Too Few Diabetes Patients Receiving Statins
Last Updated: September 13, 2016.
http://www.doctorslounge.com/index.php/news/pb/66457
Nearly all middle-aged patients with diabetes should be taking statins, but cardiologists fail to prescribe these medications for two out of every five such patients in their care, according to a study published in the Sept. 20 issue of the Journal of the American College of Cardiology.
TUESDAY, Sept. 13, 2016 (HealthDay News) -- Nearly all middle-aged patients with diabetes should be taking statins, but cardiologists fail to prescribe these medications for two out of every five such patients in their care, according to a study published in the Sept. 20 issue of the Journal of the American College of Cardiology.
Researchers analyzed the records of 215,193 patients (age 40 to 75 years) with diabetes but no overt cardiovascular disease who visited a cardiologist between May 2008 and October 2013. The data on the patients came from 204 cardiology practices.
The researchers found that only 61.6 percent of patients were prescribed a statin. Those prescribed statins were more likely to have cardiovascular risk factors. They also were more likely to receive non-statin cholesterol-lowering therapy (28 percent, versus 13 percent for patients not receiving a statin) and had lower mean low-density lipoprotein cholesterol (90 versus 103 mg/dL). The team noted a 57 percent variation in statin prescribing practices, even after accounting for individual patient factors such as age, gender, race, hypertension, dyslipidemia, tobacco use, and insurance coverage.
"The new cholesterol guideline recommends statin therapy in diabetic patients 40 to 75 years of age with low-density lipoprotein cholesterol 70 to 189 mg/dL without atherosclerotic cardiovascular disease," the authors write. "The current gap in care identified in this study supports national efforts to improve the use of statins in patients with diabetes."
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Showing posts with label diabetes. Show all posts
Showing posts with label diabetes. Show all posts
Tuesday, 13 September 2016
Friday, 2 August 2013
Flu Virus May Trigger Diabetes
Italian researchers have discovered that the flu virus may trigger the onset of type 1 diabetes.
Type 1 diabetes, once known as juvenile diabetes, affects as many as 3 million Americans, most of them diagnosed as children. Type 1 diabetes develops when the body’s immune system attacks and destroys insulin-producing cells found in the pancreas. The condition is genetic, but an environmental trigger is also necessary for it to appear.
Researchers have suspected the flu virus might provide this trigger since the 1970s, because type 1 diabetes often sets in after an infection.
Study author Ilaria Capua and her team from the World Organization for Animal Health infected turkeys with the flu to test their theory that it could trigger diabetes. They conducted the study on turkeys because they knew birds with the flu often have an inflamed pancreas, according to New Scientist. They found that many of the turkeys infected with flu virus developed severe pancreatic damage, as well as diabetes.
The researchers then infected human pancreatic tissue with two common flu viruses and found that both viruses grew well in the tissue. The flu virus in the pancreatic cells triggered production of inflammatory chemicals that are central to the autoimmune reactions that lead to type 1 diabetes.
Normally, in humans, the virus attacks the lungs and gut, but not typically the pancreas. But it can sometimes get into the blood and travel to the pancreas, researchers said.
Capua is now testing the dibates-producing effects of the flu on mice, according to the New Scientist.
“Our findings indicate that influenza infection may play a role as a causative agent of pancreatitis and diabetes in humans and other mammals,” the study authors concluded in their report.
Type 1 diabetes, once known as juvenile diabetes, affects as many as 3 million Americans, most of them diagnosed as children. Type 1 diabetes develops when the body’s immune system attacks and destroys insulin-producing cells found in the pancreas. The condition is genetic, but an environmental trigger is also necessary for it to appear.
Researchers have suspected the flu virus might provide this trigger since the 1970s, because type 1 diabetes often sets in after an infection.
Study author Ilaria Capua and her team from the World Organization for Animal Health infected turkeys with the flu to test their theory that it could trigger diabetes. They conducted the study on turkeys because they knew birds with the flu often have an inflamed pancreas, according to New Scientist. They found that many of the turkeys infected with flu virus developed severe pancreatic damage, as well as diabetes.
