5:16:00 AM jienceston 0 Comments

Ebola study to examine long term effects in survivors commences in Liberia

5:09:00 AM jienceston 0 Comments

The Liberia-U.S. clinical research partnership known as PREVAIL has launched a study of people in Liberia who have survived Ebola virus disease (EVD) within the past two years. The study investigators hope to better understand the long-term health consequences of EVD, determine if survivors develop immunity that will protect them from future Ebola infection, and assess whether previously EVD-infected individuals can transmit infection to close contacts and sexual partners. The study, sponsored by the Ministry of Health of Liberia and the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, will take place at various sites in Liberia and is expected to enroll approximately 7,500 people, including 1,500 people of any age who survived EVD and 6,000 of their close contacts.
“The clinical course of Ebola virus disease is reasonably well-understood, but we still have much to learn about the long-term health effects of the illness in those who recover,” said NIAID Director Anthony S. Fauci, M.D. “To unravel the many unknowns, we have expanded the focus of our partnership with Liberia’s Ministry of Health to include research on the long-term health effects of Ebola virus disease, in addition to our ongoing efforts to find an effective preventive vaccine and treatments for Ebola virus disease.”
Mosaka Fallah, Ph.D., M.P.H., former Ebola emergency-response program manager for Action Against Hunger–Liberia; Michael C. Sneller, M.D., from NIAID’s Laboratory of Immunoregulation; and Desmond Williams, M.D., Ph.D., from the U.S. Centers for Disease Control and Prevention, will serve as principal investigators for the study. Investigators from NIH’s National Eye Institute, the Johns Hopkins University Wilmer Eye Institute, Baltimore; the Ministry of Health of Liberia and the John F. Kennedy Medical Center in Sinkor, Monrovia, will also collaborate on the research. Enrollment began today at the John F. Kennedy Medical Center, and the study will open at the following sites later in June: C.H. Rennie Hospital in Kakata, Duport Road Clinic in Paynesville, and Redemption Hospital in Monrovia. Additional sites in Liberia are expected to join the study in the future.
Participants who test positive for HIV infection during the course of the study will be counseled and referred to treatment in accordance with standard medical practice in Liberia.
Study participants will undergo a medical history and physical and vision examination and have blood samples collected so researchers can identify and track any health issues, monitor organ and ocular function and record Ebola antibody levels. Some participants may also be asked to provide samples of bodily fluids, such as sweat, tears, and for adults, semen or cervical secretions. Participants will be asked if they would like to identify up to five close contacts (household members at the time of Ebola diagnosis and sexual partners after recovery from Ebola virus disease). Close contacts who agree to participate in the study will undergo a physical examination, have blood samples taken, and asked to complete a questionnaire detailing their contact with the Ebola survivor, such as touching, sleeping in the same bed and sexual intercourse. Staff from the NIH’s National Eye Institute have helped establish a new eye clinic at John F. Kennedy Medical Hospital, where ophthalmologists from NEI and Johns Hopkins will be evaluating study participants and their identified close contacts for visual problems. Treatment will be provided by Liberian ophthalmologists partnering in the study.
“There have been reports of inflammatory eye disease and vision loss among Ebola survivors,” said NEI Clinical Director Frederick Ferris, M.D. “Our goal is to determine the incidence and extent of Ebola-related eye disease among survivors, risk factors contributing to its development, and optimal treatment strategies.”
The research team will follow the Ebola survivors and their close contacts for up to five years with study visits occurring every six months. At each follow-up visit, participants will undergo a physical examination and additional blood draws, to allow study physicians to monitor and characterize any changes in Ebola antibody levels and to detect the presence of select medical conditions. This information will help scientists determine the evolution of Ebola antibodies and will provide insight on whether survivors can still transmit the virus and if so, whether these people get sick with Ebola virus disease.
Using data collected at these site visits, the researchers will calculate the incidence, prevalence and risk factors for various health issues experienced by survivors, such as vision problems; immune system changes; mental disorders; joint pain; diabetes; hypertension; and pregnancy complications. Close contacts will be used as a control group to assess whether the risks of these conditions are the same or different from those who have not had Ebola virus disease.
PREVAIL, or the Partnership for Research on Ebola Virus in Liberia, is a clinical research partnership between the U.S. Department of Health and Human Services and the Liberian Ministry of Health. The new study, an Ebola natural history study known as PREVAIL III, is one of three research projects launched by the partnership. In February 2015, PREVAIL initiated two other Ebola clinical studies. PREVAIL I is a clinical trial to assess the safety and efficacy of two experimental vaccines to prevent Ebola virus infection. A total of 1,500 participants continue to be followed in the Phase 2 segment of this study. PREVAIL II is a clinical trial designed to obtain safety and efficacy data on various investigational drugs for the treatment of Ebola virus disease. The trial is ongoing in Liberia, Sierra Leone and the United States

