Aspirin Use In Patients With Diabetes Requires Careful Consideration

ASPRIN has been proven to be effective in reducing the risk for cardiovascular events; however, patients with diabetes are a unique population that requires special considerations before treatment. While aspirin therapy is recommended, further exploration into dosing strategies, stronger antiplatelet therapy and the clinical interaction between aspirin and patients with diabetes is essential.

“A landmark stage published in 1990 really set the stage as to why diabetics are different and why antiplatelet therapy may be effective in this population,” Jeffrey S. Berger, MD, of the NYU Cardiac and Vascular Institute at the NYU Langone Medical Center in New York, said during a presentation. “Compared with non-diabetics, diabetics had greater platelet activity.” He was speaking at the American College of Cardiology (ACC) 60th Annual Scientific Sessions in New Orleans earlier this week.

Berger noted that one study currently being conducted at NYU suggests that markers of platelet activity correspond well with an increasing prevalence of diabetes. Data from other trials support this association, and these results raised an important question: Can measuring platelet activity prevent a future event? At present, this question remains unanswered but warrants further investigation, he said.

A Closer Look

In addition, physicians must consider dosing when treating with aspirin. Berger explained that aspirin inhibits COX-1 and, thus, reduces amounts of platelet activation and vasal constriction. However, aspirin also reportedly inhibits prostacyclin, which causes the opposite effect on thromboxane. Therefore, Berger emphasized that physicians be careful not to prescribe too much aspirin, even among patients with diabetes.

Many physicians believe that patients with diabetes respond differently to aspirin than those without the disease. Berger pointed out that this is a misconception, however, and cited data from one study indicating no significant differences in aspirin’s interaction in patients with diabetes compared with those without the disease. Most importantly, he said, research showed no significant differences in how aspirin prevents cardiovascular (CV) events between patients with the disease and those without.

Despite aspirin’s efficacy, the medication has been linked with serious adverse events, such as hemorrhagic stroke, with research showing a low number needed to treat and a low number needed to harm.

“Thinking about it this way, for every 1,000 patients treated for 5 years, three ischemic events are avoided, but three major bleeds are caused,” Berger said. “So when you’re thinking about who should get aspirin, you should think about the absolute benefit and the absolute risk.”

Future Studies

Because patients with diabetes are a special population, researchers and physicians should consider whether stronger antiplatelet therapies are required. Berger said future studies must take other medications into account. Statins, fish oil and ACE inhibitors, for example, have antiplatelet activity and this effect may be sufficient for patients with diabetes.

He also noted that dosing strategies may have to be altered, such as administering aspirin twice a day instead of once daily. Additionally, improved tools for monitoring aspirin’s effect on preventing CV events would also be extremely valuable, according to Berger.

“There is no significant clinical interaction between diabetics and non-diabetics regarding the effect of aspirin, how diabetics may need a different strategy of dosing or a stronger antiplatelet therapy, and I think future clinical trials should address these issues,” Berger said.

Commenting, Rhonda Cooper-DeHoff, Associate Professor in the Department of Pharmacotherapy and Translational Research at the Colleges of Pharmacy and Medicine, University of Florida, said: “Dr. Berger raised some very provocative points, particularly about what dose of aspirin should be used. The fact that he showed data that suggest that a lower dose of 81 mg may not be as effective as we think in patients with diabetes is an important take-home message. I don’t think that message is really out there.

“The other very provocative point he raised is that we need better tools to monitor the effect of aspirin like we have to monitor the effect of cholesterol-lowering and blood pressure-lowering drugs. We are really missing that with aspirin. Some of the focus for future trials that he discussed would be incredibly useful to the overall care for the patient with diabetes.”

Reported by Endocrine Today

Controlling Diabetes May Reduce Cancer Risk and Death

There are myriad benefits from avoiding diabetes through exercise, diet and maintaining a healthy body weight. A new NIH-AARP Diet and Health Study has confirmed additional benefits in the form of reduced morbidity and mortality from certain cancers.

Diabetes is associated with lower risk of prostate cancer in men but with higher risk of other cancers in both men and women, and the results provide further evidence that abnormal insulin and glucose signaling may contribute to cancer initiation and development. Previous epidemiologic studies have also shown an association between diabetes and an increased risk for cancers including colorectal, liver and pancreas.

Diabetes Associated With Increased Cancer Risk

The 11-year prospective study followed more than 500,000 patients ‒ predominantly white, non-Hispanic men and women aged 50 to 71 years ‒ from 1995 to 1996. The results showed that diabetes was associated with an 8 percent increased risk for cancer among women and a 4 percent decreased risk for men.

In previous research, a decreased risk for prostate cancer was associated with diabetes, which researchers believe might be due to the lower testosterone levels associated with diabetes. After excluding prostate cancer from their evaluation, the researchers found that diabetes was associated with a 9 percent increased risk for cancer in men.

As for mortality, diabetes was associated with an 11 percent increased risk in women and a 17 percent increased risk in men. These risks appeared independent from other cancer risk factors, such as obesity and cigarette smoking.

