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Climate Change and the Law

Even the Bush administration has started to recognize U.S. legal obligations to fight global warming


Global negotiations on stabilizing greenhouse gas emissions in the period after 2012 will commence in Bali in December 2007. The main emitting nations—including Brazil, Canada, China, the European Union, India, Mexico, South Africa and the U.S.—have recently affirmed their commitment to reach a “comprehensive agreement” in these negotiations. They also promised to contribute their “fair share” to stabilize greenhouse gases to prevent “dangerous anthropogenic interference with the climate system.” 

Of course, one of the biggest obstacles, if not the very biggest, to such an international agreement has been the U.S. itself. The U.S. not only failed to ratify the Kyoto Protocol—the international framework to limit emissions up to the year 2012—but has also failed to put forward any meaningful stabilization strategy in its place. One of the most shocking aspects of the U.S. failure has been the country’s disregard for both international and domestic law. Yet this lawlessness looks set to change.

In recent years, the unilateralist foreign policy of the U.S. government has brazenly ignored or contravened countless aspects of international law, ranging from the Geneva Conventions to multilateral environmental treaties to which the U.S. is a signatory. This brazenness has infected the very core of policy discussions in our country. Consider an opinion piece by two distinguished professors of law at the University of Chicago, who argued in the Financial Times on August 5 that the U.S. has no obligations to control greenhouse gases, and that if other countries don’t like how the U.S. behaves and how that behavior affects them, they might think about paying the U.S. to cut its emissions. In other words, the U.S. should behave as it likes. It is up to the others to induce the U.S. to change course. 

Stunningly, the law professors completely neglected that the U.S. is already bound by international law to take steps to stabilize greenhouse gases in the atmosphere under the United Nations Framework Convention on Climate Change, signed by President George H. W. Bush and ratified by the U.S. Senate in 1992, and which entered into force in 1994. The treaty holds specifically that the developed countries should take the lead in combating climate change, and should “adopt national policies . . . consistent with the objective of the Convention,” which is the stabilization of greenhouse gases at a level that prevents dangerous interferences in the climate system. 

The claim of these law professors that the U.S. has no duty to avoid damaging the climate of others is flatly contradicted by the Convention and by international law. The parties to the Convention, including of course the U.S., recall in its preamble that “in accordance with the Charter of the United Nations and the principles of international law…. [States have] the responsibility to ensure that activities within their jurisdiction or control do not cause damage to the environment of other States or areas beyond the limits of national jurisdiction.”

Ironically, those law professors are running away from international law even faster than the Bush administration. John B. Bellinger III, a legal advisor to the State department, recently emphasized the administration’s commitment to international law and referred to its allegiance to a post-2012 climate change framework in that context. He quoted Secretary of State Condoleezza Rice’s statement that “America’s moral authority in international politics also rests on our ability to defend international laws and treaties.”

The Supreme Court also weighed in recently to emphasize that U.S. domestic law also compels stronger federal action to mitigate climate change. The Commonwealth of Massachusetts, among a number of plaintiffs, sued the Environmental Protection Agency (EPA) for its failure to regulate the emission of carbon dioxide by automobiles. The EPA had argued that carbon dioxide was not a pollutant under the Clean Air Act, that Massachusetts could not sue the EPA because it lacked legal standing to do so, and that any action by the EPA would have minimal effect on climate change. 

The court firmly struck down all the EPA’s defenses for inaction: it noted that the EPA is obliged to regulate any deleterious pollutant emitted by motor vehicles; that carbon dioxide clearly falls within that category; that Massachusetts had standing to sue because climate change was already claiming part of the state’s coastline, and that the state was vulnerable to considerably greater coastal losses this century if climate change is not mitigated. Moreover, it emphasized that mitigating U.S. auto emissions would have a meaningful effect on the pace of climate change. For all of these reasons, the Court ruled that the EPA was obligated to act.

The obligation to limit greenhouse gas emissions is therefore already the law of the land, vis-à-vis both international and domestic law, and it’s high time we begin respecting those laws. We should do so not only because it is important that we recognize and honor our legal commitments, but also because we made those commitments for powerful reasons of our own survival and wellbeing. Even an administration that has dragged its feet for seven years is finally beginning to face that reality. 

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Brightest Supernova May Reignite

New supernova mechanism would set off repeat explosions 

SN 2006gy 
BRIGHTEST SUPERNOVA: SN 2006gy, discovered last September, may have exploded by a process known as pair-instability, in which gamma rays turn to short-lived particles instead of providing heat and pressure to support the star.

