Category: Diabetes 101

A new study published in Annals on Oncology, a cancer-focused research journal, has found that trastuzumab (Herceptin) — a breast cancer drug — increases the risk of heart complications. Women who have diabetes and women with a history of heart disease are especially at risk.

The study analyzed the medical data of 45 women between the ages of 70 and 92 who had been treated with trastuzumab starting in 2005. Researchers found that 26.7% of the patients demonstrated heart problems that were caused by the drug. This rate was slightly higher than the rate demonstrated in younger and healthier women during the drug’s clinical testing phase. Trastuzumab caused 33% of the women with histories of heart disease to develop asymptomatic or symptomatic heart problems while only 9.1% of women without a history of heart disease developed those problems. Similarly, 33.1% of women with diabetes experienced new heart problems compared to only 6.1% of non-diabetic women. All but one of the women recovered fully once treatment with the drug was discontinued; five of the women renewed their treatment with the drug upon the disappearance of the problems.

Trastuzumab is currently the most-used medication for treating women with HER2 positive breast cancer, or the type of cancer that causes expression of the HER2 protein on the surface of the cancer cells. Elderly women are most at risk for breast cancer but trastuzumab has also been tested on younger, healthy women in clinical trials.

The study was conducted by Dr. César Serrano, a clinical fellow in Barcelona, Spain at the University Hospital Department of Medical Oncology Breast Cancer Centre. “This is the first study to specifically assess trastuzumab-related cardiac toxicity and the cardiovascular factors that are associated with an increased risk in a selected population of elderly breast cancer patients,” said Serrano of the study.

“Trastuzumab is generally well-tolerated and, although there are some concerns about it causing heart problems, until now few risk factors have been identified among patients in clinical trials, most of whom are usually younger than 70 years and have good general health,” continued Serrano. “Our study has demonstrated a significantly increased incidence of cardiac events among patients aged 70 and over with cardiovascular risk factors such as a history of cardiac disease and diabetes.

“Approximately 70% of all newly diagnosed cancers occur in patients older than 65 and, given the expected increase in the absolute number of elderly cancer patients over the coming decades in Western countries, there is an unmet need for information about the efficacy and safety of anti-cancer treatments in daily clinical practice. Data obtained in this report can serve to advise clinicians to be aware of symptomatic and asymptomatic cardiac dysfunction in elderly patients. We think that it is reasonable to refer elderly breast cancer patients to a cardiologist if one or more cardiovascular risk factors are present before or during treatment with trastuzumab. Moreover, a closer surveillance of early symptoms and cardiac function is highly recommended.”

Patients developed both asymptomatic and symptomatic cardiotoxicity after administration of trastumuzab. Asymptomatic cardiotoxicity occurs when no obvious symptoms of heart problems are apparent but scanning or echocardiography reveals that the heart’s left ventrible drops in function by 10% or more. Symptomatic cardiotoxicity shows apparent physical symptoms such as swelling of the limbs and shortness of breath; this type of cardiotoxicity includes congestive heart failure.

“One of the main characteristics of trastuzumab cardiotoxicity is its reversibility,” said Serrano. “It is a well-known phenomenon that differs from other chemotherapeutic agents such as anthracyclines. Reversibility normally happens with treatment discontinuation, but also can also occur spontaneously. The decision to reintroduce trastuzumab, or to continue with it, must be taken case-by-case together with a cardiologist.”

A research team at Vienna General Hospital’s University Department of Internal Medicine III has found that preemptive insulin therapy drastically lowers the risk of patients developing diabetes mellitus, or Type 2 diabetes, after a kidney transplant. As of now, up to 30 percent of patients receiving kidney transplants develop diabetes within a year of the transplant.

“We give the patients insulin immediately after the transplant even before diabetes mellitus occurs,” says Marcus Säemann of the Clinical Department of Nephrology and Dialysis. “The new thing about this is that we are giving insulin to non-diabetics and are hereby treating patients preventatively.”

