Fair Use Notice

FAIR USE NOTICE


OCCUPY WELLNESS

This site may contain copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in an effort to advance understanding of environmental, political, human rights, economic, democracy, scientific, and social justice issues, etc. we believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law.

In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes. For more information go to: http://www.law.cornell.edu/uscode/17/107.shtml

If you wish to use copyrighted material from this site for purposes of your own that go beyond ‘fair use’, you must obtain permission from the copyright owner.

FAIR USE NOTICE FAIR USE NOTICE: This page may contain copyrighted material the use of which has not been specifically authorized by the copyright owner. This website distributes this material without profit to those who have expressed a prior interest in receiving the included information for scientific, research and educational purposes. We believe this constitutes a fair use of any such copyrighted material as provided for in 17 U.S.C § 107.

Read more at: http://www.etupdates.com/fair-use-notice/#.UpzWQRL3l5M | ET. Updates
FAIR USE NOTICE FAIR USE NOTICE: This page may contain copyrighted material the use of which has not been specifically authorized by the copyright owner. This website distributes this material without profit to those who have expressed a prior interest in receiving the included information for scientific, research and educational purposes. We believe this constitutes a fair use of any such copyrighted material as provided for in 17 U.S.C § 107.

Read more at: http://www.etupdates.com/fair-use-notice/#.UpzWQRL3l5M | ET. Updates

All Blogs licensed under Creative Commons Attribution 3.0

Thursday, May 3, 2012

Hate Meat? It May Be in Your Genes



WebMD: Better information. Better health.

Healthy Eating & Diet

Hate Meat? It May Be in Your Genes

Study Shows Some People Carry Genes That Make the Smell of Meat More Intense and Unpleasant

By
WebMD Health News
 
grilled steak 
 
May 2, 2012 -- Whether we like or loathe the smell of a frying pork chop may depend on our genes, a new study shows.

The study, published in the journal PLoS ONE, is one of the first to show how genes may shape our food choices.

"People who are instinctively vegetarian or vegan or instinctively heavy meat-eaters, it could definitely have some sort of underlying biological component to it," says Kara Hoover, PhD, a biological anthropologist and assistant professor at the University of Alaska Fairbanks. She was not involved in the current research.

"When you consider that our food preferences are driven by flavor, which is the intersection of taste and odor, with a heavier emphasis on odor, clearly genetic variation in humans is going to make a difference in how we prefer food," Hoover tells WebMD.

How Genes Influence Smell

People detect odors thanks to tiny chemical receptors that sit on nerve cells inside the nose. In total, we have genes for about 400 different smell receptors that help sense about 10,000 different odors.

Some of those receptors detect the steroid androstenone, which is found in high concentrations in male pigs.

Farmers have known for some time that uncastrated male pigs can produce meat with a strong odor, so most commercially raised animals in the U.S. are castrated to get rid of the smell, which is known as boar taint.

Previous research found that people who have two copies of a gene that helps sense androstenone -- scientists think that's about 70% of the population -- are able to smell the chemical. These people can have a mixed reaction to the pork.
"For those who are very sensitive to it, it's really disgusting. It's a sweaty, urine-like odor," says researcher Hiroaki Matsunami, PhD, an associate professor of molecular genetics and microbiology at Duke University in Durham, N.C. "For others, you can smell it, but it's not as bad. Those people say it smells fragrant, chemical, or sweet."

In contrast, people with only one copy of the gene or who carry another gene variant for the receptor aren't as bothered by the aroma of androstenone. They find the odor to be weak or unnoticeable.

Genes and Food Preference

In the new study, researchers wondered whether a simple smell test could predict who carries the single copy of the gene, and whether the gene influences the sniffer's perceptions of cooked meat.

It wasn't an entirely academic question. Europe is considering banning a practice that allows farmers to control the amount of androstenone in pork by castrating male pigs. Farmers are worried that consumers will turn their noses up at meat that contains higher levels of the hormone.

For the study, researchers recruited 23 healthy participants: 13 average eaters and 10 trained "sensory assessors," people with sensitive noses that can reliably pick out certain smells.

First, researchers added purified androstenone to two of three cups of water. People were asked to smell each cup and pick out the one that was different. If they were right, researchers classified them as sensitive. If they were wrong, they were considered insensitive.

Next, researchers had the study subjects eat cooked ground pork that had varying levels of androstenone added to it. They kept the levels within the range that might be naturally found in meat.

People were asked to rate the smell and the taste of the meat samples.
Next, researchers tested their genes. They found that all the people who could smell the androstenone had two copies of the gene needed to pick up the scent. These folks were also more likely to rate the taste of the pork with added androstenone as bad.

And everyone who had one copy of the gene could not smell the hormone. They were more likely to say the pork tasted good.

Still, "for those who cannot [initially] smell androstenone, if you try to smell this chemical every day for three weeks, about half of these non-smellers can acquire the ability to smell it," Matsunami says.

That suggests the ability to smell things isn't driven entirely by genes, but also by experience.

But, "it's a gene that's certainly influencing this preference, and I think people need to consider that fact," he says.

Tuesday, May 1, 2012

Cancer Wars: An Outcast Researcher’s New Theory

PACIFIC STANDARD

Cancer Wars: An Outcast Researcher’s New Theory

The scientific community disowned Professor Peter Duesberg for denying that HIV causes AIDS. But is there something to his new theory on cancer?


Peter Duesberg, a professor at the University of California, Berkeley. (Timothy Archibald)
 

Compact and white-haired at 75, Peter Duesberg has wide-set blue eyes magnified by corrective lenses as thick as his German accent. He is the picture of a courtly Old World scientist. But Duesberg is given to through-the-looking-glass scientific theories, the most recent of which, about the origins of cancer, could turn an accepted truth of molecular biology on its head. Viruses like hepatitis C don’t cause cancer, he says, and neither do collections of mutated genes — as nearly every other scientist believes. Instead, he argues, cancer arises when the number and appearance of a cell’s chromosomes become disrupted, leading to a tumor that has, in effect, evolved into a parasitic new species.

Some scientists think he could have a point. “There is something to what Peter Duesberg says,” says Mark David Vincent, a Canadian researcher and oncologist whose own unconventional theories about cancer overlap with Duesberg’s. But most others are skeptical. One reason may be that Duesberg is a pariah for his​ tenaciously held theory that HIV does not cause AIDS.
Duesberg works in a shabby laboratory on the campus of the University of California, Berkeley. He runs his experiments virtually alone. He has no graduate students and little staff support, and virtually no research budget, apart from some limited private funding. Duesberg acknowledges that if he weren’t a tenured full professor, he probably would have been gone long ago.
Duesberg once was highly respected by his peers. After arriving at Berkeley in 1964 with a doctorate in chemistry from the University of Frankfurt, he, in short order, extracted the RNA of the Rous sarcoma virus, shown to cause tumors in chickens, and in 1970 co-discovered a viral gene that seemed to promote cancer. He also helped plot the retroviral genome and won election to the National Academy of Sciences. “For a while I was the blue-eyed boy,” he says. “Now I’m the traitor from within.”

