Diabetes Diet?

The Sweet Truth about Diabetes?

What Kind of Diabetes Do You Have?

 Kinds of Diabetes 

 Diabetes is not a single disease with a single cause. Rather, it is a collection of diseases, some more difficult to control than others. All forms of diabetes involve a hormone (body regulator) from the pancreas called insulin. If you have diabetes, either you lack insulin or the insulin you have is not doing its job properly. The result is that instead of being stored for energy through the action of insulin, the foods you eat (primarily the starches or carbohydrates) raise your blood sugar to higher-than-normal levels. Without treatment, your blood sugar remains high and has the potential of adversely affecting every organ and system in your body. With treatment, the insulin problem can be solved, and your blood sugar can be brought down or normalized so that the body is not damaged. A person with diabetes can thus remain healthy and look forward to a normal life span.

Information written on ancient Egyptian papyrus described diabetes as a disease that caused a person to melt into the loins and the resulting urine to attract ants (because of the sugar content). The name itself indicates the loss of valuable body fluids: diabetes is from a Greek word, meaning "to siphon." Mellitus, a Latin word, relates to a word meaning "honey" or "sweet tasting." Yes, due to the high sugar content and the lack of earlier testing methodologies, actually tasting the urine did give an indication that the person had sugar diabetes! In fact, Mother Nature was fooling the disease's early observers, who saw the crystalline content of the urine after its liquid contents had evaporated. In the fourteenth century, this was actually thought to be a salt (people were not into taste-testing at that time, we suppose).

Diabetes mellitus was treated, over time, by various means aimed at lowering the sugar content in the urine or decreasing the loss of fluid. Some patients fasted and feasted on alternating days, weeks, or months. Others were taught to eat rancid meat or vegetables cooked three times in their own water. Others survived on eggs or cereal. The association of food and fluid was passed down through time. Eventually, the discovery was made that the hormone insulin, secreted by cells called beta cells in the islets of Langerhans, needed to be replaced in the body in order for normal blood-glucose levels to be achieved.

Many people contributed to the knowledge about monitoring blood-glucose levels. Insulin could not be analyzed or its significant content noted until the 1960s. We learned that other hormones, such as glucagon, might help cause the disease. We also learned that diabetes is not the result of a single event in the body but of several events that lead to a series of immune responses, with the end result being that the majority of insulin-making cells (beta cells, found in the islets of Langerhans) are no longer working.

With the discovery of insulin, many people believed that diabetes had been cured. The medical community soon discovered that if the person lived longer, and especially when the blood-glucose levels were not significantly controlled or normalized the majority of the time, complications occurred (for example, blindness, heart disease, or the need for amputation). Many of these complications can now be prevented through present knowledge of this process or through getting to the doctor in time. Eyes (retinopathy) are being stabilized and vision returned (a risk reduction of 76 percent). In one case, a young man had 350/20 vision in the right eye, 400/20 in the left eye, a detached retina in the left eye, cataract development in both eyes, and cloudy fluid in the eyes due to past hemorrhages. With the lasering of the total retina surface, a procedure that reattached the retina to the back surface of the eye, replacement of the eye fluid, and lens removal and implant of a new lens, the eyes changed to 30/20 in the left eye and 40/20 in the right eye. Amputation, a procedure most associated with diabetes in its earlier days, can be prevented in an increasing number of cases (risk reduction of nerve disease or neuropathy: 60 percent). Other problems associated with other parts of the body (i.e., risk of kidney disease or nephropathy: 56 percent) are reversed earlier or treated with transplantation, something unheard of twenty-five or more years ago.

Education of the diabetes patient is one of the major keys to attaining such high degrees of control. Since health professionals cannot be with the person and his or her family on a day-in, day-out basis, self-management education is a must. Demand it.

Diabetes has been divided into three groups: Type 1, or insulin-dependent diabetes mellitus, in which insulin must be injected daily; Type 2, or insulin-resistant diabetes mellitus, in which insulin injection is usually not necessary; and secondary diabetes (due to pancreatic surgery or overactive glands, such as the pituitary or the adrenals). We are concerned here only with Type 1 and Type 2 diabetes.

