“Barbara Corkey is one of the few people who really understand and integrate metabolism into diabetes research,” says Ronald Kahn, past president of the Joslin Diabetes Center. “For the last 30 years, metabolism has been a lost science. She helped keep the field alive.” Photo by Vernon Doucette
We all know why Americans are fat, right? We gobble chips and chug 16-ounce sodas and then park our butts in front of the TV. Seems pretty straightforward. But what if that’s not the whole story? Biochemist Barbara Corkey has an idea that turns this conventional wisdom on its head.
What if, asks Corkey, obesity isn’t simply about eating too much and exercising too little? What if there’s something more subtle at work? Maybe it isn’t extra calories that make us fat, she says, but food additives like saccharin and emulsifiers.
“I don’t believe that overeating causes obesity,” says Corkey flatly. “During my lifetime I have seen tremendous differences in food preparation and food packaging....When that novelty is associated with an increase in obesity and diabetes, is it rocket science to ask whether these things are related?”
Corkey’s suspected connection may seem like a stretch, but she is not one to oversimplify science. Corkey is a respected scientist with five decades of metabolism research under her belt. She’s the vice chair of research at the School of Medicine department of medicine, and in November was appointed MED’s Zoltan Kohn Professor in Medicine. She’s the former director of the Obesity Research Center at Boston Medical Center and recent past editor of the medical journal Obesity, and last year she was awarded the Banting Medal for Scientific Achievement Award, the American Diabetes Association’s highest scientific honor and one of the world’s top science awards.
“Barbara is out of the box—completely,” says collaborator Orian Shirihai, a MED associate professor of medicine. “She doesn’t even know what’s in the box. What she does is turn the box upside down and put it onto other scientists’ heads.”
Through March, Barbara Corkey will answer your questions about diet and obesity.
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MED’s Barbara Corkey talks about the influence of her painting on her research.
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Corkey’s area of expertise is metabolism: she studies how cells, specifically cells involved in diabetes and obesity, communicate. “Metabolic disease has always interested me,” she says. “It’s a system where pathways all interconnect and talk to each other. And so if you push on one button over here, it has consequences everywhere else.”
A key player in her research is the pancreatic beta cell, which produces insulin, a hormone that converts food into energy and stores it as either fat or glucose. In diabetics, the beta cells usually produce too much, too little, or no insulin. The reasons for beta cell breakdown are complicated, and that’s what attracts Corkey.
“Barbara is one of the few people who really understand and integrate metabolism into diabetes research,” says Ronald Kahn, past president of the Joslin Diabetes Center and a professor of medicine at Harvard Medical School. “Metabolism is coming back now, but for the last 30 years it has been a lost science.” Kahn, who calls Corkey “the queen of metabolism,” says that “she helped keep the field alive.”
Fortuitously, it turns out. Diabetes now threatens to become a worldwide epidemic. According to the U.S. Centers for Disease Control and Prevention (CDC), 25.8 million children and adults in the United States—8.3 percent of the population—have the disease, which is the leading cause of kidney failure and blindness among adults. If current trends continue, a third of U.S. adults could have diabetes by 2050. Outside the United States, the numbers are equally grim. According to the World Health Organization (WHO), 346 million people worldwide—5 percent of all humans—have diabetes, and diabetes deaths will likely double by 2030.
Decades ago, when the disease was not well understood, scientists knew that two types of diabetes existed—type 1 and type 2—but they didn’t have a clear picture of the underlying causes. People with type 1 diabetes, which is usually diagnosed in children, cannot produce insulin and must inject it to survive. Scientists thought that type 2 diabetics, who are usually adults and often obese, had a less dramatic deficit: some insulin but not enough. But when scientists came up with a way to measure insulin levels, they found that people with type 2 diabetes actually had too much insulin.
If they had plenty of insulin, what caused the diabetes? The researchers theorized that insulin receptors in the muscle and fat tissue, bombarded by an excess of the hormone, became desensitized and didn’t work as they should. This “insulin resistance” causes the beta cell to crank out more insulin, and sometimes to stop working altogether. By the 1980s, the idea that insulin resistance alone causes type 2 diabetes had solidified into scientific dogma.
There was only one catch: nobody knew which came first, the broken beta cells or the insulin resistance. Corkey was determined to find out. “I think perversely,” she says. “Why is the beta cell secreting more insulin? The glucose isn’t elevated. How can we explain this?” She suspected that the beta cells were partly responsible for triggering diabetes. And she spent the next two decades trying to prove it.
The role of outsider suits her. “I like to be in a comfortable place where we don’t have to compete and rush, and we can do our science in a thoughtful and leisurely manner,” she says. By all accounts Corkey also enjoys the role of scientific gadfly.