Duesberg’s career took a turn in March 1987, when he published a paper in Cancer Research that made two sensational claims: One was that retroviruses did not activate cancer-promoting genes; the other was that the newly identified HIV retrovirus did not cause AIDS. It did cause minor mononucleosis-like illness, he conceded, but not the lethal AIDS symptoms. As he explains it, “These questions were lingering in my mind. Why do we say these retroviruses are so bad when they’re found everywhere and hardly anyone ever gets sick?”
He would subsequently argue that gay men were dying as a result of their allegedly prodigious drug use rather than AIDS. Later, as the HIV genome was sequenced and antiretroviral drugs were introduced, he contended that the drugs themselves were causing the symptoms attributed to AIDS. Hemophiliacs who became infected through blood transfusions were already sick, he argued, and in sub-Saharan Africa, where AIDS was spreading among heterosexuals, malnutrition and parasites were the real culprits.

These ideas were discarded as further research supported the HIV hypothesis. But Duesberg seemed immune to the evidence, raising ever-flimsier objections to each new finding. He argues, for example, that Africa’s population wouldn’t have continued growing over the past few decades if AIDS really is a lethal communicable disease. Other scientists stopped taking him seriously. His government research funding dried up, and, for many years, most peer-reviewed scientific journals refused to publish his papers. So he took his case to the public, publishing a book and developing a small but devoted following, particularly among conspiracy theorists.

One of those followers was South Africa’s President Thabo Mbeki, who, in 2000, invited Duesberg, among other HIV skeptics, to serve as a consultant in shaping his government’s AIDS policies. Over the next few years, government officials cited Duesberg when refusing to promote the use of antiretroviral drugs. A 2008 study by two Harvard School of Public Health researchers, Pride Chigwedere and Max Essex, estimated that more than 330,000 South Africans had lost their lives to HIV/AIDS between 2000 and 2005 because of these policies, and it mentioned Duesberg by name. “The science behind Mbeki was Duesberg and other denialists,” Chigwedere and Essex wrote in a 2010 follow-up article.
• • • • • • • • • • • • • • •
Duesberg remains unrepentant. And he’s been equally stubborn about his radical theories on the origins of cancer.

His research in the 1970s had focused on tumor viruses because they were thought to alter human genes, thereby causing cancer. But as other scientists found evidence that humans carried genes that could mutate and drive cancer, Duesberg grew skeptical. For one thing, an ever-growing number of mutations seemed to be needed — dozens, in some cases — which he found implausible. Meanwhile, in Duesberg’s view, the mutation theory was further undermined by studies showing that many known carcinogens did not cause gene mutations in the first place.

Billions had been spent on the war on cancer, yet scientists had made little progress toward a cure. Could the research establishment be on the wrong track? “Nobody asks these questions,” Duesberg says. “People are so well trained not to ask negative questions.”

His focus shifted to the abnormal number of chromosomes that virtually every cancer tumor has — an observation first made by German scientist Theodor Boveri in the early 20th century. Most human cells have 23 pairs of matched chromosomes, half inherited from each parent, for a total of 46. This pattern is preserved each time the trillions of cells in our body divide and replicate. But in cancer cells something goes awry: there might be three or four chromosomes where there should be a single pair, or the chromosomes might be abnormally foreshortened. Such cells are described as “aneuploid.”

In a paper he published last summer in the journal Cell Cycle, Duesberg theorized that carcinogens might cause chromosomes to divide abnormally during cell division, creating extra copies of thousands of genes and disrupting the cellular machinery — an idea with parallels to a theory floated by Julian Huxley in 1956. These aneuploid cells usually die, but every so often the new genetic arrangement — called the karyotype — might enhance a cell’s ability to survive and clone itself. As these clones multiply, a tumor can emerge with a new, stable karyotype. The way Duesberg sees it, that tumor would essentially be a unique species, a parasite that feeds off its host.

Duesberg’s model resembles ideas advanced by some other researchers, including Henry H.Q. Heng, a molecular geneticist at Wayne State University, as well as Mark David Vincent, who treats lung cancer patients at the London Health Sciences Centre in Ontario, Canada. Vincent, who has referenced Duesberg’s theory in his own papers, believes that cancerous cells exploit an ancient survival mechanism, reverting to the form of protozoa-like organisms from before the time when single cells began cooperating to create multicellular organisms like us. “It became clear to me that the process of carcinogenesis involved a form of life emerging that was different from the host,” Vincent says. “We sort of converged on the same thing but from a somewhat different perspective.” Vincent sides with mainstream researchers in believing that genetic mutations are one of the things that initially turn normal cells cancerous. But he agrees with Duesberg that aneuploidy, which can entail a rapid reshuffling of genes, likely helps drive the growth and spread of tumors.
Vincent, who says people have warned him that Duesberg is “radioactive,” disagrees with the Berkeley scientist’s HIV/AIDS claims. But, he adds, those ideas don’t make Duesberg’s cancer theories wrong. “Anybody who thinks courageously outside the box and in a different way is an extraordinarily important resource,” he says. Besides, whatever the error of Duesberg’s views, “we should not censor people intellectually.”
• • • • • • • • • • • • • • •
Duesberg sometimes seems to relish his status as an outsider, portraying himself as a victim of groupthink who has been persecuted for daring to question the status quo. Other times, he sounds almost wistful. “I was immensely popular,” he says of the days when he found the first cancer-causing oncogene in the Rous sarcoma virus. “I would have been served so much better if I had stayed with oncogenes as the cause of cancer.”

Now, he says, even his Berkeley colleagues largely shun him. As recently as 2010, he says, the university investigated complaints that he had published a paper containing false claims—a response of sorts to the Chigwedere and Essex findings — in a non-peer-reviewed publication. A university spokesman says no action was taken because tenured faculty members are guaranteed academic freedom to advance their theories — with the peer-review process serving to safeguard accuracy.

He hasn’t trained any graduate students in 15 years and only recently was permitted to begin teaching an undergraduate course called “The Cancer Karyotype: What It Is and What It Does.” He runs a few experiments in his lab, almost single-handedly (sometimes with help from an undergraduate student or two), but it’s evident the fall has been painful.

“I think I was even close to a Nobel,” Duesberg says. “If I had just shut up, I would have been much better off.”

