Insulin: What It Is, What It Does Atthe centerof diabetes is the pancreas, a large glandabout the size of your hand, which is located towardthe back of the abdominal cavity and is responsible for manufacturing, storing, and releasing the hor mone insulin.
The pancreas also makes several other hormones, as well as digestive enzymes.
Even if you don't know much about dia betes,in all likelihoodyou'veheard of insulin and probably know that we all have to have insulin to survive.
What you might not realize is that only a small percentageof diabetics must have insulin shots.
Insulin is a hormone produced by the beta cells of the pancreas.In sulin's major function is to regulate the level of glucose in the blood stream, which it does primarily by facilitating the transport of blood glucose into most of the billions of cells that make up the body.
The presenceof insulin stimulates glucosetransporters to move to the sur face of cells to facilitate glucose entry into the cells.
Insulin also stimu-
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lates centers in the hypothalamus of the brain responsible for hunger and satiety.
Indeed, there is some insulin production even as one be gins to eat, before glucose hits the bloodstream.
Insulin also instructs fat cells to convert glucose and fatty acids from the blood into fat, which the fat cells then store until needed.
Insulin is an anabolic hor mone, which is to saythat it is essential for the growth of many tissues and organs.* In excess, it can cause excessive growth, as,for exam ple, of body fat and of cells that line blood vessels.
Finally, insulin helps to regulate, or counterregulate, the balance of certainother hor mones in the body.
More about those later.
One of the ways insulin maintainsthe narrow range of normal lev els of glucose in thebloodisbyregulation of the liver and muscles, di recting them to manufacture and store glycogen, a starchysubstance the body uses when blood sugar falls too low.
If blood sugar does fall even slightlytoo low, as may occur after strenuous exercise or fast ing , the alpha cells of the pancreas release glucagon, another hor mone involved in the regulation of blood sugarlevels.
Glucagonsignals the muscles and liver to convert their stored glycogen back into glu cose (a processcalledglycogenolysis), which raises blood sugar.When the body's stores of glucose and glycogen have been exhausted, the liver, and to a lesser extent the kidneys and small intestines, can trans form some of the body's protein stores , muscle mass and vital or gans , into glucose.
Insulin and Type 1 Diabetes As recently as eighty-five years ago, before the clinical availabiHty of insulin, the diagnosis of type 1 diabetes , which involves a severely diminished or absent capacityto produce insulin , was a death sen tence.Most peopledied within a few months of diagnosis. Without in sulin, glucose accumulates in the blood to extremelyhigh toxic levels; yet since it cannot be utilized by the cells, many cell types will starve. Absent or lowered fasting (basal) levels of insulin also lead the liver, kidneys, and intestines to performgluconeogenesis, turning the body's protein store , the muscles and vital organs, into even more glu cose that the body cannot utilize.Meanwhile,the kidneys, the filters of the blood, try to rid the body of inappropriately high levels of sugar.
*Anabolicand catabolichormones normallywork in harmony,building up and breaking down tissues, respectively.
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Frequent urination causes insatiable thirst and dehydration.
Eventu ally, the starving bodyturns more and more protein to sugar.
The ancient Greeks described diabetes as a disease that causes the body to melt into sugar water.
When tissues cannot utilize glucose, theywill metabolize fat for energy, generating by-products called ke tones, which are toxic at very high levels and cause further water loss asthe kidneys try to eliminatethem (see the discussion of ketoacido sis and hyperosmolar coma, in Chapter 21, "How to Cope with Dehy dration,Dehydrating Illness, and Infection").
Today type 1diabetes isstill avery serious disease, andstill eventually fatal if not properly treated with insulin.
It can kill you rapidly when your blood glucose level is too low, throughimpaired judgment or loss of consciousness while driving, for example , or it can kill you slowly, by heart orkidneydisease, whichare commonlyassociated with long-term blood sugar elevation.
Until I broughtmy blood sugars un der control, I had numerous automobile accidents due to hypogly cemia, and it's only through sheer luck that I'm hereto talk about it.
The causes of type 1 diabetes havenot yet been fullyunraveled.
Re search indicates that it's an autoimmune disorder in which the body's immune system attacks the pancreatic beta cells that produce insulin.
Whatever causes type 1 diabetes, its deleterious effects can absolutely be prevented.
The earlier it's diagnosed, and the earlier blood sugars arenormalized, the better off you will be.
At the time they are diagnosed, many type 1 diabetics still produce a small amount of insulin.
It's important to recognize that if they are treated early enough and treated properly, what's left of their insulin- producing capabilityfrequently can be preserved.
Type 1 diabetes typi cally occurs before the age of forty-five and usually makes itself apparentquite suddenly,with such symptoms asdramaticweight loss and frequent thirst and urination.We now know, however,that assud den asits appearance may be, its onset is actually quite slow.
