Eat Your Heart Out

Please note I have reposted this NYTimes article because it is such an important topic to understand and something that comes up often in my counseling sessions with clients. Enjoy and if you want to see the original, please click here.

Over the last several decades, it has become accepted wisdom that consuming saturated fat, the type found in meat and butter, is bad for you. Starting in the 1960s, studies showed convincingly that saturated fat raises cholesterol levels and that these elevated levels, especially of low-density lipoprotein cholesterol, or LDL (the so-called bad cholesterol), increase heart disease. Studies also showed that consuming polyunsaturated fats — safflower, corn and soybean oils — reduced people’s levels of overall cholesterol and LDL and should be encouraged.

But new studies may be upending those assumptions. Researchers with the National Institutes of Health and other organizations recently resurrected the results of a long-overlooked Australian study conducted from 1966 to 1973, in which one group of men with heart disease increased omega-6-rich polyunsaturated fat intake to 15 percent of calories, while reducing saturated fat intake to less than 10 percent. Another group of men with heart disease continued their normal diets.

The men were followed for an average of 39 months, and those on the polyunsaturated-rich diet lowered their cholesterol levels by an average of 13 percent. But they also were more likely to die, and in particular to die of a heart attack, than those who stuck with their usual diet, which consisted of about 15 percent saturated fat.

This study — the results of which weren’t fully analyzed when it was conducted in the early days of enthusiasm for polyunsaturated oils — adds to a small but unsettling body of data suggesting that consuming polyunsaturated oils, even though they reliably lower cholesterol, may nevertheless increase your risk of heart disease.

In broader terms, the new analysis muddies the already murky issue of just how diet affects heart-disease risk and health in general. Polyunsaturated oils, while decreasing cholesterol, may simultaneously promote inflammation throughout the body, says Philip C. Calder, a professor of nutritional immunology at the University of Southampton, in England, who wrote an editorial accompanying the new analysis. This inflammation may initiate heart disease and “outweigh any possible good effect” of the oils.

More fundamentally, we don’t fully understand how high cholesterol levels contribute to heart disease. Some would argue, Calder wrote in an e-mail, that “the link between cholesterol and heart disease is not actually as strong as we think.” That possibility, while startling, lends credence to other studies showing that assiduously sticking to a diet rich in fish oils, another heart-healthful fat, doesn’t necessarily protect people from heart attacks or strokes; and that those who carry extra pounds, even to the point of being slightly obese, may live longer than people who weigh less.

None of this is to say that there are no links between diet and heart disease or longevity. We know that synthetic trans fats seem particularly risky. And that the interplay between what you eat and your particular genetics may be primary. But the truth is, at this point, we don’t truly understand how it all works. Calder said the new analysis might prompt some people to recommend lowering the use of vegetable oils, substituting animal fats instead, but that he wasn’t ready to come to that conclusion.

A version of this article appeared in print on 03/10/2013, on page MM14 of the NewYork edition with the headline: Eat your heart out.

 

New Approach to Treating Type I Diabetes?

Columbia Scientists Transform Gut Cells into Insulin Factories

A study by Columbia researchers suggests that cells in the patient’s intestine could be coaxed into making insulin, circumventing the need for a stem cell transplant. Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

The research—conducted in mice—was published 11 March 2012 in the journalNature Genetics.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose. Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

Gut insulin cells express glucokinase, a key enzyme for glucose processing. Immunostaining detected insulin in red and glucokinase in green. Yellow marked merged colors.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed. Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels. If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, professor of medicine at Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells. Dr. Talchai, who works in Dr. Accili’s lab, is a New York Stem Cell Foundation-Druckenmiller Fellow.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

Inactivation of Foxo1, a gene important for metabolism generated insulin producing cells in small intestines of newborn mice, as detected by immunofluorescence in red.Drs. Talchai and Accili found that when they turned off a gene known to play a role in cell fate decisions—Foxo1—the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.

“Our results show that it could be possible to regrow insulin-producing cells in the GI tracts of our pediatric and adult patients,” Dr. Accili says.

