could tell she was getting bad again when she couldn't sleep," Gary said. "That was the red flag. She'd be around the house all night, watching TV, up worried, cleaning. Then she'd get worse each day. Her eyes got that sunken look. Those were the scariest times, when she was getting like that and I would drop the kids at school and go to work and know she was home alone."

During the bad periods, which was much of the time, Deanna thought about suicide almost constantly. Through the windows of the locked ward she could see Lake Ontario, cold and immense. While she was there, one patient managed to reach the lake, beyond the parking lot and a grove of trees, and drown himself. Deanna thought obsessively of doing the same.

"I imagined that all the time," she said. "That I would walk out there and walk into the lake and that would be it."

As the months and years passed and all treatments failed, it began to feel as if there were only one way out.

"It started to seem like, this is not going to stop," Gary said. "This is our life now. There were times I thought that it was going to end" — he

looked across the table at Deanna — "only when you committed suicide."

"The worst part for me," Deanna said, "was not being able to feel anything for my children. To hug them, to have them hug me, and feel nothing. That was devastating. An awful, awful place to be."

The D.B.S. operation involves an intrusion that is delicate but brutal. The patients are kept awake so they can describe any changes, and the only drug administered is a local anesthetic. The surgical team shaves much of the patient's head and attaches to the skull, with four screws drilled through skin into bone, the stereotactic frame that will hold the head steady against the operating table and serve as a navigational aid. Mounting the frame takes only about 10 minutes. But because it involves driving screws into the skull ("You can't truly feel it," as one patient said, "but you can hear it and see it and smell it"), and because it leaves you with a steel frame around the head, many patients find this the most distressing part of the whole business.

Gary found the frame more than he could take. He kissed his wife and went elsewhere, hoping she wouldn't be a vegetable when he next saw her. Then Deanna was rolled to an M.R.I. machine, where scans would be taken; the scans would help guide Lozano in placing the electrodes.

During the hour or so while the computer processed the scans, Deanna chatted with Mayberg. The day before, she told Mayberg, on video, that what she most wanted was to hold her children and feel it.

When the scans were ready, she went to the operating room. She was placed on a table, which was tilted back like a La-Z-Boy. Lozano and his team bolted the stereotactic frame to the table, as it was described to me later. There was some scrubbing on her head, some chitchat among the surgical team, much fiddling with sterile drapes and instruments. Then Lozano fit a half-inch burred bit into a drill, turned it on and started drilling. He drilled right into the top of Deanna's skull, which brought a rattling sensation and a sound like that made by an air wrench removing the lugs off a car's wheel. Then he did it again.

Now Lozano threaded a guide tube — "It's a straight shot," he said later, "really quite easy" — down between crevices and seams to one side of Area 25, which is in two small lobes at the midline of the brain. He slid the first electrode and its lead down the tube, then repeated this for the other side. All this took nearly two hours. After he double-checked his locations, he wired the leads to a pacemaker and gave Mayberg a nod. They could turn it on anytime now.

Mayberg had squeezed into a spot at Deanna's side some time before. She had told Deanna that if anything felt different, she should say so. Mayberg wasn't going to tell her when the device was activated. "Don't try to decide what's important," Mayberg told her. "If your nose itches, I want to know." Now and then the two would chat. But so far Deanna hadn't said much.

"So we turn it on," Mayberg told me later, "and all of a sudden she says to me, 'It's very strange,' she says, 'I know you've been with me in the operating room this whole time. I know you care about me. But it's not that. I don't know what you just did. But I'm looking at you, and it's like I just feel suddenly more connected to you.' "

Mayberg, stunned, signaled with her hand to the others, out of Deanna's view, to turn the stimulator off.

"And they turn it off," Mayberg said, "and she goes: 'God, it's just so odd. You just went away again. I guess it wasn't really anything.'

"It was subtle like a brick," Mayberg told me. "There's no reason for her to say that. Zero. And all through those tapes I have of her, every time she's in the clinic beforehand, she always talks about this disconnect, this closeness and sense of affiliation she misses, that was so agonizingly painful for her to lose. And there it was. It was back in an instant."

Deanna later described it in similar terms. "It was literally like a switch being turned on that had been held down for years," she said. "All of a sudden they hit the spot, and I feel so calm and so peaceful. It was overwhelming to be able to process emotion on somebody's face. I'd been numb to that for so long."