Type 1 diabetes is believed to be caused by a combination of genetics and environmental stressors. The individual who develops Type 1 diabetes has an inability to make insulin. When insulin is absent, the cells are in a state of starvation, while an excess of sugar in the form of glucose is available in the blood. This state of high blood-glucose is called hyperglycemia or, in this case, diabetes mellitus. (Hyperglycemia may be caused by a number of stressors, but when it is due to problems with insulin it is called diabetes mellitus.) Despite eating vast amounts of food the person remains in a condition of starvation until adequate insulin is available and can get the food into the cells. Body fat is burned as an alternate fuel to sugar; a by-product, ketone bodies, is created as a source of energy. But ketones cause the accumulation of acids and upset the body's buffer system. The body develops a serious problem known as ketoacidosis, a chemical imbalance of the body accompanied by high blood sugar and also excess acid. This creates the classic symptoms of out-of-control diabetes: frequent urination (polyuria), excessive thirst (polydipsia), and excessive hunger (polyphagia). If neglected, ketoacidosis can eventually lead to death.

Type 2 diabetes, besides being called non-insulin dependent diabetes, has also been known by many other names, such as maturity onset diabetes, insulin resistant diabetes, non-ketosis prone, ketosis resistant, and even MODY or Maturity Onset Diabetes in the Young. Eighty to 85 percent of the diabetes population is diagnosed as having Type 2 diabetes. Of these, 88 percent or so are overweight. Many of the so-called borderline diabetics are Type 2s who have been mislabeled.

Insulin is still the key factor in this disease, but often there is an excess rather than a lack. The increase in insulin is believed to be the result of overeating. The excess insulin causes a decrease in the cell's number of insulin-receptor sites (that is, links to get the insulin into the cell). In the absence of receptor sites, the insulin does not work, and the result is diabetes (hyperglycemia). While the elevation in blood-glucose levels may lead to polyuria, polydipsia, and polyphagia, as in Type 1 diabetes, a key difference exists.

Insulin is the key factor in all forms of diabetes. In the case of Type 1 diabetes the problem is the lack of insulin. With Type 2 diabetes there may, at least early in the course of the disease, be an excess of the hormone. The cause of this excess is not entirely understood, but at least in part is due to an interaction of inherited characteristics interacting with some lifestyle problems. The life problems are aging, obesity, and inactivity. Though the inheritance for Type 2 diabetes is probably widespread through all peoples of the world, the disease is primarily seen in industrialized countries. This is thought to be due to the insulin resistance that comes from the excess food intake and decreased energy expenditure that results in obesity. When there is obesity in persons who have the inheritance for diabetes 2, for some reason the insulin does not work right at the periferal (muscle and fat) cell, and the pancreas must then produce more insulin to get the same result. This excess insulin production ultimately leads to exhaustion of the insulin-producing cells leading to decreased production. Now we have two defects: insulin resistance with increased insulin need, and insulin deficiency due to lack of production. The result will be increased blood sugar and diabetes with its resulting symptoms of excess urination (polyuria), excess thirst (polydipsia), and excess hunger (polyphagia). These symptoms are very prominent in Type 1 diabetes but may not be present in Type 2 diabetes until very late in the course of the disease when there is a marked lack of insulin.

In Type 1 diabetes there is a lack of insulin and polyphagia is usually accompanied by weight loss, but with Type 2 diabetes there more likely will be weight gain. The major function of insulin is storage of excess food so the weight gain is easily understandable. Overeating and obesity cause excess insulin that stores the excess food, causing more fat, which causes more insulin resistance and more insulin secretion, which stores more food, and so on. Decreasing food intake and increasing energy expenditure (exercising) to reduce obesity and take the strain off the pancreas to produce extra insulin are vital to treating this disease.

The cause of the insulin resistance is not known. We know there is an inherited defect, but its actual identity, is not known. Indeed there may be many inherited defects that can cause insulin resistance in the presence of obesity. These defects may include a defect in the number or shape of the chemical on the cell membrane which accepts the insulin (called a receptor) or in a variety of defects that can occur inside the cell so that the insulin cannot work properly. Many possible defects have been identified so that there can be many kinds of Type 2 diabetes. All, though, are related to obesity as the precipitating phenomenon leading to insulin resistance, excess insulin production, beta cell exhaustion, and decreased insulin production, (i.e. insulin deficiency). The result is high blood sugar which itself can be toxic to the insulin-producing cell and further damage them, leading to a greater decrease in insulin production, more insulin deficiency, and more increase in the blood sugar, resulting in a vicious cycle. Treatment should occur as early as possible to preserve the beta cell function and insulin production.