“She likes to be provocative,” says Sarah Krawczyk (MED’11), one of Corkey’s postdoctoral students. “Lots of her theories challenge dogma, though they’re always backed up by sound science.” For two decades, while insulin resistance dominated diabetes research in the United States, Corkey stuck stubbornly with the beta cell theory. “I just thought the whole United States was wrong,” she says.
She was right. Scientists now widely accept that a person can’t get type 2 diabetes without malfunctioning beta cells, a paradigm shift largely precipitated by Corkey.
“She just really changed that field and put metabolism into it, and she’s basically regarded as the expert,” says Susan K. Fried, a MED professor of endocrinology, diabetes, and nutrition. The beta cell research, along with similar work on fat cell metabolism, helped Corkey win the 2011 Banting Medal. “She was such a perfect choice,” says Kahn. “She is an excellent scientist with a huge body of work, and she has been such an important catalyst in diabetes research.”
Giving Wing to Her Intellect
Corkey remembers the moment she decided to become a scientist. She was a teenager at New York University, majoring in fine arts while simultaneously pursuing an accelerated path to medical school. She loved painting, but considered it a “hedonistic pleasure” rather than a career, and had set her sights on medicine.
Click the image above to see a diagram of how additives may lead to diabetes. Diagram by Ed Wiederer
Walking to class one day, she glanced into a tiny lab and saw a fascinating sight: a small beating heart, dangling on a string over a dish. She stopped in her tracks. Intrigued, Corkey asked the professor why the disembodied heart was still thumping away. “It’s calcium,” he told her. As she watched, he changed the calcium levels in the solution. The heart stopped beating, then started again. “That’s when I knew that medical school was not for me,” she says. She was so smitten by biochemistry that she dropped out of NYU without finishing a bachelor’s degree and joined a laboratory. That job, in 1957, marked her first foray into diabetes metabolism.
From there her career followed an extraordinary path. Corkey married a Hungarian refugee at age 19 and had her first child, a son, at age 20. Her father, disapproving of the marriage and of foreigners in general, stopped speaking to his daughter. The young family moved to the University of Pennsylvania, where Corkey got a full-time job as a lab technician. After her second child was born, her husband walked out, leaving her with two small children and a mountain of debt.
“It was almost impossible to live on my income,” says Corkey. “I couldn’t afford babysitters. I couldn’t afford anything.” Her daughter Valerie remembers her mother struggling to provide for the family, shuttling her around on the back of a bicycle because they didn’t own a car. “But I don’t remember wanting for anything,” she says.
On the contrary, Valerie and her sister, Pamela, share happy memories of playing in their mother’s lab, spinning magnets on the centrifuge and snapping tiny plastic vials together into necklaces. “I wouldn’t trade her for any other parent,” says Valerie.
While Corkey remembers those years as lonely and stressful, they shaped the woman she is today. “I realized that I am in charge of me, and I’m responsible for my life,” she says. “No one’s going to take care of me except me. And no one’s going to take care of my kids except me. So get over it.”
Corkey dug her way out with characteristic optimism and energy. Her second husband, a medical student, encouraged her to get a PhD, and she persuaded the University of Pennsylvania to admit her without a bachelor’s degree. She was awarded a doctorate in 1981, the same year her son graduated from college. She was 43 years old—ancient in scientist years.
“It’s almost unprecedented to start a scientific career so late and achieve so much,” says Richard Bergman, director of the Cedars-Sinai Diabetes and Obesity Research Institute in Los Angeles. “Barbara is one of the greatest role models for women in science—and for scientists in general—that I know.”
Pamela frames her mother’s accomplishments another way. “Having a bunch of kids and giving them home-cooked pot roast seven nights a week is one way to make a contribution to the world,” she says. “But when your brain is capable of understanding and breaking down metabolic regulation, that’s what you should be doing. I can’t imagine how miserable she would have been if she hadn’t given wing to her intellect.”
The Fine Art of Science
Biochemist Barbara Corkey explains how painting complements her work as a scientist.
Last Remaining Bigotry
Corkey is now 73, and with her cropped white hair and funky earrings she looks more Greenwich Village grandma than top-tier biochemist. She radiates an aura of competence, kindness, and joie de vivre that endears her to both students and colleagues.
At BU, she is known as a generous collaborator and a beloved but tough mentor. “The best mentors give you a hammer on the head and then a hug,” says Shirihai. “With Barbara, you never know which it’s going to be.” As the department of medicine vice chair of research since 2007, Corkey helped build major research “cores” that allow scientists to use expensive equipment they can’t afford in their own labs, such as cell imaging and high-throughput screening machines. She helped write a strategic plan for the department that included specific language to protect postdocs and junior faculty from exploitation. A gourmet cook and wine connoisseur, she encourages fraternization through food, from pairing wine and cheese for faculty gatherings to organizing an annual dim sum lunch, which draws hundreds of faculty and staff and their families.
