WHAT IT MEANS TO BE A DIABETIC
Nobody is delighted to be diagnosed as a diabetic. After all, diabetes is a chronic disease with serious consequences and complications if it isn’t kept under control. You must watch what you eat, get regular exercise, and maybe take pills or insulin injections. It is a condition that you will have for the rest of your days. So far, there is no cure.
But diabetes is the one major disorder whose effects on your lifestyle depend to a remarkable degree on how much you know, and how much effort and time you are willing to spend paying attention to it. You can minimize the impact it has on your daily life as well as your future health simply by learning all about it and then living with a few rules that actually would make everyone in the world healthier if they, too, abided by them. At best, you may lose all evidence of diabetes and indeed the disease itself. At least, you may be able to reduce the amount of medication you require—all as the result of eating sensibly. The easy-to-follow plan presented here may change your life.
About 21 million Americans, 7 percent of the population, have diabetes, although many of them are not aware of it. Another 47 million, including 2 million adolescents ages twelve to nineteen, have prediabetes, a condition that may lead to type 2 diabetes later in life. The prevalence of the disease nearly doubled in the American adult population from 1990 to 2002 and has risen by more than 14 percent since 2003. In adults older than sixty, nearly one in every five has diabetes, and the incidence is rapidly rising in children and adolescents.
Studies estimate the cost of diabetes to be over $132 billion a year, some in direct costs, including hospitalization and treatment, and the rest in lost productivity, disability payments, loss of work time, and premature deaths. Diabetes, with its consequences and complications, consumes $1 out of every $10 spent on health care in the United States.
To give you all the bad news at once, Diabetes is the only major disease with a death rate that is still rising. Diabetics are much more likely than others to become blind, lose a foot or a leg, have kidney failure, develop coronary heart disease and stroke, and have other difficulties.
Now for the good news. Tremendous progress has been made in only the last few years in the prevention and treatment of the disease. It is very likely that a cure will be discovered soon. Most diabetics who not long ago would have died at an early age or would have existed with such dire complications that life would have been hardly worth living, can now lead almost normal lives and can look forward to a respectable, reasonably healthy old age.
the facts about diabetes
• More than nine out of ten of the diagnosed diabetics in the United States have type 2, or noninsulin- dependent diabetes mellitus (NIDDM). If they follow the correct diet, this group—formerly known as “adult-onset diabetics” because the disease usually strikes adults over the age of forty and most commonly over fifty-five—may never need insulin injections except perhaps during periods of stress. The remaining less than 10 percent of diagnosed diabetics have type 1, or insulin-dependent diabetes mellitus (IDDM). Once called “juvenile-onset diabetics” because it typically strikes in childhood, this group will always require insulin and cannot get along with diet alone or even with oral antidiabetic agents. Type 1 and type 2 are two separate disorders, although they share many of the very same problems.
• In the U.S. each year, over thirteen thousand children are diagnosed with type 1 diabetes. And more and more children and teens have type 2, with some clinics reporting that one-third to one-half of all new cases of childhood diabetes are now type 2. According to the American Heart Association, those at especially high risk are African American, Latino, Asian American, and Native American Indian children who are obese and have a family history of type 2.
• All type 1 diabetics require insulin injections because they make little or no insulin themselves.
• Ten to 20 percent of the diagnosed type 2 diabetics are treated with diet and exercise. Thirty to 40 percent take oral drugs to keep their blood sugar within acceptable limits. And 30 to 40 percent require insulin injections or a combination of insulin and oral medications.
• Type 1 diabetes is more prevalent among whites than other racial groups.
• About 11 percent of white Americans ages forty-five to seventy-four have type 2 diabetes, according to the National Institutes of Health. Among African Americans, however, the rate is over 18 percent in the same age range and black women are particularly vulnerable; one in four over the age of fifty-five has diabetes. The forecast is even bleaker for Latinos, especially Mexican Americans and Puerto Ricans, who suffer from diabetes at twice the rate of whites. There is a disproportionately high prevalence of the disease, more than twice that of U.S. adults overall, in Native American and Alaska Native adults. This is true, too, of Asian Americans who have abandoned their traditional foods and adopted a Western diet, high in fat and sugar. They are particularly susceptible to type 2 diabetes and often develop it at much lower weights than people of other races.
• The chances of developing diabetes double with every 20 percent of excess weight and with every ten years of increasing age. They also increase with the accumulation of fat around the middle. A recent study suggests that men with a waist size of 40 inches or more have the highest risk of type 2 diabetes, twelve times more likely than those with a size of 34 inches or less.