After evaluating by cancer site, the researchers found diabetes was associated with a significant increase in risk for colon, rectal and liver cancers among men and women. In men, diabetes was associated with an increased risk for pancreatic and bladder cancers. In women, it was associated with an increased risk for stomach, anal and endometrial cancers. No association was found between diabetes and lung, skin or other cancers.

Earlier research has also linked obesity, diabetes and metabolism to cancer risk with the findings linking weight gain and diabetes to a variety of cancers affecting both men and women, including breast, prostate and colorectal cancer.

Colorectal Cancer & Type 2 Diabetes Share Common Factors

Women with diabetes are 1.5 times more likely to develop colorectal cancer than those who do not have the metabolic disorder. The findings add to the complex body of evidence linking diet and colorectal cancer and also provide new evidence that furthers our understanding of the role of insulin in cancer promotion.

It has been determined that colorectal cancer and type 2 diabetes share a number of common factors, including obesity, so it is interesting to see the direct line between these two conditions. In general, the idea is that if elevated insulin levels create a biochemical environment conducive to cancer growth, it provides one mechanism by which diet and lifestyle can really influence cancer risk.

Data from a massive screening study called the Breast Cancer Detection Demonstration Project, initiated at 29 centers throughout the United States in the 1970s involving more than 45,000 study participants with no history of colorectal cancer or self-reported diabetes for eight years (from 1987-1989 and from 1995-1998), was used to identify which of them subsequently developed colorectal cancer.

According to the findings, women with diabetes had a greatly increased risk of developing colorectal cancer. These results remained statistically significant even after controlling for all known and suspected confounding variables.

However, it is not exactly clear what aspect of diabetes is the underlying cause for this increased risk but one hypothesis centers on the elevated concentration of insulin typically seen in people with type 2 diabetes. In the early stages of the disease process, people become insulin resistant, meaning they must produce more and more insulin to regulate their blood sugar.

Pre-Diabetics Also at Increased Risk

Even after frank diabetes begins, insulin levels remain chronically elevated for extended periods before the pancreas can no longer supply the level of insulin the body demands. So, if the elevated insulin is the problem, then pre-diabetics, who are also hyper-insulinemic, should also be at increased risk for developing colorectal cancer.

To test that idea, the researchers re-analyzed the data, this time including women who were likely pre-diabetic at the beginning of the follow-up period. The idea was that these women were likely hyper-insulinemic at that stage. Surprisingly, the elevated risk, while still significant, had dropped slightly in comparison with that of known diabetics.

This suggests that either the pre-diabetic women had not had elevated insulin long enough or intensely enough to increase risk as they observed in the diabetic women, or alternatively, something other than or in addition to hyper-insulinemia could explain the significant, increased risk for colorectal cancer observed in people with diabetes.

Diabetics May Have Increased Risk of Developing Parkinson’s Disease

The two diseases share some underlying mechanisms, study of 289,000 adults suggests

Diabetes and Parkinson’s disease would seem, at first, to be unrelated. Diabetes arises when the body can no longer properly use the blood-sugar-regulating hormone insulin. Parkinson’s is a brain disease in which movement-regulating cells in the brain die off or become disabled, leading to symptoms like tremors, rigidity in the joints, slowed movement and balance problems. But there seems to be a connection.

A new study ‒ published in the April issue of the journal Diabetes Care ‒ suggests that diabetics may have a slightly increased risk of developing Parkinson’s disease. Though the reasons for the link are far from clear, the connection between diabetes and Parkinson’s risk could mean that the two diseases share some underlying mechanisms.

One possibility is chronic, low-level inflammation throughout the body, which is suspected of contributing to a number of chronic diseases by damaging cells. Oxidation ‒ the process fought by anti-oxidants ‒ is another.

The study, of nearly 289,000 older U.S. adults, found that those with diabetes at the outset were more likely to be diagnosed with Parkinson’s over the next 15 years. Of 21,600 participants with diabetes, 172 (0.8 percent) were eventually diagnosed with Parkinson’s. That compared with 1,393 cases (0.5 percent) among the 267,000 men and women who were diabetes-free at the study’s start.

When the researchers accounted for other factors ‒ like age, weight and smoking habits ‒ diabetes itself was linked to a 41 percent increase in the risk of future Parkinson’s. That, however, does not prove that diabetes is a cause of Parkinson’s, and the reasons for the connection remain unknown.

Other large studies, too, have looked at the diabetes-Parkinson’s link before, with conflicting results. However, the current study included a larger number of people with Parkinson’s. And unlike most past studies, it looked at the duration of people’s diabetes.

In general, the researchers found, the higher Parkinson’s risk was largely seen among people who’d had diabetes for more than 10 years before the start of the study. That supports the idea that diabetes came first, before Parkinson’s, rather than the other way around. But more studies are needed to understand why the connection exists, and what, if anything, can be done about it.

The evidence at this time is very preliminary, the researchers say, and diabetics should simply continue to do the things already recommended for their overall health ‒ eating a well-balanced diet and getting regular exercise. Still, there might be something about diabetes ‒ like a problem regulating insulin ‒ that contributes to Parkinson’s. But that remains to be proven.