Corkey is a modest woman who avoids the limelight and disdains what she calls the “billy goats” who often dominate science. She enjoys spending time alone, cherishing the quiet Friday afternoons when she can paint in her studio.
The role of outsider suits Corkey. “She likes to be provocative. Lots of her theories challenge dogma, though they’re always backed up by sound science.”
Krawczyk, who earned a PhD under Corkey, was unaware of her boss’ status in the scientific world until they started attending conferences together and she saw other scientists treat Corkey like a superstar.
As the winner of the Banting Medal, Corkey had to give an hour-long talk to a crowd of 6,000 last June, and she did not relish the prospect. Shirihai, on the other hand, looked forward to it. “I wanted to see how she would use it to hammer 6,000 people simultaneously,” he says. He was not disappointed. Instead of simply recapping her career, Corkey spent an hour discussing a controversial new direction for her research: whether the 4,000 additives in the U.S. food supply might be contributing to diabetes and obesity. “For those people who never got out of the box,” Shirihai says with a laugh, “it was like having a high-volume enema.”
Obesity statistics are troubling. One-third of American adults are obese, and the numbers are growing, according to the CDC, which describes the cost to the American health care system as “staggering”—an estimated $147 billion in 2008 dollars. And the rest of the world is catching up. According to the WHO, worldwide obesity has more than doubled since 1980.
Corkey believes that extra calories alone can’t possibly be causing this epidemic. “This gets to the last remaining bigotry in the world, which is against obesity,” she says. “If you’re a good person and you do all the right things, you’re going to be lean. And if you’re a bad person and you eat like a pig and you don’t do any exercise, you’re going to be fat. It is the only body function that we look at this way.”
This bigotry “has slowed the field down incredibly,” she says. “We don’t spend enough money on research. This is the main disease that is growing the health care budget in our society, and we don’t even really consider it a disease. We don’t study it. We don’t understand it. We have no effective treatments, because if you say, ‘Control yourself,’ and think that’s an effective treatment, then you’re sticking your head in the sand.”
Corkey is not alone in her suspicion that environmental factors may contribute to diabetes and obesity. Earlier this year, the National Toxicology Program, part of the U.S. Department of Health and Human Services, reported that certain environmental triggers, like arsenic poisoning and some pesticides, are associated with type 1 diabetes. It also found that children of mothers who smoked during pregnancy were more likely to be obese.
“There are many factors in the environment that are probably provoking this epidemic,” says Harvard’s Kahn. “Most researchers have focused on the obvious things: you eat at McDonald’s, you sit at your computer, you get fat. I think it’s much more complicated than that.”
Many scientists and public health experts are skeptical. Nutrition expert Marion Nestle, Paulette Goddard Professor of Nutrition, Food Studies, and Public Health at New York University and coauthor of the forthcoming book Why Calories Count: From Science to Politics, says people are getting fatter simply because they eat too much.
“It’s almost unprecedented to start a scientific career so late and achieve so much. Barbara is one of the greatest role models for women in science.”
As for possible environmental factors, Nestle says, “it’s an Occam’s razor situation—the simplest explanation is often the one that works. I still vote for calories, but that, of course, doesn’t give researchers much to do.”
Such criticism only galvanizes Corkey, who began her newest line of research by screening about 500 food additives for effects on liver, fat, or beta cell tissues. Two hits proved especially interesting: a class of widely used emulsifiers called monoglycerides, often found in processed baked goods, and the artificial sweetener saccharin. Both additives made beta cells secrete insulin, but not in the normal way. Usually, says Corkey, calcium is involved in stimulating beta cells to produce insulin, and when stimulated they increase their oxygen consumption. But when monoglycerides and saccharin were put to the test, neither of these things happened. Instead, the beta cells underwent some unexpected chemical changes and released molecules called reactive oxygen species, which have been implicated in cell damage, inflammation, and obesity.
What do these intriguing—but preliminary—findings mean? At this stage, Corkey says, it’s impossible to know. But she suspects that background levels of certain food additives could cause subtle but critical changes in our metabolic tissues, possibly contributing to diabetes and obesity. Many caveats remain: perhaps the additives never reach levels in the food supply that could hurt an actual human, or perhaps the cellular changes that Corkey observed are beneficial.
“I have a model of how things might be happening,” she says. “It’s a hypothesis that needs testing. And it needs to be carefully tested.”
While it’s extremely unlikely that a single food additive could be the villain that causes obesity and diabetes, Corkey hopes to identify a handful of problem additives that could be removed from the food supply. She also knows that in the end, the additives themselves might not be the key. Rather, her research might lead to a new understanding of a metabolic pathway that could be modified to treat obesity and diabetes or to a better understanding of how individual people respond to certain chemicals.