• Two in three people with diabetes will develop heart disease. Nearly 80 percent of diabetics die of heart disease or stroke. Adult diabetics are two to four times more likely to have a heart attack or stroke than other people, the same risk as if they have already had a heart attack, according to the American Diabetes Association.
• Gender matters. Before menopause, women have built-in protection against heart attacks, but they lose that protection if they have diabetes.
The DIABETES epidemic
Diabetes in the United States has reached epidemic proportions, with over a million new cases diagnosed every year. What’s more, although type 2 diabetes mostly continues to strike older people, more children and teenagers are getting it and much of the blame has been attributed to the long hours they spend in front of the computer or the TV set instead of on their feet.
America’s children are growing fatter. The Centers for Disease Control estimates that one in three Americans born in the year 2000 will develop diabetes in their lifetime. Women and minorities face the greatest risk.
WHAT IS DIABETES?
Diabetes mellitus is a metabolic disorder that results in persistent hyperglycemia—an abnormally high amount of sugar in the blood. (On the other hand, hypoglycemia means the opposite—an abnormally low blood-sugar level.) It is thought today that diabetes is actually several different diseases with different causes, all with the same result: the inability of the body to efficiently utilize the carbohydrates we eat as a source of fuel.
Glucose, the sugar molecule that is the end product of carbohydrate metabolism, is the body’s primary fuel. It is used immediately for energy, or it is stored in the liver in the form of glycogen to be called upon at a later time. When the body is unable to metabolize carbohydrates, which are derived mainly from sugars and starches, the blood becomes overloaded with glucose. The kidneys are unable to handle the excess and in most cases it “spills” into the urine.
WHAT’S GONE WRONG?
If you have diabetes, something has gone awry in the elaborate system of metabolic checks and balances that the normal body uses to maintain a safe blood-sugar level. Sometimes the pancreas, a large gland located on the left side under the ribs, completely abdicates its job of turning out insulin, the hormone that helps the cells to use glucose as their fuel. Sometimes the pancreas secretes an inadequate amount of insulin, not enough to cope with the carbohydrates you eat. And sometimes the pancreas is unable to “recognize” the high blood-sugar level and so does not produce enough insulin in response to it even though the capacity is there.
In most cases, however, especially in older overweight diabetics, the pancreas continues to produce plenty of insulin, often much more than normal, but it can’t perform its function of helping the cells use glucose. So plenty of insulin floats uselessly in the blood, unable to penetrate the cells, while sugar piles up but cannot be utilized.
The reason for this was once thought to be a deficient number of insulin receptors, but it is turning out to be more complex. One important factor seems to be the fat cell that we used to think was nothing but a stain on your shirt. In fact, it is a tiny factory that puts out twelve different substances, including adiponectin and resistin. Not producing enough adiponectin, which prevents diabetes, or putting out too much resistin, which resists the action of insulin, is probably what occurs in diabetics.
HOW DOES YOUR BODY MAKE INSULIN?
Insulin is manufactured by complicated little biochemical “factories” in the pancreas. These are the beta cells, responsible for so much of our well-being. They are located in the islets of Langerhans, one to two million tiny areas of the pancreas comprising maybe 2 percent of the entire gland.
The islets also secrete other hormones—glucagon from the alpha cells, somatostatin from the delta cells, and amylin from the beta cells, for example—which are deposited along with insulin, the main component, into the bloodstream via the tiny blood vessels that surround them. All of these hormones are involved in maintaining normal blood-sugar levels.
When it is working normally, the pancreas responds to every tiny fluctuation in blood sugar, releasing insulin whenever it is needed just as a thermostat turns a furnace off and on to maintain a constant temperature in your house. When the blood sugar rises after we eat, a signal goes to the pancreas, alerting it to move some insulin out.
When there is not enough glucose in the bloodstream to be used for fuel, the liver, stimulated by the glucagon from the islets’ alpha cells, releases glucose from its warehouse of stored glycogen. At the same time, amylin alters the sensitivity and secretion of insulin and may help slow the absorption of sugar through the intestines. When a sufficient amount of glucose has been secreted by the liver, somatostatin is responsible for turning off the production before it goes too high.
It takes most people about two to three hours to return to the normal fasting blood-sugar level after a high-carbohydrate meal.
HOW IS INSULIN USED?
