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by Marley » Thu May 26, 2016 1:30 pm
by Maer » Thu May 26, 2016 6:28 pm
by patty » Thu May 26, 2016 8:15 pm
FOR DOCTORS ONLY (BUT NONPHYSICIANS CAN READ IT TOO)
After adequate discussion, let patients know how much more rewarding and exciting it is for you as a physician to watch people getting well and beating diabetes and their other medical issues. After all, did we get into medicine to watch people deteriorate, or did we do it to help people get better?
Make a goal with the patient to shoot for at the next visit. Make it absolutely clear to the patient that diet and exercise are now the main means of glucose control, not drugs. Without an explanation and understanding of the futility of the drug-only approach and the absolute necessity of using diet and exercise to protect against further damage, patients are not given the proper opportunity to protect themselves. High glucose readings can be treated with enhancements in exercise and dietary adjustments much in the same manner doctors use medications. Medication used in the interim period until sufficient weight is lost should be limited to those drugs that are not counterproductive to losing weight or to saving and restoring pancreatic function, or at least moving in this direction.
This protocol essentially rules out the use of sulfonylureas and insulin, except considering insulin in very small amounts when the pancreatic beta reserve is unusually depleted. When the proper eating style is combined with the proper exercise program, medications are rarely needed, and even then only in small amounts. We also want to discontinue or at least reduce medications that can cause hypoglycemia since caloric reduction and increased exercise can reduce glucose so dramatically. Glucophage (metformin) and Januvia (sitagliptin) do not cause hypoglycemia and are safe medical options when medications are needed. Byetta (exenatide) is an option when the glucose is running too high on metformin and something stronger is needed, as it does not cause weight gain.
At the first visit, when patients begin this protocol, insulin and sulfonylureas should be reduced by at least one-half and discontinued in the weeks that follow, if possible. A very low dose of 250 milligrams of Glucophage three times daily can help people who experienced indigestion from higher dosages in the past. If the dose is increased slowly, the side effects are minimized. Byetta— injections of 5 milligrams twice a day— can be used in place of insulin in the initial phase if the glucose levels are unfavorable. In most cases, the oral medications such as Glucophage, Prandin (repaglinide), and Januvia can be used because they do not induce hypoglycemia or weight gain.
MOST FAVORABLE MEDICATIONS FOR USE IN CONJUNCTION WITH DIETARY TREATMENT OF DIABETES
Less Likely to Cause Hypoglycemia or Weight Gain
Glucophage Januvia
(metformin) (sitaglitin)
Byetta Prandin
(eventide) (repaglinide)
Starlix Precose
((nateglinide) (acarbose)
Glyset (miglitol)
LEAST FAVORABLE MEDICATIONS FOR USE IN CONJUNCTION WITH DIETARY TREATMENT OF DIABETES
More Likely to Cause Hypoglycemia and Weight Gain
Insulin (various types); ultra-long-acting Lantus and Levemir cause less weight gain
Amaryl (glimpiride) Diabenese
(glimpiride) (chlorpropamide)
Glucotrol Diabeta, Glynase
(glipizide) (glyburide)
Actos Avandia
(pioglitazone) (rosiglitazone)
The goal is to avoid having a hypoglycemic event in the first week of dietary change. The glucose readings in the first few days of dietary adjustment should run 125 to 175; do not attempt tight glucose control.
It is safer to allow the patient to run a little high than to risk a hypoglycemic event when they start a diet this aggressive. I always give the first-time diabetic patients my cell phone number and ask them to call me every day for the first three days after their visit. On the third call, I determine when the next call will be or if they can wait until their follow-up appointment in two weeks.
I also instruct the patients who are reducing their insulin dose to cut back their dose considerably each time they get even one reading below 120. I emphasize strongly that if they don’t, the next reading may have them in a dangerous hypoglycemic episode. I write out exactly which insulin to cut back on and by how much, reducing both the long-acting (Lantus or Levemir) and the short-acting meal-time insulin (usually Lispro).
I carefully watch their morning fasting readings for guidance on the reduction of the long-acting insulin dose. The most physiological insulin regimen is to use four shots a day: one of the long-acting, twenty-four-hour insulins (such as Levemir or Lantus) before dinner or at bedtime, and one short-acting insulin immediately before each meal.
This most accurately mimics what a normal, nondiabetic pancreas would supply. Long-acting and short-acting insulins cannot be combined in the same shot, thus four shots are required per day, not three. The nighttime long-acting insulin dose is usually cut back by 40 percent at the first visit, and the pre-meal (quick-acting) insulin is reduced by 30 percent. Because regular insulin extends its action beyond mealtime needs and can lead to hypoglycemia, it is no longer recommended as the medication of choice— especially for my patients, whose mealtime insulin requirements are even shorter lived.
Reviewing the morning fasting and preprandial glucose levels will help the physician adjust the bedtime long-acting dose, and the two-hour postprandial glucose readings will help further adjust the mealtime quick-acting insulin dose.
