Health – Page 42 – artdiamondblog.com

“A Foolish Faith in Authority Is the Worst Enemy of Truth”

(p. A21) Several years ago I grew concerned about my postmenopausal mother’s risk of osteoporosis. I tried to convince her to initiate hormone replacement therapy. She didn’t listen to me. Instead, she spoke with her gynecologist, who–contrary to best medical evidence at the time–recommended against such treatment. I would eventually be thankful my mother listened to the gynecologist who had known her for decades instead of me and the published medical reviews I was relying on. Some years later my mother was diagnosed with early breast cancer. Had she been on estrogen replacement, it is likely that her tumor would have progressed more rapidly. The gynecologist likely saved my mother’s life.

Studies published in the medical literature are mostly produced by academics who face an imperative to publish or watch their careers perish. These academics aren’t basing their careers on their clinical skills and experiences. Paradoxically, if we allow the academic literature to set guidelines for accepted practices, we are allowing those who are often academics first and clinicians second to determine what clinical care is appropriate.
Consciously or not, those who provide the peer review for medical journals are influenced by whether the work they are reviewing will impact their standing in the medical community. This is a dilemma. The experts who serve as reviewers compete with the work they are reviewing. Leaders in every community, therefore, exert disproportional influence on what gets published. We expect reviewers to be objective and free of conflicts, but in truth, only rarely is that the case.
Albert Einstein once noted that “a foolish faith in authority is the worst enemy of truth.”

For the full commentary, see:

NORBERT GLEICHER. “‘Expert Panels’ Won’t Improve Health Care; Government reliance on medical studies will make it harder to discard false prophecies and dogmas.” The Wall Street Journal (Mon., October 19, 2009): A21.
(Note: the online version of the commentary is dated Sun., Oct. 18.)

John Mackey: “I Believe in the Dynamic Creativity of Capitalism”

Whole Foods CEO John Mackey. Source of the caricature: online version of the WSJ interview quoted and cited below.

(p. A11) “I honestly don’t know why the article became such a lightning rod,” says John Mackey, CEO and founder of Whole Foods Market Inc., as he tries to explain the firestorm caused by his August op-ed on these pages opposing government-run health care.
. . .
. . . his now famous op-ed incited a boycott of Whole Foods by some of his left-wing customers. His piece advised that “the last thing our country needs is a massive new health-care entitlement that will create hundreds of billions of dollars of new unfunded deficits and move us closer to a complete government takeover of our health-care system.” Free-market groups retaliated with a “buy-cott,” encouraging people to purchase more groceries at Whole Foods.
. . .
What Mr. Mackey is proposing is more or less what he has already implemented at his company–a plan that would allow more health savings accounts (HSAs), more low-premium, high-deductible plans, more incentives for wellness, and medical malpractice reform. None of these initiatives are in any of the Democratic bills winding their way through Congress. In fact, the Democrats want to kill HSAs and high-deductible plans and mandate coverage options that would inflate health insurance costs.
. . .
Mr. Mackey’s latest crusade involves traveling to college campuses across the country, trying to persuade young people that business, profits and capitalism aren’t forces of evil. He calls his concept “conscious capitalism.”
What is that? “It means that business has the potential to have a deeper purpose. I mean, Whole Foods has a deeper purpose,” he says, now sounding very much like a philosopher. “Most of the companies I most admire in the world I think have a deeper purpose.” He continues, “I’ve met a lot of successful entrepreneurs. They all started their businesses not to maximize shareholder value or money but because they were pursuing a dream.”
Mr. Mackey tells me he is trying to save capitalism: “I think that business has a noble purpose. It’s not that there’s anything wrong with making money. It’s one of the important things that business contributes to society. But it’s not the sole reason that businesses exist.”
What does he mean by a “noble purpose”? “It means that just like every other profession, business serves society. They produce goods and services that make people’s lives better. Doctors heal the sick. Teachers educate people. Architects design buildings. Lawyers promote justice. Whole Foods puts food on people’s tables and we improve people’s health.”
Then he adds: “And we provide jobs. And we provide capital through profits that spur improvements in the world.
. . .
“I don’t think anybody’s too big to fail,” he says. “If a business fails, what happens is, there are still assets, and those assets get reorganized. Either new management comes in or it’s sold off to another business or it’s bid on and the good assets are retained and the bad assets are eliminated. I believe in the dynamic creativity of capitalism, and it’s self-correcting, if you just allow it to self-correct.”
That’s something Washington won’t let happen these days, which helps explain why Mr. Mackey felt compelled to write that the Whole Foods health-insurance program is smarter and cheaper than the latest government proposals.