“What I want is to find the cure, but what I don’t want to do is get people all fired up in a direction that will be misleading,” she says. “Important work needs to be done to prove or disprove what’s right and what’s wrong.”
Corkey’s colleagues describe her as a classic biochemist. She comes up with a hypothesis, tests it, and evaluates the data. “She has a vision, she’s going about it systematically, and the science will take her where it takes her,” says MED’s Fried. “In her mind, it’s as simple as that. If we don’t do the experiment and find out, we will never know.” ■
Ask the Expert: Barbara Corkey
Readers took advantage of our invitation to ask Barbara Corkey about diet and obesity. Here are some of those questions, along with Corkey's responses.
QAs we age, as a general observation, we all seem to acquire fat in the belly just under the ribs in front and
distributed in the mid-back. Is there anything known about its cause and how to alter our behaviors to reduce it?
ABelly fat in men is associated with a decrease in testosterone. Similarly, in women, a little more central fat is associated with menopause (a fall in estrogen). The mechanisms by which sex steroids affect fat distribution are poorly understood. However, testosterone treatment in men and estrogen treatment in postmenopausal women do not reliably reduce this fat in older adults, despite the fact that a drop in either hormone promotes belly fat distribution. Growth hormone can prevent it but can also cause diabetes. So the advice from one of our endocrine doctors is to enter your older years as fit as possible and with strong bones and hope for the best as far as what your body will look like at 80!
QI read with interest the article about insulin. A few years ago I discovered very high levels of glucagon, the hormone that works in opposition to insulin. I’m insulin resistant, and doctors say I’ll suffer from diabetes. They searched pancreatic cells in my body for pancreatic cancer before declaring nothing is abnormal in me, just this kind of sugar intolerance. — Elena
AMost insulin-resistant patients with prediabetes or diabetes are relatively hyperglucagonemic, so it is not a useful test in most patients for that reason. Glucagonomas (pancreatic tumors) are extremely rare, almost always seen along with a specific rash, and usually patients have mild diabetes and weight loss. Our local doctors recommend exercise and a low carbohydrate diet to treat insulin resistance.
Q
Barbara, your research is fascinating, and I’m curious to know if you have out-of-the-box answers to these questions:
I have had patients ask why their blood glucose rises after aerobic exercise. If the liver is putting out excessive glucose during exercise, what is the reason?
How does chronic strength training help to lower HbA1C in type 2 diabetics (what is the mechanism)? — Reba Schecter
A
The short answer to the first question is that we do not know. I can suggest some possibilities that are worth testing:
1. Fat is being used instead of glucose.
2. Muscle glycogen is being used instead of glucose.
3. Epinephrine or norepinephrine is being released, which inhibits insulin secretion and stimulates liver glycogen breakdown.
My answer to the second question is that exercise promotes insulin independent glucose use. Thus, any exercise spares insulin and uses glucose—a very beneficial process for diabetics.
Q How do metabolic and hormonal changes found in the menopausal transitioning process in women affect obesity? What are the specific chemical changes that occur, and how do they affect metabolism?— Barbara Fernie
A You ask a very complicated question. It is clear from the work of Professor Susan Fried that great differences occur in fat storage between men and woman. Some of these changes involve estrogen and estrogen receptors. Since menopause involves a dramatic but normal decrease in estrogen production, many of the postmenopausal changes in fat storage may be a result. One of the most notable changes involves the unfortunate migration of fat from under the skin, particularly in the face and neck, to the belly. I wish I knew how to send it back to the skin.
Q How can we recognize mono-oleol-glycerides on lists of ingredients on foods? Are all artificial sweeteners like Stevia, Splenda, and Equal suspected of triggering overproduction of insulin, like saccharin?
A
1. Monoglycerides are usually listed among the ingredients.
2. Not all artificial sweeteners are the same. In our studies only saccharin appears likely to reach levels that could affect insulin secretion, but more studies are needed since we don’t really know the blood levels of the others in heavy users.
Q How do you explain people who eat the same saccharin and emulsifiers but do not become obese or get diabetes? Also, when you travel a lot, you get the benefit of observing other diets and it seems Americans not only eat a lot of fatty food, but the portion sizes are markedly different here versus other countries. Americans eat huge portions comparatively.— Caroline
A
1. The actual dietary intake of lean versus obese on similar diets is not well documented, although if that were found, it could be due to differences in efficiency of using food to make energy or differences in heat production: some people generate heat and others are always cold with a sweater on.
2. I do travel a lot, and appallingly food portions seem to be growing everywhere. The real question is why do people eat more than they need. They didn’t use to, even when food was available.