The research group has proven this approach to be successful. A selection of 25 patients who were treated with preventative insulin therapy for three months after the transplant showed about a 75% decrease in their chances of developing diabetes. A control group that was not administered insulin treatment but treated according to the current standards for kidney transplant patients had a 45% chance of developing diabetes within the year following the transplant. “This is sensational data that we have obtained from thousands of blood sugar measurements,” said Manfred Hecking, a supervisor for the study.

The research team’s efforts did not go unnoticed. Their initial results caught the attention of the University of Michigan as a research partner. Starting at the end of 2011 the United States National Institutes of Health (NIH) will sponsor the study and expand upon it across multiple research facilities throughout the world. The study will last three to five years and will be coordinated by Hecking and Säemann. Research facilities in Germany, France, Italy and Spain will contribute to the effort.

Kidney transplant patients often develop diabetes mellitus in the year following the transplant because of increased stress from the surgery and also from the high levels of immunosuppressant drugs given to the patient to prevent acute organ rejection. “The patient shall be, so to say, swept away from a wave of acute disease,” says Säemann. There are currently no effective treatments in use for the development of diabetes following a transplant. Diabetes drastically shortens the patient’s life expectancy and quality of life in addition to reducing the lifespan of the transplant organ. The results of this new study provide hope for those waiting on kidney transplants that they may not have to face diabetes in their lifetimes.
Kidney transplants typically extend the life of patients by 10-15 years. Even elderly patients who receive transplants live four more years on average than if they had stayed on dialysis. Patients who receive kidney transplants see their quality of life improve greatly. They feel less fatigued and can eat a less restrictive diet.

Kidney transplant patients must take a variety of immunosuppressant medications to prevent the body from rejecting the new kidney. The most common combination of medications includes tacrolimus, mycophenolate, and prednisone; patients have to take these expensive medications for the remainder of their lives. Amid the chances of organ rejection and development of diabetes, kidney transplant patients are also at risk of infections and sepsis, lymphoma, hair loss, acne, obesity, and raised cholesterol. Preventative insulin therapy may one day eliminate the development of Type 2 diabetes as a risk that kidney transplant patients must take.

“Our study is a great advance for transplant medicine generally,” said Säemann. The Vienna General Hospital currently treats about 1,100 patients who received kidney transplants with outpatient therapy.

Physicist Aaron Keller and his colleagues at the Helmholtz-Zentrum Dresden-Rossendorf in Germany and at Aarhus University in Denmark have reported a significant advancement in the possibility of treatment for Type 2 diabetes and Alzheimer’s disease. The researchers are studying amyloids, or clumps of proteins that form in the body, which seem to be closely related to the development of these diseases. If doctors could prevent these clumps from forming they might have an effective defense against diabetes and Alzheimer’s.

Amyloids form on the surfaces of different types of cells, namely the cells of the pancreas in diabetes and the brain in Alzheimer’s. Physicians currently do not have imaging technology that can view these processes as they occur, but Adrian Keller and his colleagues are working to recreate these processes artificially in tests at the Interdisciplinary Nanoscience Center in Aarhus, known as “iNano.”

Recreating the processes on an artificial surface is difficult because of the properties of the cell surfaces in organisms. Cells can be hydrophilic or hydrophobic, which means they either attract water or repel water, respectively.

Adrian Keller has used mica crystal to recreate the amyloid-forming process. He has configured the surface of the mica so that positively-charged atoms of argon gas are only able to slightly penetrate into the surface of the material. “This chemically activates the surface without significantly changing the roughness,” said Keller of the first step of the process. The roughness of the surface would also influence the possibility that amyloids could form there.

Next, Keller places the processed mica into boxes and stores them in the lab for several weeks. While stored away, the surface of the mica adsorbs hydrocarbons in the air around it. The surface of the mica gradually becomes hydrophobic instead of hydrophilic; after about three months, the mica is totally hydrophobic (water repellent).