For the full interview, see:
STEPHEN MOORE. “The Conscience of a Capitalist; The Whole Foods founder talks about his Journal health-care op-ed that spawned a boycott, how he deals with unions, and why he thinks CEOs are overpaid.” The Wall Street Journal (Sat., OCTOBER 3, 2009): A11.
(Note: ellipses added.)

New Scientific Optimism on Life Extension

Source of photo: online version of the NYT article quoted and cited below.

(p. D1) It may be the ultimate free lunch — how to reap all the advantages of a calorically restricted diet, including freedom from disease and an extended healthy life span, without eating one fewer calorie. Just take a drug that tricks the body into thinking it’s on such a diet.

It sounds too good to be true, and maybe it is. Yet such drugs are now in clinical trials. Even if they should fail, as most candidate drugs do, their development represents a new optimism among research biologists that aging is not immutable, that the body has resources that can be mobilized into resisting disease and averting the adversities of old age.
This optimism, however, is not fully shared. Evolutionary biologists, the experts on the theory of aging, have strong reasons to suppose that human life span cannot be altered in any quick and easy way. But they have been confounded by experiments with small laboratory animals, like roundworms, fruit flies and mice. In all these species, the change of single genes has brought noticeable increases in life span.
With theorists’ and their gloomy predictions cast in the shade, at least for the time being, experimental biologists are pushing confidently into the tangle of linkages that evolution has woven among food intake, fertility and life span. “My rule of thumb is to ignore the evolutionary biologists — they’re constantly telling you what you can’t think,” Gary Ruvkun of the Massachusetts General Hospital remarked this June after making an unusual discovery about longevity.
Excitement among researchers on aging has picked up in the last few years with the apparent convergence of two lines of inquiry: single gene changes and the diet known as caloric restriction.
. . .
In the view of evolutionary biologists, the life span of each species is adapted to the nature of its environment. Mice live at most a year in the wild because owls, cats and freezing to death are such frequent hazards. Mice with genes that allow longer life can rarely be favored by natural selection. Rather, the mice that leave the most progeny are those that devote resources to breeding at as early an age as possible.
According to this theory, if mice had wings and could escape their usual predators, natural selection ought to favor longer life. And indeed the maximum life span of bats is 3.5 times greater than flightless mammals of the same size, according to research by Gerald S. Wilkinson of the University of Maryland.
In this view, cells are so robust that they do not limit life span. Instead the problem, especially for longer-lived species, is to keep them under control lest they cause cancer. Cells have not blocked the evolution of extremely long life spans, like that of the bristlecone pine, which lives 5,000 years, or certain deep sea corals, whose age has been found to exceed 4,000 years.
Some species seem to be imperishable. A tiny freshwater animal known as a hydra can regenerate itself from almost any part of its body, apparently because it makes no distinction between its germ cells and its ordinary body cells. In people the germ cells, the egg and sperm, do not age; babies are born equally young, whatever the age of their parents. The genesis of aging was the division of labor in the first multicellular animals between the germ cells and the body cells.
That division put the role of maintaining the species on the germ cells and left the body cells free to become specialized, like neurons or skin cells. But in doing so the body cells made themselves disposable. The reason we die, in the view of Thomas Kirkwood, an expert on the theory of aging, is that constant effort is required to keep the body cells going. “This, in the long run, is unwarranted — in terms of natural selection, there are more important things to do,” he writes.
All that seems clear about life span is that it is not fixed. And if it is not fixed, there may indeed be ways to extend it.

For the full story, see:
NICHOLAS WADE. “Tests Begin on Drugs That May Slow Aging.” The New York Times (Tues., August 18, 2009): D1 & D?.
(Note: ellipsis added.)
(Note: thanks to Luis Locay for calling my attention to the article quoted above.)

How “Free” Government Health Care Works

“Michael Kellerman and daughter Jovi, 1, wait in line near 69th and Underwood for a flu shot Thursday morning.” Source of caption and photo: online version of the Omaha World-Herald article quoted and cited below.

Thousands turned out this morning for Douglas County’s first public clinic for H1N1 flu vaccinations.