Routine commercial laboratory studies are available that can detect it earlier, and it may be possible to arrest it in these early stages by aggressive treatment.
My own body no longer produces any detectable insulin at all.
The high blood sugars I experienced during my first year with diabetes burned out, or exhausted, the ability of my pancreas to pro duce insuhn.
I must have insulin shots or I will rapidly die.
I firmly believe , and know from experience with my patients , that if the kind of diet and medical regimen I prescribe for my patients had been utilized when I was diagnosed,the insulin-producing capabilityleft to
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me at diagnosis would likely have been preserved. My requirements for injected insulinwouldhave beenlessened, and it would havebeen much easier for me to keep my blood sugars normal.
Blood Sugar Normalization: Restoring the Balance According to the NIH, approximately 225,000 people died in 2002 from diabetes, but it is likely that deaths due to diabetes are under- reported. (Is a diabetic's death from heart disease, kidney disease, or stroke, for example,really a death from diabetes?) It is the NIH's con tention that "the risk for death among people with diabetes is about twice that of peoplewithout diabetes of a similarage." Certainlyeveryone hasto die of something,but you needn't die the slow, torturous death of diabetic complications, which often include blindness and amputations.
My history and that of my patients sup port this.
The Diabetes Control and Complication Trial (DCCT), conducted by the NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), began in 1983 asa ten-yearstudy of type 1 diabet ics to gauge the effects of improved control of blood sugar levels.
Pa tients whose blood sugars were nearly "normalized" (my patients' blood sugars are usually closer to normal than were those in the in tensivecare arm of the trial because ofour low-carbohydrate diet) had dramatic reductions of long-term complications.
Researchers began the DCCT trying to seeif they could, forexample,lessenthe frequency of diabetic retinopathy by at least 33.5 percent.
Instead of a one-third reduction in retinopathy, they found more than a 75percent reduction in the progression of early retinopathy.
They found similarlydramatic results in other diabetic complications and announced the results of the study early in order to make the good news immediately available to all.
They found a 50 percent reduction of risk for kidney disease, a 60 percent reduction of risk for nerve damage,and a 35 percentreduction of risk for cardiovascular disease.
This reduction continues to this day, many years after the study was terminated.
I believe that with truly normal blood sugars, which many of my patients have,these reductionscanbe 100 percent.
The patients followed in the DCCT averaged twenty-seven years of age at the beginning of the trial, so reductions could easilyhave been greater in areas such ascardiovascular disease if they had been older or followed for a longer period of time.
The implication is that full nor-
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malization of blood sugar could totally prevent these complications. In anycase, the results of the DCCT aregood reason to begin aggres sively to monitor and normalize blood sugar levels. The effort and dollar cost ofdoing sodoes nothave toberemotely as high as was sug gested in the DCCT'sfindings.
The Insulin-Resistant Diabetic: Type 2 Different from type 1 diabetes is what is officially known as type 2.
This isbyfarthe moreprevalent form of the disease.
According to sta tisticsfrom the American Diabetes Association, 90-95 percent of dia betics are type 2.
Furthermore, as many as a quarter of Americans between the ages of sixty-five and seventy-four have type 2 diabetes.
A study published by Yale University found that 25 percent of obese teenagers now have type 2 diabetes. (A new category of "pre-diabetes" has been recently called latent autoimmune diabetes, or LADA.
This category applies to mild dia betes with onset after the age of thirty-five, in which the patient has been found to produce an antibody to the pancreatic beta cell protein called GADA, just as in type 1 diabetes.
Eventually these people may develop overt diabetes and require insulin.
When the symptoms of di abetes finally occur, they are often more severe than at the "onset" of type 1 diabetes.) Approximately 80 percent of those with type 2 diabetes are over weight and are affected by a particular form of obesity variously known as abdominal, truncal, or visceral obesity.
It is quite possible that the 20 percent of the so-called type 2 diabetics who do not have visceral obesity actually suffer from a mild form of type 1 diabetes that causes only partial loss of the pancreatic beta cells that produce insulin.* If this proves to be the case, then fully all of those who have true type 2 diabetes may be overweight. (Obesity is usually defined as being at least 20 percent over the ideal body weight for one's height, build, and sex.) Whilethe causeof type 1 diabetes maystillbe somewhatmysterious, the cause of type 2 is less so.
As noted previously, another designation for type 2 diabetes is insulin-resistant diabetes.
Obesity, particularlyvis ceral obesity, and insulin resistance , the inability to fully utilize the glucose-transporting effects of insulin, are interlinked.
For reasons
Recentstudies show that even type 2 diabeticsexperiencesome degree of im mune attack on their beta cells.
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