Q
It is great to learn of your innovative thinking on what has always seemed to me a profoundly deficient analysis of the obesity/diabetes epidemic. All the dieticians and health care establishment yammering about exercise and healthy snacks, and the food industry response of creating more packaged foods with more additives. What is so scary about whole foods to these gurus? What scares me is that many things have entered our bodies without testing whether they are good or bad.
Anyway, I just wondered what your opinion is of the value of pursuing the role of some of the ubiquitous toxic molecules such as plastics, and in particular Bisphenol A, in cell metabolism gone wrong. It seems there is accumulating evidence that it is involved. Do you have any plans to research this or its relatives? Since certain professions expose workers to inordinate amounts of it (e.g., store clerks handling heat-sensitive register receipts), human subjects might be easy to find. — Cyndy Stancioff
A The data on BPA are pretty convincingly bad. Let’s work together to eliminate it or prove that it’s OK and to test others that have not been tested.
Q
My grandson was born on October 26, 2011. On December 25, he had a major epileptic seizure and was rushed to the hospital in Washington, D.C. They have tried several exotic medicines to stop the infantile spasms, mostly to no avail. Now, he is preparing to re-enter the D.C. Children’s Medical Center to start the ketogenic diet. This is a diet in which carbohydrates are eliminated and the patient is fed only fat and protein. For some reason, this diet has had great success in treating childhood epilepsy. We are hoping for the best, as he is running out of options. If the seizures continue, the brain damage will be irreversible, and the quality of his life will be very poor.
Can you tell me if there is any ongoing research being conducted on this ketogenic diet or other similar regimes to control seizures?
Any information that you could give us would be greatly appreciated by. — Nancy Muirhead Marsh
A My research has not addressed seizure disorders. However, I am impressed with the data that has been published on ketogenic diets. It’s interesting that low-carb diets and the Atkins and South Beach diets are ketogenic. I don’t see a negative aspect to such diets as long as they contain adequate protein, since the body has no requirement for carbohydrates. Historically, carbohydrates have made up a large part of our diet, mainly because they are cheap and available.
Q
I am fascinated by your research and your passion for "thinking outside the box." I, too, am a scientist by training, a veterinarian, and I am also an "obesity survivor.”
I have recently recovered from a path of self-destruction—slow death by compulsive overeating—and was headed on the fast track to type 2 diabetes. It's a miracle that my beta cells still work!
I come from a family of diabetics. My grandmother died at the age of 48 from obesity/diabetes, and my mother is part of the diabetes prevention research program at Northwestern University, as she was prediabetic.
I believe in your research 100 percent and know without a doubt that the food additives and amounts of sugars and refined carbohydrates that I used to consume contributed to my being 100 pounds overweight without having any means to stop eating. And I felt overwhelmed with self-loathing and was filled with shame about my inability to stay on a diet. I was a five-time Weight Watcher flunkee.
I hope that you may have already come across the program of Overeaters Anonymous (OA) in your thinking-outside-the-box approach to metabolism and obesity research, that you may have opened your mind to the possibility that obese people are "addicts," and that you are not put off by the spiritual aspect of the OA recovery program.
I feel that OA has saved my life, and that it could do so for many hundreds of others, if they learned and accepted the idea that their obesity is directly correlated to the substances in (as well as quantity of) the foods that they eat.
I learned (by chance) that I personally used food substances like an alcoholic uses alcohol—to change the way I felt or to "decompress" or unwind after a long day at work. Many people call this "stress eating.” However, the more I did it, the more I "had" to keep doing it. I became addicted to these foods, most of which you can find at a gas station and are filled with the chemical additives and sugars that you are looking at.
I soon began to understand that the food I was eating was a "chemical" that I could become dependent on.
Then I started to see that my inability to just stop eating these foods, which were killing me, was due to a chemical dependency on these foods. I was able to accept the idea that I had a disease (addiction) and stop hating myself because of that obesity bigotry that I had learned from society. I was then ready and willing to accept the idea that I would have to identify all of those foods, and practice total abstinence. They all broke down to carbohydrates or were foods rich in the chemical additives and artificial sweeteners and sugars that you are now researching in your lab. I never in my wildest dreams thought that I would ever be able to give these foods up—but what I learned was that once I gave them up and they were out of my system for period of time, my physical cravings for these foods was removed.
I believe 100 percent that my ability to lose 80 pounds (and to keep it off) for the past four years is a direct result of my understanding that these foods were chemicals that I was physically addicted to, and that I had to abstain from these foods to acquire the ability to stop eating them.