Without prompting, he ticks off the names of scientists who’ve won Nobel Prizes for contributing to the standard mutation model of cancer genetics. “All the sheep think the same thing: mutations cause cancer, and HIV causes AIDS,” he says. But he maintains that in his acid skepticism he’s upholding the purity of the scientific method. “Science is absolute,” he says. “You question things that you were taught or were told by your priest, your führer, or your teacher — or anyone.” Whenever a scientist worries about what others will think or the moral implications of his work, “it’s not good science anymore,” he asserts. “It should be amoral — without morals.”

This article appeared in the May-June issue of Pacific Standard under the title “The Heretic.”

Turning Diabetes Treatment Upside Down


PACIFIC STANDARD


Turning Diabetes Treatment Upside Down

Dr. Jay Shubrook is flipping conventional insulin treatment upside-down — with startling results.


Jay Shubrook
Dr. Jay Shubrook

There is something eerily familiar about Athens, Ohio, even if you grew up in New York City. It’s the accessible beauty of Appalachia, which surrounds the town — the gentle hills, the long, flat fields, the meandering brooks and neat, smallish farms.

It’s something more nefarious as well: the profound rural poverty vivid in the mini-malls and convenience stores on the outskirts of town. It’s the curse of plenty — the deal with the devil that this area made long ago with large mining corporations and fast-food chains. And it’s the number of overweight and obese people of all ages in stores and on the streets. People in Athens are pleasant and helpful, but they seem exhausted and desperate, both from generations of poverty and hard physical labor on farms and in mines, but also from the hard work of moving with extra weight. The self seems buried, like a trapped animal, in the body.

The data is mind-numbing: two-thirds of all Americans are overweight or obese, putting them at increased risk for diabetes. Many of us already have the disease and don’t know it. It’s an epidemic: according to the Centers for Disease Control and Prevention, in 2010, one in 10 Americans had type 2 diabetes. And roughly one in every 10 health-care dollars is spent on diabetes every year.

Today, if you’re diagnosed with type 2 diabetes — the most common form — your treatment would likely go like this: Your doctor would tell you to change your lifestyle, exercise more, lose weight, eat more fruits and vegetables. You’d be given a device to check your blood-glucose levels, and you’d be told to come back in a couple of months. After an average of two years of checking your glucose levels, you’d be put on metformin, the most common medicine for type 2 diabetics. Then the disheartening process of “stacking meds” would start. In addition to metformin, which lowers blood sugar by reducing the amount of sugar produced by the liver and helps the body better use its own insulin, you’d be put on sulfonylureas, drugs that stimulate the pancreas to release additional insulin. As this combination became ineffective, you would be put on any of nine other classes of drugs, an average of one additional med every two years. At the end of 10 years, you’d finally be shown how to inject insulin several times a day to lower your blood sugar. If you’re like most patients, this is when you’d feel like a failure. And you’d have spent 10 years thinking you were the victim of a disease.

But Athens resident Jay Shubrook, an associate professor of family medicine and director of clinical research at Ohio University Heritage College of Osteopathic Medicine, is developing another story.
• • • • • • • • • • • • • • •
When Shubrook goes to the grocery store, people stop him in the aisles to ask questions, or often to just say thank you. Although his two teenage daughters have come to dread these trips (a run to the store is never quick), he doesn’t mind: the encounters mean his patients trust him. And trust is critical for doctors working with patients who have a chronic disease, because success depends on the patients’ ability to manage their own health.

That ability is particularly important to Shubrook, because the multipronged approach he’s taking in his research on diabetes is revolutionary. He refuses to treat his patients as passive victims. He asks them to fight — to take certain risks, and face deep fears. And he is turning the practice of stacking meds upside down.
• • • • • • • • • • • • • • •
In 1991, fresh out of the University of California, Santa Cruz, with an undergraduate degree in psychobiology, Jay Shubrook got on his bike and pedaled to Appalachia and Ohio University’s medical school. Shubrook can seem Zelig-like. With his blond hair, boyish face, and freckles, he’d fit right in on the beaches of Southern California. His succinct delivery wouldn’t be out of place in a fast-paced city. But he chose small-town Athens because Ohio University had an osteopathic medical school where the students were trained to look at the whole person rather than the specific problem or disease.

When he was a fourth-year medical student, Shubrook did an endocrinology rotation with Frank Schwartz, a doctor in private practice in nearby West Virginia. It was a pivotal meeting for Shubrook: Schwartz had spent almost two decades helping people with diabetes. “I loved my time with him,” Shubrook says. So much so that, in 1998, as a resident, Shubrook requested another rotation with Schwartz.

At the time, many people saw diabetes as a hopeless death sentence. “When I was in school, and even after, the more chronic the disease was, the less sexy — precisely because there is no magic pill,” Shubrook says. “My predecessors were fascinated with medicines. No one wanted to work on diabetes.”

Type 1 diabetes, an autoimmune disease that accounts for 5 to 10 percent of all cases, is diagnosed most often in children and teenagers. In this form of the disease, the immune system mistakenly attacks the beta cells in the pancreas that produce the insulin needed to maintain normal blood sugar, effectively shutting down insulin production. But 90 to 95 percent of all diabetes diagnoses are type 2 — the kind that can be brought on by obesity. People with type 2 can produce insulin, but their cells don’t recognize it, so blood sugar isn’t metabolized properly and rises and falls to dangerous levels.

Frank Schwartz
Dr. Frank Schwartz in his lab at Ohio University in Athens. (John Sattler/Ohio University)

In reality, Shubrook explains, there are more than just two types of diabetes; there are many types — and many misconceptions about them. A lot of people think only adults get type 2 diabetes and only kids get type 1. And a lot of people think you can treat all kinds of diabetes the same way. “I have had some families think they can cure their child who has type 1 diabetes with diet and exercise,” Shubrook says, “and this is just not the case.”

Type 2 diabetes rates have increased for all ages in this country, and among people in their 30s, it has risen by 70 percent in just the past 10 years. That has meant increases in the ghastly problems that can accompany diabetes: dental disease, kidney disease, nervous-system disorders, blindness, limb amputation, heart disease, and strokes. Because of the nation’s high obesity rates, type 2 diabetes — once only seen in adults — has become a common diagnosis in teenagers. In Ohio, more than 10 percent of the population has diabetes, and in Appalachian Ohio, that rate can be twice as high as in other regions of the state.
• • • • • • • • • • • • • • •
In 2003, Schwartz was asked by Ohio University to start a diabetes center — which gave him an opportunity to return to diabetes research. Looking to develop a diabetes practice that focused on health and prevention, Shubrook and Schwartz opened the Appalachian Rural Health Institute Diabetes/Endocrine Center.