It worked that way for other patients too. For those for whom it worked, the first surges of mood and sensation were peculiar to their natures. Patient 4, for instance, was fond of taking walks, and she had previously told Mayberg that she knew she was getting ill when whole landscapes turned dim, as if "half the pixels went dark." Her first comment when the stimulator went on was to ask what they'd done to the lights, for everything seemed much brighter. Patient 5, an elite bicycle racer before his depression, told me that a pulling that he had long felt in his legs and gut, "as if death were pulling me downward," had instantly ceased. Patient 1, who in predepression days was an avid gardener, amazed the operating room by announcing that she suddenly felt as if she were walking through a field of wildflowers. Two days after going home, she put a scarf over her shaved, stitched head, found her tools and went out to reclaim her long-neglected gardens.

Not all was light and flowers. On a purely biological level, the improvement made by D.B.S. sometimes amplified the side effects of the high doses of medication the patients had been taking. Doctors don't quite understand this phenomenon, but they see it happen in other instances too; it is as if the patient, deadened, is again made sensate. Deanna broke out in hives and felt nauseated; her hands shook. These symptoms eased when she (as several of the patients have done) reduced her meds — slowly, so as not to introduce new variables. She now takes standard doses of Effexor, an antidepressant, and Seroquel, an anti-psychotic drug.

The cure also brought challenges at home. As with other disabilities, any partner turned caretaker gets used to calling the shots, and rearranging power, dependencies and expectations after a sudden recovery can prove hard. One patient, the cyclist, faced this challenge starkly, for he had started a relationship and married while he was depressed. "Frankly," he told me, "I'm not sure we've quite finished working this out." All the patients have benefited from coordinated assistance from psychiatrists, social workers and occupational therapists who try to smooth the transition.

"That help is crucial," says Mayberg, who is now a professor of psychiatry and neurology at Emory University in Atlanta. "We're just fixing the circuit. The patient's life still needs work. It's like fixing a knee. They need that high-quality physical and supportive therapy afterward if they're really going to move around again."

This transition is not back to a former self and family but to a new one. Gary Benjamin says he sees similar things in military families. "These soldiers get sent away for six months, they come back and all they want to do is return to their old home. But their old home isn't there, because everybody's changed. It takes some tough rearranging sometimes."

For a change so profound, these seem acceptable adjustments. And the treatment so far seems remarkably free of side effects. No one has suffered significant neural complications, probably because, unlike ECT, which sends 70 to 150 volts through the entire brain, these electrodes deliver only about 4 volts to an area about the size of a pea.

But what will happen when larger groups are treated? The team is continuing to operate on depressed patients, with a goal of 20. And would the successes stay high and the side effects low in a large, placebo-controlled trial? Neither Mayberg nor any of the other collaborators cares to guess. Other treatments have started this well and fizzled. For instance, vagus nerve stimulation, which sends a low current to the brain via a major nerve with connections to various brain areas, appeared to help about half of the patients in a small, initial, uncontrolled trial, but failed its only placebo-controlled trial. (In a controversial move, the Food and Drug Administration overruled its own reviewers and approved the device as a depression treatment anyway.)

"What if you do a hundred patients," I asked Mayberg one day, "and they do no better than placebo?"

"I suppose that's possible," she said. But she doesn't think that will be the case. The several authorities I talked to agree that the high success rate so far, along with the soundness of the theoretical base and D.B.S.'s track record with Parkinson's, suggests that this isn't just a lucky run.

"This just makes so much sense," says Dr. Antonio Damasio, director of the University of Southern California's Brain and Creativity Institute and a renowned neurologist, "and the weight of the results is so sizable. I would be surprised if they had no results with a larger body of patients."

On the other hand, even if it works, no one sees this becoming the new Prozac. The procedure costs too much (around $40,000) to use on anyone who hasn't tried everything else. The appropriate candidates for D.B.S. probably number in the thousands, not the millions. Perhaps the most sensible worry is that if the thing works, doctors might use it too freely, as they tend to do with successful new treatments; witness the problematic boom in D.B.S. for Parkinson's.

In the end, the procedure's greatest clinical value may lie in inspiring less intrusive ways of tweaking key nodes — localized delivery of drug or gene therapies, or other means still to come. Such possibilities probably lie at least a decade away.

Regardless of how it pans out in the clinic, Mayberg and Lozano's D.B.S. study is already changing how neuroscientists and psychiatrists think about depression. One possibility, for instance, is that refining the networks that go awry in depression may reveal neurological subtypes of depression that can be diagnosed and treated differently. For example, Mayberg has already found that patients who respond well to Prozac usually show a change in their brain scans only a week after they start medication — even though they don't feel a difference for 3 to 10 weeks (a long and sometimes dangerous wait). She's done preliminary work suggesting she might be able to identify such Prozac-friendly patients before they even start the drug. If she or others can replicate and elaborate on this diagnostic ability, doctors might be able to characterize a patient's depression and choose a best-odds therapy — Prozac for one patient, talk therapy for a second, both for a third — at the very beginning of treatment, savings weeks or months of trial and error.