A new type of ultrapowerful supernova discovered last year may blow its top again, according to a new study. Researchers report that supernova 2006gy fits a model of star explosion that should have produced two flare-ups already and may culminate in a third before the star fizzles out. A second study proposes that the explosion might have come about from the marriage of multiple stars.

SN 2006gy first caught astronomers' eyes in September. Burning 100 times brighter than a typical supernova, it maintained full strength for an amazing three months, by which point most of its counterparts would have begun fading. Even eight months later it was as brilliant as a so-called type II supernova, the most common variety. The energy unleashed implied that the exploding star was a behemoth of at least 100 solar masses (suns).

Supernovas typically occur after a star bigger than 10 suns has gradually exhausted its supply of hydrogen and helium, which have fused into progressively heavier elements. Unable to muster the heat to support its outer layers, the burnt-out star implodes, blasting its envelope outward in a last gasp of nuclear energy.

To explain SN 2006gy's massive outburst, researchers invoked a competing mechanism called pair-instability, which theoretically kicks in for stars larger than 90 suns. In this scenario, dating to 1967, high-energy gamma rays inside the star convert into pairs of electrons and positrons, draining stellar energy that would normally help maintain its internal pressure, eventually leading to a premature collapse that liberates vast amounts of energy and light.

In a new Nature paper, astrophysicist Stan Woosely of the University of California, Santa Cruz, and his colleagues report that the observed changes in SN 2006gy's brightness fit a model of pulsating pair-instability, assuming the star was initially 95 to 130 solar masses, with a helium-rich core of about 50 suns.

Developed by Woosely and co-author Alexander Heger in 2002, the model predicts that the initial implosion of a 110–solar mass star would shed several sun's worth of mass before igniting the star's carbon and oxygen fuel and temporarily halting the collapse. Roughly seven years later, pair-instability would cause a second breakdown that emits a smaller but faster pulse of material.

Normally, Woosely says, the star itself, bloated with age, would soak up most of such a shockwave's energy without releasing light. But in this case, the two pulses would slam into each other, sparking fireworks.

"Essentially [the first pulse] could act like a sponge to soak up the energy—and then reradiate that energy as light," says Nathan Smith of U.C. Berkeley, a member of the group that first pointed out SN 2006gy's peculiar brightness. The new study "gives a nice numerical confirmation of the empirical model we proposed initially."

Woosely says he "wouldn't want to bet the house" on the model, partly because it requires the initial star to lose mass slower than predicted by calculations of stellar evolution, but adds that "it's the best model going." He notes that if the model is correct, SN 2006gy might flare up again or it might quietly collapse into a black hole.

Whatever the mechanism behind the explosion, a second Nature paper this week proposes that the initial star may have formed from the collision of a large, older star and a small, younger one. This would explain the presence of hydrogen in SN 2006gy, even though big stars are thought to run out of hydrogen hundreds of thousands of years before going supernova, says co-author Simon Portegies Zwart of the University of Amsterdam.

Since SN 2006gy was discovered, astronomers have noticed a second, even brighter supernova that was first observed in 2005 but lasted for an ordinary amount of time. Smith notes that a third explosion nearly matched the brilliance and duration of SN 2006gy, which has hogged the spotlight. 

New Blood Substitutes Promise Relief for Sagging Blood Banks

HemoBioTech says it has solved the toxicity issues that have plagued its predecessors

 

HELP ON THE WAY: HemoBioTech, Inc.'s HemoTech is expected to not only suppress hemoglobin's inherent toxicity but also serve to improve blood flow and even spur the creation of new red blood cells. Courtesy of HemoBioTech, Inc.

Researchers are stepping up efforts to develop a safe blood substitute amid a growing demand and dwindling supply of the real thing to treat trauma victims and blood disorders such as potentially deadly types of anemia.

Their major hurdle: to come up with a replacement for hemoglobin (an iron-enriched protein in red blood cells that transports oxygen from the lungs to the rest of the body) that can be directly introduced into the human circulatory system. The problem is that the body breaks down and eliminates real hemoglobin that is not protected by red blood cells, a process that can be toxic to the kidneys, constrict blood vessels (resulting in hypertension), and cause inflammation.