In the normal person, starches, sugars, and proteins (58 percent of which is eventually converted into carbohydrate) are broken down by the intestines into glucose, a form of sugar. The glucose is carried throughout the body by the bloodstream, entering the cells with the help of insulin, then burned for energy by the muscles. Some of the leftovers are stored in the muscle cells or converted into fat. The rest is stockpiled in the liver in the form of glycogen, to be called upon later if the blood sugar falls too low.
If there is not enough insulin or if the insulin available cannot help the glucose permeate the cells, this sugar accumulates in the blood, often in very high concentrations. The result is diabetes.
In a nondiabetic, glucose concentration is usually below 100 milligrams per 100 milliliters of blood plasma, and even after a huge overload of sugar rarely goes above 160 to 180 mgs. In uncontrolled diabetics, it can go much higher, frequently reaching 800 or even 1,000 mgs. Though there’s obviously plenty of glucose available to feed the body’s hungry tissues, it cannot be used effectively and the cells can literally starve, no matter how much you eat.
At the same time, the liver is stimulated to release its stores of sugar and then to begin a process called gluconeogenesis. In a response to an emergency call for more fuel, this important organ takes the huge amounts of amino acids produced by the starving tissues and changes them into more glucose. Fats are also transported to the liver. Now ketones, the end products of the burning of fat instead of carbohydrate for fuel, also overload the kidneys and spill into the urine. This is called ketoacidosis. When this happens, and nothing is done to remedy the situation, the body lapses into a diabetic coma—a real emergency.
By the way, people who are trying to lose weight on a high-fat diet such as Atkins also produce ketones, but this is not dangerous as long as their blood sugar remains normal. It is only when ketones are combined with high blood sugar that ketoacidosis becomes a problem.
TYPE 2 (NONINSULIN–DEPENDENT DIABETES MELLITUS, OR NIDDM)
About 92 percent of diabetics are type 2. If you are in this category, you continue to manufacture insulin, perhaps not enough to cover your needs, or perhaps more than enough, but it cannot be efficiently utilized. You can probably control your diabetes with diet and exercise, or diet combined with oral hypoglycemic drugs that stimulate the release of insulin, delay the absorption of carbohydrates, or lower your blood sugar by suppressing the liver’s output of glucose. Or you may require insulin injections to supplement your own supply, or use the new drugs called incretins to make your available insulin more effective.
Although your diabetes may have been discovered after you developed specific symptoms such as excessive thirst and urination, more likely you were diagnosed during a routine medical checkup. Or maybe your eye doctor or dentist was the first to suspect it. Most cases of type 2 occur gradually, and never present obvious warning signals.
Heredity plays a very important role for type 2s. We know there must be a genetic predisposition, perhaps resulting in early aging of the pancreatic cells or the shutdown of insulin receptors. When some kind of stress—overweight or pregnancy, for example—is added to the genetic tendency, diabetes is the result. The sumo wrestlers of Japan are programmed by their genes to gain tremendous amounts of weight. They are adored by the sportsmen of Japan, but develop diabetes and heart disease early in their lives. They blaze like meteors across the sky, but the trip is short.
The genetically isolated Pima Indians who live in a remote river valley in the Arizona desert tend to be sedentary, overweight, and diabetic. Half of the Pimas over thirty-five have diabetes, 15 times the incidence among the general population in the United States, the highest rate ever recorded. Yet those Pimas who live in Mexico and work the land usually remain thin and do not have evidence of increased diabetes.
Both groups are good examples of the inherited tendencies toward this disease combined with obesity. If you have a family history of diabetes, it would be extremely wise not to get fat.
Even teenagers may have this variety of diabetes (about 5 percent of type 2s are under twenty), more and more of them every year, but statistically it is probably likely to occur in people over forty, becoming more common by age fifty or sixty.
Eighty-five percent of type 2s have a diabetic parent, sibling, or other close relative. Those with an identical twin who is diagnosed with type 2 are almost certain to develop it, too, within a few years.
who are the culprits?
The genetics of type 2 diabetes turns out to be very complicated and the disease is thought to be caused, along with excess weight and a faulty lifestyle, by a variety of genes. A major development, reported in 2005, was the discovery of a variant gene—designated TCF7L2—that increases the risk of diabetes significantly and is thought to be carried by more than a third of the American population. According to Iceland-based research team that identified it, people with one copy of the gene are estimated to have a 45 percent greater risk of type 2, while those who have inherited two copies, one from each parent, are 141 percent more likely to develop the disease.