The line ran out of the First United Methodist Church to the east, then down 69th Street before hooking west along Cass Street toward 72nd Street.
Police estimated that 4,000 people had gathered by 9:20 a.m.
Phil Rooney of the Douglas County Health Department said the turnout was no surprise.
“There hasn’t been a clinic this size done in the county or in the surrounding counties recently, so we were prepared for a very large crowd, and that’s what we’ve got,” he said.
He said 252 people were vaccinated in the clinic’s first hour. “The pace the first hour was slower than we wanted, so we’re trying to pick that up,” he added.

For the full story, see:
John Keenan and Rick Ruggles. “Long line for flu shots.” Omaha World-Herald online edition (Thurs., Nov. 5, 2009).
(Note: as far as I can tell, having checked several online e-editions for Nov. 5 and Nov. 6, this version of the article was never published in any of the print editions of the paper.)
(Note: at some point the title of the online version of this article was changed to “Flu shot seekers turned away.”)

“A Man of Science Past Sixty Does More Harm than Good” (Unless His Name is “Avery”)

(p. 421) . . . , in 1928, Fred Griffith in Britain published a striking and puzzling finding. Earlier Griffith had discovered that all known types of pneumococci could exist with or without capsules. Virulent pneumococci had capsules; pneumococci without capsules could be easily destroyed by the immune system. Now he found something much stranger. He killed virulent pneumococci, ones surrounded by capsules, and injected them into mice. Since the bacteria were dead, all the mice survived. He also injected living pneumococci that had no capsules, that were not virulent. Again the mice lived. Their immune systems devoured the unencapsulated pneumococci. But then he injected dead pneumococci surrounded by capsules and living pneumococci without capsules.
The mice died. Somehow the living pneumococci had acquired cap-(p. 422)sules. Somehow they had changed. And, when isolated from the mice, they continued to grow with the capsule–as if they had inherited it.
Griffith’s report seemed to make meaningless years of Avery’s work– and life. The immune system was based on specificity. Avery believed that the capsule was key to that specificity. But if the pneumococcus could change, that seemed to undermine everything Avery believed and thought he had proved. For months he dismissed Griffith’s work as unsound. But Avery’s despair seemed overwhelming. He left the laboratory for six months, suffering from Graves’ disease, a disease likely related to stress. By the time he returned, Michael Dawson, a junior colleague he had asked to check Griffith’s results, had confirmed them. Avery had to accept them.
His work now turned in a different direction. He had to understand how one kind of pneumococcus was transformed into another. He was now almost sixty years old. Thomas Huxley said, “A man of science past sixty does more harm than good.” But now, more than ever, Avery focused on his task.

Source:
Barry, John M. The Great Influenza: The Story of the Deadliest Pandemic in History. Revised ed. New York: Penguin Books, 2005.
(Note: ellipsis added.)
(Note: italics in original.)

Health Care Incentives and Information Improve When Patients Are Payers

Nobel Prize winning economist Vernon Smith sees that the current health care system is an incentive and information “nightmare.” The third parties, who pay, have neither the incentive nor the information to reward the providers who do a good job. And patients, who have the information, do not have the power or incentives to reward those who do a good job. And since providers are not being rewarded for doing a good job, they will only avoid becoming cynical bureaucrats as long as they are mission-driven saints.
A better system, that goes a long way toward Smith’s “solution,” has been suggested by Susan Feigenbaum, who suggests that third parties provide payments directly to patients, who then may choose what services to buy from which providers.
Here is the core of Smith’s analysis:

(p. A11) The health-care provider, A, is in the position of recommending to the patient, B, what B should buy from A. A third party–the insurance company or the government–is paying A for it.

This structure defines an incentive nightmare.
. . .

I don’t know whether this problem has a solution. If it does, I think it requires us to find mechanisms whereby third-party payment is made to the patient, B, who in turn pays A, supplemented with any co-payment from B for services. Hence, from the moment B seeks services from A both know who is going to be paying A for what is delivered. A and B each has need for what the other brings to the table, and this structure carries the potential for nurturing the relationship between A and B. B is empowered to become better informed about the services recommended by various A’s that he might choose among, and the A’s might find it particularly important to build good reputations with B’s.

For the full commentary, see:
VERNON L. SMITH. “The ABC Dilemma of Health Reform; Third-party payment creates a big incentive problem.” The Wall Street Journal (Sat., OCTOBER 16, 2009): A11.
(Note: ellipsis added.)