Keller conducts experiments during these three months. He places amylin, a small protein, on the mica. This protein is also produced by certain pancreatic cells along with insulin. When an organism develops Type 2 diabetes, its body’s reaction to insulin becomes less effective. The organism’s blood sugar elevates and the pancreas produces more insulin and amylin in response to the increased blood sugar. Some of the amylin proteins assume a concave “bowl” shape and influence nearby amylin proteins to follow suit.

The misshapen amyloid proteins begin to stick together, forming amyloids. These clumps destroy pancreatic cells and reduce insulin production, which causes the other cells to ramp up their own insulin produciton. The cycle continues and the organism’s insulin production mechanism can be devastated.

In Keller’s experiments, the amylins clump together on the surface of the mica according to the nature of the crystal’s surface. If the experiment has just been started and the surface is still hydrophilic, the amylin proteins form clusters called “fibrils.” However, if the mica has been gathering hydrocarbons and the surface is becoming hydrophobic, the amylins increasingly form clumps called “oligomers.” Both oligomers and fibrils work to destroy the surface of the cells, though they work through different mechanisms. In either case, when the clumps form on pancreatic cells, they inhibit insulin production.

Keller’s experiments have allowed researchers to view the creation of amyloid clumps for the first time in history. This new technology may pave the way for researchers to develop methods of preventing the clumping process and thus preventing diabetes and Alzheimer’s.

Tampa Bay Rays outfielder Sam Fuld made the day of one six-year-old boy when he visited Andrew Cordovez in an examination room. Fuld had one special connection with the young boy: they both have Type 1 diabetes.

Andrew received an autograph picture of Fuld and a baseball. “That was cool,” said Andrew. “He’s a really good player.”

Fuld visited the newly-founded diabetes center at the University of South Florida, taking a two-hour tour of the 10,000 square foot facility. The diabetes center, which opened last month, is part of the Carol & Frank Morsani Center for Advanced Healthcare.

Officials at the University of South Florida hope that the facility will propel them to the forefront of research, education and treatment of diabetes. The disease affects more than 23 million people around the country.

According to the dean of the USF College of Medicine, Dr. Stephen Klasko, the university is quickly becoming a national leader in diabetes research. The university has received more than $400 million for its efforts in studying diabetes but did not have a clinical facility. The new diabetes center cost $2 million; university funds and donations paid for the facility.

Facility officials who met Fuld included Dr. Klasko, Judy Genshaft (USF President) and Drs. Jeffrey Krischer and Henry Rodriguez (heads of the new center). The group all wore Tampa Bay jerseys.

Fuld visited the center with wife, Sarah, and son, Charlie, in tow. Charlie is 20 months old and does not have diabetes but his parents are wary since the disease is hereditary and Charlie is at increased risk.

“It’s a cause near and dear to my heart,” said Fuld of diabetes. He was diagnosed with Type 1 diabetes at only 10 years old. But like Andrew Cordovez, Fuld was visited by an athlete with Type 1 diabetes when as a young boy. Fuld met Bill Gullickson, a professional pitcher who also had Type 1 diabetes, when Fuld was 12 years old.

Gullickson had encouraging words for Fuld. “He told me I could do anything, academically and athletically, I wanted to,” said Fuld of the meeting.

Fuld took the advice to heart and made the best of his situation. Now 29 years old and known as “Super Sam,” Fuld’s athletic style of fielding has garnered attention and adoration from fans. His athleticism belies the fact that his diabetes requires him to perform regular blood sugar checks on himself, six to seven times a day, including two to three times in the middle of games. Fuld also administers his own insulin shots four to five times every day. “I keep those up in the clubhouse in the locker room. So if you see me running up the tunnel to go to the locker room, that’s probably why,” said Fuld.