Diabetes: Autonomic Neuropathy Far Worse Than ‘Pins & Needles’ in the Feet

For around 50 percent diabetics, living with diabetic peripheral neuropathy ‒ that “pins and needles” feeling you get after your foot falls asleep, along with a burning sensation, and possibly numbness and loss of balance and no way to relieve it ‒ is a daily reality. When the peripheral nervous system fails, the patient becomes a vegetable.

Diabetic neuropathy is categorized as autonomic and peripheral diabetic neuropathy, depending on which particular nervous system it affects. The third category, focal diabetic neuropathy, affects individual nerves, not a system.

Diabetes can cause dysfunction of any or every part of the autonomic nervous system, leading to a wide range of disorders. And these are serious. Among the most troublesome and dangerous of the conditions linked to autonomic neuropathy are known: silent myocardial infarction (MI), cardiac arrhythmias (abnormal heart rhythm), ulceration (formation or development of an ulcer), gangrene, and nephropathy (damage to or disease of the kidney).

The prognosis is bleak: While treatment relieves pain and can control some symptoms, the disease generally continues to get worse.

What is Autonomic Neuropathy?

The peripheral nervous system controls the sensory and motor functions. This helps us to become aware of our environment and to control muscular activity. Patients with diabetic neuropathy might also develop autonomic neuropathy, leading to incontinence, constipation, diarrhea, acid reflux, difficulty breathing, sexual dysfunction (impotence) and inability to regulate blood pressure.

This happens because autonomic neuropathies affect the nerves that regulate vital functions, including the heart muscle and smooth muscles. Indeed, the autonomic nervous system is at the very core of our existence. It controls the vital life functions like heartbeat and respiration. So, when the autonomic nervous system fails, the patient dies.

In other words, autonomic neuropathy is a form of peripheral neuropathy. It is a group of symptoms, not a specific disease. There are many causes. Damage to the autonomic nerves affects the function of areas connected to the problem nerve. For example, damage to the nerves of the gastrointestinal tract makes it harder to move food during digestion (decreased gastric motility). Damage to the nerves supplying blood vessels also causes problems with blood pressure and body temperature.

Essentially, diabetic autonomic neuropathy impairs the ability to conduct activities of daily living and lowers quality of life. Autonomic neuropathy is also associated with an increased risk of sudden death. It also accounts for a large portion of the cost of care. (See my earlier related post ‘Don’t Ignore Diabetic Nerve Pain’ here.)

Remember, diabetic autonomic neuropathy is a stealthy complication of diabetes, developing slowly over the years and quietly robbing diabetic patients of their ability to sense when they are becoming hypoglycemic or having a heart attack. It can affect any organ of the body, from the gastrointestinal system to the skin, and its appearance portends a marked increase in the mortality risk of diabetic patients.

Eventually, autonomic neuropathy damages the nerves that run through a part of the peripheral nervous system and are used for communication to and from the brain and spinal cord (central nervous system) and all other parts of the body, including the internal organs, muscles, skin, and blood vessels.

Telltale Signs

Clinical symptoms generally do not develop for many years after the onset of diabetes. However, subclinical autonomic neuropathy can often be identified by quantitative functional testing within 1 year of diagnosis in patients with type 2 diabetes and within 2 years in those with type 1 diabetes. The most important causative factors are poor glycemic control, long duration of diabetes, increasing age, female sex, and higher body mass index. (See my earlier related post ‘All Eyes on Research That May Provide Cure for Diabetic Neuropathy’ here.)

Leading causes of death in diabetic patients with either symptomatic or asymptomatic autonomic neuropathy are heart disease and nephropathy. Increased urinary albumin excretion is related to autonomic neuropathy in diabetic patients.

Impairments in the autonomic nervous system may also contribute to the pathogenesis of diabetic nephropathy and cardiovascular disease. Autonomic neuropathy is also an independent risk factor for stroke.

Consequences

The cardiovascular manifestations of autonomic neuropathy appear to be the most widely studied ones and justifiably so because they are likely to be potentially lethal. Postural giddiness and syncope (temporary loss of consciousness and posture, described as “fainting” or “passing out”) are the only autonomic symptoms referable to the cardiovascular systems.

Undeniably, the cardiovascular system bears the brunt of autonomic neuropathy in diabetics and this may be responsible for certain disabling symptoms, painless myocardial infarction and even sudden death during surgery. (It is therefore desirable to evaluate in detail the cardiovascular and autonomic status of all diabetics before major surgery.)

Cardiovascular autonomic neuropathy causes abnormalities of heart-rate control and vascular dynamics. It has been linked to postural hypotension, exercise intolerance, enhanced intraoperative cardiovascular lability (susceptible to change, error or instability), increased incidence of asymptomatic ischemia (showing no evidence of inadequate blood supply), myocardial infarction (heart attack), and decreased likelihood of survival after myocardial infarction.

Besides, failure to recognize symptoms in a diabetic as due to autonomic neuropathy may lead to a lot of unnecessary investigations and sometimes to wasteful treatment such as testosterone in sexual impotence.  Indeed, sexual impotence is now recognized to be a common and sometimes the only manifestation of autonomic neuropathy followed closely by nocturnal polyuria (passing large volumes of urine at night but normal amounts during the day).