The Texas Tech University Health Sciences Center in Lubbock and Dallas-based blood substitute developer HemoBioTech, Inc., believe they have a chemically modified bovine hemoglobin called HemoTech that not only suppresses hemoglobin's inherent toxicity but also serves to improve blood flow and even spur the creation of new red blood cells. "This represents a learning from all of the failures that have proceeded us over the past 35 years," says Arthur Bollon, HemoBioTech's chairman and chief executive officer. Texas Tech University spun off HemoBioTech in 2002 to commercialize HemoTech.

"Creating an effective substitute for human blood has been an elusive dream for many decades," says Jan Simoni, associate research professor in Texas Tech's surgery department and HemoBioTech's acting vice president for research and development. "Our product addresses all the intrinsic toxicity issues."

HemoBioTech's use of modified bovine hemoglobin addresses the two biggest issues affecting today's blood supply: There is not enough to go around and the available blood runs the risk of contamination. "Bovine hemoglobin is an unlimited source of raw material for making blood substitutes," Simoni says. Hemoglobin from bovines (which include antelopes, bison and cattle) also does not carry human-born viruses such as HIV and hepatitis. It could, however, potentially carry other pathogens that might be transmitted to humans, such as the protein that causes mad cow disease. But Simoni says Texas Tech scientists have developed a method to effectively filter out such threats.

He adds that real blood must be carefully screened, noting that one in every 60,000 units may carry hepatitis B and one in every 500,000 units, HIV; other contaminants of concern are hepatitis C and the human T-cell leukemia virus.

"The World Health Organization estimates that 100 million units (45 million liters) of blood are needed worldwide per year," Simoni says. "There are not enough blood donations to meet the demand when you consider that the demand is increasing by 1 percent per year, while donations are decreasing by 1 percent per year." The U.S. alone annually uses about 12 million units, and by 2030 it is projected that there will be a shortage of as much as four million units of blood.

HemoTech also eliminates the need to match blood types between patients and donors, because pure hemoglobin is not affected by varying factors found in human blood. In addition, HemoTech has a shelf life of at least 180 days—significantly longer than the typical 42-day period during which donated blood can be used.

In the early 1990s HemoTech was used in Zaire to successfully treat nine children with sickle-cell anemia. In fact, HemoTech constituted 25 percent of each patient's blood volume during the treatment. None of the patients suffered toxic side effects, Bollon says.

But it could be years before the product is approved for other than experimental use. HemoBioTech is in the process of obtaining permission from the Food and Drug Administration (FDA) to conduct clinical trials in the U.S. The company hopes that early next year it will initiate clinical trials on product safety, which will pave the way for human efficacy testing that could be completed by 2011. Clinical trials are set to begin in India early next year. If all goes according to plan, HemoTech is expected to be a cheaper alternative to treating patients with donated red blood cells.

While HemoBioTech is not alone in its quest to create a blood substitute, others have run into difficulty during clinical testing. Northfield Laboratories, Inc., in Evanston, Ill., has been conducting clinical trials for its oxygen-carrying red blood cell substitute, PolyHeme, but in May said the product failed to meet the primary goals of mortality and safety in an important phase III study. Biopure Corporation in Cambridge, Mass., is working on FDA approval for its "oxygen therapeutics," which are intravenously administered to deliver oxygen to the body's tissues, after the agency in July 2005 put the company's clinical trials on hold, citing safety issues. Last month, Biopure launched a revamped clinical development program, emphasizing testing in Europe, with three phase II clinical trials planned for 2008 to study the impact of its product on heart attack patients, chemotherapy patients with anemia and the terminally ill.

Another blood substitute provider, Synthetic Blood International, Inc., in Costa Mesa, Calif., has thus far successfully navigated the clinical trial waters with Oxycyte, an oxygen-carrying intravenous emulsion that the company says can carry up to four times more oxygen than hemoglobin. In May, Synthetic Blood announced its phase II study in patients with traumatic brain injury indicated Oxycyte helped increase blood oxygen levels.

Although there is no guarantee that any of these blood substitutes will make the grade, each holds the promise of bringing relief to the health care organizations and their patients that rely on rapidly declining supplies of donated blood.

Double Trouble: What Really Killed the Dinosaurs

Instead of being driven to extinction by death from above, dinosaurs might have ultimately been doomed by death from below in the form of monumental volcanic eruptions.

The suggestion is based on new research that is part of a growing body of evidence indicating a space rock alone did not wipe out the giant reptiles.