I am mostly writing in the hopes that I may find a scientist who understands that processed foods are very much a chemical substance that not only leads to diabetes but that has an addictive property, and that those who suffer from morbid obesity may be considered addicts by medical professionals so that they may receive referrals to OA or other 12-step food recovery programs.
I believe that medical professionals will still want to help people with their focus on medically managed weight loss programs, in which they feed people liquid diets made up of sugars and other addictive chemicals, believing that the solution is in the actual physical weight loss. I believe that solution lies in treating obesity like an addictive disorder, which deserves the same understanding that other chemical dependency programs give to alcoholics, narcotics addicts, and even to nicotine addicts.
I thank you for your time. — Ilana Strubel
A Thank you for sharing your story with me. I am impressed that you found a solution that works for you. I hope that your story and mine will motivate further research into the addictive aspects of foods. Still a wild frontier. OA has been a lifesaver for many but not all. I am committed to continue my quest to understand how the food and our environment have created the problems we now face. Congratulations on your success.
Q I just read your article in Bostonia magazine and was very intrigued by your research on the connection between food additives and obesity. My question concerns soy protein isolates: are you aware of any potential metabolic problems with these food substances? I appreciate your stated willingness to answer question from the readership. Good luck to you on your research. — Fran Kaplan
A Thanks for reading my story. I have not yet studied soy protein isolates, but like many things neither have others. I would like to see a time when everything that enters our food supply undergoes testing for its effect on metabolic health. We have a long way to go and could use your help.
Q
As a person who has been diagnosed with metabolic syndrome, I am extremely interested in your work and felt compelled to correspond with you.
Four years ago, I experienced a significant lifestyle change, which had a profound impact on my health. Prior to this change, I was at least 30 pounds overweight, had high total cholesterol and high triglycerides as well. My good cholesterol was low and my bad cholesterol was high. I was very active and worked out regularly, seemingly with no effect. I am currently 52 years old.
I was advised by my doctor, based on my family history and my blood results, that I was in a high-risk group to develop heart disease, type 2 diabetes, or a whole host of other health issues.
His recommendation was to attend an Overeaters Anonymous meeting and to seek out a sponsor who follows what is called the 90-day plan. The gist of the program is eliminating ALL refined carbohydrates and sugars from my diet. I eat no flour or sugar and do not drink alcohol. Since making these changes, I lost 30 pounds and all my blood chemistry has moved to normal, healthy levels. These results are absolutely a miracle.
I have a number of friends in the program who have experienced similar miraculous results, with weight losses exceeding 150 pounds and completely restored health.
The OA90 program addresses the problem from the perspective of addiction with the “drug” being flour and sugar. I speak from my direct experience that these chemicals in food, when consumed in any form, have the power to produce uncontrollable craving and the desire for more. The typical American diet is loaded with these chemicals in all forms and fashion, and they are also hidden in the sauces, additives, and preservatives, etc.
To avoid such foods takes concerted and focused effort. I would not be able to do this without the aid of OA90.
I am confident that your research investigation is conducted by the highest professional scientific standards and will yield at least a biochemical explanation for the phenomena that we are witnessing. My experience tells me that the answer to why Americans are fat lies not only in the scientific reasons but also the mental and spiritual aspects of human beings and their attitude toward food.
I have not kept the statistics, but the number of people I encounter on a daily basis who are overweight, even by only 20 or 30 pounds, is astounding. Many people comment that they need to lose weight, but few even make the effort. The typical American diet consists of an excess of refined carbohydrates and sugars with very few, if any, fresh fruits and vegetables. Fast food restaurants and packaged unnatural foods are rampant. The rate at which people develop diabetes is accelerating. If the refined carbohydrates and sugars are eliminated, people experience dramatic weight loss, generally reduce cholesterol and triglycerides, and limit their risk of developing diabetes.
I hope that you read this e-mail and that you are at least intrigued to inquire and explore a little deeper into what I have expressed. I suggest that you attend an OA90 meeting just out of curiosity and talk to some of the people to get a perspective. I know that the organization exists in greater Boston. I think you will find it fascinating and pertinent to your work. — Andrew
A Thanks for sharing your story. As a scientist, I need to test ideas carefully before promoting a conclusion, but I share your suspicion that something in our processed food is causing a problem for many people. It is my goal to test this idea and provide the evidence, if found. Interestingly, I think major food companies would rapidly remove harmful substances from our food supply if provided evidence.
Q Dieting and intentional weight loss seem to provoke later weight gain. Is there a biological mechanism to explain this or why, at the very least, do between 80 percent and 95 percent of people put the weight back on? If this is so, should people who have gained weight just live with it and try and get as healthy as possible through other means, rather than try and reduce their fat?
A I agree with your last suggestion since most people do regain all the weight they lost quite rapidly. Unfortunately, we do not know why. My suspicion is that there is a mechanism that stimulates eating until the last spontaneously achieved weight is regained, but we need to learn how.