Gastrointestinal manifestations of autonomic neuropathy also include nausea and vomiting due to diminished gastric motility (the ability to move spontaneously); diarrhea and nocturnal fecal incontinence (bedwetting) due to exaggerated sympathetic hypofunction (a diminished or inadequate level of activity of an organ system or its parts) during sleep; and asymptomatic, functional disturbances of the gall bladders and the esophagus. Localized bouts of sweating on the face during eating are also reported to be diagnostic of diabetic autonomic neuropathy.

Outlook (Prognosis)

Once autonomic abnormalities are present, they are permanent, sometimes showing progressive deterioration but rarely, if ever, improving. They can affect multiple organ systems in the body, can cause disabling symptoms and have a lethal potential. It is therefore, necessary to be constantly aware of them and to screen the diabetics periodically, and most certainly pre-operatively. Therein lies their safety.

Of patients with symptomatic autonomic dysfunction, 25% to 50% die within 5 to 10 years of diagnosis. The 5-year mortality rate in patients with diabetic autonomic neuropathy is three times higher than in diabetic patients without autonomic involvement.

Undeniably, neuropathy is one of the most common complications of diabetes. And when it affects the autonomic nervous system, it can damage the cardiovascular, gastrointestinal, and genitourinary (reproductive and urinary) systems and impair metabolic functions (necessary for the maintenance of a living organism) such as glucose counter-regulation (unrestrained eating).

This is because the autonomic nervous system is primarily efferent (conveying away from a center), transmitting impulses from the central nervous system to peripheral organs. However, it also has an afferent (carrying toward the center) component. Its two divisions—the parasympathetic (part of nervous system that serves to slow the heart rate, increase intestinal and gland activity, and relax the sphincter muscles) and the sympathetic (that accelerates the heart rate, constricts blood vessels, and raises blood pressure) nervous systems— work in balanced opposition to control the heart rate, force of cardiac contraction, dilatation and constriction of blood vessels, contraction and relaxation of smooth muscle in the digestive and urogenital systems, the secretions of glands, and pupillary (affecting the pupil of the eye) size.

Ipso facto, the reported prevalence of diabetic autonomic neuropathy varies, with community-based studies finding lower rates than clinic-based and hospital-based studies, in which the prevalence may be as high as 100%.

Prevention

Intensive glycemic control is critical in preventing the onset and slowing the progression of diabetic autonomic neuropathy. The Diabetes Complications and Control Trial (DCCT) showed that intensive glycemic control reduced the prevalence of autonomic dysfunction by 53%.

It is also the first therapy to be considered when diabetic autonomic neuropathy is diagnosed. In addition, a variety of pharmacologic and nonpharmacologic therapies are available to treat the symptoms of autonomic neuropathy.

In addition, regular foot care can prevent a small infection from getting worse. This is why no appointment for diabetes care is complete without a thorough foot examination.

Treatment

For patients with both type 1 or type 2 diabetes, glycemic control is important, although methods to achieve target levels may differ. The methods for achieving euglycemia (normal glucose content of the blood) and the target blood glucose and HbA1c levels are given in a position statement from the American Diabetes Association.

The goals of treating diabetic neuropathy are to prevent the disease from getting worse and to reduce the symptoms of the disease. Tight control of blood sugar (glucose) is important to prevent symptoms and problems from getting worse.

Medications may be used to reduce the symptoms in the feet, legs, and arms. These medications include antidepressant drugs, such as amitriptyline (Elavil), doxepin (Sinequan), or duloxetine (Cymbalta); antiseizure medications, such as gabapentin (Neurontin), pregabalin (Lyrica), carbamazepine (Tegretol), and valproate (Depakote); drugs that block bladder contractions may be used to help with urinary control problems.

Erythromycin, domperidone (Motilium), or metoclopramide (Reglan) may help with nausea and vomiting. Pain medications (analgesics) may work for some patients on a short-term basis, but in most cases they do not provide much benefit. Capsaicin can be used topically to reduce pain.

Phosphodiesterase type 5 (PDE-5) drugs, such as sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) are safe and effective for treating impotence in patients with diabetes.

Regular foot exams are important to identify small infections and prevent foot injuries from getting worse. If foot injuries go unnoticed for too long, amputation may be required.

Possible Complications

Injury to the feet due to loss of feeling; muscle breakdown and imbalance; poor blood sugar control due to nausea and vomiting; skin and soft tissue breakdown (ulceration) that may require amputation.

In addition, neuropathy may mask angina, the warning chest pain for heart disease and heart attack.

When to Contact a Medical Professional

Promptly call your health care provider if you develop symptoms of diabetic neuropathy.

Sources: American Diabetes Association (ADA), Neurology, National Institute of Health (NIH), Aaron I Vinik, National Diabetes Information Clearinghouse (NDIC)

Diabetes Management: Tight Cholesterol, BP Control Does Little Good for Diabetics

Lower isn’t always better in diabetes management. In fact, pushing too hard may not help, and may actually hurt in some cases. This has been proved, once again, by the landmark Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, results released last week reveal. Indeed, the new lipid and blood pressure results round out the negative portrait of aggressive risk factor management in diabetes patients.