According to Fuld, he has an advantage in that baseball is more flexible in addressing his diabetes. “All that down time in the dugout. So I get plenty of time to check my sugar. And I give myself shots probably four to five times a day.”

“My outlook on it, all along was just look at it as a challenge,” Fuld said of living with diabetes.

Fuld isn’t the only athlete who achieved success despite being diagnosed with diabetes. Other diabetic athletes include NFL quarterback Jay Cutler, Indy car driver Charlie Kimball, Olympic gold medalist swimmer Gary Hall Jr. and two tennis Hall of Famers: Billie Jean King and Arthur Ashe.

Mannkind (MKND) stock rose more than 20%, showing increased investor confidence after the fledgling pharmaceutical company confirmed that it has received approval from the FDA for clinical trials on its key product. Mannkind received FDA clearance to conduct efficacy trials on a new inhaled insulin product dubbed Afrezza, designed to treat patients with both Type 1 and Type 2 diabetes.

Mannkind has navigated rough financial waters, seeing its stock fall upon news of delays in developing the drug but the company has seen its fortunes reversed in light of the new agreement regarding the design of the clinical trials. One trial will compare Mannkind’s new inhaler design with the MedTone inhaler, subject of previous trials. The FDA has requested data on the impact of various inhalers on the cardiovascular systems of users.

Mannkind’s fortunes have hinged on Afrezza and the market for inhaled insulin. The company has suffered numerous setbacks to the development and approval of Afrezza amidst a general reduction in interest of inhaled insulin. Eli Lilly and Pfizer backed out of the inhaled insulin race; chairman and CEO of Mannkind, Alfred Mann, believes that there is a market for inhaled insulin. Mannkind currently has no products on the market.

“We are very encouraged and pleased with this outcome,” said Mann of the FDA approval. “Our attention now turns to the execution of these trials. The protocol for Study 171 has already been sent to Institutional Review Boards and the protocol for Study 174 is being finalized and will be distributed to our sites shortly,” Mann said, referring to the two recently approved trials.

Mannkind focuses primarily on treating patients with cancer and diabetes. While it has no products on the market, it is hopeful that Afrezza will give it a heady boost. The medication is an meal-time inhaled insulin.

Inhaled insulin was on the market in the United States from September 2006 through October 2007. The first FDA-approved inhaled insulin product, called Exubera, was approved in January 2006 and marketed by Pfizer. Studies determined that inhaled insulin was no more effective than subcutaneously injected insulin. Both Type 1 and Type 2 diabetics would still require injections of long-lasting insulin in addition to inhaled insulin. The possibly of dosing errors with inhaled insulin, along with its prohibitive cost, caused major players Pfizer and Eli Lilly to discontinue their programs and market interest in the product dwindled. Mannkind is the only company still pursuing production of inhaled insulin with its Afrezza product.

Mannkind received notification from the FDA in January that additional clinical trials would need to be performed before Mannkind received the green light for marketing Afrezza. The product was first submitted for approval in March of 2009, when the FDA notified Mannkind that it would need to provide additional data before trial approval was granted.

The approval of the trials is a boon for Mannkind, which saw losses of $44.5 million in the second quarter of 2011 and $42.3 million in the same quarter last year. Per-share losses saw no change at 37 cents. Mannkind did not see any revenue in the second quarter of 2011 compared with revenue of $93,000 in the same quarter of 2010.

In the wake of the news, company shares rose 47 cents to $2.84.

Mannkind has its corporate headquarters located in Valencia, California, with the manufacturing facility for Afrezza located in Danbury, Connecticut. Though technically founded in 1991, the current form of Mannkind was founded in 2003 with a merger between three of Alfred Mann’s companies. Mann has invested over $900 million in the company.

Researchers at York University have discovered a new protein that might hold the answer to the problem of controlling blood sugar and appetite.