Q I’ve been studying for 15 years the relationship between environment (internal and external) and obesity. I’m so excited, because Dr. Corkey is on the right track. She might want to look at a possible intervening variable that produces changes in metabolism—oxygen or lack of it in blood and muscles. In other words, what is the effect of exercise on the beta cells that underwent chemical changes? What is prompting cell damage and inflamation and preventing oxygen consumption? My theory is, certain additives cause the cells to go haywire. Could it be, Dr. Corkey, that doubling the amount of oxygen in a cell could speed up pumping more sugar and starch out of the blood and muscles of an individual? That is to say, given the increase of additives and other toxins in our internal and external environment, we might well need to save the pancreas by aggressively increasing our daily movement? As a social scientist, my inquiring mind wants to know. Thank you for the splendid thought-provoking work you’re doing.
A My expectation is that increasing oxygen would only be beneficial if there wasn't enough to begin with. It is unusual in most cells to have too little. The main thing that limits respiration is need. If one is doing work or in a cold environment, we burn fuel, otherwise we don’t need to. Only fat is meant to be stored in large amounts, so we only take up enough carbohydrate to use for energy and maintain small stores that are usually full. Exercise is great, especially in stimulating fuel use by muscle without the need for insulin. That benefits the ß-cells, because they don't have to work as hard.
Q
I just wanted to tell you to keep doing your research, as I believe you are on the right track. I realize that this is only anecdotal, but I have had the experience of being overweight in this country all but five years of my adult life.
However, I lose weight dramatically when traveling and living in
Sweden, all the while consuming MORE calories (particularly their delicious candy and pastries and alcoholic beverages), doing about the same exercise as I have here. On one two-week trip, in 2000, I lost my freshman 15 pounds, all while eating all the local goodies, drinking alcohol, having a fourth meal (coffee) every day and doing some walking through sightseeing, but not much more than I did back home. I then weighed 130 pounds and was borderline underweight! Anytime I have gone there, I lose weight effortlessly and I eat pretty much the same foods I do here.
The only thing I can come up with is despite having the same eating and activity habits there as I do here, is Sweden’s restrictions on additives and hormones in their food. I believe that the next decade or two will reveal some shocking things about how hormones are affecting everything, from weight gain to early puberty onset in our children, and even some illnesses.
As you say it, most doctors believe it boils down to diet and exercise. I was 192 pounds on my 5-foot-8-inch frame when a doctor at Boston Medical Center advised me to start a 1,200-calorie-a-day diet, with no more than 30 percent of my calories deriving from fat in early 2005. I religiously recorded my meals in a diary to keep track. In addition, I worked out at least two hours nearly every day (at least five days a week, usually six). Through those next months, the weight came off extremely slowly, and so I hired at very great expense a personal trainer. Ultimately, I got down to about 164 (only one pound less than being overweight per BMI charts) after nine long months of eating practically nothing and working out constantly. After my wedding, I went on a 2,000-calorie-a-day diet because I wanted to keep my weight the same and because I was literally starving! Three months after my wedding I was at 175, another few months 185. Disheartened, I simply gave up. Today, I weigh 226 after having my first child in 2010 and am lucky with my busy lifestyle to have one full meal a day! I have found that eating more meals during my times abroad correlated with my healthier, leaner frame. Unfortunately, this country doesn’t support additive-free foods, and meals are always on the run as well!
A Your experiences are very interesting and contrary to what most clinicians would expect. Perhaps you have an unusual reaction to something in your diet in the United States but not in Sweden. It will require some research to determine if such agents can be identified, and I would be happy to test them in my cells. If you live in or near Boston, I would recommend trying an all-natural diet to test the effect. Such foods are available from farm markets and Russos.
Q How much of a role do you think high fructose corn syrup plays in the increase in obesity and diabetes? I have seen some information that links the metabolism of HFCS to high blood pressure, diabetes, inhibited leptin response (weight gain), hyperlipidemia, fatty liver, and hardening of the liver. Have you done any research into the role of HFCS?
A I have not researched it yet but plan to test diets with different glycemic index on metabolic health in animals. Studies in humans have not been conclusive to the best of my knowledge, however, I see no value in consuming HFCS.
Q I’m fascinated by your investigations into metabolism. My son has a mitochondrial disorder, was an intermittently floppy baby, and still has muscle weakness. The interesting thing that possibly relates to your research is the way that during stomach illness, mito kids have to be treated with glucose infusion, even though their blood sugar isn’t a problem in itself. I wonder if muscle myopathies could lead to a craving for “energy,” even in a larger population?