(ACCORD is one of the largest studies ever conducted in adults with type 2 diabetes who were at especially high risk of cardiovascular events, such as heart attacks, stroke, or death from cardiovascular disease.  The multicenter clinical trial tested three potential strategies to lower the risk of major cardiovascular events: intensive control of blood sugar, intensive control of blood pressure, and treatment of multiple blood lipids. The lipids targeted for intensive treatment were high density lipoprotein (HDL) cholesterol and triglycerides, in addition to standard therapy of lowering low density lipoprotein (LDL) cholesterol. Read the Questions & Answers about the ACCORD Trial here.)

According to received wisdom, intensive blood pressure and blood fat management could drive down diabetics’ higher risks of heart problems. But results from the ACCORD trial prove that when it comes to traditional measurements of heart disease risk, a blood pressure target of 120 mm Hg rather than the general population standard of 140 did not reduce nonfatal heart attacks, nonfatal strokes or death from cardiovascular causes.

Likewise, adding the cholesterol-busting drug fenofibrate to standard statin therapy did not reduce the chances of major adverse cardiovascular events. Indeed, tribal behavior by physicians that is no doubt driven by the big pharma marketing machinery, has raised concerns about the ramifications of recommending costly medications that don’t confer real benefits to patients. (See my post ‘Increased Use of Fibrates in US Could Be A Triumph Of Marketing Over Medicine’ here.)

Both studies ‒ part of the complex ACCORD trial ‒ were presented at the American College of Cardiology meeting in Atlanta, Ga. and released simultaneously online in the New England Journal of Medicine.

[A third part of this research ‒ one which examined intensive lowering of blood sugar to see if this had a positive effect ‒ was prematurely halted in 2008 because it turned out that patients receiving this approach actually had an increased, instead of decreased, risk of death. (See a related post ‘Aggressive Diabetes Therapy May Raise Death Risk’ here.)]

As for the newly released findings, the lipid arm of ACCORD included 5,518 patients with high risk of heart problems because of cardiovascular disease or at least two risk factors. LDL, or bad, cholesterol levels had to be between 60 and 180 mg/dL; HDL, or good cholesterol, levels had to be under 50 mg/dL or 55 mg/dL for women and blacks; and triglycerides had to be under 750 mg/dL if the patients were not on any therapy, or 400 mg/dL otherwise. Patients either received fenofibrate or a placebo in addition to statins.

What the researchers found was that lipid and triglyceride levels responded as expected. Despite this, however, the patients appeared to receive no benefit when it came to major heart problems such as heart failure, stroke and nonfatal heart attacks.

Meanwhile, the  blood pressure portion of ACCORD compared a strategy of keeping systolic blood pressure under 120 mm Hg to one of under 140 mm Hg in 4,733 diabetes patients with high risk of cardiovascular events because of clinical or subclinical heart disease or at least two risk factors. In this trial, treatment effectively lowered blood pressure. But again, there was no impact on aspects of patient health including death risk, death related to heart problems and nonfatal heart attacks.

ABC News reported that the U.S. Food and Drug Administration will conduct a full review of findings from the ACCORD study. An FDA spokesperson said the agency planned to include a review of the labeling and indications for fenofibric acid (Trilipix) ‒ even though the trial used fenobrate (TriCor). Asked about the timing of the announcement, the spokesperson said the FDA was attempting to be more proactive.

Both Trilipix and TriCor are marketed by Abbott, and Trilipix is “the active metabolite of TriCor,” according to Dr. Marshall Elam of the Memphis VA Medical Center. Elam, who was involved in the design of the lipid treatment arm of ACCORD said that “neither TriCor nor Trilipix has a label indication for cardiovascular disease.”

In a statement released after the ACCORD results were reported, but before the FDA said it would conduct a review of the ACCORD findings, Abbott said the data from the ACCORD Lipid trial “supports the appropriate patient type and current treatment guidelines for fibrates. The top-line results of the study were widely expected, given that two-thirds of patients in the trial would not be recommended for fibrate therapy under current guidelines.”

Diabetes: Increased Use of Fibrates in US Could Be A Triumph Of ‘Marketing Over Medicine’

U.S. prescriptions for cholesterol-lowering medications predating statins have increased steadily despite uncertain benefit, suggesting that aggressive marketing has trumped scientific evidence.

These drugs, called fibrates, modestly reduce blood levels of artery-clogging bad cholesterol, raise good cholesterol and are most effective at lowering levels of other damaging blood fats called triglycerides, although the overall picture from clinical trials remains confusing.

Fibrates include gemfibrozil (Lopid), which got the regulatory nod in 1981; fenofibrate (TriCor, Triglide), approved in 2007, and the closely related drug fenofibric acid (TriLipix, Fibricor), which entered the U.S. pharmaceutical marketplace in December 2008. In 2009, fenofibrate and fenofibric acid together accounted for almost 74 percent of the U.S. market share of fibrates.