Feigenbaum’s prescient suggestion for reform can be found in:
Feigenbaum, Susan. “Body Shop’ Economics: What’s Good for Our Cars May Be Good for Our Health.” Regulation 15, no. 4 (Fall 1992): 26-27.

Harvard Medical School Conference on the Quest for Eternal Life

“AGE WELL. David Sinclair, left, and Christoph Westphal, co-founders of Sitris Pharmaceuticals, in Dr. Sinclair’s laboratory in Cambrdge, Mass. The company develops drugs that mimic resveratrol, a chemical found in some red wines.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. D4) BOSTON — Who would have thought it? The quest for eternal life, or at least prolonged youthfulness, has now migrated from the outer fringes of alternative medicine to the halls of Harvard Medical School.

At a conference on aging held here last week, the medical school’s dean, Jeffrey Flier, was to be seen greeting participants who ranged from members of the 120 club (they intend to live at least that long) to devotees of very low calorie diets.
. . .

Dr. Gallagher said that unpublished tests in mice showed that another chemical mimic, SRT-1720, increased both health and lifespan; after two years, twice as many mice taking the drug were alive compared with the undosed animals. Resveratrol itself has not been shown to increase lifespan in normal mice, although it does so in obese mice, laboratory roundworms and flies.
Sirtris has so far been doubly fortunate. No severe side effects have yet emerged from the clinical trials. The company has also been lucky in having apparently picked the right horse, or at least a good one, in a fast-developing field.
Besides the sirtuins, several other proteins are now known to influence longevity, energy use and the response to caloric restriction. These include the receptors for insulin and for another hormone called IGF-1, and a protein of increasing interest called TOR (“target of rapamycin”). Rapamycin is an antimicrobial that was recently found to extend lifespan significantly, even when given to mice at an advanced age. Since TOR is involved in the response to caloric restriction, rapamycin may extend life through this pathway.
. . .

“In five or six or seven years,” said Christoph Westphal, Sirtris’s other co-founder, “there will be drugs that prolong longevity.”
But neither Dr. Sinclair nor Dr. Westphal was the most optimistic person at the conference. That status belonged to the English gerontologist Aubrey de Grey, who sports a beard so luxuriant that it is hard to see if he is wearing a tie. His goal is “negligible senescence.”
. . .

Sirtris’s quest for longevity drugs is founded on solid and promising research. But most drugs fail at some stage during trials. So there is no guarantee that any of Sirtris’s candidate compounds will work in people. The first result from a Phase 2 clinical trial is not expected until the end of next year at the earliest.
Meanwhile, it is a pleasant and not wholly unfounded thought that, just possibly, a single drug might combat every degenerative disease of Western civilization.

For the full story, see:
NICHOLAS WADE. “Quest for a Long Life Gains Scientific Respect.” The New York Times (Tues., September 28, 2009): D4.
(Note: ellipses added.)

Rapid Mutation of RNA-Based Flu Virus Allows Rapid Adaptation to Immune System Response

I found the passage quoted below to be especially illuminating on how rapid mutation helps explain why the flu virus is so successful and dangerous. (An additional important factor is that the virus can survive in birds, without killing them.)
It occurs to me that something akin to rapid mutation (e.g., rapid experimentation) has also been advocated as a way to quickly advance science (Karl Popper), or enterprise (George Gilder).

(p. 105) Whenever an organism reproduces, its genes try to make exact copies of themselves. But sometimes mistakes–mutations–occur in this process.