Type 1 diabetes is most often diagnosed in children with a peak incidence during the pre-adolescent growth spurt. The disease can occur at any age and must never be misdiagnosed just because the person is older. Type 2 diabetes is more common in people over age 35, but it can also occur at any age. We are in fact seeing an increase in this form of the disease in children associated with an increase in obesity of our children. People with newly diagnosed Type 1 diabetes have a tendency to be thin and have lost weight. People with Type 2 diabetes are usually obese and will have gradually gained weight. Both types may require insulin for treatment. Type 1 patients are insulin dependent, i.e. they will die without the hormone replacement, while Type 2 may require insulin to control the blood sugar but will not die soon without it, although they will develop the long-term complications that ultimately will be fatal. Sometimes these two forms of diabetes are difficult to tell apart. Some tests can be done to differentiate them but these tests can be expensive, and family history and symptoms are more often used and are usually effective in differentiating the two types.

In 1997, new criteria for diagnosis and classification terminology were developed. These are shown in Tables 1-1 and 1-2. All diabetes is diagnosed by one of three criteria: (1) a fasting plasma glucose level (FPG) of 126 mg/dl or 7 mmol (the measure used in most countries other than the USA- the conversion factor is 18) on two occasions, (2) a value of 200 mg/dl or 11 mmol at two hours after an oral glucose load (rarely used anymore), or (3) a random value greater than 200 mg/dl or 11 mmol if associated with symptoms usually associated with diabetes. These are the criteria that should be used today for diagnosis in all patients. If the FPG is greater than normal (105 mg/dl-6 mmol) but less than (126 mg/dl-7 mmol) or the 2-hour value on the oral glucose tolerance test is greater than 140 mg/dl-7.08 mmol but less than 199 mg/dl-11.1 mmol, the diagnosis is Impaired Fasting Glucose or Impaired Glucose Tolerance. We no longer use the term a borderline diabetic which used to be used for these intermediate states since that term has no meaningful criteria and is subject to any physician's interpretation. The above terms have precise definitions and are the same from doctor to doctor.

Type 1 diabetes has two subcategories: (1) autoimmune and (2) ideopathic. By this we mean that class 1 are of known cause in that there is absolute insulin deficiency caused by a defect in the immune system that destroys the beta cells of the pancreas. Ideopathic means that some other cause such as removal of the pancreas, destruction of the pancreas by infection, inflammation or chemicals, or some unknown cause has destroyed the beta cells or the entire pancreas so again there is complete insulin deficiency but not from destruction by the immune system. Type 2 diabetes can be subclassed as well but the subclasses are still being developed. Most are adult and most are obese. The next classification is Impaired Fasting Glucose (IFG) or Impaired Glucose Tolerance (IGT), and the last class is Gestational Diabetes, which will be discussed later.

With Type 1 (insulin-dependent) diabetes, after the acute episode (diabetic ketoacidosis) or early symptoms leading to the diagnosis (frequent passing of urine, normal eating with weight loss, extreme thirst), there may be a partial remission period (the honeymoon) in which the body appears to be able to make some insulin again. This period usually lasts from three to six months, but it may last longer, depending on the suppression of the insulin-making ability of the beta cells through an external insulin-injection program. Illness, poor blood sugar control, or extreme emotional stress appear to aid in further destruction of the beta cells, as does growth, and may shorten the remission period. Eventually, the person becomes totally insulin dependent, especially if more than 90 percent of the beta cells become inactive. Except during the honeymoon or period of partial remission, people with Type 1 diabetes cannot make insulin. There will be no measurable insulin levels except that which is injected and no measurable levels of any of the by-products of internal insulin secretion such as a protein called C-Peptide which can differentiate internal and external insulin when it is present.

C-Peptide is present in persons with Type 2 diabetes often in large amounts consistent with the elevated insulin levels and can be used to differentiate Type 1 from Type 2 diabetes. As time goes on and insulin secretion is decreased in Type 2 diabetes, C-Peptide will decrease as well and make this tool use less to differentiate the different kinds of diabetes. C-Peptide is expensive and not of much value except in a research setting.