Complications After Ebola Survival

5:07:00 AM jienceston 0 Comments

A new report in the New England Journal of Medicine documents the lasting effects of survival from the Ebola virus, including muscle pains, nerve damage, and vision loss.
Ebola, a single stranded negative sense RNA virus of the family Filoviridae, is a hemorrhagic virus that caused thousands of deaths through most of 2014 and into 2015. There is no known cure for the virus, though there have been vaccine and pill successes in the past year. Patients are instead put on palliative care and treated for complications such as dehydration, a process that puts a significant strain on hospital systems and which only half of patients survive.
Those that survive the illness in past outbreaks have complained of after-effects, but this new report in NEJM is the first comprehensive analysis of all patients treated in the United States to determine the most prevalent and debilitating post-infection issues. The questionnaire and analysis were initially performed in March 2015.
SOURECE; OUTBREAK NEWS TUDAY
Of the physical symptoms, arthralgia (joint pain), alopecia (hair loss), and general muscle fatigue were the most common (75% of patients).  Neurological issues, such as insomnia and depression/anxiety, occurred in 62% and 50% of patients, respectively. Other symptoms included heart problems (50%), shortness of breath (38%), and hearing loss (12%).
Interestingly, 62% of patients had general blurriness in vision, and 40% of those patients had to eventually be treated for severe eye inflammation. It has been recently found that the eye is “immunoprotected”, meaning the immune system rarely mobilizes to the ocular cavity. While this fact is taken advantage of in stem cell treatments for diseases like macular degeneration, it also allows viruses and bacteria to live in and around the eye without any competition. As documented in National Geographic’s Breakthrough series’ highlight of Dr. Ian Crozier, an Ebola survivor, those that are infected with Ebola can harbor live virus in their eyes, making their tears and ocular secretions potentially infectious. Ongoing tests are still working to determine how infectious these individuals are.
Overall, most of the symptoms were present months after initial onset and some, like hair loss, never went away. While these are small issues compared to the debilitating and deadly effects of Ebola infection, they can still be life altering and should be studied further to aid the thousands of potential sufferers in West Africa.
Edward Marks is a PhD student at the University of Delaware.  His research involves the healing of myocardial tissue after major cardiac events using nanomedicine techniques, with the goal of pushing any advancement directly into the clinic.  Edward received his BS from Rutgers University and Masters from the University of Delaware.

NIDDK staff help combat Ebola in West Africa

4:53:00 AM jienceston 0 Comments

n the midst of the ongoing Ebola crisis in West Africa, during which more than 25,000 people to date have contracted the deadly virus, three intramural NIDDK staff answered the call to volunteer their services in some of the worst-affected areas. Nurse practitioners Michelle Braun and Michael Davis and registered nurse Megan Mattingly – all active members of the U.S. Public Health Service – each spent eight weeks in Liberia with their respective teams working to treat health care workers who became infected with Ebola.

Causes of Diabetes

4:45:00 AM jienceston 0 Comments

What is diabetes?

Diabetes is a complex group of diseases with a variety of causes. People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.
Diabetes is a disorder of metabolism—the way the body uses digested food for energy. The digestive tract breaks down carbohydrates—sugars and starches found in many foods—into glucose, a form of sugar that enters the bloodstream. With the help of the hormone insulin, cells throughout the body absorb glucose and use it for energy. Diabetes develops when the body doesn’t make enough insulin or is not able to use insulin effectively, or both.
Insulin is made in the pancreas, an organ located behind the stomach. The pancreas contains clusters of cells called islets. Beta cells within the islets make insulin and release it into the blood
 Islets within the pancreas contain beta cells, which make insulin and release it into the blood.
If beta cells don’t produce enough insulin, or the body doesn’t respond to the insulin that is present, glucose builds up in the blood instead of being absorbed by cells in the body, leading to prediabetes or diabetes. Prediabetes is a condition in which blood glucose levels or A1C levels—which reflect average blood glucose levels—are higher than normal but not high enough to be diagnosed as diabetes. In diabetes, the body’s cells are starved of energy despite high blood glucose levels.
Over time, high blood glucose damages nerves and blood vessels, leading to complications such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other complications of diabetes may include increased susceptibility to other diseases, loss of mobility with aging, depression, and pregnancy problems. No one is certain what starts the processes that cause diabetes, but scientists believe genes and environmental factors interact to cause diabetes in most cases.
The two main types of diabetes are type 1 diabetes and type 2 diabetes. A third type, gestational diabetes, develops only during pregnancy. Other types of diabetes are caused by defects in specific genes, diseases of the pancreas, certain drugs or chemicals, infections, and other conditions. Some people show signs of both type 1 and type 2 diabetes.