According to Dr. Cam Patterson, cardiology chief and physician-in-chief of the Center for Heart and Vascular Care at the University of North Carolina, Chapel Hill, “Statins are the only cholesterol-lowering drugs that have been shown conclusively to save lives. Fibrates may be an option as add-on therapy, but there is no compelling case to use them as first-line therapy” for patients with elevated cholesterol, he warns.

Patterson feels the substantial increase in fibrate use demonstrated “unfortunate tribal behavior by physicians that is no doubt driven by the big pharma marketing machinery” and expressed concern about the ramifications of “recommending costly medications that don’t confer real benefits to our patients. We’ve been burned before.”

“The use of fibrates in America is very troubling,” says Dr. Steven E. Nissen, chairman of cardiovascular medicine at the Cleveland Clinic Foundation. Describing the increasing use of fibrates as an expensive failure to educate doctors and regulators, he notes that fibrates are among medications advertised directly to consumers. “This is a classical example of marketing triumphing over science,” he feels.

Dr. James H. Stein, director of preventive cardiology at the University of Wisconsin-Madison School of Medicine and Public Health, says most people don’t realize the influence of marketing on health care. Pointing out that negative studies about fibrates have been “spun to focus on the possible benefits”, he cautions that fenofibrate is associated with significant side effects, including “increased creatinine, which might indicate kidney dysfunction; gallstones, and more serious complications like pancreatitis, blood clots, and pulmonary embolism.”

In the past five years, two major studies have found fenofibrate failed to reduce heart disease risks among diabetic men and women. Last year, the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, which involved 10,000 patients with diabetes, found that those who took both simvastatin and fenofibrate suffered about as many heart attacks, strokes and deaths as diabetic patients treated with simvastatin alone.

The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial, which involved nearly 10,000 patients and has reported results since 2005, found that fenofibrate failed to decrease cardiovascular deaths more than a placebo.

Yet a new study published in the current issue of the Journal of the American Medical Association found that U.S. prescriptions for fibrates grew from 336 per 100,000 people in January 2002, to 730 per 100,000 people in December 2009. That’s a 117.1 percent hike. At the same time, Canadian prescriptions for fibrates held nearly steady, at 402 per 100,000 in early 2002 and 474 per 100,000 in late 2009.

The increase in fibrate prescriptions, driven by a 200 percent jump in the use of fenofibrate, has outpaced the growth of statins. But, to keep things in perspective: statins, which are among the most commonly prescribed medications, remain blockbuster drugs that dominate lipid-lowering treatment, with fibrates accounting for just 9.4 percent of the U.S. lipid-lowering market in 2009.

Based on a news report in ABC News

Wake-up Call: 50% Adult Americans Face Serious Health Risk

Nearly 50 percent of all adult Americans have high cholesterol, high blood pressure or diabetes. All conditions increase the risk of cardiovascular disease. Diabetics, of course, are at greater risk of having the other two conditions as well, and heart disease is one of the most common complications resulting from poor diabetes management.

A report released online Monday by the national Centers for Disease Control and Prevention said nearly 13 percent Americans have at least two of the conditions and three percent have all three, sharply increasing their risk. Of those with at least one condition, 15 per cent have not been diagnosed.

(Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2011. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects a whopping 35 percent of adults aged 20 and older.)

“The number that really surprises me is the penetration of these conditions into the U.S. population,” said Dr. Clyde Yancy of Baylor University Medical Center, president of the American Heart Association. “When that number is nearly 50%, that’s a huge wake-up call.” It means there are a large number of people “who think they are healthy…but are working under a terrible misconception.”

The data come from the ongoing National Health and Nutrition Examination Survey, which releases new figures every two years. The survey consists of interviews conducted in participants’ homes, standardized physical examinations given to some participants and laboratory tests using blood and urine specimens.

“This report is so timely and important because it crystallizes exactly what the burden is,” Yancy said. “It tells us the challenge we now face that could stress and potentially defeat any healthcare system we could come up with.”

Personal responsibility plays a big role in creating these three health problems, he said. “This trio begins with a quartet of smoking, a junk diet, physical inactivity and obesity. Those are all things we can do something about.”

Though researchers should be able to use the new data to plan interventions, “the main thing here is for people to be aware that they have these conditions and know that lifestyle modifications and medications can control them and reduce their risk for cardiovascular disease,” said epidemiologist Cheryl D. Fryar of the CDC’s National Center for Health Statistics, one of the study’s authors.

Peer Support Improves Diabetes Self-Management

Diabetes patients who receive peer support benefit from improved control of their blood sugar levels. Research carried out at the University of Michigan Medical School and published in the Annals of Internal Medicine reveals that phone calls to peers facing the same self-management challenges helped diabetics manage their conditions better than those who used traditional nursing care management services.

For the study, researchers randomly assigned 244 male patients with uncontrolled diabetes to either peer support or nurse care management. After six months, those in the peer-support group saw a significant drop in their HbA1c levels (a measure of blood sugar over time) ‒ from an average of 8.02 to 7.73 per cent, which represented a 0.58 per cent decrease from those who received care from a nurse.