The immediate practical effect of this discovery is that it may lead to diagnostic tests that can identify people with this gene, inspiring them to watch their weight, get plenty of exercise, and eat healthy diets.
Similar work goes on in many places. One study at the University of Texas Southwestern Medical Center has shown that a variation in the gene ENPPI is much more common in people with type 2 diabetes and those at greater risk for the disease. It may explain why certain ethnic groups have a higher risk even when they are thin. Changes in the gene PTPN1 are another possibility that may affect the production of a protein important in insulin activity. Variations in HNF4A, a gene that seems to act as a master regulator of insulin-making cells, seem to be much more common in type 2 diabetes. And Dr. C. Ronald Kahn of the Joslin Clinic has identified genes specifically involving PI3K that are defective in some type 2 diabetics.
What’s more, type 2s are almost always overweight. The vast majority of adult diabetics are too heavy or even obese. Many overweight type 2s can lose their diabetes by losing weight. Sometimes a loss of even a few pounds is sufficient to accomplish this miracle because now you may produce enough of your own insulin to keep your blood sugar normal or decrease the visceral fat around your abdomen that interferes with the action of insulin.
In controlled studies, it has been discovered that regular, vigorous exercise can lower or even eliminate the need for pills or injections.
Not all type 2 diabetes, however, is the result of overweight in a predisposed person. Sometimes it’s simply the result of an inefficient pancreas. The beta cells become unable to sense the sugar molecules and so can’t respond accurately to their presence; or they simply cannot produce enough insulin. In these cases, losing weight won’t help but eating correctly and enough exercising will, perhaps supplemented by oral agents or insulin.
TYPE 1 (INSULIN-DEPENDENT DIABETES MELLITUS, OR IDDM)
Type 1 diabetes, once known as juvenile diabetes, is quite another story and may even be another disease with a similar outcome. There are comparatively few type 1s—less than 10 percent of the total number of diabetics.
Type 1 can strike at any age, and about 15 to 20 percent of IDDMs are adults when they are diagnosed. But it happens for most people before they are twenty, and most commonly around the ages of eight, twelve, and puberty, when dramatic growth spurts take place. For every 100,000 people in the country, there are 50 diagnosed diabetics under the age of five; there are 150 under age ten; 270 below age fifteen; and 325 per 100,000 population by the age of eighteen.
Type 1 diabetes affects about one million Americans, with about thirteen thousand new cases each year, making it the second largest childhood disease in the U.S. after asthma.
It is now understood to be an autoimmune disease in which a body’s germ-fighting defenses mistakenly attack organs and tissues; in this case, the insulin-producing beta cells of the pancreas. Theory today is that the disease is usually triggered by a virus—perhaps a virus that is fairly benign for most people—that sets off an unrelenting immune response in a person who is genetically susceptible, knocking the beta cells permanently out of commission.
This kind of diabetes develops only in children and some adults who carry a very specific genetic make-up.
If you are a type 1, you have a marked insufficiency in the number of beta cells your pancreas possesses and you produce little or no insulin of your own. That means you must take insulin injections to compensate. Except in extremely rare cases, the oral drugs, designed to stimulate production in a pancreas that has the capability to make its own insulin, won’t work for you.
Unlike type 2, type 1 diabetes generally shows up very abruptly and dramatically, with unmistakable symptoms—excessive urination and thirst, dramatic weight loss, weakness, irritability. If these symptoms go untreated, they rapidly progress into acidosis (see Chapter 9) and finally coma in only a few days or weeks.
As a type 1, a person with the severest form of diabetes, you probably do not have diabetic parents, though there is a genetic factor here, too, as studies with identical twins have shown. Far from overweight, you are probably very thin and perhaps wan. There is no way for you to lose your symptoms by losing weight and eating sanely. But supplementary insulin, aided by good diet and plenty of exercise, will keep your blood sugar relatively normal.
Genes Play a Role
Many genetic markers for type 1 diabetes have been identified only recently. If a child has genes HLA-DR3 or HLA-DR4 on his sixth chromosome, inherited from both parents, he has 21?2 times more chance of becoming a type 1 diabetic after a viral infection. Eighty-five to 90 percent of all type 1 diabetics have DR3 and/or DR4. And if aspartic acid is not found in position 57 in these genes, the risk of diabetes increases even more. The worst-case scenario is to have both DR3 and DR4. But remember, even if a youngster has DR3 or DR4 genes, it is not inevitable that he or she will develop the disease.
