A growing number of people in the U.S. and throughout the world are overweight and more prone to develop Type 2 diabetes, particularly if they have the genetics for it. "Type 2 diabetes can be caused by genetic inheritance, but by far the obesity epidemic has created massive increases in the occurrence of Type 2 diabetes. This is due to the major insulin resistance that is created by obesity," Gage says.
A. Diabetes is the inability of the body to ‘produce insulin - type 1 diabetes’ or ‘proper use of insulin - type 2 diabetes, gestational diabetes and pre-diabetes’. Diabetes is often goes undiagnosed because many of the symptoms of diabetes seems harmless. The causes of diabetes continues to be a mystery, pancreas it the organ whose defect causes diabetes.
Insulin is needed to allow glucose to pass from the blood into most of the body cells. Only the cells of the brain and central nervous system can use glucose from the blood in the absence of insulin. Without insulin, most body cells metabolize substances other than glucose for energy. However, fat metabolism in the absence of glucose metabolism, creates ketone bodies which are poisonous and their build up is associated with hyperglycemic coma. In the absence of sufficient insulin, unmetabolized glucose builds up in the blood. Water is drawn from body cells by osmosis to dilute the highly concentrated blood, and is then excreted along with much of the glucose, once the renal threshold for glucose (usually 10 mmol/L) is exceeded. Dehydration follows.
Every cell in the human body needs energy in order to function. The body's primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.
Can you “exercise your way” out of this problem? Sometimes you can; however, the key is exercising properly. For younger patients, it is best to exercise briefly and intensely. Within the first 20 minutes of intense exercise, your body burns its sugar stores, which are hanging out in liver and muscle again. After that, you start burning fat. Although this sounds good; and to some extent it is, if you spend hours running or exercising excessively, you train your body to burn fat efficiently, which subsequently lead to also training your body to store fat efficiently.
Beta cells are vulnerable to more than just bad genes, which may explain the associations between type 2 diabetes and environmental factors that aren't related to how much fat a body has or where it is stored. Beta cells carry vitamin D receptors on their surface, and people with vitamin D deficiency are at increased risk for type 2. Plus, several studies have shown that people with higher levels of toxic substances in their blood—such as from the PCBs found in fish fat—are at increased risk of type 2 diabetes, though a cause-and-effect relationship hasn't been proved. (Toxic substances and vitamin D have also been implicated in type 1 diabetes, but the disease mechanism may be unrelated to what's going on in type 2.)
After a diagnosis of diabetes mellitus has been made, and treatment with insulin therapy has begun, a so-called ‘honeymoon stage’ may develop. This stage is characterised by a reduction in insulin requirements which may last from weeks to months. Some patients may require no insulin at all. This stage is always transient (short-lasting) and is due to production of insulin by the remaining surviving pancreatic beta cells. Eventually, these cells will be destroyed by the on-going auto-immune process, and the patient will be dependent on exogenous (artificial) insulin.
Insulin is a hormone that — in people without diabetes — ferries glucose, or blood sugar, to cells for energy or to be stored for later use. In people with diabetes, cells are resistant to insulin; as a result of this insulin resistance, sugar accumulates in the blood. While eating sugar by itself does not cause insulin resistance, Grieger says, foods with sugar and fat can contribute to weight gain, thereby reducing insulin sensitivity in the body.
Commonly, diabetic patients’ random blood glucose measurement will be greater than 200 mg/dL. Additionally, diabetic patients’ urinalysis will be positive for greater than 30 mg/g of microalbumin on at least two of three consecutive sampling dates. Type 2 diabetics who have had diabetes mellitus for more than 2 years will usually have a fasting C-peptide level greater than 1.0 ng/dL. Patients with type 1 diabetes will have islet cell and anti-insulin autoantibodies present in their blood within 6 months of diagnosis. These antibodies, though, usually fade after 6 months.
Being too heavy gets the bulk of the blame for triggering type 2 diabetes. According to the National Institutes of Health, about 85 percent of people with type 2 diabetes are overweight or obese. But consider that the remaining 15 percent are not. Consider, too, that roughly two-thirds of overweight people and a third of those who are obese will never develop diabetes. In other words, normal-weight and thin people also develop type 2, while heavy people won't necessarily. Clearly, there is more to the connection between lifestyle and type 2 diabetes than just body size.
Diabetic foot disease, due to changes in blood vessels and nerves, often leads to ulceration and subsequent limb amputation. It is one of the most costly complications of diabetes, especially in communities with inadequate footwear. It results from both vascular and neurological disease processes. Diabetes is the most common cause of non-traumatic amputation of the lower limb, which may be prevented by regular inspection and good care of the foot.