The protein is called nesfatin-1 and Suraj Unniappan, an associate professor in the York Department of Biology, Faculty of Science & Engineering, is exploring its characteristics. The protein occurs naturally in large amounts in the brain; Unniappan administered rats with the protein and found that they were more active and ate less while their metabolisms were more likely to use stored body fat to generate energy. The administration of the protein in rats and mice also stimulated pancreatic beta cells into secreting insulin.

“[The rats] actually ate more frequently but in lesser amounts,” said Unniappan, who was chosen by York’s neuroscience graduate diploma program and also received the Canadian Institutes of Health Research New Investigator Award. “In addition, they were more active and we found that their fatty acid oxidization was increased,” added Unniappan. “In other words, the energy reserve being preferably used during nesfatin-1 treatment was fat. This suggests more fat loss, which could eventually result in body weight loss.” The rats’ metabolisms switched to using fat as their preferred energy resource, making it more likely that body fat would be reduced through activity.

Unniappan’s findings were published in the form of two recent articles in Endocrinology and in the Journal of Endocrinology.

A research team from Japan discovered nesfatin-1 in 2006. It has been shown in the past that nesfatin-1 regulates appetite and the storage of body fat when it is injected into the brains of rats and mice.

Unniappan showed through his research that, in addition to regulating body fat, nesfatin-1 stimulates the islets of Langerhans in the pancreas into producing several hormones, including insulin. The pancreas then secretes the insulin into the bloodstream, which works to reduce blood sugar levels.

Unniappan’s research team had previously shown the link between nesfatin-1 and diabetes in mice. Not only could nesfatin-1 be used to stimulate the production of insulin in mice, but the islets of Langerhans in mice with Type 1 diabetes showed decreased nesfatin-1 production while those in mice with Type 2 diabetes displayed increased nesfatin-1 production. In patients with Type 1 diabetes, the destruction of pancreatic cells causes the body to stop producing insulin while Type 2 diabetes sees patients becoming insulin resistant.

Unniappan focuses his research on discovering and analyzing metabolic hormones on fish and mammals. “We call this the gut-brain axis,” he says. “While the brain is involved in many factors that regulate our energy balance, the gut is also responsible for many neural and endocrine signals responsible for regulating hunger, satiety and blood sugar levels. A major question we’re trying to address is how these peptides act and interact with other peptides in the endocrine network – which is so complex – in order to maintain steady blood glucose levels and body weight.”

Unniappan believes that understanding this gut-brain axis is the key to developing new medications and treatments for obesity and diabetes. However, he warns that nesfatin-1 may not be used pharmacologically any time soon. “New hormone-based treatments that would suppress body weight and blood sugar would be very desirable. However, we are far from developing nesfatin-1 as a candidate molecule. Our current research focuses on further exploring the therapeutic potential of nesfatin-1 in metabolic diseases with debilitating complications.”

Patients suffering with Type 2 diabetes are commonly prescribed a combination of medications designed to lower LDL cholesterol, or bad cholesterol, and their triglyceride levels while simultaneously raising HDL cholesterol, or good cholesterol. It has been accepted by the medical community for quite a while that this combination of medication mitigates the effects of diabetes by lowering the risk of heart attacks.

However, that knowledge has been challenged recently in the New England Journal of Medicine. The combination of medication was recently evaluated for effectiveness by a Food and Drug Administration panel and three physicians who served on the panel say that these drugs have not demonstrated any effectiveness in lowering the risk of heart attacks in Type 2 diabetics who have higher levels of cholesterol.

The drugs are called fibrates and doctors prescribe them to raise HDL cholesterol levels while lowering blood triglyceride levels.

Fibrates are commonly prescribed to diabetics as companion medications to statins — drugs that lower levels of LDL cholesterol. There are three fibrates approved for use in the United States by the FDA, including gemfibrozil (Lopid), fenofibrate (Tricor) and fenofibric acid (Trillipix). The sales of these three drugs run into the billions of dollars, reflecting their popularity with physicians prescribing them for patients with diabetes or obesity.