“Nobody would have predicted this result,” Dr. Accili adds. “Many things could have happened after we knocked out Foxo1. In the pancreas, when we knock out Foxo1, nothing happens. So why does something happen in the gut? Why don’t we get a cell that produces some other hormone? We don’t yet know.”

Insulin-producing cells in the gut would be hazardous if they did not release insulin in response to blood glucose levels. But the researchers say that the new intestinal cells have glucose-sensing receptors and do exactly that.

The insulin made by the gut cells also was released into the bloodstream, worked as well as normal insulin, and was made in sufficient quantity to nearly normalize blood glucose levels in otherwise diabetic mice.

“All these findings make us think that coaxing a patient’s gut to make insulin-producing cells would be a better way to treat diabetes than therapies based on embryonic or iPS stem cells,” Dr. Accili says. The location of the cells in the gut may also prevent the diabetes from destroying the new insulin-producing cells, since the gastrointestinal tract is partly protected from attack by the immune system.

The key to turning the finding into a viable therapy, Dr. Accili says, will be to find a drug that has the same effect on the gastrointestinal progenitor cells in people as knocking out the Foxo1 gene does in mice. That should be possible, he says, since the researchers found that they could also create insulin-producing cells from progenitor cells by inhibiting Foxo1 with a chemical.

“It’s important to realize that a new treatment for type I diabetes needs to be just as safe as, and more effective than, insulin,” Dr. Accili says. “We can’t test treatments that are risky just to remove the burden of daily injections. Insulin is not simple or perfect, but it works and it is safe.”

Additional contributors are Shouhong Xuan (CUMC)Tadahiro Kitamura (Gunma University, Maebashi, Japan), and Ronald A DePinho (Harvard Medical School).

The research was supported by the NIH (DK58282, DK64819, DK63608), the New York Stem Cell Foundation, and the Russell Berrie Foundation.

The authors report no financial or other conflict of interest.

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Upon its official opening in October 1998, the Naomi Berrie Diabetes Centerat Columbia University Medical Center established a new standard of care for the 1.6 million people with diabetes in the New York area—combining world-class diabetes research and education programs with unprecedented family-oriented patient care. Named for the mother of the late Russell Berrie, founder of RUSS™ Toys, the center is today recognized as the most comprehensive diabetes research and treatment center in the tri-state region and has been designated a national “Diabetes Center of Excellence” – one of only three in the state of New York. Approximately one hundred faculty and students, affiliated with the Center, conduct basic and clinical research related to the pathogenesis and treatment of all forms of diabetes and its complications. For more information, visit www.nbdiabetes.org.

Why Is Type 1 Diabetes Rising Worldwide?

We’ve gotten sadly accustomed by now to warnings about obesity and its effect on health: joint damage, heart disease, stroke, diabetes and its complications such as blindness and amputation. We almost take for granted that as obesity increases worldwide, diabetes will also, and it is. That is, type 2 diabetes — the kind that is linked to obesity and used to be called adult-onset diabetes — is rising as obesity does.

But here’s a puzzle: Type 1 diabetes — the autoimmune disease that begins in childhood and used to be called juvenile-onset diabetes — is rising too, around the globe, at 3 percent to 5 percent per year. And at this point, no one can quite say why.

I have a column in the February Scientific American, on newsstands now and live on the web, exploring this conundrum. There is a raft of researchers exploring the issue, but so far there is only one thing they can say for sure: The increase, which began in the 1950s and accelerated in about the 1980s, is happening too fast to be due solely to genetic change. Something in the environment is driving the increase. But what?

The challenge for explaining the rising trend in type 1 diabetes is that if the increases are occurring worldwide, the causes must also be. So investigators have had to look for influences that stretch globally and consider the possibility that different factors may be more important in some regions than in others.

The list of possible culprits is long. Researchers have, for example, suggested that gluten, the protein in wheat, may play a role because type 1 patients seem to be at higher risk for celiac disease and the amount of gluten most people consume (in highly processed foods) has grown over the decades. Scientists have also inquired into how soon infants are fed root vegetables. Stored tubers can be contaminated with microscopic fungi that seem to promote the development of diabetes in mice.