What causes type 1 diabetes?

Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells in the pancreas. In type 1 diabetes—an autoimmune disease—the body’s immune system attacks and destroys the beta cells. Normally, the immune system protects the body from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. But in autoimmune diseases, the immune system attacks the body’s own cells. In type 1 diabetes, beta cell destruction may take place over several years, but symptoms of the disease usually develop over a short period of time.
Type 1 diabetes typically occurs in children and young adults, though it can appear at any age. In the past, type 1 diabetes was called juvenile diabetes or insulin-dependent diabetes mellitus.
Latent autoimmune diabetes in adults (LADA) may be a slowly developing kind of type 1 diabetes. Diagnosis usually occurs after age 30. In LADA, as in type 1 diabetes, the body’s immune system destroys the beta cells. At the time of diagnosis, people with LADA may still produce their own insulin, but eventually most will need insulin shots or an insulin pump to control blood glucose levels.

Genetic Susceptibility

Heredity plays an important part in determining who is likely to develop type 1 diabetes. Genes are passed down from biological parent to child. Genes carry instructions for making proteins that are needed for the body’s cells to function. Many genes, as well as interactions among genes, are thought to influence susceptibility to and protection from type 1 diabetes. The key genes may vary in different population groups. Variations in genes that affect more than 1 percent of a population group are called gene variants.
Certain gene variants that carry instructions for making proteins called human leukocyte antigens (HLAs) on white blood cells are linked to the risk of developing type 1 diabetes. The proteins produced by HLA genes help determine whether the immune system recognizes a cell as part of the body or as foreign material. Some combinations of HLA gene variants predict that a person will be at higher risk for type 1 diabetes, while other combinations are protective or have no effect on risk.
While HLA genes are the major risk genes for type 1 diabetes, many additional risk genes or gene regions have been found. Not only can these genes help identify people at risk for type 1 diabetes, but they also provide important clues to help scientists better understand how the disease develops and identify potential targets for therapy and prevention.
Genetic testing can show what types of HLA genes a person carries and can reveal other genes linked to diabetes. However, most genetic testing is done in a research setting and is not yet available to individuals. Scientists are studying how the results of genetic testing can be used to improve type 1 diabetes prevention or treatment.

Autoimmune Destruction of Beta Cells

In type 1 diabetes, white blood cells called T cells attack and destroy beta cells. The process begins well before diabetes symptoms appear and continues after diagnosis. Often, type 1 diabetes is not diagnosed until most beta cells have already been destroyed. At this point, a person needs daily insulin treatment to survive. Finding ways to modify or stop this autoimmune process and preserve beta cell function is a major focus of current scientific research.
Recent research suggests insulin itself may be a key trigger of the immune attack on beta cells. The immune systems of people who are susceptible to developing type 1 diabetes respond to insulin as if it were a foreign substance, or antigen. To combat antigens, the body makes proteins called antibodies. Antibodies to insulin and other proteins produced by beta cells are found in people with type 1 diabetes. Researchers test for these antibodies to help identify people at increased risk of developing the disease. Testing the types and levels of antibodies in the blood can help determine whether a person has type 1 diabetes, LADA, or another type of diabetes.

Environmental Factors

Environmental factors, such as foods, viruses, and toxins, may play a role in the development of type 1 diabetes, but the exact nature of their role has not been determined. Some theories suggest that environmental factors trigger the autoimmune destruction of beta cells in people with a genetic susceptibility to diabetes. Other theories suggest that environmental factors play an ongoing role in diabetes, even after diagnosis.
Viruses and infections. A virus cannot cause diabetes on its own, but people are sometimes diagnosed with type 1 diabetes during or after a viral infection, suggesting a link between the two. Also, the onset of type 1 diabetes occurs more frequently during the winter when viral infections are more common. Viruses possibly associated with type 1 diabetes include coxsackievirus B, cytomegalovirus, adenovirus, rubella, and mumps. Scientists have described several ways these viruses may damage or destroy beta cells or possibly trigger an autoimmune response in susceptible people. For example, anti-islet antibodies have been found in patients with congenital rubella syndrome, and cytomegalovirus has been associated with significant beta cell damage and acute pancreatitis––inflammation of the pancreas. Scientists are trying to identify a virus that can cause type 1 diabetes so that a vaccine might be developed to prevent the disease.
Infant feeding practices. Some studies have suggested that dietary factors may raise or lower the risk of developing type 1 diabetes. For example, breastfed infants and infants receiving vitamin D supplements may have a reduced risk of developing type 1 diabetes, while early exposure to cow’s milk and cereal proteins may increase risk. More research is needed to clarify how infant nutrition affects the risk for type 1 diabetes.