Since then, Shubrook, Schwartz, and the teams they hired have been transforming diabetes care in Appalachian Ohio. With nearly $1.3 million in funding from the National Institutes of Health, they partnered with Mary de Groot, of the Diabetes Translational Research Center at Indiana University, to start Program ACTIVE, which combines talk therapy and exercise for patients with type 2. The team also opened Athens’s Diabetes Free Clinic for people without insurance. And Shubrook launched programs for health-care workers and educators, and for obese children and their parents.

Schwartz and Shubrook also pursued new research. In 2004, Schwartz and a team of computer engineers, biologists, endocrinologists, and others began working on, among other things, artificial-intelligence software and smartphone applications that will automatically detect blood-glucose problems and recommend solutions. In 2009, Schwartz and a team of researchers received nearly $900,000 to develop a natural compound called phenylmethimazole (C10), which blocks proteins that can trigger abnormal cell responses and that play a role in a number of diseases.

Their work has won some 30 awards in the past decade. “Frank is the gas, and I am the brakes,” Shubrook says. Shubrook’s energy never seems to lag, so this statement seemed questionable. But then I spent a day following Schwartz: a 6 a.m. lecture, followed by a seminar, followed by a development meeting, followed by a lab meeting where Schwartz, who’d had only one cup of coffee, quietly directed scientists, facilitators, and students.
• • • • • • • • • • • • • • •
All the while, Shubrook was well aware that patients were frustrated with the stacking of meds and how long lifestyle changes can take to have an effect. “We were always a step behind,” he says. “We were chasing the disease. The burden on patients was significant.”

Diabetes doctors sometimes see patients with such high levels of glucose, or hyperglycemia, that the treatment has to be aggressive, which means insulin is the only option. “We had these people who were really hyperglycemic, so we knew meds would not work quickly enough,” says Shubrook. “We put them on insulin first. We knew it wouldn’t harm them.”

Artificial Pancreas
How the Artificial Pancreas Eases Diabetes Therapy
A handful of researchers in America and Europe aim to change type 1 diabetes treatment with a simple-sounding solution: an artificial pancreas.
(Click the image to read the story.)

Shubrook wondered whether using insulin first would also work in patients who weren’t severely hyperglycemic. “That made a lot of people nervous,” he says. “I was told, ‘You can’t do that, because [blood-glucose levels] will drop too low,’ ” making the patient hypoglycemic, the opposite of hyperglycemic. Other doctors and researchers saw it as a shockingly aggressive approach. Shubrook almost didn’t get funding for his Insulin First study, because funders thought he’d never find participants who were willing to try first what had long been a last resort. But Shubrook understood his patients in this corner of Appalachia; he knew they were ready to try something, anything, different.

In 2006, Shubrook began a series of trials with a group of patients who’d been newly diagnosed with type 2. Instead of 10 years to build up to insulin, they were taught to give themselves four shots a day almost immediately.

The results were undeniable. In six to eight weeks, the patients’ blood-sugar levels started to normalize. Shubrook and his team then, with close monitoring, started to withdraw the insulin. In three to four months, the patients no longer needed the injections to regulate their blood sugar. And many were able to stay off all medicines for up to three or more years. Shubrook asked people to work at maintaining a balanced diet and as much exercise as they could do, but, “We did not ask them to do any more than we ask of all our patients,” he explains.

“I love taking people off medicine,” Shubrook says. When blood sugar gets high, he adds, it’s toxic to the pancreas; using insulin to get rid of that toxicity allows the pancreas to work again. “In the old way of thinking, it was just a matter of time before the toxicity would return. We believe that a pulse of 12 to 16 weeks of complete insulin replacement allows the pancreas to rest and recover. We see dramatic drops in glucose in the first few weeks.” He adds, “What is surprising is we tell patients that this may not last, and, at some point, we will likely need to treat them with some medications. But all of them have said they would prefer insulin if they need treatment. They like the lack of side effects and the control it gives them, and they prefer the notion of a ‘booster’ treatment.” Even if patients have to come in for insulin treatment every three to four years, he says, that’s still better than the slow stacking of increasingly ineffective meds.

Today, Shubrook is nearing the end of his second trial,  with 30 type 2 patients who were randomly chosen to receive either the standard care or a course of insulin replacement. Shubrook can’t release the full results until the summer of 2013, but he says that, so far, the rate of hypoglycemia, the dropping of glucose levels feared by doctors and funders, has been extremely low among the patients given insulin.

“We have learned that it is safe and effective to start with insulin,” he says. “We do not see increased rates of hypoglycemia, and we do not see the weight gain typically seen when insulin is used as a last treatment.”

What surprised Shubrook was that several of his other diabetes patients wanted to join the trial but didn’t want to run the risk of not getting insulin first by being randomly assigned to a meds-first group. Those patients are now part of his case-study work on insulin-first treatment. Their openness to using insulin as a first course of treatment amazed Shubrook and a lot of other diabetes health workers, because injecting insulin carries so much social stigma: it’s seen as a last resort and considered tantamount to an admission of failure.

“There’s always been a lot of fatalism in diabetes patients,” Shubrook says. “A kind of ‘it’s just a question of how long you keep them alive’ mentality. So many of our assumptions, including assumptions about the role of genes, no longer hold true. Many people assume that if they start on insulin, they’ll be on it for the rest of their lives. We don’t believe this is true.”

I got a sense of the shame that can come with diabetes when, as an experiment, a nurse at Shubrook’s clinic inserted a glucose sensor in my abdomen so that we could watch my blood-glucose levels for 24 hours. Keenly aware of the extra 10 pounds I was carrying, I kept a food and activity journal to see how I reacted to meals, exercise, and sleep. A glass of red wine caused a vivid spike on the graph that night, followed by a spike in the morning after coffee and a muffin. Normal, randomly taken blood-sugar levels range from around 70 to 145. My cup of coffee brought my blood sugar up to a whopping 170. Then Shubrook showed me how to inject myself (though not with insulin). The shot was painless, but there was a certain shame in grabbing the fat and puncturing it. I felt acutely aware of all the excesses in my life. I felt that I had abandoned my body, my health, for childish appetites and a lifestyle that wasn’t of my own design. I could imagine how closely depression and self-hatred might shadow this disease.
• • • • • • • • • • • • • • •
Shubrook is “one of those oddballs that crosses disciplines,” says Darlene Berryman, associate professor of food and nutrition at Ohio University. “In just five years, he has brought these two cultures together.” She adds, “From a cultural perspective, it’s considered OK to be overweight here. There’s a real distrust of doctors. Jay is able to cross that barrier. He connects with the people in this community.”