The Age of Dinosaurs ended roughly 65 million years ago with the K-T or Cretaceous-Tertiary extinction event, which killed off all dinosaurs save those that became birds, as well as roughly half of all species on the planet, including pterosaurs. The prime suspect in this ancient murder mystery is an asteroid or comet impact, which left a vast crater at Chicxulub on the coast of Mexico.

Another leading culprit is a series of colossal volcanic eruptions that occurred between 63 million to 67 million years ago. These created the gigantic Deccan Traps lava beds in India, whose original extent may have covered as much as 580,000 square miles (1.5 million square kilometers), or more than twice the area of Texas.

Arguments over which disaster killed the
dinosaurs often revolve around when each happened and whether extinctions followed. Previous work had only narrowed the timing of the Deccan eruptions to within 300,000 to 500,000 years of the extinction event.

Now research suggests the mass extinction happened at or just after the biggest phase of the Deccan eruptions, which spewed 80 percent of the lava found at the Deccan Traps.

"It's the first time we can directly link the main phase of the Deccan Traps to
the mass extinction," said Princeton University paleontologist Gerta Keller.

Clues in other life forms


Keller and colleagues focused on marine fossils excavated at quarries at Rajahmundry, India, near the Bay of Bengal, about 600 miles (1,000 kilometers) southeast of the center of the Deccan Traps near Mumbai. Specifically, they looked at the remains of microscopic shell-forming organisms known as foraminifera.

"Before the
mass extinction, most of the foraminifera species were comparatively large, very flamboyant, very specialized, very ornate, with many chambers," Keller explained. These foraminifera were roughly 200 to 350 microns large, or a fifth to a third of a millimeter long.

These showy foraminifera were very specialized for particular ecological niches.

"When the environment changed, as it did around K-T, that prompted their extinction," she added. "The foraminifera that followed were extremely tiny, one-twentieth the size of the species before, with absolutely no ornamentation, just a few chambers." As such, these puny foraminifera serve as very distinct tags of when the K-T extinction event started.

The researchers found these simple foraminifera seem to have popped up right after the main phase of the Deccan volcanism. This in turn hints these eruptions came immediately before the mass extinction, and might have caused it.

Double trouble

Both an impact from space and
volcanic eruptions would have injected vast clouds of dust and other emissions into the sky, dramatically altering global climate and triggering die-offs. Keller's collaborator, volcanologist Vincent Courtillot at the Institute of Geophysics in Paris, noted upcoming work from her collaborators suggests the Deccan eruptions could have quickly released 10 times more climate-altering emissions than the nearly simultaneous Chicxulub impact.

Keller stressed these findings do not deny that an impact occurred around the K-T boundary, and noted that one or possibly several impacts may have had a hand in the mass extinction. "The dinosaurs might have faced an unfortunate coincidence of a one-two punch—of Deccan volcanism and then a hit from space," she explained. "We just show the Deccan eruptions might have had a significant impact—no pun intended."

Although paleontologist Kirk Johnson at the Denver Museum of Nature and Science called these new findings "significant," he noted a great deal of evidence connected a single massive impact with the K-T extinction event. He suggested that advances in radioisotope dating could now hone down when the Deccan eruptions occurred to within 30,000 to 65,000 years. "That could help put to bed some of the disputes regarding the issue," he said.

 
Diabetes 'revolution' is cutting both ways
Diabetes expert John Buse recalls looking into his office's waiting room in the early 1990s and seeing it filled with people suffering the long-term complications of the disease. They would be blind, have legs missing from emergency amputations or be on kidney dialysis.

Not anymore.

Diabetes rates continue to skyrocket, but "most days in the clinic, I see no one disabled with diabetes," Buse says. "No one."

The Centers for Disease Control and Prevention reported this month that the prevalence of heart disease dropped 14% in diabetics ages 35-64 from 1997-2005. Since the mid-1990s, rates of other complications such as diabetic kidney failure, blindness and deaths caused by a lack of insulin have declined, the CDC reports. It reflects what Buse calls a "revolution" in diabetes treatments during the past decade.

That's the good news. The bad: Not everyone is reaping the benefits. Heart deaths have declined in men with diabetes, but not in women; kidney failure rates among diabetics are much higher in blacks and Hispanics than in whites. Meanwhile, the disease is increasing worldwide at such an alarming rate that the number of new cases is outpacing the number of those benefiting from gains made in treatment. That's largely because obesity, the chief risk factor for the most common form of diabetes, is a growing problem.