This is true whether the genes belong to people, plants, or viruses. The more advanced the organism, however, the more mechanisms exist to prevent mutations. A person mutates at a much slower rate than bacteria, bacteria mutates at a much slower rate than a virus–and a DNA virus mutates at a much slower rate than an RNA virus.
DNA has a kind of built-in proofreading mechanism to cut down on copying mistakes. RNA has no proofreading mechanism whatsoever, no way to protect against mutation. So viruses that use RNA to carry their genetic information mutate much faster–from 10,000 to 1 million times faster–than any DNA virus.
Different RNA viruses mutate at different rates as well. A few mutate so rapidly that virologists consider them not so much a population of copies of the same virus as what they call a “quasi species” or a “mutant swarm.”
These mutant swarms contain trillions and trillions of closely related but different viruses. Even the viruses produced from a single cell will include many different versions of themselves, and the swarm as a whole will routinely contain almost every possible permutation of its genetic code.
Most of these mutations interfere with the functioning of the virus and will either destroy the virus outright or destroy its ability to infect. But other mutations, sometimes in a single base, a single letter, in its genetic code will allow the virus to adapt rapidly to a new situation. It is this adaptability that explains why these quasi species, these mutant swarms, can move rapidly back and forth between different environments and also develop extraordinarily rapid drug resistance. As one investigator has observed, the rapid mutation “confers a certain randomness to the disease processes that accompany RNA [viral] infections.”
Influenza is an RNA virus. So is HIV and the coronavirus. And of all RNA viruses, influenza and HIV are among those that mutate the fastest. The influenza virus mutates so fast that 99 percent of the 100,000 to 1 million new viruses that burst out of a cell in the reproduction process (p. 106) are too defective to infect another cell and reproduce again. But that still leaves between 1,000 and 10,000 viruses that can infect another cell.
Both influenza and HIV fit the concept of a quasi species, of a mutant swarm. In both, a drug-resistant mutation can emerge within days. And the influenza virus reproduces rapidly–far faster than HIV. Therefore it adapts rapidly as well, often too rapidly for the immune system to respond.

Source:
Barry, John M. The Great Influenza: The Story of the Deadliest Pandemic in History. Revised ed. New York: Penguin Books, 2005.
(Note: italics in original.)

How Wilson and the Feds Turned “Only Influenza” into “The Great Influenza”

Here is the core of John Barry’s account of how President Woodrow Wilson, and his administration, turned what might have been an ordinary flu, into what, by some measures, was the worst pandemic in human history:

(p. 396) . . . , whoever held power, whether a city government or some private gathering of the locals, they generally failed to keep the community together. They failed because they lost trust. They lost trust because they lied. (San Francisco was a rare exception; its leaders told the truth, and the city responded heroically.) And they lied for the war effort, for the propaganda machine that Wilson had created.

It is impossible to quantify how many deaths the lies caused. It is impossible to quantify how many young men died because the army refused to follow the advice of its own surgeon general. But while those in authority were reassuring people that this was influenza, only influenza, nothing different from ordinary “la grippe,’ at least some people must have believed them, at least some people must have exposed themselves to the virus in ways they would not have otherwise, and at least some of these people must have died who would otherwise have lived. And fear really did kill people. It killed them because those who feared would not care for many of those who needed but could not find care, those who needed only hydration, food, and rest to survive.

Source:
Barry, John M. The Great Influenza: The Story of the Deadliest Pandemic in History. Revised ed. New York: Penguin Books, 2005.
(Note: ellipsis added.)

How Government Universal Health Care Works in India

“Amir Jahan found her health insurance wouldn’t pay for all of her $200 stomach surgery; she continues to work with an untreated tumor.” Source of caption: print version of the WSJ article quoted and cited below. Source of photo: online version of the WSJ article quoted and cited below.

(p. A14) PANIPAT, India — Amir Jahan can spin thick, white thread into magnificent cloth, but the 46-year-old weaver has been unable to unravel her health plan to pay for stomach surgery.

Under a health-insurance program introduced a few years ago, the Indian government has provided health-insurance coverage for the country’s hand-loom weavers, a group of 6.5 million workers, 60% of them female, who are mostly illiterate and invariably poor. Yet holding an insurance card hasn’t helped Ms. Jahan, who says the coverage only pays for minor ailments and not for major problems, such as the removal of a stomach tumor.
“The health care is all a sham,” Ms. Jahan says angrily. “I was refused treatment on grounds of huge expense. I won’t ever go to be humiliated again.”
Ms. Jahan’s health-care issues represent the problems that come with trying to provide insurance to India’s poor. Access to quality care remains a distant dream for many in this country of 1.1 billion.
Last year, the Indian government launched the National Health Insurance Program on (sic) promised health coverage of $700 per person for families earning less than $100 a year.
Holders of health cards have to register in their home states to access benefits, thereby precluding a large population of migrant laborers. Those who can get past the complex state-identification and qualification process often can’t cope with hospital bureaucracies.

For the full story, see:
VIBHUTI AGARWAL. “Indian Weavers Shun Health Plan.” The Wall Street Journal (Sat., Sept., 2009): A14.