“There have been few studies regarding the clinical outcome efficacy of fibrates,” said Sanjay Kaul, MD. Kaul is one of the doctors challenging the hypothesis that fibrates reduce risk of heart attacks and is director of the Cardiology Fellowship Training Program at Cedars-Sinai Heart Institute. According to Kaul, “Thousands and thousands of Americans take fibrates every day but so far, there are no long-term studies showing that fibrates lower cardiovascular risk or improve survival among diabetes patients who are also on statins.”

The doctors have suggested that more studies be performed to determine the efficacy of fibrates. However, they did recommend that doctors continue to prescribe the fibrate-statin combination of medication to diabetics who are at elevated risk for heart attacks, but only after the patients have been treated with statins to establish control of LDL cholesterol levels.

High blood triglyceride levels have been demonstrated to be a risk factor for heart disease and stroke as well as atherosclerosis, or hardening of the arteries. Triglyceride levels are increased by diets heavy in carbohydrates, such as those where carbohydrates make up 60 percent or more of caloric intake, especially in patients who already exhibit insulin resistance. Patients with high triglyceride levels can reduce those levels with exercise and by consuming omega-3 fatty acids from sources such as fish and flax seed oil. While United States residents are recommended to eat 3 grams of omega-3 fatty acids every day, most people do not consume that amount. Consumption of omega-3 fatty acids should also be balanced with consumption of omega-6 acids.

Clinical trials have shown that although treatment with fibrates alone does reduce the risk of non-fatal heart attacks, it does not reduce the risk of mortality. Fibrates have been used since the 1930s but their mechanism of reducing LDL cholesterol was not fully understood until the 1990s, when it was shown that they activate a type of cellular receptor called PPARs that regulate carbohydrate and fat metabolism. When activated, PPARs actually alter cellular DNA to increase fat metabolism, or the body’s use of stores of body fat to provide energy.

Fat Levels Higher in Thin Children” width=”290″ height=”249″ />A study conducted by Children’s Hospital Boston and the Joslin Diabetes Center has revealed that levels of “brown fat,” a healthy type of fat that appears in children, increase in puberty and then decrease after. The study also showed that thinner children have higher levels of brown fat. The study was published in the Journal of Pediatrics.

Researchers used PET scans to reveal the locations and concentrations of brown fat in children. Brown fat is unlike white fat in that it actually contributes to the burn-off of energy instead of functioning as an energy storage mechanism.

The study has important implications for fighting diabetes in children. “Increasing the amount of brown fat in children may be an effective approach at combating the ever increasing rate of obesity and diabetes in children,” said Aaron Cypess, MD, PhD. Cypess was the senior author of the paper in addition to being assistant investigator and staff physician at the Joslin Diabetes Center.

This is not Cypress’ first time investigating the role of brown fat in metabolism. His team showed in a 2009 study published in the New England Journal of Medicine that brown fat plays a role in the metabolism of adults as well. Prior to this study, it was accepted that brown fat appeared only in children and babies, but the study proved that brown fat is also found in between 3 and 7.5 percent of adults. Women have a greater chance of storing brown fat.

Cypess’ newest study involved PET scans of 127 children from ages 5 to 21. The researchers found active brown fat in 44 percent of the children; the incidence of brown fat was about the same for boys and girls. Children in the 13 to 15 year old range were most likely to have active brown fat stores, and theirs were the most active. The study also showed that BMI seemed to have an effect on the activity of brown fat: the heaviest children showed the least amount of brown fat activity.

Cypess’ previous study of brown fat in adults showed that brown fat stores were more active in the winter since it had to burn more energy to maintain homeostasis, or the “stabilization” of body temperature. The study of brown fat in children, however, showed that their brown fat stores were active at the same rate throughout the year. The authors of the study said that the decrease in brown fat activity from childhood to adulthood shows that it plays a role in the metabolism of children in addition to weight maintenance and energy balance.