The network model — which some scientists also call a "systems" model — also offers an organizing principle for research. Andreas Meyer-Lindenberg, a researcher with the N.I.M.H., points out that research on depression has so far followed clues left by drugs that were found to be effective only by chance. "We'd find a drug that helped depression, figure out how it works and make hypotheses from that about how the brain works," he says. The effectiveness of selective serotonin reuptake inhibitors (S.S.R.I.'s) like Prozac, for instance, inspired piles of research showing that mood regulation depends heavily on the availability of the neurotransmitter serotonin. (Neurotransmitters are chemicals that help carry messages across the spaces between neurons; S.S.R.I.'s treat depression by making more serotonin available in those spaces.)

This focus on neurotransmitters is the "bowl of soup" approach that Mayberg speaks of, and it has formed the bulk of depression research for more than two decades. Defining the networks the neurotransmitters move within, however — and in particular identifying Area 25 as a key gateway within the depression network — will let researchers bring their neurochemical knowledge to bear on specific targets.

"With this D.B.S. work," Meyer-Lindenberg says, "they have characterized in detail a system" — or network — "underlying a major disorder. It's not a simplistic thing where you're saying it's all about this one area and you inject a current and everything's fine. It's a very complicated system. But this D.B.S. work shows us that amid this complicated system there is a place of overlap, a common denominator" — Area 25 — "that's a very attractive treatment target." Here, Meyer-Lindenberg says, researchers can try to apply the knowledge they've gained about neurochemistry and genetics. The network theory presents a framework around which to apply these perspectives.

Meyer-Lindenberg's own work shows the power of this approach. Last June he published a study on the serotonin transporter gene, or sert gene, which helps determine serotonin availability. Other research had shown that people with the "short" version of the sert gene run more depression risk. Meyer-Lindenberg found a way to identify how various brain areas were affected by having that short version. Then he took 112 patients, half with the long version and half with the short, scanned their brains and asked the computer to find areas that scanned differently in the two groups. The area showing the most difference was Area 25.

Along with redirecting research, the quieting of Area 25 may also change our conception of depression from a condition in which something is lacking — self-esteem, resilience, optimism, energy, serotonin, you name it — to one in which an active agent makes a person sick.

"Most people think of depression as a deficit state," Mayberg says. "You're low, you're negative. But in fact, talk to a depressed person, and you have this bizarre combination of numbness and what William James called 'an active anguish.' 'A sort of psychical neuralgia,' he said, 'wholly unknown to healthy life.' You're numb but you hurt. You can't think, but you are in pain. Now, how does your psyche hurt? What a weird choice of words. But it's not an arbitrary choice. It's there. These people are feeling a particular, indescribable kind of pain."

This anguish, Mayberg suggests, is the manifestation of a neural circuit run amok. For doctors, establishing this should focus research and care. For those of us who've never known depression, recognizing it may help us see depression not as a dead absence but as a live affliction. We might even stop indulging the romantic notion of depression as intrinsic to one's identity. For this notion, too, was tested by Mayberg's experiment. When a steady, 4-volt thrum calmed these patients' anguish, they did not lose their identities. They regained them, feeling again the engagements with the world that most define them: flowers for the gardener, lightness for the cyclist and, for Deanna, a long-missed connection to others.

When Deanna, Gary and I finally finished talking, they insisted on driving me to my hotel. Halfway through town, Gary pulled off the main road, drove up a long, sinuous driveway and parked in a lot facing a dark, rambling building.

"This is the hospital," Gary said. "You see where Deanna stayed."

In the winter dark, the secure ward, off to the left, was easily discerned. It was a low wing, the only one with a few lights still on inside. Outside, bright flood lamps illuminated an exercise yard ringed by 20-foot-tall cyclone fencing topped with razor wire.

"And there's the lake," Gary said, motioning behind us. Through trees I could make out its blackness.

We sat several minutes, but no one said much.

"Well," Gary said, putting the minivan in gear. "We'd better get home."

David Dobbs writes on science, medicine and culture. His last article for the magazine was about autopsy.
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Sleep Tight

More folks I know have sleep disorders than any other type of maladjustment problem. They simply don't get enough rest. This article raises awareness on that matter. Enjoy !

The New York Times
April 2, 2006
Can't Sleep? Read This
By WILLIAM L. HAMILTON

TRY this sometime.

Plaster about two dozen electrodes to your face and head and tape some more to your chest and legs. Give yourself two to three feet of wire on each, and attach the other ends to the wall next to a bed, so they tug tightly when you move. Make sure the bed is in a room that you've never seen before, something that looks like a hospital room disguised as a hotel room. A kind of Soviet-era bugged spy box for information gathering, with a video camera, pointed at the bed, blinking silently from the ceiling.