On a crisp fall day, the Diabetes Center Clinic is in full swing by 7:30 a.m. Shubrook, who’s already been for a long run, has an appointment with the first patient in his second trial: Laura, a student who has type 2 diabetes. Laura went through the typical frustrating rounds with medication: she’d start on a new drug, but inevitably her blood sugar would go up again. “I felt like a failure,” she says. Shubrook put her on insulin, and her blood sugar stabilized. She’s now coming off the insulin trial, and Shubrook has put her on a brief fast. “Here, more than anywhere else, it’s not a blame game,” she says. “On the insulin, I felt energized, relaxed, and more able to focus. I ate better, exercised more because walking was easier, and I lost weight.”

Robert, another of Shubrook’s patients (a case-study patient), was put on insulin more than three years ago. Robert is a slurry technician in a brickyard, where a workday can include moving tons of shale manually. “Jay is an unusual doctor,” he says. “Old school. He doesn’t use big medical terms. He listens to me, and I can talk to him.” After six weeks of insulin shots, Robert says, he was sleeping better and had more energy. “We’re not calling it a cure,” he says. “We’re giving my pancreas a rest and calling it remission.”
• • • • • • • • • • • • • • •
More-aggressive interventions at early stages of type 2 diabetes have gained in popularity, but Shubrook’s trials will need to be repeated and expanded before the use of insulin as a first response could be widely adopted. Finding better treatments is critical. Since Shubrook started studying diabetes, the number of people with the disease has only risen. The CDC predicts that by 2050, one in three Americans will develop diabetes if current trends continue. The rates probably will be higher in minority populations and in underserved areas such as Appalachia.

“We have our work cut out for us,” Shubrook says. “People have free will,” he adds, then shrugs. It’s an unusual gesture for such an impassioned man. “It’s not my disease. I give them information. I can’t do it all for them.”

Yet he’s committed to giving patients as much information as he can and to showing them how much they can do for themselves.

Shubrook and Schwartz dream of building a wellness center like the Joslin Diabetes Center in Boston or the International Diabetes Center in Minnesota. But they think their incarnation would be better. It would be a one-stop shop for people with diabetes. Patients would come in for several-hour appointments and leave with a medical strategy and a plan for changing their lifestyle. The clinic would be a place to exercise, read, learn to cook, undergo supervised physical activity in a gym. And there would be a restaurant with healthy choices and carbohydrate counts on the menu. There would be laboratories where researchers could do cutting-edge work, such as stem-cell research. There would be fellowships for visiting nurses and doctors. As Shubrook sums it up: “What if you came to the hospital four times a year to get well?”

This article appeared in the May-June issue of Pacific Standard under the title “Reversing the Course.”

Monday, April 30, 2012

End of Illness': Hidden Health Cues in Hair, Nails, Feet?


ABC News

End of Illness': Hidden Health Cues in Hair, Nails, Feet?

Friday, April 27, 2012

Scientists Cry Fowl Over the FDA's Regulatory Failure

CommonDreams.org


Overuse of antibiotics in factory farming kills thousands every year, yet the industry is force-feeding chickens pharmaceuticals

 
In 2005, the antibiotic fluoroquinolone was banned by the FDA for use in poultry production. The reason for the ban was an alarming increase in antibiotic-resistant campylobacter bacteria in the meat of chickens and turkeys – "superbugs", which can lead to a lethal form of meningitis that our current antibiotics are no longer effective against.
 
 

We create hellish conditions for our livestock, then we drug them to keep them numb. Then we drug them again to wake them from their pharmaceutical stupor. Then we drug them to grow faster. Then we drug them so their flesh will look healthier. Then we drug them to withstand the disease epidemics that our overcrowding has created. Then, of course, we drug ourselves every time we take a bite of factory-farmed poultry.Antibiotic-resistant infections kill tens of thousands of people every year, more than die of AIDS, according to the Infectious Diseases Society of America. This problem is on the rise because antibiotics are recklessly overused, especially in the commercial livestock industry, where 80% of all antibiotics manufactured in the US end up.

Fluoroquinolone used to be fed to chickens primarily to stimulate their growth. But why did the banned substance show up recently in eight of 12 samples of "feather meal", the ground-down plumage leftover from commercial poultry production?

This was just one of the mysteries uncovered in a study conducted jointly by the Johns Hopkins Center for a Livable Future and Arizona State University. The research, published last month in the journal Environmental Science & Technology, uncovered a whole slew of other drugs in the feather meal that the scientists had not expected to find there.

Traces of the arsenic compound Roxarsone, for example, were present in almost all of the samples. Farms administer arsenic to chickens to turn their flesh just the right shade of pink that consumers find attractive. Yet, in June 2011, the FDA gave Pfizer 30 days to discontinue selling Roxarsone, a proven carcinogen. So why is it still showing up in our chickens?

Other substances that the scientists found include acetaminophen, the active ingredient in Tylenol, Benadryl, an antihistamine, even Prozac, an antidepressant. Farms feed chickens these mood-altering drugs to reduce their anxiety. Chickens are anxious because they are bred on overcrowded and filthy factory farms. Stressed-out birds develop meat that is tough and unpalatable, so they need to be sedated. Yet, chickens on tranquilizers sleep all the time and do not eat enough. So they are given high doses of caffeine (which was also found in the feather meal) to keep them awake at night to feed and fatten up.
So, here is the deal. We create hellish conditions for our livestock, then we drug them to keep them numb. Then we drug them again to wake them from their pharmaceutical stupor. Then we drug them to grow faster. Then we drug them so their flesh will look healthier. Then we drug them to withstand the disease epidemics that our overcrowding has created.

Then, of course, we drug ourselves every time we take a bite of factory-farmed poultry.

"We were kind of floored," Keeve E Nachman, a co-author of the study told the New York Times. "It's unbelievable what we found." While Nachman says that the levels of arsenic and the witches' brew of other drugs and chemicals in the chicken samples may not be high enough to harm humans, he is not betting his own health on it.

"I've been studying food-animal production for some time," the researcher said, "and the more I study, the more I'm drawn to organic. We buy organic [in my family]."

"So, here is the deal. We create hellish conditions for our livestock, then we drug them to keep them numb. Then we drug them again to wake them from their pharmaceutical stupor. Then we drug them to grow faster. Then we drug them so their flesh will look healthier. Then we drug them to withstand the disease epidemics that our overcrowding has created... Then, of course, we drug ourselves every time we take a bite of factory-farmed poultry."Organic chickens are bred without artificial growth hormones and antibiotics. They are fed organically grown vegetable foods rather than the ground-up animal products – bones, feathers, blood, excrement, fishmeal and diseased animal parts – which their conventionally grown brethren receive. They are also raised free-range with plenty of space, sunlight and opportunities for exercise to keep them healthy. A 2001 study conducted at the University of Perugia found that chickens produced this way actually taste better than conventionally bred birds.