Diabetes, caused by the body's inability to produce or use insulin effectively to prevent a buildup of sugar in the blood, now afflicts nearly 21 million in the USA and roughly 250 million worldwide. Health analysts project that by 2025, 50 million Americans and up to 380 million people globally will have diabetes. So even as treatments for diabetes complications improve, the disease's rising prevalence means there will be more people disabled by it and more who eventually will die from it.

During the past decade, medical studies have shown that by reducing high blood pressure and cholesterol and keeping blood sugar levels as close to normal as possible, diabetics can forestall many of the disabling complications that once seemed inevitable. This knowledge, along with simpler, more accurate blood tests and better drugs, has improved treatment, says Buse, an endocrinologist at the University of North Carolina at Chapel Hill.

But the soaring rate of people with diabetes threatens to overwhelm health systems and undermine economies, health specialists say. The problem has mobilized world health leaders, who are marking World Diabetes Day on Wednesday to draw attention to the issue. For the first time, the United Nations is taking part in such activities and has passed a resolution encouraging member states to develop national policies to prevent and treat diabetes.

The International Diabetes Federation, which tracks global diabetes, says the disease will cause 3.8 million deaths worldwide this year, nearly equal to HIV/AIDS and malaria combined. In the USA, the CDC says, it is the sixth leading cause of death, contributing to nearly 225,000 deaths in 2002, up from 213,064 in 2000.

"The prevalence of diabetes is going up because obesity is going up," says Judith Fradkin, director of the National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health. "But if we hadn't made the prog-ress we have, things would be much worse."

New drug treatments, more accurate methods for monitoring blood sugar levels and assessing control of diabetes, and practical steps that patients can take are more common than ever, she says.

A disease with no respect

Buse, president of the American Diabetes Association, says it wasn't so long ago that diabetes treatments weren't much of a priority in the medical community.

"It was the Rodney Dangerfield of human disorders," Buse says. "Ten or 15 years ago at ADA, we were talking about what message we want to convey (to the public), and a decision was made not to convey the message that diabetes was serious," because there was so little doctors could do to prevent complications.

"It would have been like saying: 'Bad news, your house is on fire, and worse, there's no water for miles,' " he says. Until 1993, it wasn't clear that lowering blood sugar prevented or delayed complications, and it's only within the past decade that doctors learned that managing blood pressure and cholesterol reduced complications, he says. "Until 1995, there had been no substantial advance in drug management of diabetes since the 1950s."

Diabetes, like other chronic diseases, is caused by a combination of genetics and environment. It results in a high level of sugar in the blood, which over time clogs vessels the way gummy oil clogs a car engine, leading to poor circulation that affects everything from brain to feet, increasing the risk of heart disease and damage to kidneys, eyes and nerves.

There are two major forms of diabetes: type 1, an autoimmune disease that results in loss of the insulin-producing cells in the pancreas and usually occurs in children or young adults, who need daily insulin shots; and type 2, which accounts for 90% of diabetes cases and is associated with obesity and inactivity and reduces the ability to use insulin efficiently.

American Indians, blacks, Asians and Latinos are believed to carry a higher genetic risk for type 2 diabetes. That, along with increasingly fatty diets, has helped to trigger an explosion of diabetes in those communities — even as treatments for complications from diabetes have improved.

Dorothy Becker, chief of the division of pediatric endocrinology and diabetes at Children's Hospital Pittsburgh, treats children, most of whom have type 1 diabetes.

"I used to see major complications in kids," she says. "Now, I can't make my kids understand what complications are. We used to see kidney damage, now we're not. We used to see protein in the urine (an indicator of decline in kidney function), but now we don't see it at all. We're just not seeing what we used to see."

Doctors say these changes are the result of improvements in:

•Diagnosis. Greater awareness of diabetes has prompted increased screening and earlier diagnosis of type 2 diabetes. One example: The Blood Bank of Delmarva, which serves Delaware and the Eastern Shore of Maryland and Virginia, last month began offering free, non-fasting blood sugar tests to donors. Donors will have access to a secure site online to see their results and get more information on their diabetes risks. Those whose tests indicate dangerously high blood sugar levels will be contacted by the blood bank.

•Drug treatments. Once, there was a single type of insulin. Now there are six types and several classes of drugs, including those that boost the body's own insulin production, reduce the need for extra insulin or lower the risk of complications. The most recent entries are drugs that act on gut hormones to keep blood sugar levels steady without causing weight gain or hypoglycemia, a low-sugar condition that can be dangerous.