Then turn out the lights and go to sleep.

I'm not a very cooperative lab rat, but this would describe a typical night at a sleep clinic, where data is gathered on how you sleep. This describes my night at the Center for Sleep Medicine at the Mount Sinai Medical Center in Manhattan. I woke up the next morning at 7 with someone misting my head. That softens the glue on the electrodes. On the subway ride home I looked like an escapee, discs of plaster crusted on my skull. Just another alien abduction.

I have joined the national discussion on sleep, a statistic in what is being called an epidemic of sleeplessness, or the growing perception that in bed, extracurriculars aside, we're not being our personal best.

It is a discussion being conducted in doctors' offices, at dinner tables, on Web sites like talkaboutsleep.com and sandiegodreamcatchers.org, and in chat rooms, where people call themselves "midnightclyde" and "sleepymoon."

"Nutrition, physical fitness, now sleep," said Dr. William C. Dement, director of the Sleep Disorders Clinic and Research Center at Stanford University, of the modern history of the American obsession with wellness.

Dr. Dement, who basically founded the idea of sleep medicine, is, at 77, the Sandman. He said the only periods during which he ever recalling losing sleep were when applying for grant money. "Twenty-five years ago everyone started jogging, worried about fitness," he said. "Now sleep is having its moment. Ninety percent of your waking health is dependent on your sleep."

Since 1970, when Dr. Dement founded his clinic, the nation's first, sleep has spawned university departments, associations, journals, conventions, academies and foundations like the National Sleep Foundation, which declared last week National Sleep Awareness week, ending today with daylight saving time, when we lose an hour of sleep by the clock whether we normally snooze with the gods or not.

Like many others, I complained to my doctor of poor sleep, and of tiredness during the day. He prescribed a sleep evaluation, to be conducted at a sleep clinic.

With baby boomers again leading the charge (I'm 54; you lose your natural gift for sleep as you age), sleep has become a commercial industry. In addition to pills (more popular than ever), breathing masks, nose pillows, hypnotic podcasts, aromatherapies and specialty bedding, there are sleep clinics like Mount Sinai's, which are proliferating.

With a tantalizing promise of self-improvement, like a day spa crossed with a night class, accredited facilities in the United States have tripled in number, to 963, in the last 10 years. (There are roughly 900 more unaccredited centers.) Sleep doctors warn that a shortage of trained, certified personnel like the technicians who administer the overnight testing could be sleep's next crisis.

"Think you have a sleep disorder?" asks the American Academy of Sleep Medicine, which accredits sleep centers, at its Web site, www.aasmnet.org. "Find a sleep center near you!"

Dr. Stasia J. Wieber, director of the Comprehensive Center for Sleep Medicine at Mount Sinai, said of evaluations: "A lot of people do it because their friends did it. But we only do an overnight sleep study when it's indicated. Everyone leaves with a diagnosis, but not everyone gets thrown into the lab. A physician has to order the study."

The overnight evaluation at Mount Sinai costs $1,500; most insurance companies cover it.

I arrived at 8 in the evening with an overnight bag, filled out a form on my sleep habits to determine my overall sleep "hygiene," then changed into my nightwear (tattered workout clothes) and sat in a chair watching "Armageddon" without sound on a corner television while a technician worked behind me, wiring my head.

Mount Sinai also evaluates pediatric sleep disorders. Down the hall, someone sang a lullaby, with the soft disembodiment that foreshadows horrible events in movies. On the television Bruce Willis said goodbye to Earth, his finger on the bomb.

Lights out. During the night, as I traveled between wakefulness and sleep, sending back streams of data like a space probe, the technician appeared and disappeared, adjusting my wires, and exiting my consciousness in a ring of light — the door to the corridor — like a spectral visitor, a goblin that only the sixth-sensed see. He monitored my voyage from a desk somewhere in the clinic, taking notes as I sped through the blackness.

The next morning, miles from a cup of coffee, my head damp with mist and dotted with what looked like old toothpaste, I filled out another form, asking, among other things, what I had dreamed about.

"I dreamed I was wired to a bunch of wires, in a threatening tangle, that pulled me back to a wall every time I tried to escape," I wrote, truthfully.

"Perhaps it was not a dream," the technician said, reviewing my responses, with a graveyard humor that was also chilly and serious. Working nights will do it to you.

During an office visit with Dr. Wieber two weeks later, I was told I have sleep apnea. I stop breathing 16 times an hour as I sleep, which she explained is considered moderate.

When you stop breathing, because of an inadequate passage for air between your tongue and the back of your throat, your body sends a message to your brain that something is going wrong, and your brain, in an emergency response, wakes you up. You lose sleep. And you are at increased risk for heart attack and stroke, studies have shown.