The researchers then infected human pancreatic tissue with two common flu viruses and found that both viruses grew well in the tissue. The flu virus in the pancreatic cells triggered production of inflammatory chemicals that are central to the autoimmune reactions that lead to type 1 diabetes.
Normally, in humans, the virus attacks the lungs and gut, but not typically the pancreas. But it can sometimes get into the blood and travel to the pancreas, researchers said.
Capua is now testing the dibates-producing effects of the flu on mice, according to the New Scientist.
“Our findings indicate that influenza infection may play a role as a causative agent of pancreatitis and diabetes in humans and other mammals,” the study authors concluded in their report.
Thursday, 29 March 2012
Alzheimer's and Diabetes: Finding the Common Origin
Learn more about the pathological links between Alzheimer’s and diabetes, and how understanding more about them could lead to effective therapies for both.
Alzheimer's Reading Room
Join Cure Alzheimer’s Fund Research Consortium member Sam Gandy, M.D., Ph.D., and David Shenk, author of the national bestseller, The Forgetting, for a free webinar about the linkage between Alzheimer’s disease and diabetes.
Alzheimer’s disease and Type II diabetes have been observed to have a clinical connection. Patients with diabetes are more than twice as likely to develop Alzheimer’s, as those without diabetes.
The precise nature of this connection has been a mystery until recently.
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Over the last few years, research projects funded by Cure Alzheimer’s Fund and others have helped bring us much closer to an understanding of the molecular connection—and, potentially, to effective treatments for both Alzheimer's and diabetes.
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Sam Gandy, MD, PhD, is Mount Sinai Professor of Alzheimer's Disease Research, Professor of Neurology and Psychiatry, Associate Director of the Mount Sinai Alzheimer's Disease Research Center in New York City, and Chairman Emeritus of the National Medical and Scientific Advisory Council of the Alzheimer's Association. Dr. Gandy is an international expert in the metabolism of the sticky substance called amyloid that clogs the brain in patients with Alzheimer's. In 1989, Gandy and his team discovered the first drugs that could lower formation of amyloid. Dr. Gandy has written more than 150 original papers, chapters and reviews on this topic. Dr. Gandy has received continuous NIH funding for his research on amyloid metabolism since 1986.
David Shenk is the award-winning and national-bestselling author of six books, including The Genius in All of Us ("deeply interesting and important" - New York Times), The Forgetting ("remarkable" - Los Angeles Times), Data Smog ("indispensable" - New York Times), and The Immortal Game ("superb" - Wall Street Journal). He is a popular lecturer, a short-film director, and a correspondent for TheAtlantic.com. He has contributed to National Geographic, Slate, The New York Times, The Wall Street Journal, Gourmet, Harper's, Spy, The New Yorker, NPR, and PBS. Shenk lives in Brooklyn.
More Insight and Advice from the Alzheimer's Reading Room
- How Alzheimer's Spreads Throughout the Brain
- Test Your Memory for Alzheimer's (5 Best Self Assessment Tests)
- What is Alzheimer's Disease?
- What is Dementia?
- What’s the Difference Between Alzheimer’s Disease and Dementia
- Communicating in Alzheimer's World
- How the Loss of Memory Works in Alzheimer’s Disease, and How Understanding This Could Help You
- Learning How to Communicate with Someone Suffering From Alzheimer's Disease
- Alzheimer's World -- Trying to Reconnect with Someone Suffering from Alzheimer's Disease
- Does the Combination of Aricept and Namenda Help Slow the Rate of Decline in Alzheimer's Patients
- Driving with Alzheimer's Can Mean Death
- About the Alzheimer's Reading Room
Original content Bob DeMarco, the Alzheimer's Reading Room
Sunday, 25 March 2012
Brain Insulin Resistance Contributes to Cognitive Decline in Alzheimer's Disease
This is the first study to directly demonstrate that insulin resistance occurs in the brains of people with Alzheimer's disease.