“We believe that the ability to non-invasively evaluate brown fat activity in vivo with PET imaging provides a better understanding of its prominent role in pediatric physiology, and may possibly provide insights into the treatment of childhood obesity,” said Laura Drubach, MD, first author of the study and physician at the Children’s Hospital program in Nuclear Medicine and Molecular Imaging.

Cypess said that treating childhood obesity through this new knowledge would likely involve attempting to increase the activity of brown fat through non-pharmacological methods, such as by lowering the temperature in households or through the intake of certain foods. If those methods were not successful, medication may be necessary.

The Joslin Diabetes Center conducted a study in 2010 which showed that certain mice cells could be turned into brown fat cells. Cypess has hope that the studies will provide new answers in treating childhood obesity: “We might be able to combat the obesity and diabetes epidemics if we find safe ways of increasing brown fat activity. This might be an additional tool in the fight.”

The Journal of Sexual Medicine recently published a new study demonstrating that weight loss in men with Type 2 diabetes is more than just a healthy choice. It also improves sexual health, increasing erectile function and desire while lowering the risk of developing urinary tract symptoms.

The research team at the University of Adelaide, led by Professor Gary Wittert, MBBch, MD, FRACP, FRCP, conducted the study on 31 men who were diagnosed with Type 2 diabetes and classified as obese. The study lasted eight weeks and utilized two mechanics of weight loss: the men either ate a low-calorie diet based on meal replacements or a reduced carbohydrate, high protein, and low fat diet designed to decrease the patient’s nutritional intake by 600 calories a day.

The results of the study showed that even with just a 5 percent weight loss after eight weeks of the diet, the diabetic men demonstrated a decrease in sexual and urinary problems. The men’s’ sexual health continued to improve for a full year.

“Our findings are consistent with the evidence that not only erectile function, but also lower urinary tract symptoms are a marker of cardio-metabolic risk,” said Wittert. “The evidence that improvement can be achieved by modest weight loss, in particular when a diet is of high nutritional quality, is of public health significance in framing public health messages that resonate with men.”

Wittert hopes that framing weight loss in diabetic men as improving sexual function and health will be an effective wake-up call to men that they should work to lose weight. Since even a small amount of weight loss provides tangible benefits, Wittert believes that these findings will provide new data that will motivate men, especially those with diabetes, to take control of their weight loss and make a concerted effort.

“This important paper supports earlier publications that lifestyle is relevant and can positively affect sexual function,” said Irwin Goldstein, Editor-in-Chief of the Journal of Sexual Medicine, where the study was published. “At a time when oral drugs are very popular, it can now be shown that weight loss is an important non-pharmacologic therapeutic intervention in restoring erectile and urinary function and cardiovascular health,” continued Goldstein. “Obesity is an epidemic, and such data reinforce the positive relationship between eating right, losing weight, improved sexual function and voiding and overall cardiovascular health.”

According to the Harvard Medical School Joslin Diabetes Center, diabetes is commonly associated with sexual dysfunction in not only men but women as well. Thirty million American men experience impotence (or erectile dysfunction, the inability to achieve or maintain an erection); half of the 10 million American men diagnosed with Type 2 diabetes will suffer from impotence. Men with diabetes are two to three times more likely to suffer from impotence than non-diabetics. However, if a man’s diabetes is under control, he only has a 30 percent chance of suffering impotence.

Nerve damage is another risk factor in sexual for men with diabetes, with 50 to 70 percent of men with nerve damage experiencing impotence. Since sexual arousal occurs when a sexual stimulus causes the body’s autonomic nerves to signal more blood flow to the erectile tissue in the genitals, damage to the nervous system can impair this process and prevent the signals from ever reaching their destination.