Yet, organic poultry is a lot more expensive to raise. While the market is growing steadily for organic birds, it still comprises less than 1% of the poultry sold in the US today (pdf). So, food scientists argue that the standards for conventional chickens and turkeys need to be strengthened.

"We strongly believe that the FDA should monitor what drugs are going into animal feed," Keeve Nachman urged, adding that, based on what the researchers discovered, they had little confidence that the animal food production industry could be left to regulate itself.

Earlier this month, the FDA announced what looked at first glance like sweeping new guidelines on the use of antibiotics in livestock. The new rules, however, are strictly "voluntary", and, while they do recommend restricting the use of antibiotics to stimulate growth, they would still allow them to be prescribed by a veterinarian for animals that are "either sick or at risk of getting a specific illness".

Critics contend that the words "at risk of getting a specific illness" provide factory poultry farms a loophole big enough to drive a truck through. Margaret Mellon, senior scientist at the Union of Concerned Scientists, said in a press statement:
"The outlined process appears to give the companies the opportunity to relabel drugs currently slated for growth promotion for disease prevention instead. Such relabeling could allow them to sell the exact same drugs in the very same amounts."
Public interest groups like the Union of Concerned Scientists say the time has come for the FDA to stop proposing half-measures and demonstrate that it is serious about preventing a looming public health disaster. It needs to ban dangerous antibiotic use in the raising of livestock, and to conduct rigorous on-site inspections to insure that the ban is enforced.
Richard Schiffman
Richard Schiffman is the author of two books and a former journalist whose work has appeared in, amongst other outlets, the New York Times and on a variety of National Public Radio shows including Morning Edition and All Things Considered.

Thursday, April 26, 2012

America's Mad Cow Crisis

CommonDreams.org


 
Americans might remember that when the first mad cow was confirmed in the United States in December, 2003, it was major news.  The United States Department of Agriculture (USDA) and the Food and Drug Administration (FDA) had been petitioned for years by lawyers from farm and consumer groups I worked with to stop the cannibal feeding practices that transmit this horrible, always fatal, human and animal dementia.  When the first cow was found in Washington state, the government said it would stop such feeding, and the media went away.  But once the cameras were off and the reporters were gone nothing substantial changed.

 

In the United States, dairy calves are still taken from their mothers and fed the blood and fat of dead cattle.  This is no doubt a way to infect them with the mad cow disease that has now been incubating here for decades, spread through such animal feeding practices.  No one knows how the latest dairy cow was infected, the fourth confirmed in the United States.  Maybe it was nursed on cow's blood.  Perhaps it was fed feed containing cattle fat with traces of cattle protein.  Or perhaps there is a mad cow disease in pigs in the United States, which simply has not been found yet, because pigs are not tested for it at all, even though pigs are fed both pig and cattle byproducts, and then the blood, fat and other waste parts of these pigs are fed to cattle.

All these U.S. cattle feeding methods are long banned and illegal in other countries that suffered through but eventually dealt properly with mad cow disease.  Here, rather than stopping the transmission of the disease by stopping the cannibal feeding, mad cow is simply covered up with inadequate testing and very adequate public relations.  US cattle are still fed mammalian blood, fat and protein, risking human deaths and threatening the long term safety of human blood products, simply to provide the U.S. livestock industry with a cheap protein source and a cheap way to get rid of dead animal waste.Docile, eating what they are fed, trusting the rancher all the way to the slaughterhouse.  Is that just the cows, or is it us too?

I began researching this issue around 1989, long before the disease was confirmed to have jumped from cattle to the people eating them, as announced by the British government in 1996.  In 1997 I co-authored Mad Cow USA, warning that the disease was likely already here and spreading, since the animal cannibalism that caused its outbreak in Britain and spread it to other countries was actually more widespread in the United States than anywhere.

Some years ago responsible U.S. beef companies wanted to test their animals for mad cow disease and label their beef as being disease free, but they were forbidden under penalty of law from doing so.  Only the USDA can test for mad cows in America.    In 2004 and 2005, after two additional mad cows were discovered in Texas and Alabama, the United Sates government declared that obviously mad cow wasn't much of a problem and gutted it's anemic testing program.  Today only about 40,000 cattle a year are tested, out of tens of millions slaughtered.  It's amazing that the California cow was even detected given this pathetic testing program that seems well designed to hide rather than find mad cows. 

The prevention of mad cow disease is relatively  simple.  If your country has it, test each animal before it goes to slaughter to keep the diseased animals out of the food chain.  Cheap, accurate and easy tests are now available in other countries but illegal here.  Testing cattle both identifies the true extent of the disease, and keeps infected animals from being eaten in your sausage or hamburger.  In this manner countries like Britain, Germany, France and Japan have controlled their problem through testing and a strict ban on cannibal feed.

Once mad cow disease moves into the human population of a country, all bets are off as to what could happen next.  It's a very slow disease, it develops invisibly over decades in someone who has been infected, and it is always fatal.  We'll know a lot more in fifty years, but the future looks worrisome.  In Britain people are dying from mad cow disease, people who never consumed infected meat.  They used medical products containing human blood, and that blood was infected because it was from infected people.  There is no test to identify infectious prions, the causal agent, in blood.

Almost none of this information appeared in news stories about the California mad cow.  Instead the headlines and the talking heads fed us the line that the United States fixed this problem long ago, and the fact that only 4 mad cows have been detected so far is proof of our success.   Oprah Winfrey once tried via her talk show to warn about this, way back in 1996,  but Texas cattlemen dragged her and her guest Howard Lyman into court and she had to spend many millions of dollars defending herself from the supposed crime of slandering meat.

Oprah won her case, which was probably unfortunate for the rest of us because had she been convicted the ensuing appeals court trial might have gotten enough attention to wake up Americans to the truth.  Instead Oprah learned her lesson - shut up and you won't get sued.   Other media learned too that if the government and industry can silence Oprah, they can muzzle anyone. (One of the 4 confirmed U.S. mad cows was later found in Texas, appropriately enough.)

There are a handful of dedicated activists such as Howard Lyman who have been sounding the alarm on this.  They include the ecologist Dr. Michael Hansen of Consumers Union and Dr. Michael Greger, a physician.  Terry S. Singeltary Sr., whose mom died of a version of the human form of mad cow disease, has been a relentless, unpaid activist on this issue.

Despite their dedicated work,  there is no indication that anything is going to change here in America.  The U.S. government refuses to implement the feed ban and the animal testing necessary.   It doesn't matter if the President is named Clinton, Bush or Obama because their bureaucrats in the USDA and FDA stay the course and keep the cover up going.  Docile, eating what they are fed, trusting the rancher all the way to the slaughterhouse.  Is that just the cows, or is it us too?