What causes type 2 diabetes?

Type 2 diabetes—the most common form of diabetes—is caused by a combination of factors, including insulin resistance, a condition in which the body’s muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin. Symptoms of type 2 diabetes may develop gradually and can be subtle; some people with type 2 diabetes remain undiagnosed for years.
Type 2 diabetes develops most often in middle-aged and older people who are also overweight or obese. The disease, once rare in youth, is becoming more common in overweight and obese children and adolescents. Scientists think genetic susceptibility and environmental factors are the most likely triggers of type 2 diabetes.

Genetic Susceptibility

Genes play a significant part in susceptibility to type 2 diabetes. Having certain genes or combinations of genes may increase or decrease a person’s risk for developing the disease. The role of genes is suggested by the high rate of type 2 diabetes in families and identical twins and wide variations in diabetes prevalence by ethnicity. Type 2 diabetes occurs more frequently in African Americans, Alaska Natives, American Indians, Hispanics/Latinos, and some Asian Americans, Native Hawaiians, and Pacific Islander Americans than it does in non-Hispanic whites.
Recent studies have combined genetic data from large numbers of people, accelerating the pace of gene discovery. Though scientists have now identified many gene variants that increase susceptibility to type 2 diabetes, the majority have yet to be discovered. The known genes appear to affect insulin production rather than insulin resistance. Researchers are working to identify additional gene variants and to learn how they interact with one another and with environmental factors to cause diabetes.
Studies have shown that variants of the TCF7L2 gene increase susceptibility to type 2 diabetes. For people who inherit two copies of the variants, the risk of developing type 2 diabetes is about 80 percent higher than for those who do not carry the gene variant.¹ However, even in those with the variant, diet and physical activity leading to weight loss help delay diabetes, according to the Diabetes Prevention Program (DPP), a major clinical trial involving people at high risk.
Genes can also increase the risk of diabetes by increasing a person’s tendency to become overweight or obese. One theory, known as the “thrifty gene” hypothesis, suggests certain genes increase the efficiency of metabolism to extract energy from food and store the energy for later use. This survival trait was advantageous for populations whose food supplies were scarce or unpredictable and could help keep people alive during famine. In modern times, however, when high-calorie foods are plentiful, such a trait can promote obesity and type 2 diabetes.

Obesity and Physical Inactivity

Physical inactivity and obesity are strongly associated with the development of type 2 diabetes. People who are genetically susceptible to type 2 diabetes are more vulnerable when these risk factors are present.
An imbalance between caloric intake and physical activity can lead to obesity, which causes insulin resistance and is common in people with type 2 diabetes. Central obesity, in which a person has excess abdominal fat, is a major risk factor not only for insulin resistance and type 2 diabetes but also for heart and blood vessel disease, also called cardiovascular disease (CVD). This excess “belly fat” produces hormones and other substances that can cause harmful, chronic effects in the body such as damage to blood vessels.
The DPP and other studies show that millions of people can lower their risk for type 2 diabetes by making lifestyle changes and losing weight. The DPP proved that people with prediabetes—at high risk of developing type 2 diabetes—could sharply lower their risk by losing weight through regular physical activity and a diet low in fat and calories. In 2009, a follow-up study of DPP participants—the Diabetes Prevention Program Outcomes Study (DPPOS)—showed that the benefits of weight loss lasted for at least 10 years after the original study began.

Insulin Resistance

Insulin resistance is a common condition in people who are overweight or obese, have excess abdominal fat, and are not physically active. Muscle, fat, and liver cells stop responding properly to insulin, forcing the pancreas to compensate by producing extra insulin. As long as beta cells are able to produce enough insulin, blood glucose levels stay in the normal range. But when insulin production falters because of beta cell dysfunction, glucose levels rise, leading to prediabetes or diabetes.