By Bob DeMarco
Alzheimer's Reading Room
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| Steven E. Arnold |
Insulin is an important hormone in many bodily functions, including the health of brain cells.
The team identified extensive abnormalities in the activity of two major signaling pathways for insulin and insulin-like growth factor in non-diabetic people with Alzheimer's disease. These pathways could be targeted with new or existing medicines to potentially help resensitize the brain to insulin and possibly slow down or even improve cognitive decline.
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Brain Insulin Resistance Contributes to Cognitive Decline in Alzheimer's Disease
This is the first study to directly demonstrate that insulin resistance occurs in the brains of people with Alzheimer's disease. The study is now online in the Journal of Clinical Investigation.
"Our research clearly shows that the brain's ability to respond to insulin, which is important for normal brain function, is going offline at some point. Insulin in the brain not only modulates glucose uptake, but also promotes the health of brain cells — their growth, survival, remodeling, and normal functioning.
We believe that brain insulin resistance may be an important contributor to the cognitive decline associated with Alzheimer's disease," said senior author, Steven E. Arnold, MD, professor of Psychiatry and Neurology. Arnold is also the director of the Penn Memory Center, a National Institute on Aging-designated Alzheimer's Disease Core Center.
"If we can prevent brain insulin resistance from occurring, or re-sensitize brain cells to insulin with any of the currently available insulin-sensitizing diabetes medicines, we may be able to slow down, prevent, or perhaps even improve cognitive decline".
The risk of developing Alzheimer's disease is increased by 50 percent in people with diabetes.
Type 2 diabetes is due to insulin resistance and accounts for 90 percent of all diabetes. The defining clinical feature of Type 2 diabetes (and Type 1 "juvenile" diabetes) is hyperglycemia — high levels of sugar in the blood — but there is no evidence that the brain in Alzheimer's is hyperglycemic. Insulin acts differently in the brain than in the rest of the body. Researchers found that insulin resistance of the brain occurs in Alzheimer's disease independent of whether someone has diabetes, by excluding people with a history of diabetes from this study.
The investigators used samples of postmortem brain tissue from non-diabetics who had died with Alzheimer's disease, stimulated the tissue with insulin, and measured how much the insulin activated various proteins in the insulin-signaling pathways. There was less insulin activation in Alzheimer's cases than in tissue from people who had died without brain disease. Other proteins linked to insulin action in the brain were abnormal in Alzheimer's disease samples. These abnormalities were highly correlated with episodic memory and other cognitive disabilities in the Alzheimer's disease patients.
In tissue from people with Alzheimer's disease and mild cognitive impairment (MCI), researchers found that changes to a protein called insulin receptor substrate-1 (IRS-1 pS636/639 and pS616) in brain cells were linked to the severity of memory impairments regardless of age, sex, diabetes history, or apolipoprotein E (APOE) gene status. Levels of IRS-1 were also significantly associated with, but not likely to affect, the presence of amyloid beta plaques and neurofibrillary tangles, the signature markers of Alzheimer's disease. This suggests that insulin resistance contributes to cognitive decline independent of the classical pathology of Alzheimer's disease.
Researchers noted that three insulin-sensitizing medicines are already approved by the FDA for treatment of diabetes. These drugs readily cross the blood-brain barrier and may have therapeutic potential to correct insulin resistance in Alzheimer's disease and MCI. "Clinical trials would need to be conducted to determine the impact the drugs have on Alzheimer's disease and MCI in non-diabetic patients," said Dr. Arnold.
The study's lead author, Konrad Talbot, PhD, is a Research Assistant Professor in Penn's Psychiatry department and co-lead author, Hoau-Yan Wang, Ph.D. is an Associate Medical Professor of Physiology and Pharmacology at the City University of New York. Along with Drs. Talbot and Arnold, the Perelman School of Medicine research team from Penn includes: Hala Kazi, Li-Ying Han, Robert L. Fuino, Krista R. Kawaguchi, Andrew J. Samoyed, from Psychiatry; Bryan A. Wolf (from Children's Hospital of Philadelphia) and John Q. Trojanowski, both from Penn's Department of Pathology and Laboratory Medicine. In addition, other researchers from the City University of New York Medical School and the Rush Alzheimer’s Disease Center from Rush University Medical Center contributed equally to this work.