The researchers also monitored changes in insulin therapy, blood pressure and adherence to oral treatment regimens, and found that patients who received peer support managed their conditions better.

Michele Heisler, lead author of the study, said “Our model was testing the hypothesis that a good way to activate patients was to give them some skills and encouragement to both help and be helped. Just as in education they say that the best way to learn something is to try to teach it.”

“Our program hoped to mobilize patients themselves to realize how much they themselves had to offer another person with diabetes and enjoy the sense of meaning and pleasure that being needed and helping another can provide. That’s why I think people did well – they were very motivated when they felt they were helping someone else.”

She concluded: “Most chronically ill patients need more support for self-care than most health care systems can provide. That’s why programs like this, that increase the quality and intensity of assistance through peer support, deserve further exploration.”

 

All Eyes on Research That May Provide Cure for Diabetic Neuropathy

An Australian optometrist researching how contact lenses affect the eye accidentally discovered a new way to study diabetic neuropathy. The discovery holds the key to monitor nerve degeneration over time.

The extreme magnification of a special microscope, called a corneal confocal microscope, allowed Nathan Efron, a professor at the Queensland University of Technology’s School of Optometry at Brisbane, Australia, to see fine nerves in the cornea that had never been seen before.

Efron found that the nerves affected by neuropathy are an exact match to nerves found in front of the eye, and is testing whether looking at their level of degeneration in these nerves over a period of time would match the nerve degeneration found in arms and legs.

“We want to see how well the degeneration of the nerves in the cornea matches the degeneration of nerves throughout the body, and if it matches it will mean that we can monitor diabetic neuropathy using a simple eye test,” Efron says.

The breakthrough is so profound and important that Efron was honored last November with the Glenn A. Fry Lecture Award from the American Academy of Optometry for his research into non-invasive ophthalmic diagnosis of diabetic nerve damage.

As the principal researcher of a five-year study ‒ Expanding the Role of Optometry in Diabetes Management: Determining the Discrimination Capacity of a Novel New Ophthalmic Marker of Diabetic Neuropathy ‒ Efron says early indications are promising and he is presenting his findings at the Asia Pacific Academy of Opthamology Congress in Sydney this week.

When he first saw the nerves, Efron, who has type 2 diabetes, knew at once that what he was seeing was something unique. One of the serious consequences of the disease is diabetic neuropathy – a condition that causes nerve damage and can result in ulcers and amputations ‒ that affects about half of diabetics in varying degrees of severity, which causes the degeneration of nerves, mostly in the arms and leg. (See my post ‘Don’t Ignore Diabetic Nerve Pain’ here.)

“I wondered if my own diabetes specialist might be interested in the technology and it turned out he was a world authority on diabetic neuropathy. He thought it was astonishing,” recalls Efron. It was ideas generated by discussions with his diabetes specialist that led Efron to investigate linkages between the nerves in the eyes and nerves elsewhere in the body with the aim of developing a relatively simple and non-invasive eye test to identify neuropathy (or diabetic nerve disease).

Neuropathy is typically measured by taking skin biopsies from the foot and running a series of specialized tests that can take up to a week to complete. In many cases, this debilitating condition is not identified until serious, and irreparable, damage has already been done.

On the other hand, the quick and non-invasive eye tests would see results in a matter of minutes. In short, the importance of Efron’s discovery lies in the fact that since the eye is a transparent structure, it is the only place in the body where you can look directly at nerves and their degeneration over time.

Efron and his team have established a four-year clinical trial assessing the optimal method of ophthalmic neuropathy diagnosis. This will hopefully lead to a standard protocol for optometrists and ophthalmologists to quickly and simply identify people at risk of neuropathy, anticipate the level of damage and assess treatment outcomes.

There are multiple benefits of being able to measure the onset of neuropathy, one being that there are drugs in development that aim to cure diabetic neuropathy. “When these drugs are ready to come onto the market, we will, using our method, be able to detect nerve degeneration early and then hopefully cure it,” he says.

For the tests, patients would receive a drop of anesthetic in the eye, then a corneal confocal microscope would capture a 20 second “movie” of their eye for analysis.

There are also three more tests being looked at – the first, called non-contact corneal aesthesiometry, measures how nerve degeneration is affecting the function of the cornea, by projecting tiny puffs of air into the eye, growing progressively stronger until the patient can feel it.

Two more eye tests will look at the effect of nerve degeneration on the retina.

“Diabetic patients currently go for yearly eye tests anyway, so we are saying that these tests could be done at the same time, and only take a few minutes,” Efron says.

Efron hopes his discoveries will lead to early testing for diabetic neuropathy that will motivate sufferers to better manage their disease. Testing could be carried out at the same time as diabetes patients are tested for other eye problems caused by the disease.

The test has been used to monitor nerve regeneration in patients who have undergone kidney and pancreas transplants, and it could help track the effects of new treatments.

Based on a news report in Sunday Star Times

Diabetes: Is the ADA Shifting its Stance About Carbs?