Variants of another HLA gene may also play a role in this kind of diabetes. Researchers have recently found that DQA1 (0301) and DQB1 (0302), again on the sixth chromosome, are strong predictors of diabetes when passed along by two parents. Others—for example, DQB1 (0201) and DQB1 (0602)—are the most protective against it.
A second indicator is the presence of cytoplasmic pancreatic-islet-cell antibodies, found in 80 to 90 percent of children destined to become diabetics. If, in addition to these antibodies, the presence of genes ILA2 and GAD65 let us know when to start treatment. The likelihood of a child with all three indicators of becoming diabetic is almost 100 percent; with two of the three, it’s 80 percent. Tests are currently underway at Columbia Presbyterean Medical Center in New York to determine whether treating new-onset or recently diagnosed children with the antibody HOKT3Y (Ala-Ala) can preserve their beta cells.
But if, like the Inuits, a child has B7 on the sixth chromosome, his chances of diabetes are decreased. And if he has DR2, it is extremely doubtful he will get diabetes. Though people with DR2 make up a quarter of the population, only a few cases of diabetes have ever been reported among them.
Occasionally, diabetes is the result of another physical condition: pancreatitis, tumors, adrenal imbalance, injury to or removal of the pancreas, or damage caused by one of several drugs.
Double Dose: type 11?2
Many people, perhaps 5 to 10 percent of all diabetics, do not fit neatly into the categories of type 1 or type 2. Instead, they have characteristics of both varieties. Like type 1, they harbor antibodies that attack the beta cells, reducing their insulin production to little or none. And like type 2, their disease develops slowly as they gradually lose their insulin-producing capability and eventually require insulin. They are usually overweight and have insulin resistance. The standard oral medications are usually not effective with this group, and they often need insulin to bring their sugar level down enough to ward off later complications.
Prediabetics are people who have blood glucose levels that are higher than normal but not high enough to qualify them as true diabetics. With a fasting plasma glucose level between 100 mg/dl and 125 mg/dl, they have “impaired glucose tolerance” (IGT) and about half of them will be diagnosed as diabetics within ten years.
If you are in this category, you should be treated as a diabetic because you may already be on your way to its many unpleasant complications such as cardiovascular disease, kidney failure, and vision loss. You can lower your risk of continuing down the path to big trouble by losing weight (if you are too heavy), exercising regularly, cutting back on fats, eating judiciously (see Chapter 3), and maybe even taking an insulin-sensitizing medication (see Chapter 16 for more about stopping diabetes in its tracks).
WHO GETS DIABETES?
Diabetes gives geneticists headaches because it is almost impossible to predict, even in the presence of defective genes, who will eventually become diabetic, although many risk factors have recently been determined (see Chapter 16).
It was once thought that all the children of two diabetic parents would eventually become diabetic. Today it is thought that 60 percent is a more accurate figure. With one diabetic parent, sibling, or child, there is a 3 percent chance of diabetes by the age of forty to fifty-nine, a 10 percent chance after sixty.
The identical twin of a person who becomes diabetic before forty has a 30 percent likelihood of developing the disease. If the disease has its onset after forty, the chance an identical twin will have it increases to close to 100 percent, but if the disease does not occur within three years, the identical twin is probably home free. Fraternal twins, by the way, have about the same risk as other family members—about 10 percent.
EVERYTHING’S UNDER CONTROL
Diabetes is all about managing sugar. Once you know you are diabetic, you’ve got a new goal in life: to keep your blood sugar as close to normal as you possibly can. That means, ideally, between 70 mgs percent fasting and 150 mgs after a meal. That’s not easy, especially in times of stress when every diabetic’s blood sugar runs rampant, but you can stay within that range most of the time if you remember your future depends on it.
For many years, it was thought that this “tight control” was not too important as long as you felt well and functioned normally. Today we know differently.
Good Control or Else
Uncontrolled diabetes—consistently high blood sugars—can eventually affect every system of the body, resulting in many exotic varieties of diabetic complications. For example, people with diabetes are 21?2 times more likely to suffer from strokes and 2 to 4 times more likely to develop cardiovascular disease. Over 60 percent of diabetics have high blood pressure and 60 to 70 percent have nerve disease. Diabetes is the leading cause of new cases of blindness in adults and of end-stage kidney disease. It is the primary cause of amputations, an estimated 82,000 of them in the U.S. in 2002. That’s ten times the number of amputations for other reasons.