Medically, the first line of defense is a machine with a mask called a CPAP (continuous positive airway pressure) device. Then there is a Clockwork Orange-like dental device, which is not effective in every case, explained Dr. Wieber. And there was a surgical procedure, for select cases.

Rock, hard place.

The CPAP (pronounced SEE-pap) mask was simpler and showed great success, she said. But it meant snorkeling your way down into the deep of sleep, more scuba diving than sheep counting. Every single night. And you look like Dennis Hopper in "Blue Velvet," to yourself and anyone else. I freaked out.

In a subsequent telephone conversation, Dr. Wieber assured me I was not alone.

"It's hard to wear a mask every night," she said, adding that for patients who are hearing of apnea and its treatments for the first time, the mask "might come as a shock." But she added that 70 to 75 percent adopt it, and compliance is good.

"For people walking around tired all day, it's a no-brainer," said David Schneiderman, 44, chief operating officer for a commodities clearing corporation in New York, with assurance. Mr. Schneiderman, who was diagnosed with apnea in 2002 and who wears a CPAP mask every night, recalled his wife and daughter telling him that before he was evaluated, he slept like a man in a cartoon.

"The dresser drawers would pull out and push in, from my snoring," he said. Now, with his snorkel-like CPAP in place as he prepares for bed, "my daughter comes in to kiss me goodnight: 'Goodnight Darth,' she says." Mr. Schneiderman added that he slept so well that he could no longer nap during the day.

Apnea, a recognized threat, is the tip of the iceberg, say sleep doctors. There are more than 80 identifiable sleep disorders, including restless leg syndrome and classics like insomnia.

"People think if you have apnea you die," said Dr. Thomas Roth, director of the Sleep Disorder and Research Center at Henry Ford Hospital in Detroit, who is cynical about the nation's discussion on sleep and the fashionable interest in the subject, and recited the rest of the wives' tales that have garnered the greatest media attention. "If you have insomnia, you're neurotic. If you don't sleep a lot, you're macho."

Dr. Roth, like many sleep specialists spoken to, believes the awareness of inadequate sleep, or the importance of good sleep hygiene, is still developing.

"Go to every school in the state and see how many have taught one word about sleep," he said. "My daughter's high school hygiene and health textbook? One page. That will be hard to justify to kids, because they don't sleep well either."

In a study released on Tuesday the National Sleep Foundation reported that more than half of the teenagers polled, ages 11 to 17, said they got less sleep than they thought they should, and a third suspected they had a sleep disorder. Only 7 percent of the parents polled thought their children had problems sleeping, though 28 percent of the teenagers said they fell asleep in class and were too tired to exercise.

More than half said they had driven while drowsy during the last year. Caffeine and electronic games, computers, personal telephones and televisions in the bedroom were culprits called out in the study: familiar to teenagers, but absent in their parents' suppositions about how much, or how well, their children sleep.

"Changing human behavior is a very difficult challenge," said Dr. Roth, who expressed pessimism about people's ability to embrace better sleep habits when, like eating or exercise, changing them went to the core of how people liked to live. He compared the epidemic of sleeplessness to the national epidemic of obesity, which is worsening.

And then there is blissful denial. If only that could help you sleep. "Ninety percent of the time, people with sleep problems think they're champion sleepers, and that they're just somehow too sleepy," said Dr. Meir Kryger, director of the sleep disorder clinic at St. Boniface General Hospital in Winnipeg, Manitoba, of his adult patients.

"It's a strange business," he said of sleep.

Tell me about it. Just not before I turn out the light.
###

Brainiacs are different (yawn)

Yet another confirmation of the obvious - intelligent's children's (and i suspect adults will show similar indications) brains look different than other children's brains. Still fascinating - just not surprising. Enjoy.

The New York Times
March 30, 2006
Scans Show Different Growth for Intelligent Brains
By NICHOLAS WADE

The brains of highly intelligent children develop in a different pattern from those with more average abilities, researchers have found after analyzing a series of imaging scans collected over 17 years.

The discovery, some experts expect, will help scientists understand intelligence in terms of the genes that foster it and the childhood experiences that can promote it.

"This is the first time that anyone has shown that the brain grows differently in extremely intelligent children," said Paul M. Thompson, a brain-imaging expert at the University of California, Los Angeles.

The finding is based on 307 children in Bethesda, Md., an affluent suburb of Washington. Starting in 1989, they were given regular brain scans using magnetic resonance imaging, a project initiated by Dr. Judith Rapoport of the National Institute of Mental Health.