A I’m always amazed at the ability of children with various defects to crave what they need and avoid what harms them once they get past infancy. It’s a worthwhile thought to investigate. I think some cravings may reflect deficiencies as well.
Q After reading this article, I was moved and excited by the interesting science discoveries and new research. My question is, as a public health person, what can we do to prevent child obesity in the United States and at community level?
A You ask the impossible question. If only we knew. It is the reason I’m testing things that have entered our environment in the last 50 years. I am suspicious that some of these may be contributing to the problem.
Q Does stress enter into this equation at all? I’ve read that we can produce stress hormones that help cause fat to collect in the midriff area. When we exercise, I know that it alleviates stress, but are the benefits from the physical burning of calories or the reduction of stress hormones, or a combination of both?
A Exercise is great and it helps with weight maintenance as well as having other benefits. Unfortunately, moderate exercise does not cause weight loss in most people.
Q I have prediabetes without metabolic syndrome (normal BP, excellent lipid profile, thin). If I eat a low glycemic load diet that doesn’t cause gluose spikes (fasting glucose is normal), can I stave off diabetes? Or does a family history (mother and grandmother) mean it likely will arise no matter what I do?
A I can't predict, but you’re doing the right thing and might also benefit from mild exercise, since exercise allows food to be stored without requiring insulin and so preserves the ß-cells.
Q
As a registered dietitian, I often find myself frustrated by the “all
food fits” motto promoted by some large organizations. Even as a student, I believed and noted through experience that environment, food additives, and the processing of the foods that most Americans eat play a large role in the rising rates of obesity and pediatric diabetes specifically. I have always encouraged my clients to consume as many whole, unprocessed foods as feasible even within a budget (it is possible). My question is this: Have you done any research on the effect of infant formula ingredients/additives? The growth patterns of formula-fed infants is markedly different from breastfed infants, and I wonder if some of these ingredients play a role in turning on key genes that play a role in obesity and metabolic diseases?
Please keep doing what you are doing!
A Really good idea. I agree with you.
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On 17 June 2014 at 2:58 PM, Lydia L. Pineault (MED/BUSM’2014) wrote:
I am a frustrated woman of 63 yrs. old. I have a few health issues, I keep getting told by PCP that I am "FAT" even though I told her there is something very different and/or strange about my connective tissue that I do not understand! --- My Cohlesterol is high but not the bad one. My Glucose is great at 108 I think! My Triglicerides are high. I weigh 173 at 5'1" I don't have flab, and I have excellent muscle tone. --- I have recently read a whole bunch of information about a rather little known condition called Food Dependent Cushings where GIP receptors develop on the Adrenal glands, causing the Metabolism to kind of go into a tail spin! Maybe you could also consider this little known disorder and include it in some of your research!
On 9 December 2012 at 1:03 AM, Anonymous (SON) wrote:
Is there any way to contact you? I am a nursing student who loves to investigate and one of those investigations is about food, its additives and health issues they cause us, and I´d really love and appreciate your help in this matter. Is it possible?
On 16 March 2012 at 1:34 AM, Jennifer Glenister (SAR’87) wrote:
Not a question but a grateful comment. I relate to Ilana's story. For a long time I have thought carbohydrates triggered my food cravings, but it's not carbohydrates per se, but rather baked goods. Of course, that's where the multiplicity of additives are. Oats for breakfast have no additives. Pasta, few. I will follow your research with great interest. I am sure you are on to something important, and long ignored. Thanks for your marvelous mind.
On 12 March 2012 at 10:43 AM, PL Hayner wrote:
Hi Ms. Corkey - This is not a question, but a comment. We had four au pairs from Scandinavia each live with us a year at a time when our daughters were young. This was in the late 1990's. All four gained weight when they lived here and immediately lost it when they went back home. We always attributed it to the fact that the food in the U.S. had more preservatives in it than they were used to and also they said our food was generally much sweeter. And in our household we were able to have high-quality foods. So your research is along the lines of what we just assumed to be the case over a decade ago based on personal experience.
On 11 March 2012 at 4:56 PM, Kevin Stever (ENG’88) wrote:
This is more of a comment than a question. My diet used to consist of about 2800 calories a day, with proportion of 50/25/25 Carb/fat/protein. Over the past 3 years, I have transitioned to the Paleo diet, and my daily intake is now about 3500 calories and more like 20/60/20. Thru all of this, my weight and activity levels were reasonably constant. (I do lift weights more now than I did before). So, how frustrating do you find it when someone like Nestle calls it "... an Occam's razor situation" and his apparent claim that we get fat because we eat too much?
Also, I should add I just finished reading Gary Taubes' book, Good Calories, Bad Calories, where he expounds upon the weaknesses in current conventions regarding diet and obesity. I am glad there are scientists like you pursuing rigorous proofs of theories.
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