Abnormal Glucose Production by the Liver

In some people with diabetes, an abnormal increase in glucose production by the liver also contributes to high blood glucose levels. Normally, the pancreas releases the hormone glucagon when blood glucose and insulin levels are low. Glucagon stimulates the liver to produce glucose and release it into the bloodstream. But when blood glucose and insulin levels are high after a meal, glucagon levels drop, and the liver stores excess glucose for later, when it is needed. For reasons not completely understood, in many people with diabetes, glucagon levels stay higher than needed. High glucagon levels cause the liver to produce unneeded glucose, which contributes to high blood glucose levels. Metformin, the most commonly used drug to treat type 2 diabetes, reduces glucose production by the liver.

The Roles of Insulin and Glucagon in Normal Blood Glucose Regulation

A healthy person’s body keeps blood glucose levels in a normal range through several complex mechanisms. Insulin and glucagon, two hormones made in the pancreas, help regulate blood glucose levels:

• Insulin, made by beta cells, lowers elevated blood glucose levels.
• Glucagon, made by alpha cells, raises low blood glucose levels.

When blood glucose levels rise after a meal, the pancreas releases insulin into the blood.

• Insulin helps muscle, fat, and liver cells absorb glucose from the bloodstream, lowering blood glucose levels.
• Insulin stimulates the liver and muscle tissue to store excess glucose. The stored form of glucose is called glycogen.
• Insulin also lowers blood glucose levels by reducing glucose production in the liver.

When blood glucose levels drop overnight or due to a skipped meal or heavy exercise, the pancreas releases glucagon into the blood.

• Glucagon signals the liver and muscle tissue to break down glycogen into glucose, which enters the bloodstream and raises blood glucose levels.
• If the body needs more glucose, glucagon stimulates the liver to make glucose from amino acids.

Insulin and glucagon help regulate blood glucose levels.

Metabolic Syndrome

Metabolic syndrome, also called insulin resistance syndrome, refers to a group of conditions common in people with insulin resistance, including

• higher than normal blood glucose levels
• increased waist size due to excess abdominal fat
• high blood pressure
• abnormal levels of cholesterol and triglycerides in the blood

People with metabolic syndrome have an increased risk of developing type 2 diabetes and CVD. Many studies have found that lifestyle changes, such as being physically active and losing excess weight, are the best ways to reverse metabolic syndrome, improve the body’s response to insulin, and reduce risk for type 2 diabetes and CVD.

Cell Signaling and Regulation

Cells communicate through a complex network of molecular signaling pathways. For example, on cell surfaces, insulin receptor molecules capture, or bind, insulin molecules circulating in the bloodstream. This interaction between insulin and its receptor prompts the biochemical signals that enable the cells to absorb glucose from the blood and use it for energy.
Problems in cell signaling systems can set off a chain reaction that leads to diabetes or other diseases. Many studies have focused on how insulin signals cells to communicate and regulate action. Researchers have identified proteins and pathways that transmit the insulin signal and have mapped interactions between insulin and body tissues, including the way insulin helps the liver control blood glucose levels. Researchers have also found that key signals also come from fat cells, which produce substances that cause inflammation and insulin resistance.
This work holds the key to combating insulin resistance and diabetes. As scientists learn more about cell signaling systems involved in glucose regulation, they will have more opportunities to develop effective treatments.

Beta Cell Dysfunction

Scientists think beta cell dysfunction is a key contributor to type 2 diabetes. Beta cell impairment can cause inadequate or abnormal patterns of insulin release. Also, beta cells may be damaged by high blood glucose itself, a condition called glucose toxicity.
Scientists have not determined the causes of beta cell dysfunction in most cases. Single gene defects lead to specific forms of diabetes called maturity-onset diabetes of the young (MODY). The genes involved regulate insulin production in the beta cells. Although these forms of diabetes are rare, they provide clues as to how beta cell function may be affected by key regulatory factors. Other gene variants are involved in determining the number and function of beta cells. But these variants account for only a small percentage of type 2 diabetes cases. Malnutrition early in life is also being investigated as a cause of beta cell dysfunction. The metabolic environment of the developing fetus may also create a predisposition for diabetes later in life.