This set of scans has been analyzed by Philip Shaw, Dr. Jay Giedd and others at the institute and at McGill University in Montreal. They looked at changes in the thickness of the cerebral cortex, the thin sheet of neurons that clads the outer surface of the brain and is the seat of many higher mental processes.

The general pattern of maturation, they report in Nature today, is that the cortex grows thicker as the child ages and then thins out. The cause of the changes is unknown, because the imaging process cannot see down to the level of individual neurons.

But basically the brain seems to be rewiring itself as it matures, with the thinning of the cortex reflecting a pruning of redundant connections.

The analysis was started to check out a finding by Dr. Thompson: that parts of the frontal lobe of the cortex are larger in people with high I.Q.'s. Looking at highly intelligent 7-year-olds, the researchers said they were surprised to find that the cortex was thinner than in a comparison group of children of average intelligence.

It was only in following the scans as the children grew older that the dynamism of the developing brain became evident. The researchers found that average children (I.Q. scores 83 to 108) reached a peak of cortical thickness at age 7 or 8. Highly intelligent children (121 to 149 in I.Q.) reached a peak thickness much later, at 13, followed by a more dynamic pruning process.

One interpretation, Dr. Rapoport said, is that the brains of highly intelligent children are more plastic or changeable, swinging through a higher trajectory of cortical thickening and thinning than occurs in average children. The scans show the "sculpturing or fine tuning of parts of the cortex which support higher level thought, and maybe this is happening more efficiently in the most intelligent children," Dr. Shaw said.

The I.Q. was tested when the children entered the program. Further tests were not needed because I.Q.'s are so stable, Dr. Rapoport said.

Dr. Thompson said the new study opened huge possibilities because researchers should be able to identify the factors that influence the brain by looking at the scan patterns identified by the researchers.

The Bethesda children have had genetic samples taken from their cells, so genes that have even the mildest influence on the brain should be detectable, Dr. Thompson said. The pattern of development may also be affected by factors like diet, hours spent in school or the number of siblings, and these may come to light by asking parents how they raised their children.

"There are many enigmas of intelligence that they can now solve," he said.

I.Q. scores and measuring intelligence have long been controversial. Brain-imaging studies by Dr. Thompson and the study group have advanced the field by identifying physical features of the brain that correlate with I.Q.

In 2001, Dr. Thompson reported that based on imaging twins' brains the volume of gray matter in the frontal lobes and other areas correlated with I.Q. and was heavily influenced by genetics. Despite the great importance of genes in brain function, Dr. Thompson said experience could also change the brain.

"Unless you have strong natural potential, you won't become a world-class marathon runner," he said. "But that disillusionment is rapidly replaced by the notion that you can improve your own performance."

The institute's team has many genetic studies in progress. The analysis reported today was not intended to look at the relationship between genes and intelligence.

"A lot of research in intelligence has not been that great," Dr. Shaw said. "I would hope by this modest descriptive study to put things on an empirical footing."

One goal of the study was to establish normal development patterns, to diagnose what goes awry in children with schizophrenia or attention deficits. Dr. Shaw said his team did not have the full answers as to how the brain differed in those cases.
###

Dance around these blogs

Lots going on around my blogosphere right now.

Ever notice that there are now 10 (ten) blogs here (see list to the right - PLUS - three of the blogs aren't even listed yet - you have to peek at my profile page at the bottom to see 'em)?

Check some of these others out - they contain entries not found here at the main 3deye blog (although at times i post a particularly good entry in several blogs at once).

And since i believe in the Buddhist saying that "your most beloved teachers are your critics," please feel free to suggest improvements for your reading / viewing pleasure here.

Or you may just complain if you wish. Feels good sometime to simply vent. I have an alligator's hide, so pull no punches.

MEANWHILE

Check out OUR Constant Gardeners blog at

http://constantgarden.blogspot.com/ for the latest stuff there.

Enjoy !

p.s. Want to contribute to any of these blogs on a regular basis? That's doable. Just write to me and tell me. Welcome.

To the Ladies I love

This "hot flash" bugaboo has got to stop. Here's how to achieve that.

Enjoy, ladies.

Oh - I like dark beer (Guiness, Abita Springs, Shiner Bock, Fat Tire, etc). Call me to come over for a beer and to discuss how this treatment helped you. We'll both have a good laugh and I'll get to drink some favorite beer as well.

The New York Times
March 28, 2006
Personal Health
A Chance Find, and Voilà! Goodbye, Hot Flashes. Hello, Sleep.
By JANE E. BRODY

A widely used drug that has been mired in controversy for most of its decade-long life may now bring relief to postmenopausal women whose lives have been disrupted by unrelenting hot flashes. The relief may be especially welcome to women who have had breast cancer and cannot take estrogen.