Those are frightening facts, but here’s the good news: Control your diabetes—in other words, maintain your blood sugar at consistently normal levels—and you can avoid or minimize all of these nasty complications. A thirty-year study of 4,400 diabetics revealed that those people who had held their blood-sugar levels to below 300 mgs had three times less risk of complications after fifteen years of the disease than those with higher levels. Those with a level below 250 mgs had five to twenty times less risk. And those who kept their blood sugar below 120 on diet alone had almost no risk of complications at all.
In 1998, the United Kingdom Prospective Diabetes Study strongly proved and confirmed an earlier DCCT study that intensive treatment—be it with oral agents (sulfonylureas or metformin) or insulin—reduced diabetic complications equally but metformin seemed to be better for the heart. The study also showed reducing blood pressure greatly reduced complications.
In a study of the Pimas, it was found that complications occurred in the group with fasting sugars above 140 and above 200 two hours after eating. The higher the sugar, the more likely the complications, and follow-up data found that a long period of intensive control delayed the onset of complications for many years even when that control was later abandoned.
More recently, in December 2005, a long-awaited federally funded landmark study reported in the New England Journal of Medicine presented solid evidence that stringent blood sugar control can cut the risk of heart disease nearly in half, at least for type 1 diabetics. Type 2s are the subject of a similar large trial sponsored by the National Institutes of Health with results expected in 2009.
Of course, life is not fair. Some people who pay no attention to their control never develop complications in spite of their lack of vigilance, while others who exercise great care do get them in later years. But, in general, it is true that greater control means a better, healthier, longer life.
Nobody’s perfect, and you won’t be either. You will not always follow your diet plan, you will succumb to temptation now and then, you’ll forget to test your blood sometimes, you will let your control get out of hand. But if this becomes your pattern and not just an occasional slip-up, you will undoubtedly pay the piper later. All the health problems associated with diabetes are hastened and exacerbated by poor control.
WHO’S IN CHARGE AROUND HERE?
You are. Your doctor will diagnose and prescribe and direct your treatment, but you are the only one who can live your own life. You’re the one who puts the food into your mouth, decides how much exercise to get, takes the blood tests every day, handles the crises of hypoglycemia and high blood sugar. You can get direction and advice from your doctor and this book, but you are in charge of yourself.
This does not mean you are out there all on your own. It is very important that you see your doctor frequently, whether or not you take insulin. The doctor monitors your blood-sugar control in order to prevent complications in the future, picks up early changes, works with you on problems concerning diet, exercise, lifestyle, or whatever, and advises you on handling illnesses.
If you are a diabetic who is regulated by diet alone, see your doctor at least every three months. Don’t go whenever you feel like it, or only when trouble brews. Go regularly on a scheduled basis.
If you take oral agents or insulin, make an appointment even more often, depending on your condition. Once every one to three months is right for most people. Never skip or postpone an appointment if you can possibly avoid it. And don’t hesitate to call your physician if you see a change in the results of your home glucose monitoring.
To find a doctor who can give you good care, call your local chapter of the American Diabetes Association or the Juvenile Diabetes Foundation. You will be given the names of several doctors in your area who are the most knowledgeable about diabetes. This is a specialized field, and many general physicians are not qualified to handle your problems. Your future will be much brighter if you find a doctor who is.
It’s a Balancing Act
Living with diabetes means a constant balancing act between the food you eat and the insulin you produce yourself or take by injection, along with the exercise you get. Insulin provides the mechanism for burning the food for energy to run your complex body. Exercise lowers your blood-sugar level. If you eat more food, you will need more insulin and exercise. If you eat less food, you will require less insulin and exercise. That’s simple. What’s hard is always having to think about this balancing act, especially at times when, often through no fault of your own, this balance is thrown out of kilter.
For many people, one of the most trying aspects is the need to be consistent, to lead a structured life. Especially if you take insulin, you soon discover that you must eat a preordained amount of carbohydrate, that you must eat on time, take your medication on schedule, take constant blood tests, check in with your doctor regularly. While everyone else, it seems, can stay up all night partying, eating pizza, and drinking sodas, stuffing themselves one day and fasting the next, paying no attention to medicines or doctors, you, if you are on NPH insulin, must plod along, day after day, on three meals plus two snacks.
That can be difficult, but it will pay off. Consistency isn’t such a tremendous price to pay for feeling well now and in the future. It will eventually become a lifestyle you can live with.
Excerpted from Diabetes Survival Guide by Stanley Mirsky, M.D., and Joan Rattner Heilman. Copyright © 2006 by Stanley Mirsky. Excerpted by permission of Ballantine Books, a division of Random House LLC. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.