None of those lines of research, though, have returned results that are solid enough to motivate other scientists to stake their careers on studying them. So far, in fact, the search for a culprit resembles the next-to-last scene in an Agatha Christie mystery — the one in which the detective explains which of the many suspects could not possibly have committed the crime.

One of the best-elaborated hypotheses suggests that lack of exposure to infections in childhood keeps the various components of the immune system from learning how to hold themselves in balance. If this sounds familiar, it’s because it’s a version of the “hygiene hypothesis” (past posts here, here and here), which says that a too-clean childhood can lead to allergies later in life.

The diabetes version of this hypothesis explores whether conditions that are a proxy for exposure to infections — not having older siblings in the house, not attending day care, being born by Caesarean — can have an effect on the occurrence of diabetes. No clear culprit has been found yet.

Some researchers say it is possible that obesity may play a role. In type 2 diabetes, tissues in the body that receive the hormone insulin, which regulates blood sugar, become insensitive to it. In type 1, the body destroys the insulin-producing cells. But an “overload” hypothesis is now suggesting that if a child is obese to begin with, that could prime the insulin-producing cells for failure, with the autoimmune attack pushing them over the edge.

If obesity is an explanation, it’s not a comforting one. As the CDC’s National Center for Health Statistics noted today, a whopping percentage of United States adults — 36 percent — are obese. And the trend is not reversing. By 2048, according to Johns Hopkins researchers whose work is discussed in my story, every adult in America will be at least overweight if the current trend continues.

That’s a lot of potential diabetes cases: a lot of glucose monitors, syringe jabs and inevitable blood sugar swings, if you care for it well, and a lot of kidney disease, heart disease, amputations and blindness if you don’t. (Not to mention effects like this image of insulin lipohypertrophy published in the New England Journal of Medicine this week, from years of administering insulin injections.) Let’s hope we find, if not a cure, at least a cause for rising type 1, before the trend gets out of control.

Reference click here.

Jay Cutler: a becoming face for diabetes

Every night before Jay Cutler goes to bed, he puts a can of Coke on his nightstand. It usually sits next to a Reese’s peanut-butter cup.

Cutler keeps the junk food close in case he feels woozy in the middle of the night and needs a sugar fix due to his glucose level dropping suddenly. Like many afflicted with Type 1 diabetes, Cutler injects himself five times a day with insulin to prevent anything like that from happening.

Still, Cutler knows it could.

It might be in his bedroom on a weeknight or on the field on a Sunday afternoon. But Cutler lives every day knowing it could.

That is among the messages Cutler delivers in a webisode to be released later this month — National Diabetes Month — that the Tribune previewed Wednesday. The revealing, three-minute video is the fourth in a series that began appearing on the Web in mid-October. The final two, all produced by Eli Lilly, the pharmaceutical company that hired the Bears quarterback as a spokesman, are in the works.

“The worst thing imaginable is to get really low and pass out in the middle of a play or in the huddle or something,” Cutler said in the latest video. “I think that would scare a lot of people — not only myself but fans and the public in general. We try to avoid it as much as possible but it’s still a reality.”

Appearing more vulnerable and candid than anybody in Chicago has seen him, Cutler looked into the camera, his eyes darting back and forth, and talked about the kind of pressure that has nothing to do with getting sacked.

Seeing Cutler discuss injecting an insulin pen into his stomach put into perspective hearing him answer questions Wednesday about how sore he was after the Browns game. Bruises go away after a couple of days. Barring a cure, his diabetes never will.

“Living with diabetes in the public eye, it makes it harder,” Cutler continued in the video. “There is no real room for error. Every day I have to be on. If I go out and have a bad game and my numbers are way off I’m going to get criticized for it. I can get real low and not know exactly what’s going on and get hit the wrong way and hurt myself. There are definitely dangers out there.”

Initially after being diagnosed in April 2008, Cutler didn’t want to discuss those dangers publicly. He told the Tribune he first needed to figure out how to live with the disease before he felt comfortable educating others.