But recent reports suggesting the anti-diabetes drug Avandia increases the risk of heart attack and death from heart disease show that research is needed — not just to find new drugs but to assess the long-term effects of drugs already in use.

"We have validated the concept that lowering blood sugar is good," Buse says, "but we don't have trials that demonstrate using drug X has advantages over using drug Y. And particularly, we don't have proof we can lower the risk of heart disease or stroke in patients who have diabetes using blood-sugar-lowering drugs."

•Blood sugar control. A variety of high-tech meters and monitors that measure blood sugar in seconds, along with insulin pens, pumps and jets, have made tighter control much easier. Injected insulin has become so easy to use that a recently introduced product, the inhaled insulin Exubera, was pulled from the market last month because of poor sales.

•Diabetes management. Several studies have shown that early, intensive treatment to keep blood sugar, blood pressure and cholesterol under control has lasting benefits, giving doctors science-based ammunition to keep patients on track.

The advances mean that if patients manage their diabetes, the disease doesn't have to impose the limits it once did, says Rita Louard, director of the Clinical Diabetes Center at Montefiore Medical Center in New York.

It took Sandra Velez, 55, of Yonkers, N.Y., several years with diabetes before a family tragedy brought home to her the seriousness of the disease. She has five siblings, including a brother, Felix, 60, who lives with her, and several aunts and uncles with diabetes. Her father, an uncle and two brothers died of complications. And four years ago, her daughter, Stephanie, who also had diabetes, died at 27 of flu-related pneumonia.

Stephanie's blood sugar levels were six times above normal, Velez says, a dangerous condition because diabetes increases susceptibility to infectious diseases and makes them harder to cure. "When she passed, they said if her diabetes hadn't been so out of control, maybe something could have been done."

That was when Velez, one of Louard's patients, began to take control of her own health, though she didn't change overnight.

"I said, 'I cannot continue like this.' I would be sometimes very depressed, say, 'The heck with it, I'm going to have a cheesecake,' " she says. She is 5 feet 4 inches tall and weighed 240 pounds. She took daily insulin shots to control her blood sugar.

Finally she realized, "I was really harming myself." She got an exercise bike and some hand weights. At first, "I used them two minutes and gave up," she says. "But in the last few months, I've been using them every night. I started doing half an hour. Now I'm up to 45 to 50 minutes a night." And she spends her lunch hour walking and window-shopping. The result: Her blood sugar level is in the normal range, and she has lost almost 65 pounds. She still takes medication, but "they took my insulin away."

She watches out for her brother, a former cabdriver, who is having symptoms of nerve damage in his feet. Before she insisted he get a physical exam a year and a half ago, when his diabetes finally was diagnosed, Felix hadn't seen a doctor in 28 years. Now, she makes sure he checks his blood and takes his medicine. "I taught him about diet," she says. "He was upset in the beginning. He said, 'Why can't I eat cake?' But I said it's not my fault."

Fighting fear with information

Diabetes itself doesn't kill, doctors say. It's uncontrolled diabetes — the heart disease, kidney failure, nerve damage and increased susceptibility to infection — that causes illness, disability and death.

"Patients are terrified of diabetes and its consequences," Buse says. "Generally, the first step in treatment is to make patients believe that diabetes is a disease that can be effectively controlled. A well-informed patient is generally so highly motivated and the treatments generally so well tolerated that avoidance of complications is a reasonable expectation."

But rising obesity threatens to blunt progress on other fronts, Buse and other experts warn. They say it will take a major societal change of the kind that changed smoking habits to prevent a future of fatter, sicker people.

"I am optimistic, but I do think the problem is going to get worse before it gets better," says Ann Albright, director of the CDC's diabetes division. Prevention is key, but "it's going to take time to get policies in place, and for large numbers of people to be able to access new technologies and diabetes education."

Last month in Seattle, the Pacific Northwest Research Institute hosted a meeting of international scientists who formed an alliance aimed at thwarting what they called a "growing tsunami of diabetes."

The "amount of money it will cost in 10 years to manage diabetes is going to bust the economies" of many countries, says institute president Paul Robertson. "Governments need to jump in and understand, if they don't help, you can pay us now, or pay us later."

 
DIABETES COMPLICATIONS DECREASE
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