CSA_TX said:
If a parent lets there kids eat or feeds there kid nothing but crap then who else is there to blame? That is their business but don't come whining to me when your kid has diabetes or gets picked on for being fat. Parents should be at the schools demanding that there kids get more than 1 day a week of PE.
Ok I have to reply to a small part of this. The part about Diabetes. I want to educate you people on a subject that people commonly misunderstand, and it really pisses me. Mainly because I am diabetic, secondly because everyone thinks there is only one kind of diabeties.
So I found this artical on the causes of diabetes for everyone to read. Just for the record my brother delevoped Type 1 Diabetes when he was 5, I developed it when I was 29. Neither of us is overweight, we both grew up in the same household, same schools, eating the same foods, and pretty much doing the same thing.
While it is true that some of the causes for type 2 can be linked to diet, and exercise their are many more causes than just that. So please read and educate yourself.
From "http://my.webmd.com/content/article/3/1680_51021?src=Inktomi&condition=Health%20Topics%20A-Z"
Causes of Diabetes
Drugs such as steroids, Dilantin, and others may elevate the blood sugar through a variety of mechanisms. Certain other drugs, such as alloxan, streptozocin, and thiazide diuretics, are toxic to the beta cells of the pancreas and can cause diabetes. Certain syndromes (for example, Prader-Willi, Down's, Progeria, and Turner's) may result in a hyperglycemic state; if this state is prolonged, the result can be permanent diabetes.
Diabetes resulting in an insulin-dependent state is classified as Type 1 diabetes. While Type 1 diabetes affects only between 5 to10 percent of the diabetic population, its effects on the body can be worse than other forms of diabetes. In the past, Type 1 has been known as juvenile or juvenile-onset diabetes (because it is usually diagnosed in those under thirty), brittle diabetes, unstable diabetes, and ketosis-prone diabetes. People in this classification more frequently exhibit the classic symptoms, usually with ketones present in blood and urine. A blood-sugar level of 800 mg/dl (44 mmol) or more, especially if ketones are not present, indicates a diagnosis of hyperglycemic hyperosmolar nonketotic syndrome (a state in which the body is extremely dry (dehydrated), the chemicals in the body are concentrated, and the blood sugar is high).
As stated before, diabetes is a syndrome or group of diseases (rather than one disease), leading to the prolonged hyperglycemic state. Type 1 is most associated with the killing of the beta cells, most likely by the body's own immune system. Either the immune system cannot kill an infecting agent, which then kills the beta cells, or the immune system itself goes "wild," attacking the body's own tissue and destroying the beta cells. The cells of the islets of Langerhans are inflamed, resulting from an infectious-disease process (for example, mumps) or, more commonly, from an autoimmune (allergic to self) response.
The autoimmune process results in the circulation of antibodies that may either cause or be caused by beta-cell death. If it is found that the antibodies cause beta-cell destruction (the body fighting what it now considers foreign to itself), the body's response to the Type 1 diabetes is much less severe (i.e., easier to control) with treatment. Until then, the outcome is a lack of available insulin. While the onset is said to be sudden, changes resulting in decreased insulin availability may have occurred over a longer period of time. In short, insulin-dependent diabetes mellitus is an inherited defect of the body's immune system, resulting in destruction of the insulin-producing beta cells of the pancreas.
Heredity is a major cause of diabetes. If both parents have Type 2 diabetes, there is a chance that nearly all of their children will have diabetes. If both parents have Type 1 diabetes, fewer than 20 percent of their children will develop Type 1 diabetes. In identical twins, if one twin develops Type 2 diabetes, the chance is nearly 100 percent that the other twin will also develop it. In Type 1 diabetes, however, only 40 to 50 percent of the second twins will develop the disease, indicating that while inheritance is important, environmental factors (for example, too much food, too much stress, viral infection, and so forth) are also involved in the development of Type 1 diabetes.
Causes of Type 1 Diabetes
Type 1 diabetes is an inherited defect of the immune system triggered by an environmental stimuli. The problem may be in the on switch of the immune system in which the viral stimuli do not turn the system on. The virus is then allowed to penetrate the beta cell and cause its destruction. Conversely, the problem may be in the off switch in that the system turns on appropriately and kills the virus but then does not turn itself off. The T-cells are then allowed to attack the beta cells themselves. This is a very simplified explanation. In point of fact, it is much more complex, involving many, many steps in the immune system. The beta cells themselves may contribute to this by producing antigens or chemicals on the cell surface that stimulate the immune system, and there may be many other environmental stimuli rather than just viruses. Indeed, there is some evidence now that protein in cows' milk may cause the formation of antibodies that can attach to the beta cell or that are similar to antibodies on the beta cell. When the immune system mobilizes in response to a stimulus, these antibodies will attach to receptors on the surface of the beta cell causing the damage to occur to the beta cells of the pancreas. For whatever reason, the beta cells are then destroyed by the immune system in what is called an autoimmune phenomena, in which the body has come to recognize itself as a foreign body and begins to eliminate certain parts.