The drug, best known by its trade name, Neurontin, but now prescribed generically as gabapentin, was approved by the Food and Drug Administration in 1994 to treat epileptic seizures. In 2002, it was approved to treat postherpetic neuralgia, horrific pain that sometimes follows shingles.

Aided by the Internet and, the government has said, an illegal marketing campaign by its parent company, Neurontin sales eventually exceeded $2 billion a year before its patent expired and the generic gabapentin entered the market in 2004.

The parent company, Warner-Lambert (since bought by Pfizer), was investigated after a whistle-blower said it had paid doctors to promote Neurontin to their colleagues for a host of additional symptoms not approved by the F.D.A. The whistle-blower also said the company had paid to have research articles prepared claiming benefits of a dubious nature.

Varied Applications

As a result, Neurontin has been used for problems like migraines, social phobia, attention-deficit disorder in children, gastric ulcers, restless leg syndrome, essential tremor, osteoarthritis, backache, insomnia, anxiety, bipolar disorder, panic attacks and withdrawal from cocaine and alcohol — all known as off-label uses.

Its most frequent off-label use is as an adjunct to drugs used to treat pain, especially pain thought to have nerve involvement.

Thus, gabapentin was part of the medication prescribed for my unrelenting pain after a double knee-replacement operation last year. It was prescribed again last fall when I developed debilitating back and leg pain caused by a pinched nerve in my back.

Between the two prescriptions, I made a discovery that changed my life for the better. While taking Neurontin three times a day for the knee pain, I had none of the hot flashes that had plagued me day and night after breast cancer in 1999 made me stop postmenopausal hormones. But when I weaned myself from gabapentin last May, the hot flashes returned, resulting in three sleepless nights in a row. I wondered whether it could be a factor and decided, with my doctor's approval, to try just one 300-milligram capsule before bedtime. Voilà! No hot flashes. No waking up damp and clammy and unable to go back to sleep.

I've stayed on the drug, and this winter I've been able to wear turtlenecks. I'm sleeping much better. On the dose that helps me — 300 milligrams after breakfast and 300 or 600 milligrams at bedtime — I've noticed no unusual effects beyond an ability to sleep comfortably for seven hours a night.

Last September, I found a report in The Lancet, the medical journal, by researchers from four medical centers who conducted a clinic trial using gabapentin to treat hot flashes in women with breast cancer. In the study, 420 women having two or more hot flashes a day were randomly assigned to take 300 or 900 milligrams of gabapentin or a look-alike placebo each day in three divided doses for eight weeks.

About one patient in five on the placebo reported a decline in hot flashes, while a third of those taking 300 milligrams of gabapentin did and nearly half of those on 900 milligrams reported a benefit.

The researchers, led by Dr. Kishan J. Pandya of the James P. Wilmot Cancer Center at the University of Rochester Medical Center, found that "only the higher dose of gabapentin was associated with significant decreases in hot flash frequency and severity." They recommended that the drug "be considered for treatment of hot flashes in women with breast cancer."

Dr. Pandya undertook this study after Dr. Thomas J. Guttuso Jr., a neurologist then at the university's medical center, published findings in February 2003 in Obstetrics & Gynecology. Dr. Guttuso and his colleagues had randomly assigned 59 postmenopausal women who suffered from seven or more hot flashes a day to receive gabapentin or a placebo for 12 weeks.

Reducing the Heat

Those who took 300 milligrams of gabapentin three times a day reported a 54 percent reduction in overall hot flash activity (frequency and severity) compared with a 31 percent drop in the placebo group.

In an interview, Dr. Guttuso, now at the Jacobs Neurological Institute at the University at Buffalo, discussed a soon-to-be-published study by Dr. Sireesha Y. Reddy and colleagues that pitted 2,400 milligrams of gabapentin daily against 0.625 milligram of estrogen, the gold standard for controlling hot flashes.

Participants suffered from moderate to severe hot flashes, defined as seven or more per day, accompanied by sweating. Gabapentin relieved hot flashes as effectively as estrogen, Dr. Guttuso said. Although about 40 percent of the women taking 2,400 milligrams of gabapentin daily reported side effects (sleepiness, dizziness and swelling of the feet), they felt that the benefit of the drug outweighed them, Dr. Guttuso said.

Gabapentin has other benefits. "It does not interact with any other medications, which is very unique," Dr. Guttoso said, "so doctors don't have to worry about other drugs a patient might be taking. Also, gabapentin is not metabolized, so it has no effect on the liver. It's fully excreted in the urine." He said that it works through a receptor on the membranes of brain and peripheral nerve cells.

Estrogen normally acts as a brake on cells in the brain's temperature-regulating center through pathways called calcium channels. Gabapentin binds to a channel.