Risk Factors for Type 2 Diabetes

People who develop type 2 diabetes are more likely to have the following characteristics:

• age 45 or older
• overweight or obese
• physically inactive
• parent or sibling with diabetes
• family background that is African American, Alaska Native, American Indian, Asian American, Hispanic/Latino, or Pacific Islander American
• history of giving birth to a baby weighing more than 9 pounds
• history of gestational diabetes
• high blood pressure—140/90 or above—or being treated for high blood pressure
• high-density lipoprotein (HDL), or good, cholesterol below 35 milligrams per deciliter (mg/dL), or a triglyceride level above 250 mg/dL
• polycystic ovary syndrome, also called PCOS
• prediabetes—an A1C level of 5.7 to 6.4 percent; a fasting plasma glucose test result of 100–125 mg/dL, called impaired fasting glucose; or a 2-hour oral glucose tolerance test result of 140–199, called impaired glucose tolerance
• acanthosis nigricans, a condition associated with insulin resistance, characterized by a dark, velvety rash around the neck or armpits
• history of CVD

The American Diabetes Association (ADA) recommends that testing to detect prediabetes and type 2 diabetes be considered in adults who are overweight or obese and have one or more additional risk factors for diabetes. In adults without these risk factors, testing should begin at age 45.

What causes gestational diabetes?

Scientists believe gestational diabetes is caused by the hormonal changes and metabolic demands of pregnancy together with genetic and environmental factors.

Insulin Resistance and Beta Cell Dysfunction

Hormones produced by the placenta and other pregnancy-related factors contribute to insulin resistance, which occurs in all women during late pregnancy. Insulin resistance increases the amount of insulin needed to control blood glucose levels. If the pancreas can’t produce enough insulin due to beta cell dysfunction, gestational diabetes occurs.
As with type 2 diabetes, excess weight is linked to gestational diabetes. Overweight or obese women are at particularly high risk for gestational diabetes because they start pregnancy with a higher need for insulin due to insulin resistance. Excessive weight gain during pregnancy may also increase risk.

Family History

Having a family history of diabetes is also a risk factor for gestational diabetes, suggesting that genes play a role in its development. Genetics may also explain why the disorder occurs more frequently in African Americans, American Indians, and Hispanics/Latinos. Many gene variants or combinations of variants may increase a woman’s risk for developing gestational diabetes. Studies have found several gene variants associated with gestational diabetes, but these variants account for only a small fraction of women with gestational diabetes.

Future Risk of Type 2 Diabetes

Because a woman’s hormones usually return to normal levels soon after giving birth, gestational diabetes disappears in most women after delivery. However, women who have gestational diabetes are more likely to develop gestational diabetes with future pregnancies and develop type 2 diabetes.³ Women with gestational diabetes should be tested for persistent diabetes 6 to 12 weeks after delivery and at least every 3 years thereafter.
Also, exposure to high glucose levels during gestation increases a child’s risk for becoming overweight or obese and for developing type 2 diabetes later on. The result may be a cycle of diabetes affecting multiple generations in a family. For both mother and child, maintaining a healthy body weight and being physically active may help prevent type 2 diabetes

Other Types and Causes of Diabetes

Other types of diabetes have a variety of possible causes.

Genetic Mutations Affecting Beta Cells, Insulin, and Insulin Action

Some relatively uncommon forms of diabetes known as monogenic diabetes are caused by mutations, or changes, in a single gene. These mutations are usually inherited, but sometimes the gene mutation occurs spontaneously. Most of these gene mutations cause diabetes by reducing beta cells’ ability to produce insulin.
The most common types of monogenic diabetes are neonatal diabetes mellitus (NDM) and MODY. NDM occurs in the first 6 months of life. MODY is usually found during adolescence or early adulthood but sometimes is not diagnosed until later in life. More information about NDM and MODY is provided in the NIDDK health topic, Monogenic Forms of Diabetes.
Other rare genetic mutations can cause diabetes by damaging the quality of insulin the body produces or by causing abnormalities in insulin receptors.

Other Genetic Diseases

Diabetes occurs in people with Down syndrome, Klinefelter syndrome, and Turner syndrome at higher rates than the general population. Scientists are investigating whether genes that may predispose people to genetic syndromes also predispose them to diabetes.
The genetic disorders cystic fibrosis and hemochromatosis are linked to diabetes. Cystic fibrosis produces abnormally thick mucus, which blocks the pancreas. The risk of diabetes increases with age in people with cystic fibrosis. Hemochromatosis causes the body to store too much iron. If the disorder is not treated, iron can build up in and damage the pancreas and other organs.

Damage to or Removal of the Pancreas

Pancreatitis, cancer, and trauma can all harm the pancreatic beta cells or impair insulin production, thus causing diabetes. If the damaged pancreas is removed, diabetes will occur due to the loss of the beta cells.