John Stauber
John Stauber founded the non-profit, non-partisan Center for Media & Democracy and its newsmagazine PR Watch in 1993 in Madison, Wisconsin. Prior to his retirement from CMD in 2009, Stauber co-authored six books for them including the 2003 New York Times bestseller Weapons of Mass Deception: The Uses of Propaganda in Bush's War on Iraq. He continues now as an independent investigative writer, public speaker and democracy advocate whose leadership on controversial public issues began in high school when he organized to end the U.S. war in Vietnam and for the first Earth Day. He has begun or worked with many non-profit public interest groups.

Sunday, April 1, 2012

Is sugar toxic?

CBS News.com


HealthWatch

April 1, 2012 7:07 PM 

 

 (CBS)

Watch the Episode »

Dr. Sanjay Gupta reports on new research showing that beyond weight gain, sugar can take a serious toll on your health, worsening conditions ranging from heart disease to cancer.
(CBS News) If you are what you eat, then what does it mean that the average American consumes 130 pounds of sugar a year? Sanjay Gupta reports on new research showing that beyond weight gain, sugar can take a serious toll on your health, worsening conditions ranging from heart disease to cancer. Some physicians go so far as to call sugar a toxin.

The following script is from "Sugar" which aired on April 1, 2012. Dr. Sanjay Gupta is the correspondent. Denise Schrier Cetta and Sumi Aggarwal, producers.
The chances are good that sugar is a bigger part of your daily diet than you may realize which is why our story tonight is so important. New research coming out of some of America's most respected institutions is starting to find that sugar, the way many people are eating it today, is a toxin and could be a driving force behind some of this country's leading killers, including heart disease.
As a result of these findings, an anti-sugar campaign has sprung up, led by Dr. Robert Lustig, a California endocrinologist, who believes the consumption of added sugars has plunged America into a public health crisis.
Dr. Sanjay Gupta: Is sugar toxic?
Dr. Robert Lustig: I believe it is.
Dr. Sanjay Gupta: Do you ever worry that that's-- it just sounds a little bit over the top?
Dr. Robert Lustig: Sure. All the time. But it's the truth.
Dr. Robert Lustig is a pediatric endocrinologist at the University of California, San Francisco and a pioneer in what is becoming a war against sugar.
Motivated by his own patients -- too many sick and obese children - Dr. Lustig has concluded that sugar, more than any other substance, is to blame.
Dr. Sanjay Gupta: What are all these various diseases that you say are linked to sugar?
Dr. Robert Lustig: Obesity, type II diabetes, hypertension, and heart disease itself.
Lustig says the American lifestyle is killing us.
Dr. Sanjay Gupta: And most of it you say is preventable?
Dr. Robert Lustig: Seventy-five percent of it is preventable.
While Dr. Lustig has published a dozen scientific articles on the evils of sugar, it was his lecture on YouTube, called "Sugar: The Bitter Truth," that brought his message to the masses.
[YouTube Video: I'm standing here today to recruit you in the war against bad food.]
By "bad food" Dr. Lustig means the obvious things such as table sugar, honey, syrup, sugary drinks and desserts, but also just about every processed food you can imagine, where sugar is often hidden: yogurts and sauces, bread, and even peanut butter. And what about the man-made, often vilified sweetener, high fructose corn syrup?
Dr. Sanjay Gupta: Is it worse than just table sugar?
Dr. Robert Lustig: No. 'Cause it's the exact same. They are basically equivalent. The problem is they're both bad. They're both equally toxic.
Since the 1970s, sugar consumption has gone down nearly 40 percent, but high fructose corn syrup has more than made up the difference. Dr. Lustig says they are both toxic because they both contain fructose -- that's what makes them sweet and irresistible.
Dr. Robert Lustig: We love it. We go out of our way to find it. I think one of the reasons evolutionarily is because there is no food stuff on the planet that has fructose that is poisonous to you. It is all good. So when you taste something that's sweet, it's an evolutionary Darwinian signal that this is a safe food.
Dr. Sanjay Gupta: We were born this way?
Dr. Robert Lustig: We were born this way.
Central to Dr. Lustig's theory is that we used to get our fructose mostly in small amounts of fruit -- which came loaded with fiber that slows absorption and consumption -- after all, who can eat 10 oranges at a time? But as sugar and high fructose corn syrup became cheaper to refine and produce, we started gorging on them. Americans now consume 130 pounds per person a year -- that's a third of a pound every day.
Dr. Lustig believes those sweeteners are helping fuel an increase in the most deadly disease in America: heart disease. For years, he's been a controversial voice.
[Kimber Stanhope: Here is our oral isotope...]
But now, studies done by Kimber Stanhope, a nutritional biologist at the University of California, Davis are starting to back him up. She's in the middle of a groundbreaking, five-year study which has already shown strong evidence linking excess high fructose corn syrup consumption to an increase in risk factors for heart disease and stroke. That suggests calories from added sugars are different than calories from other foods.
Dr. Sanjay Gupta: The mantra that you hear from most nutritionists is that a calorie is a calorie is a calorie.
Kimber Stanhope: And I think the results of the study showed clearly that is not true.
Stanhope's conclusions weren't easy to come by. Nutrition studies are expensive and difficult. Stanhope has paid groups of research subjects to live in this hospital wing for weeks at a time, under a sort of 24-hour lockdown. They undergo scans and blood tests - every calorie they ingest, meticulously weighed and prepared.
Kimber Stanhope: They're never out of our sight. So we do know that they are consuming exactly what we need them to consume.
Dr. Sanjay Gupta: And they're not sneaking any candy bars on the side.
Kimber Stanhope: Yeah, right, exactly.
For the first few days, participants eat a diet low in added sugars, so baseline blood levels can be measured.
[Research assistant: So remember you guys have to finish all of your Kool-Aid. ]
Then, 25 percent of their calories are replaced with sweetened drinks and Stanhope's team starts drawing blood every 30 minutes around the clock. And those blood samples? They revealed something disturbing.
Dr. Sanjay Gupta: And what are you starting to see?
Kimber Stanhope: We found that the subjects who consumed high fructose corn syrup had increased blood levels of LDL cholesterol and other risk factors for cardiovascular disease.
Dr. Sanjay Gupta: How quickly did these changes occur?
Kimber Stanhope: Within two weeks.
Kimber Stanhope's study suggests that when a person consumes too much sweet stuff, the liver gets overloaded with fructose and converts some of it into fat. Some of that fat ends up in the bloodstream and helps generate a dangerous kind of cholesterol called small dense LDL. These particles are known to lodge in blood vessels, form plaque and are associated with heart attacksDr. Sanjay Gupta: Did it surprise you when you first got these results back?
Kimber Stanhope: I would have to say I was surprised because when I saw our data, I started drinking and eating a whole lot less sugar. I would say our data surprised me.
So imagine, for these healthy young people, drinking a sweetened drink might be just as bad for their hearts as the fatty cheeseburgers we've all been warned about since the 1970s. That's when a government commission mandated that we lower fat consumption to try and reduce heart disease.
Dr. Sanjay Gupta: So with the best of intentions, they say, "Time to reduce fat in the American diet?"
Dr. Robert Lustig: Exactly. And we did. And guess what? Heart disease, metabolic syndrome, diabetes and death are skyrocketing.
Dr. Lustig believes that's primarily because we replaced a lot of that fat with added sugars.
Dr. Robert Lustig: Take the fat out of food, it tastes like cardboard. And the food industry knew that. So they replaced it with sugar.
Dr. Sanjay Gupta: This idea that sugar increases this particularly bad LDL, the small dense particles that are associated with heart disease. Do most doctors-- do they know this?
Dr. Robert Lustig: No, they do not know this. This is new.
And it turns out, sugar has become a major focus in cancer research too. Lewis Cantley, is looking at the connection.
Dr. Sanjay Gupta: If you limit your sugar you decrease your chances of developing cancer?
Lewis Cantley: Absolutely.
Cantley, a Harvard professor and the head of the Beth Israel Deaconess Cancer Center, says when we eat or drink sugar, it causes a sudden spike in the hormone insulin, which can serve as a catalyst to fuel certain types of cancers.
Lewis Cantley: What we're beginning to learn is that insulin can cause adverse effects in the various tissues. And of particular concern is cancer.
Why? Nearly a third of some common cancers -- including breast and colon cancers -- have something called insulin receptors on their surface. Insulin binds to these receptors and signals the tumor to start consuming glucose.
Lewis Cantley: This is your body...
Every cell in our body needs glucose to survive. But the trouble is, these cancer cells also use it to grow.
Lewis Cantley: So if you happen to have the tumor that has insulin receptors on it then it will get stimulated to take up the glucose that's in the bloodstream rather than go into fat or muscle, the glucose goes into the tumor. And the tumor uses it to grow.
Dr. Sanjay Gupta: So you've just seen that tumor turn blue which is essentially reflective of glucose going into it.
Lewis Cantley: That's right.
Dr. Sanjay Gupta: So these cancers, much in the same way that muscle will say, "Hey, I'd like some of that glucose, the fat says, "I would like some of that glucose," the cancers have learned how to do this themselves as well?
Lewis Cantley: Yes. So they have evolved the ability to hijack that flow of glucose that's going by in the bloodstream into the tumor itself.
Lewis Cantley's research team is working on developing drugs that will cut off the glucose supply to cancer cells and keep them from growing. But until there's a breakthrough, Cantley's advice? Don't eat sugar. And if you must, keep it to a minimum.
Lewis Cantley: In fact-- I-- you know, I live my life that way. I rarely eat sugar.
Dr. Sanjay Gupta: When you see a sugary drink or if I were to offer you one, what-- with all that you know, what's going through your mind?
Lewis Cantley: I probably would turn it down and get a glass of water.
But for most of us, that's easier said than done...
Eric Stice: It turns out sugar is much more addictive than I think we had sort of realized early on.
Eric Stice, a neuroscientist at the Oregon Research Institute, is using functional MRI scanners to learn how our brains respond to sweetness.
Eric Stice: Sugar activates our brain in a special way. That's very reminiscent of, you know, drugs like cocaine.
That's right. Cocaine.
Dr. Sanjay Gupta: Let's give it a shot...
I climbed into the MRI scanner to see how my brain would respond. That's a straw that's been rigged to deliver a tiny sip of soda into my mouth.
Eric Stice: Stay as still as you can, ok?
Just as it hit my tongue, the scanner detected increased blood rushing to certain regions of my brain. In these images, the yellow areas show that my reward region is responding to the sweet taste. Dopamine - a chemical that controls the brain's pleasure center - is being released, just as it would in response to drugs or alcohol.