Recently researchers have been attempting to locate the genes for diabetes. As a part of the genome project, in which researchers around the world are attempting to map the entire gene structure of all the human chromosomes, they have isolated 18 genes that appear to be involved in the production of Type 1 diabetes. Not all of these genes have equal potency. Two of them appear to be most potent, some others are least potent, and others are simply auxiliary or helper genes that seem to have some assisting effect in the process. There are also genes which are protective so that one might inherit the genes for diabetes, but if you also inherited the protective genes, you would not develop the disease. Thus, development of the disease is not 100 percent in those who have inherited the genetics for the disease. Those people may have the genes but may either have protector genes or may be fortunate enough to avoid the environmental stimuli.
The cause of Type 1 diabetes, then, is an inherited defect in the immune system that interacts in some way with environmental factors. These factors may be viruses or chemicals in the environment or perhaps other environmental factors that we have not yet identified, which team up together to result in the eventual complete destruction of the beta cells and the loss of insulin secretion.
Causes of Type 2 Diabetes
The cause of Type 2 diabetes is not as well understood. Two factors appear to be important in Type 2 diabetes. These are insulin resistance and insulin deficiency. There is a debate over which comes first, but the general consensus of the moment is that insulin resistance is the first factor. Type 2 diabetes is also a genetic disease, although the genes are carried on entirely different chromosomes than those for Type 1 diabetes. There are probably multiple genes involved in this disease. For whatever reason, this genetic factor, perhaps interacting with some environmental factors such as obesity, excess caloric intake, deficient caloric expenditure, and aging, may result then in a resistance to insulin. That is, the peripheral cell, a muscle or fat or other cell, does not respond appropriately to the insulin present. The body then begins to produce more insulin in order to try to overcome the insulin resistance. The next part of the sequence may involve two factors. One is that the increasing insulin secretion may ultimately exhaust the beta cells, thus resulting in insulin deficiency. Another factor has been identified recently and this is called glucotoxicity. It turns out that sugar in high amounts can be toxic or poisonous to the cells of the body. In the person with insulin resistance who is running high blood sugars that have been undetected and untreated, or even in the person who know he or she has the disease but does not treat it appropriately, the continuing high levels of sugar have a toxic effect on the insulin-producing cells of the pancreas, thus damaging those cells and reducing insulin secretion. So we then end up with a combination of peripheral resistance to the action of insulin and at the same time insulin deficiency, and those two can then precipitate a severe case of Type 2 diabetes that may in fact require insulin for treatment. There are many steps in the action of insulin at the peripheral cell level, and each of those steps is stimulated by a different enzyme, and each enzyme is controlled by a different gene. Therefore, there are many potential places where the defects can occur, resulting in the same ultimate end: resistance of the peripheral cell to the action of insulin. This is probably the precipitating factor in Type 2 diabetes.
There is an increase in the diabetes for both Type 1 and Type 2 disease but a more pronounced increase in Type 2. The increase is at the rate of about 6 percent per year, which means the number of people with diabetes will double every 15 years. In the United States this increase is occurring predominately in the non-white ethnic populations. The prevalence of diabetes in the Caucasian population is approximately 5 to 6 percent; in the black population it is somewhere between 12 to 15 percent; in the Hispanic population it is around 20 percent; and in the Native American population it frequently exceeds 30 percent. Indeed, there are tribes in which the prevalence may be as high as 65 percent. Likewise, diabetes is increasing in the world, particularly in developing countries. The disease is very rare in third world or undeveloped countries. But as these countries begin to develop and achieve industrial prominence and economic stability there is a mushrooming of the amount of diabetes occurring in these cultures. This was seen in Japan after World War II and most recently in Korea and Taiwan, and it is now occurring in other Southeast Asian countries as the standard of living begins to increase. It is thought that this increase is probably related to increased caloric intake associated with decreased caloric expenditure. The genes for Type 2 diabetes are probably widespread throughout the world in equal amounts for all races and ethnic groups, but the change in lifestyle from manual labor with a low caloric intake to industrial labor with a high caloric intake and reduced caloric expenditure, because of the use of machinery, can then result in a virtual explosion of Type 2 diabetes.
Type 1 diabetes is pervalent in certain geographic areas that are closest to the equator, and as one moves farther north to the arctic circle the prevalence of the disease increases. The highest incidence occurs in the Scandinavian countries; the lowest in the Mediterranean area except for the Island of Sardinia which has an incidence equal to that of Finland. The reasons for these differences are not well understood but it is believed to be due to a change in diet from Brahman cows to English cows a few years ago. It is believed that there may be in English cows used throughout Europe and the Western Hemisphere a protein that may somehow cause the damage to the pancreas and that this protein is lacking in the milk of Brahman cows used in Africa and Asia. Time and research will tell if this is a causative factor in Type 1 diabetes in Europe and North America.