Endocrine Diseases

Endocrine diseases affect organs that produce hormones. Cushing’s syndrome and acromegaly are examples of hormonal disorders that can cause prediabetes and diabetes by inducing insulin resistance. Cushing’s syndrome is marked by excessive production of cortisol—sometimes called the “stress hormone.” Acromegaly occurs when the body produces too much growth hormone. Glucagonoma, a rare tumor of the pancreas, can also cause diabetes. The tumor causes the body to produce too much glucagon. Hyperthyroidism, a disorder that occurs when the thyroid gland produces too much thyroid hormone, can also cause elevated blood glucose levels.

Autoimmune Disorders

Rare disorders characterized by antibodies that disrupt insulin action can lead to diabetes. This kind of diabetes is often associated with other autoimmune disorders such as lupus erythematosus. Another rare autoimmune disorder called stiff-man syndrome is associated with antibodies that attack the beta cells, similar to type 1 diabetes.

Medications and Chemical Toxins

Some medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. Pentamidine, a drug prescribed to treat a type of pneumonia, can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoids—steroid hormones that are chemically similar to naturally produced cortisol—may impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.
Many chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxin—a contaminant of the herbicide Agent Orange, used during the Vietnam War—may be linked to the development of type 2 diabetes. In 2000, based on a report from the Institute of Medicine, the U.S. Department of Veterans Affairs (VA) added diabetes to the list of conditions for which Vietnam veterans are eligible for disability compensation. Also, a chemical in a rat poison no longer in use has been shown to cause diabetes if ingested. Some studies suggest a high intake of nitrogen-containing chemicals such as nitrates and nitrites might increase the risk of diabetes. Arsenic has also been studied for possible links to diabetes.

Lipodystrophy

Lipodystrophy is a condition in which fat tissue is lost or redistributed in the body. The condition is associated with insulin resistance and type 2 diabete

Points to Remember

• Diabetes is a complex group of diseases with a variety of causes. Scientists believe genes and environmental factors interact to cause diabetes in most cases.
• People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia. Diabetes develops when the body doesn’t make enough insulin or is not able to use insulin effectively, or both.
• Insulin is a hormone made by beta cells in the pancreas. Insulin helps cells throughout the body absorb and use glucose for energy. If the body does not produce enough insulin or cannot use insulin effectively, glucose builds up in the blood instead of being absorbed by cells in the body, and the body is starved of energy.
• Prediabetes is a condition in which blood glucose levels or A1C levels are higher than normal but not high enough to be diagnosed as diabetes. People with prediabetes can substantially reduce their risk of developing diabetes by losing weight and increasing physical activity.
• The two main types of diabetes are type 1 diabetes and type 2 diabetes. Gestational diabetes is a third form of diabetes that develops only during pregnancy.
• Type 1 diabetes is caused by a lack of insulin due to the destruction of insulin-producing beta cells. In type 1 diabetes—an autoimmune disease—the body’s immune system attacks and destroys the beta cells.
• Type 2 diabetes—the most common form of diabetes—is caused by a combination of factors, including insulin resistance, a condition in which the body’s muscle, fat, and liver cells do not use insulin effectively. Type 2 diabetes develops when the body can no longer produce enough insulin to compensate for the impaired ability to use insulin.
• Scientists believe gestational diabetes is caused by the hormonal changes and metabolic demands of pregnancy together with genetic and environmental factors. Risk factors for gestational diabetes include being overweight and having a family history of diabetes.
• Monogenic forms of diabetes are relatively uncommon and are caused by mutations in single genes that limit insulin production, quality, or action in the body.
• Other types of diabetes are caused by diseases and injuries that damage the pancreas; certain chemical toxins and medications; infections; and other conditions.
•  

Diabetes Increases Dementia Risk in Women

4:38:00 AM jienceston 0 Comments

Women with type 2 diabetes may be at risk of developing a type of dementia resulting from damaged or blocked blood vessels to the brain, a new research review suggests.

Analyzing data from nearly 2.5 million participants in 14 studies, an international team of scientists found that women with type 2 diabetes may have a nearly 20 percent higher risk of developing vascular dementia than men with diabetes. Vascular dementia is characterized by memory, thinking and language difficulties due to reduced blood flow to the brain, according to the Alzheimer's Association.

But the risk for any form of dementia was the same for both sexes -- about 60 percent higher for diabetics than for people without the disease, according to the research, published online Dec. 17 in the journal Diabetes Care.

Why Some Kids Face This Adult Health Problem;(hypertension)

5:34:00 AM jienceston 0 Comments

What parents can do to prevent and treat the issue.

Hypertension can put a man at more serious danger for a scope of cardiovascular issues – from heart assault to stroke. In any case, on the off chance that you believe it's just a grown-up issue, reconsider.