Gabapentin was developed to help avoid the addictive quality of drugs called GABA analogues (Valium, Ativan and Xanax) used for anxiety and seizure disorders. The modified drug proved nonaddictive.

Properly designed clinical trials are needed to show just how helpful gabapentin is against various conditions and whether prolonged use may have unexpected adverse effects. At high doses, side effects like drowsiness, dizziness and weight gain from retained water can limit its usefulness.

Now that the drug is without patent protection, future F.D.A. approvals will depend on studies by two companies. One, PharmaNova, has patented a sustained-release formulation of gabapentin and is studying its role in treating hot flashes. Meanwhile, Pfizer has introduced a chemical cousin of gabapentin, sold as Lyrica and approved for treating nerve pain caused by shingles and diabetes. It should control hot flashes, too.

Lyrica is being studied in patients with hot flashes under a licensing agreement with the University of Rochester, which has patented new uses of gabapentin and other drugs that use the same mechanism.
###

Emotions Key

Dana Reeve tells viewers: “Your emotional state has a tremendous amount to do with sickness, health and well-being."

It's one of those insights which seems obvious at first, but then we don't live as if we believe it.

We must.

Enjoy.

MSNBC.com

Dana Reeve poignantly begins PBS program
Months before death, is ‘hopeful' in introduction to ‘The New Medicine’

The Associated Press
Updated: 6:08 p.m. ET March 25, 2006


CHARLOTTE, N.C. - Dana Reeve would live only about three more months after she taped an introduction to the two-hour PBS documentary “The New Medicine.”

The widow of paralyzed “Superman” actor Christopher Reeve was battling lung cancer diagnosed last summer, but was upbeat on that late November day of the taping.

“She was very hopeful at that point that she would survive,” director Muffie Meyer recalled. “She was buying Christmas presents for her son that day, and really had a tremendous amount of energy.”

In her introduction to the first segment of “The New Medicine,” Reeve tells viewers: “Your emotional state has a tremendous amount to do with sickness, health and well-being. For years, my husband and I lived on — and because of — hope. Hope continues to give me the mental strength to carry on.”

The project was the last she is known to have completed before her death March 6. “The New Medicine,” which debuts Wednesday (check local listings), looks at how mainstream doctors are embracing the idea that true healing involves treating the whole patient — not just the symptoms of a disease.

By airing after her death, Reeve’s appearance unintentionally underscores one of the central points of the documentary: Holistic medicine is a tool for fighting illness — not a cure-all.

“Part of the challenge is we get patients all the time that are really looking for a magic cure,” said Dr. Tracy Gaudet, an obstetrician-gynecologist who heads the Duke Center for Integrative Medicine in Durham and is featured in the PBS program. “We’re not in the business of magic cures; we’re in the business of good medicine.”

The idea behind her center, Gaudet said, is to use any available techniques — from alternative to mainstream — that might improve a patient’s experience. Accepted practices include herbal supplements, acupuncture, massage and meditation.

“The Science of Emotion,” the first hour of the documentary, follows Gaudet as she treats Tammy Patton following her hospitalization in the 25th week of pregnancy. Patton’s water has broken prematurely, exposing her fetus to the risk of infection and increasing the chance of premature birth.

Stress is known to raise the risk of infection and to spur early labor, so Gaudet led Patton through a series of relaxation exercises intended to hold off labor.

“We can help your mind take a little vacation,” Gaudet told her patient. Patton ended up carrying her baby boy four more weeks. So the birth was still premature, but the boy has a good chance of a healthy life.

Also featured in the program is Dr. Ralph Snyderman, the chancellor emeritus of health affairs at Duke who helped start the center. Snyderman said recently that before he was an administrator, he specialized in technology-driven, federally financed research.

“I was about as hard-nosed a physician-scientist as you could find,” he said. But he learned that patients had problems “beyond what was going to be solved through pure science and technology alone.”

Reeve, in an off-camera interview with the film’s producers on the day she taped her introductions, said she had consulted with integrative medicine guru Dr. Andrew Weil and was doing “creative image work” — a technique in which patients learn to relax by evoking images and sensations.

With her doctors’ blessing, she said, she also was taking botanical supplements along with the medicines she was prescribed at Memorial Sloan-Kettering Medical Center.

The PBS film almost consciously avoids a New Age tone. There are a few shots of yoga classes and one segment in which scientists study the brain waves of a Buddhist monk as he meditates.

But there are no magic crystals, no “cancer diets” or trips to Mexico for treatments outlawed in the United States. Just a sincere effort to find something — anything — that will lead to a better quality of life for patients.

© 2006 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

© 2006 MSNBC.com

URL: http://www.msnbc.msn.com/id/12012024/from/RS.4/