Dr. Sanjay Gupta: So dopamine is released. That sort of makes me feel good. I'm experiencing some pleasure from having this Coke.
Eric Stice: Right, that euphoric effect.
Dr. Sanjay Gupta: So far be it for people to realize this 'cause sugar is everywhere, but you're saying this is one of the most addictive substances possibly that we have?
Eric Stice: It certainly is very good at firing the reward regions in our brain.
Eric Stice says by scanning hundreds of volunteers, he's learned that people who frequently drink sodas or eat ice cream or other sweet foods may be building up a tolerance, much like drug users do. As strange as it sounds, that means the more you eat, the less you feel the reward. The result: you eat more than ever.
Eric Stice: If you overeat these on a regular basis it causes changes in the brain that basically it blunts your reward region response to the food, so then you eat more and more to achieve the same satisfaction you felt originally.
With all this new science emerging, we wanted to hear from the sugar industry, so we visited Jim Simon, who's on the board of the Sugar Association, at a sugar cane farm in Louisiana.
Dr. Sanjay Gupta: Would it surprise you that almost every scientist that we talked to in researching this story told us they are eliminating all added sugars. They're getting rid of it because they're concerned about the health impacts.
Jim Simon: To say that the American consuming public is going to completely omit, eliminate, sweeteners out of their diet I don't think gets us there.
Simon cautions that eliminating sugar wrongly vilifies one food, rather than working towards the long-term solution of reducing calories and exercising.
Dr. Sanjay Gupta: You know, a lot of people, Jim, are saying that sugar is different. That it is bad for your heart and is causing a lot of the problems we're talking about. It is addictive and in some cases might even fuel cancers. What would you - I mean you've looked at this. You must have looked at some of these studies. What do you say about that?
Jim Simon: The science is not completely clear here.
Dr. Sanjay Gupta: But some of that's, but some of these studies exist. I mean, what is a consumer, what are they to make of all that?
Jim Simon: Well, I would say to them, that they've got to approach, their diet in balance.
Dr. Robert Lustig agrees -- we need a balanced diet -- but his idea of balance is a drastic reduction in sugar consumption. To that end he co-authored an American Heart Association report recommending men should consume no more than 150 calories of added sugars a day. And women, just 100 calories. That's less than the amount in just one can of soda.
Dr. Robert Lustig: Ultimately this is a public health crisis. And when it's a public health crisis, you have to do big things and you have to do them across the board. Tobacco and alcohol are perfect examples. We have made a conscious choice that we're not going to get rid of them, but we are going to limit their consumption. I think sugar belongs in this exact same wastebasket.