The quantity of children who have hypertension and what's called prehypertension, or marginal hypertension, has expanded generously as of late. Around 1 in 10 kids and young people ages 8 to 17 has hypertension or is considered at danger for creating it, as indicated by the most recent study and research information, which finds an expected 1 to 3 percent of youngsters and youths as of now have hypertension. The issue seems to be leveling off to some degree, says Wei Perng, research right hand educator of dietary sciences and the study of disease transmission at the University of Michigan School of Public Health. "In any case, it's worried this is going on at all in kids, on the grounds that truly hypertension should be an infection of later life," she says. "The contemplation is [that] this is driven by the weight pandemic that started in the '80s and truly sort of spun wild in the '90s [and] mid 2000s."

Perng drove research distributed online this month that assessed the connection between quick weight pick up right on time in life and a tyke's danger of growing hypertension later. The study found that increments in body mass list, or BMI – a measure of muscle to fat ratio ratios taking into account weight and tallness – in 0-to 6-month-olds and 2-to 3-year-olds was connected with higher systolic circulatory strain. That is the top number in a pulse perusing, which measures weight in the supply routes when the heart thumps. "Our discoveries recommend that more fast pick up in body mass list amid the initial 6 postnatal months and in the preschool years might prompt higher systolic circulatory strain in mid-adolescence, paying little respect to size during childbirth," the analysts wrote in an American Heart Association diary Hypertension.

That is noteworthy on the grounds that kids who have hypertension are significantly more liable to face the issue sometime down the road. "It's totally steady with the pattern as of late recognizing the quick put on in weight in more youthful kids – newborn children and little children – as a danger element for the improvement of hypertension later on in young people and adulthood," says Dr. Alan Lewis, a pediatric cardiologist at Children's Hospital Los Angeles. He includes that the exploration gives extra understanding into the early age ranges where fat increase is by all accounts connected with a trek in pulse later on.

The study incorporates more than 900 members from Project Viva, a continuous, long haul research investigation of ladies and youngsters.

Specialists say it's vital to nearly screen a tyke's weight pick up with your pediatrician to guarantee it's inside of a sound reach. "Keep away from the rotund child disorder," Lewis urges folks. "Verifiably a rotund child was seen as a sound infant and a flourishing infant and something to be empowered." But later research – strengthened by the study distributed in Hypertension – has demonstrated that included fat can unfavorably influence cardiovascular wellbeing, including by prompting hypertension.

Specialists likewise call attention to, in any case, that a finding of hypertension in a tyke could owe to numerous components past weight pick up, from a family history of hypertension to a hidden therapeutic issue, similar to a heart deformity. While the study in Hypertension demonstrated a relationship between more fast weight pick up amid outset and in little children with lifted circulatory strain levels in mid-adolescence, it didn't set up circumstances and end results, notes Dr. Cynthia Pan, a pediatric nephrologist, or kidney authority, at the Children's Hospital of Wisconsin and educator of pediatrics at the Medical College of Wisconsin. "In view of this, we would not suggest [that folks place] newborn children on strict eating regimens, and once more, folks ought to dependably look for exhortation from a pediatrician about their baby's development." However, for more established children, she emphasized proposals that kids who are stout are encouraged to battle the issue with adhering to a good diet and work out.

She additionally proposed that kids ages 3 and up be routinely screened for hypertension. That is in accordance with suggestions from the American Academy of Pediatrics. Then again, the U.S. Preventive Services Task Force, a free gathering of specialists that makes suggestions on preventive consideration, says that present confirmation is deficient to measure the advantages of screening asymptomatic kids and young people against any potential damages, similar to reactions from youngsters being put on circulatory strain solution.

Dr. Joseph Block, a pediatric cardiologist at the Children's Hospital of Wisconsin and colleague teacher of pediatrics at the Medical College of Wisconsin, says especially in kids, where purported auxiliary hypertension is more basic, it's vital to first distinguish if there's a fundamental medicinal reason for hypertension and treat that issue. That can likewise offer clinicians some assistance with gaging the short-and long haul suggestions for the youngster.

Children with essential hypertension – which isn't brought about by a basic therapeutic issue however may be identified with hereditary qualities and way of life components, similar to weight pick up – can likewise confront genuine wellbeing outcomes that influence both the heart and cerebrum. Extreme circulatory strain height in kids can bring about hypertensive encephalopathy, or neurological brokenness, Block says, notwithstanding hypertension raising the danger of heart issues and stroke not far off. "We're discovering more that these children [who] have hoisted pulse [face]

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