It is a considerable challenge to obtain the goals of the intensively treated patients in the DCCT with the vast majority of people with diabetes given the more limited health care resources typically available in routine practice. If diabetes control can be improved without significant damage to quality of life, the economic, health, and quality of life savings associated with a reduction in complications in later life will be vast. Although some people who have had poorly controlled diabetes over many years do not develop complications, complications commonly arise after 15–20 years of diabetes and individuals in their 40s or even 30s may develop several complications in rapid succession. However, up until the early 1980s, patients had no way of monitoring their own blood glucose levels at home. Urine glucose monitoring only told them when their blood glucose had exceeded the renal threshold of approximately 10 mmol/L (i.e., was far too high), without being able to discriminate between the too high levels of 7–10 mmol/L or the hypoglycemic levels below 4 mmol/L. Clinics relied on random blood glucose testing and there were no measures of average blood glucose over a longer period. Since the 1980s there have been measures of glycosylated hemoglobin (GHb, HbA1, or HbA1c) which indicate average blood glucose over a six to eight week period and measures of glycosylated protein, fructosamine, which indicates average blood glucose over a two-week period. Blood-glucose meters for patients were first introduced in the early 1980s and the accuracy and convenience of the meters and the reagent strips they use has improved dramatically since early models. By the late 1990s blood-glucose monitoring is part of the daily routine for most people using insulin in developed countries. Blood-glucose monitoring is less often prescribed for tablet- and diet-alone-treated patients, financial reasons probably being allowed to outweigh the educational value of accurate feedback in improving control long term. The reduced risk of hypoglycemia and diabetic ketoacidosis in NIDDM patients not using insulin means that acute crises rarely arise in these patients though their risk of long-term complications is at least as great as in IDDM and might be expected to be reduced if feedback from blood-glucose monitoring were provided.
Diabetes that's triggered by pregnancy is called gestational diabetes (pregnancy, to some degree, leads to insulin resistance). It is often diagnosed in middle or late pregnancy. Because high blood sugar levels in a mother are circulated through the placenta to the baby, gestational diabetes must be controlled to protect the baby's growth and development.
Louis B. Malinow, MD is an MDVIP-affiliated physician that's been practicing in Baltimore for more than 20 years. He's board certified in Internal Medicine, a certified Hypertension Specialist and a Diplomate of the American Board of Clinical Lipidology. Dr. Malinow graduated from the University of Maryland School of Medicine and completed his residency at Stanford University Hospital in Stanford, CA. Dr. Malinow is one of the only physicians in Maryland that specializes in both high blood pressure and high cholesterol management. He is also a member of the prestigious Alpha Omega Alpha medical honor society and is recognized by Best Doctors and Top Doctor by U.S. News & World Report and Baltimore Magazine. Dr. Malinow has appeared on numerous news programs advocating for preventive care and wellness.
1. Monitoring of blood glucose status. In the past, urine testing was an integral part of the management of diabetes, but it has largely been replaced in recent years by self monitoring of blood glucose. Reasons for this are that blood testing is more accurate, glucose in the urine shows up only after the blood sugar level is high, and individual renal thresholds vary greatly and can change when certain medications are taken. As a person grows older and the kidney is less able to eliminate sugar in the urine, the renal threshold rises and less sugar is spilled into the urine. The position statement of the American Diabetes Association on Tests of Glycemia in Diabetes notes that urine testing still plays a role in monitoring in type 1 and gestational diabetes, and in pregnancy with pre-existing diabetes, as a way to test for ketones. All people with diabetes should test for ketones during times of acute illness or stress and when blood glucose levels are consistently elevated.
High blood sugar levels (hyperglycemia) can lead to a condition called glucose toxicity. This leads to further damage to the pancreas, and the body is less able to produce insulin. Without insulin, glucose levels continue to rise to levels that can cause damage to organs such as the eyes, nerves, and kidneys. These problems are similar to the complications associated with type 1 diabetes.
Type 2 diabetes is different. A person with type 2 diabetes still produces insulin but the body doesn't respond to it normally. Glucose is less able to enter the cells and do its job of supplying energy (a problem called insulin resistance). This raises the blood sugar level, so the pancreas works hard to make even more insulin. Eventually, this strain can make the pancreas unable to produce enough insulin to keep blood sugar levels normal.
Type 1 diabetes is always treated with insulin, a life-saving treatment. Patients will need to take insulin several times a day for the rest of their lives. They will usually learn how to self-administer this. Insulin is usually given through injections under the skin, normally two to four times a day. An increasing number of patients with type 1 diabetes are being treated with ‘insulin pumps’, which provide a continuous supply of insulin.
People with diabetes either don't make insulin or their body's cells no longer are able to use the insulin, leading to high blood sugars. By definition, diabetes is having a blood glucose level of greater than or equal to126 milligrams per deciliter (mg/dL) after an 8-hour fast (not eating anything), or by having a non-fasting glucose level greater than or equal to 200 mg/dL along with symptoms of diabetes, or a glucose level of greater than or equal to 200 mg/dL on a 2-hour glucose tolerance test, or an A1C greater than or equal to 6.5%. Unless the person is having obvious symptoms of diabetes or is in a diabetic crisis, the diagnosis must be confirmed with a repeat test.
A chronic metabolic disorder in which the use of carbohydrate is impaired and that of lipid and protein is enhanced. It is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma. Long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
In type 2 diabetes (formerly called non– insulin-dependent diabetes or adult-onset diabetes), the pancreas often continues to produce insulin, sometimes even at higher-than-normal levels, especially early in the disease. However, the body develops resistance to the effects of insulin, so there is not enough insulin to meet the body’s needs. As type 2 diabetes progresses, the insulin-producing ability of the pancreas decreases.