The study was supported by the Alzheimer's Association (a T.L.L. Temple Foundation Discovery Award), the National Institute on Aging (at Penn: RO1 AG15819, P30 AG10124, at Rush: P30 AG10161) and the Allen H and Selma W. Berkman Charitable Trust. The study would not have been possible without all the patients and families that contributed to this study, as well as the volunteers in the Rush Religious Order Study.
_______________________________
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $4.3 billion enterprise.
Read More on the Alzheimer's Reading Room
- How Alzheimer's Spreads Throughout the Brain
- Test Your Memory for Alzheimer's (5 Best Self Assessment Tests)
- What is Alzheimer's Disease?
- What is Dementia?
- What’s the Difference Between Alzheimer’s Disease and Dementia
- Communicating in Alzheimers World
- How the Loss of Memory Works in Alzheimer’s Disease, and How Understanding This Could Help You
- Learning How to Communicate with Someone Suffering From Alzheimer's Disease
- Alzheimer's World -- Trying to Reconnect with Someone Suffering from Alzheimer's Disease
- About the Alzheimer's Reading Room
You are reading original content from the Alzheimer's Reading Room.
Monday, 23 January 2012
WHAT IS DIABETES
1) Type 1 diabetes is an autoimmune disease that occurs when the insulin-producing beta cells within the pancreas are destroyed and fail to produce insulin. Insulin is a hormone that helps the body's cells use glucose for energy. Blood glucose (or blood sugar) is manufactured from the food we eat (primarily carbohydrates) and by the liver. If glucose can't be absorbed by the cells, it builds up in the bloodstream instead. Untreated, the high blood sugars that result can be toxic to every system of the body, causing serious complications.
2) Type 2 diabetes is the most common form of the disease, accounting for 90 to 95% of all diabetes cases in America. Most people with type 2 diabetes are still able to produce insulin at diagnosis. However, the insulin they make does not work properly and is unable to perform its primary job, which is helping the body's cells use glucose for energy. This characteristic of type 2 diabetes is called insulin resistance.If left untreated, the high blood sugar levels from uncontrolled diabetes can cause serious long-term diabetic complications. Eventually, they damage the insulin-producing beta cells of the pancreas, reducing insulin output.
Although the majority of people with type 2 diabetes are adults, children and adolescents are increasingly at risk for the disease due to growing childhood weight problems and sedentary lifestyles.
3) GESTATIONAL DIABETES-The hormonal changes that happen in pregnancy can cause gestational diabetes in pregnant women at risk for the condition. Hormones produced by the placenta -- including estrogen, cortisol, and human placental lactogen (HPL) -- increase insulin resistance in some women, which results in high blood sugars. This usually occurs between 20 and 24 weeks of pregnancy. Gestational diabetes goes away when the baby is born, but women who have had the condition are at a higher risk of developing type 2 diabetes later in life.
4) LADA- Short for Latent Autoimmune Diabetes in Adults, LADA is also known as Slow-Onset Type 1 Diabetes, Type 1.5 Diabetes, Late-Onset Autoimmune Diabetes of Adulthood, and even "double diabetes," since it has elements of both type 1 and type 2 diabetes. LADA patients, however, are closer to type 1 patients because, just as I did, they will test positive for antibodies against insulin-producing beta cells of the pancreas.
LEARN BELOW IN THIS VIDEO -WHAT IS DIABETES
Thursday, 10 April 2008
Diabetes in Middle Age Raises Alzheimer's Risk
This a lengthy article. Follow the link for more information.
Men who develop diabetes in middle age may be at greater risk of Alzheimer's disease, a Swedish study finds.
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