The smell of that hamburger or steak (unprocessed meat) on the backyard grill is tantalizing, but we all know that we’re not supposed to have too much of it simply because it’s not great for our health for a number of reasons, to include the susceptibility to type 2 diabetes.  But, it’s now known that that hotdog (processed meat) lying beside that hamburger on the grill might be a little bit worse for your health than the burger or steak, including your susceptibility to type 2 diabetes.

A new study has shown that eating either unprocessed and/or processed meat can increase a person’s susceptibility to type 2 diabetes.  Processed meats are meats such as hotdogs, deli meats, bacon, or sausage.  Unprocessed meats are meats such as beef; in other words, that hefty steak on your plate that smells so good when it’s cooking.

But, the conclusion of this study indicates that the consumption of processed meats, which are usually high in sodium and nitrites, should be cut back dramatically, and that the intake of unprocessed red meat should be reduced.

The study was conducted at the Harvard School of Public Health and was led by An Pan, a Research Fellow in the Harvard School of Public Health’s Department of Nutrition.  The conclusion of this study will be published in the American Journal of Clinical Nutrition.

These study conclusions were cultivated from questionnaire responses that involved a long time period and a myriad of participants.  For 20 years, 37,083 men were followed in the Health Professionals Follow-Up Study; for 28 years, 79,570 women were followed in the Nurses’ Health Study 1; and for 14 years, 87,504 women were followed in the Nurses’ Health Study 11.  Included in the study’s conclusions were combined data from existing studies for a total of 442,101 participants, and 28,228 of those participants developed type 2 diabetes during the study; therefore, there were many, many people involved in these studies, and these study questionnaires covered a very long period of time.

The study concluded that one daily serving of 100 grams of unprocessed red meat (example:  steak, the size of a deck of cards) increased the percentage of a diagnosis of type 2 diabetes by 19 percent.  But, one daily serving of processed meats (example:  one hotdog) increased the percentage of a diagnosis of type 2 diabetes by 51 percent.

Senior author on the paper, Dr. Frank Hu, stated, “Clearly, the results from this study have huge public health implications given the rising type 2 diabetes epidemic and increasing consumption of red meats worldwide.”  Dr. Hu added, “The good news is that such troubling risk factors can be offset by swapping red meat for a healthier protein.”

There are many ways an individual can reduce their intake of unprocessed red meat, or that steak on your plate.  Unprocessed meats are also a big part of the backyard cookout, that famous hotdog on a bun, and it can also be swapped out for more nutritious food.

Red meat is high in protein, a necessity for the body to function properly, but protein can be found in many healthier choices.  An individual could use nuts instead of red meat on a number of occasions, switch to low-fat or fat-free dairy products, and increase one’s consumption of whole grains.  Fish is a great source of protein, as is legumes.  Nuts are a healthy option for protein, but are high in calories, so an individual would take that into account in their caloric intake for the day.

Over 25 million Americans have type 2 diabetes, which is usually controlled through diet restrictions, increased exercise, and medication, if necessary.  If left untreated, type 2 diabetes can lead to the same very serious complications of the body that type 1 diabetes causes, such as heart problems, kidney problems, vision problems and nerve problems (neuropathy).

“Our study clearly shows that eating both unprocessed and processed red meat – particularly processed – is associated with an increased risk of type 2 diabetes,” Pan stated.

This study result might make you pause a little in the supermarket and choose a salmon steak over a T-bone, scallops instead of that hotdog.  If a salmon steak isn’t to your taste, you can make salmon patties with canned salmon (good source of healthy protein) mixed with cooked brown rice (good source of whole grains), egg whites (more protein), and some grated onion and fresh ground pepper for zip.  You might even stick your nose in the air and breeze right past the processed foods case (baloney, hotdogs, bacon), and make a fat-free cottage cheese and egg white omelet instead.  Each little healthy food choice helps in the long run, but avoidance of known health hazards is a giant step in the right direction for healthy eating, which might lead to a longer and healthier life.

Support for this study was provided by the National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Diseases, and the National Heart, Lung and Blood Institute.