“It was a very personal battle so I needed to take some time,” Cutler said in an interview. “I knew there would be a time when I would want to do something, especially with kids. It’s hard enough growing up these days without having to worry about an insulin pump or pricking your finger. I wanted those kids to know I was like them.”

In the video sessions shot in the offseason with a relaxed Cutler in a white button-down shirt and khaki pants, he recalled the diagnosis bringing relief because he wasn’t dying as he feared after he lost 33 pounds. He also shared how difficult it was to tell his parents, especially his mom, Sandy, who “cried for two days straight.” When Sandy Cutler wanted to come to Denver the night he had to start injecting insulin, her son intervened by saying, “Mom, I’m 24 years old.”

The biggest mental hurdle Cutler had to clear? Jabbing himself with a needle.

Seeing Cutler discuss injecting an insulin pen into his stomach put into perspective hearing him answer questions Wednesday about how sore he was after the Browns game. Bruises go away after a couple of days. Barring a cure, his diabetes never will.

“Living with diabetes in the public eye, it makes it harder,” Cutler continued in the video. “There is no real room for error. Every day I have to be on. If I go out and have a bad game and my numbers are way off I’m going to get criticized for it. I can get real low and not know exactly what’s going on and get hit the wrong way and hurt myself. There are definitely dangers out there.”

Initially after being diagnosed in April 2008, Cutler didn’t want to discuss those dangers publicly. He told the Tribune he first needed to figure out how to live with the disease before he felt comfortable educating others.

“It was a very personal battle so I needed to take some time,” Cutler said in an interview. “I knew there would be a time when I would want to do something, especially with kids. It’s hard enough growing up these days without having to worry about an insulin pump or pricking your finger. I wanted those kids to know I was like them.”

In the video sessions shot in the offseason with a relaxed Cutler in a white button-down shirt and khaki pants, he recalled the diagnosis bringing relief because he wasn’t dying as he feared after he lost 33 pounds. He also shared how difficult it was to tell his parents, especially his mom, Sandy, who “cried for two days straight.” When Sandy Cutler wanted to come to Denver the night he had to start injecting insulin, her son intervened by saying, “Mom, I’m 24 years old.”

The biggest mental hurdle Cutler had to clear? Jabbing himself with a needle.

“That’s where it gets a little iffy,” he said.

To get him in the proper frame of mind for his new reality, Cutler thanked his quarterbacks coach at Vanderbilt, Jimmy Kiser. Kiser, 51, is one of the 3 million Americans afflicted with Type 1 diabetes and has lived with it for more than 20 years.

“The first thing he said was, ‘You’re going to be fine,’ ” Cutler said.

John Holcombe, a research physician for diabetes care affiliated with Eli Lilly, was more effusive given Cutler’s line of work.

“People like Jay Cutler are phenomenal,” Holcombe said in a phone interview. “Exercise is critical in treating it but it also plays havoc with your blood-sugar level.”

It is why Cutler pricks his finger so often to make sure his level is between the acceptable range of 90-120 or 130-150 during games. It is why Cutler might be prone to mood swings after exertion. It is why it’s hard to look at No. 6 the same without thinking of the numbers he checks five times a day.

“I’m still struggling with this,” he said in one of the webisodes. “Over time you get used to and it becomes part of you. I’m not to that point yet.”

Showing a sense of humor, Cutler recounted cleaning out his refrigerator within days of the diagnosis. Type 1 diabetes prevents the pancreas from producing insulin required to metabolize sugar from food and convert it into glucose the body uses for energy.

“I miss a lot of foods,” he said. “I used to love desserts. I miss sweet tea, lemonade. Do I ever cheat? Yes, I do. Reese’s peanut-butter cups is my cheating food.”

Sounds like a commercial pairing. But for now, Cutler is more interested in education than endorsements — a point he made directly into the camera.

“I’d love to use my story to inspire kids who get diabetes at 4 or 5 years old and they think it’s the end of the world, they can’t have dreams or do what they want to do in life,” Cutler said. “It’s entirely false.”

The truth? We have marveled at many Cutler highlights since he became a Bear. But he never has been more impressive on video than when discussing his life as a diabetic.

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