Carbohydrates are a very touchy subject with diabetics. And for me at least, understanding carbs in a diabetic diet is more difficult than quantum mechanics (or double-entry accounting if you’re not a science type). Diabetologists and dieticians, too, have differing views. I found this article by LAURA DOLSON very instructive and am reproducing it here for those who may have missed it. You can find the lively discussion that followed the article’s publication here.

You may be surprised to know that for the past couple of decades, the American Diabetes Association has been sort of a cheerleader for carbs. Yes, I’m talking about the organization who’s mission it is to promote education and research in ways aimed at preventing diabetes and alleviating the suffering of diabetics.

What is diabetes? It is essentially a disorder of the body’s ability to process carbohydrates. This includes Type 1 and Type 2 diabetes, pre-diabetes, metabolic syndrome, insulin resistance, and all the other points on the diabetes spectrum. (The Endocrine Society suggests that anyone with a fasting blood glucose of 89 or above is at risk for damage to their health.)

In light of this, you’d think that limiting carbohydrate intake would be a priority in educating people about handling these disorders. And yet, the ADA jumped right onto the Food Pyramid bandwagon and began to advise people to get at least 55% of their calories from carbohydrate, such as in the Food Pyramid for Diabetes (see illustration above).

In 2008, they made one exception: diabetics trying to lose weight could follow a low-carb diet for up to one year; this was later loosened further to two years. But still they did not recommend a low-carb diet for health, blood sugar control, or preventing progression of the diabetes.

Now, in the March 2011 edition of the ADA magazine “Diabetes Forecast” are three rather remarkable articles. The first is called The “ADA Diet” Myth, which claims that there is no such thing as the ADA Diet! (Who else was having this hallucination?) Instead, Stephanie Duncare, director of nutrition and medical affairs for the ADA says, “For more than 15 years now, ADA has recognized that people with diabetes should eat in a way that helps them reach their blood glucose, cholesterol, blood pressure, and weight goals. For some, this means a relatively higher-carbohydrate diet, and for others, the diet may be lower in carbohydrate”. Well, hallelujah to that, especially if the goal is “normal blood glucose” (normal meaning “a blood glucose level that will not cause further damage in the pancreas”).

Even more bold is an article called, “Are Carbs the Enemy?” which attempts to cover the debate. They first present a sort of wimpy pro-carb stance. This section of the article has a notable absence of anything to do with science, instead relying on statements such as “Gone are the days of ‘diabetic diets’ that were meager and confining” and “as long as people eat less or cover their carb intake with medications, they can keep blood glucose levels in check with a healthy diet” (“healthy” in this case meaning “high-carb”).

The article then goes on to describe a low-carb approach, citing Dr. Richard Bernstein. This section cites actual evidence, and makes what I think is a much stronger case for controlling blood glucose by limiting carbohydrates. The article goes on to a section on saturated fats which is much more balanced than usual, and then the normal “we don’t have the long-term studies”. The article concludes with the statement: “In the end, the best diet is the healthy one you’re able to follow.”

The only thing I would add is that people need support in making those changes, and as far as I can tell they are still leaving an awful lot up to the individual to figure it out for themselves. There has been quite a defeatist attitude coming from the organization that is supposed to be helpful – along the lines that it is asking just too much of people to cut carbs in any significant way. Are dietitians now actually going to support people in finding a diet that achieves as close to a normal blood glucose as possible? It would be a very big change if this happened any time soon.

But wait, there’s more! A follow-on short piece called “Eating With Diabetes: 3 Approaches” lists the low-carb approach first, and then follows with “Moderate-Carb” and “Vegan/High-Carb”. The weird thing is that the three approaches are described as “less than 10% carb”, “40-50% carb” and “75% carb”. What about people who normalize their blood glucose with 20% carb or 30% carb? Why not just say, “it’s a spectrum disease, with a spectrum of carb that will treat it effectively”? In any case, I don’t want to complain too loudly, because this is SO great to see in an ADA publication!

Now, to be sure, the ADA is not yet changing their basic stance. Nowhere on the latest update of the diabetes.org Web site is it stated that diabetics should follow a low-carb diet. On the other hand, there is no longer anything I can find that says to eat over half of calories from carbohydrate, either. The former food pyramid, as far as I can tell, has vanished, and there are several hints that low-carb eating is becoming a bona-fide option.

There are statements such as, “Understanding the effect of carbohydrate on blood glucose levels is key to managing diabetes. The carbohydrate in food makes blood glucose levels go up.” Although diabetics are still advised that “a place to start is at about 45-60 grams of carbohydrate at a meal.”, (yikes) it goes on to say to adjust from there. Even though this is not what most of us would call a low-carb diet, for most people it is a reduction from their previous advice.

[Side note: I also notice it doesn’t actually say 45-60 g/meal is a good place to start. If that actually controls someone’s blood glucose, that’s great, but I would think that in the cases where it doesn’t, it would be more disheartening to subsequently take more carb away. Why not start lower, and then add? Also, most likely, the person for whom this works is losing weight – a phase which doesn’t last forever.]

To me this looks like the beginnings of a real change in approach from the ADA. The Titantic may actually be turning around! This could make a difference to the health of millions of people, and nothing could make me smile more than that.

By Laura Dolson/about.com

Image courtesy about.com