For type 1 diabetics, adjust the long-acting dose so the morning and preprandial glucose readings range from 80 to 120, and adjust the preprandial insulin dose so the two-hour postprandial glucose readings hit in the 130 to 175 range.
The only way to safely achieve these results without hypoglycemic reactions is not by conventional carbohydrate counting but by stability in the diet and stability in the insulin dosage. For example, a sample dietary skeleton for a type 1 diabetic woman with a daily intake of 1,500 calories would be:
Breakfast 400 calories
Two fruits, oats and oat bran, almonds, ground flax, walnuts
Lunch 500 calories
Salad with nut/ seed-based dressing, veggie/ bean soup, one fruit
Dinner 500 calories Salad with hummus/ bean/ salsa dip, steamed greens, veggie stew, tofu or flavored beans or fish, one fruit
The consistency is in the food choices, as the carbohydrates used and the overall GI of the meal is low and the fiber is very high. The secret to the excellent control is the use of greens, beans, seeds, and nuts all together in the meal at both lunch and dinner.
This hypothetical type 1 patient will now require only 3 to 5 units of insulin before each meal and 15 to 25 units of long-acting insulin at night. Whereas under the standard carbohydrate-counting ADA regimen, the average type 1 diabetic would take 6 to 9 units before each meal and 40 to 50 units at night.
With consistency in diet and medication, precise management of type 1 diabetes is possible without highs or lows. Patients are no longer at high risk for heart disease, stroke, or other tragic complications of the condition. They are no longer overusing insulin. They are no longer destined to be overweight. Their lipids come under control, and they get better glucose management, without the risk of being hypoglycemic. Their condition is managed more physiologically, and they feel better.
Fuhrman, Joel (2012-12-26). The End of Diabetes: The Eat to Live Plan to Prevent and Reverse Diabetes (Kindle Location 2946). HarperCollins. Kindle Edition.
by patty » Fri May 27, 2016 11:45 am
Juvenile Diabetes
There are multiple forms of diabetes, and two are relevant to this chapter. The first is known as juvenile diabetes (or type 1, insulin-dependent diabetes). For reasons that are just being sorted out, in some people the immune system decides that the cells in the pancreas that secrete insulin are, in fact, foreign invaders and attacks them (such “autoimmune” diseases will be discussed in chapter 8. This destroys those cells, leaving the person with little ability to secrete insulin. For equally mysterious reasons, this tends to hit people relatively early in life (hence the “juvenile” part of the name) although, to add to the mystery, in recent decades, the rate at which adults, even middle-aged adults, are getting diagnosed with juvenile diabetes is climbing. Because the person can no longer secrete adequate amounts of insulin (if any), there is little ability to promote the uptake of glucose (and, indirectly, fatty acids) into target cells. Cells starve—big trouble, not enough energy, organs don’t function right. In addition, there’s now all that glucose and fatty acid circulating in the bloodstream—oleaginous hoodlums with no place to go, and soon there’s atherosclerotic trouble there as well. The circulating stuff gums up the blood vessels in the kidneys, causing them to fail. The same can occur in the eyes, causing blindness. Blood vessels elsewhere in the body are clogged, causing little strokes in those tissues and, often, chronic pain. With enough glucose in the circulation, it begins to stick to proteins, begins to Velcro proteins together that have no business being connected, knocking them out of business. None of this good.
And what is the best way to manage insulin-dependent diabetes? As we all know, by accommodating that dependency with insulin injections. If you’re diabetic, you never want your insulin levels to get too low—cells are deprived of energy, circulating glucose levels get too high. But you don’t want to take too much insulin. For complex reasons, this deprives the brain of energy, potentially putting you into shock or a coma and damaging neurons. The better the metabolic control in a diabetic, the fewer the complications and the longer the life expectancy. Thus, there’s a major task for this type of diabetic to keep things just right, to keep food intake and insulin dosages balanced with respect to activity, fatigue, and so on. And this is an area where there has been extraordinary technological progress enabling diabetics to monitor blood glucose levels minute by minute and make minuscule changes in insulin dosages accordingly.
How does chronic stress affect this process? First, the hormones of the stress-response cause even more glucose and fatty acids to be mobilized into the bloodstream. For a juvenile diabetic, this increases the likelihood of the now-familiar pathologies of glucose and fatty acids gumming up in the wrong places.
Another, more subtle problem occurs with chronic stress as well. When something stressful happens, you don’t just block insulin secretion. Basically, the brain doesn’t quite trust the pancreas not to keep secreting a little insulin, so a second step occurs. As noted earlier, during stress, glucocorticoids act on fat cells throughout the body to make them less sensitive to insulin, just in case there’s some still floating around. Fat cells then release some newly discovered hormones that get other tissues, like muscle and liver, to stop responding to insulin as well. Stress promotes insulin resistance. (And when people get into this diabetic state because they are taking large amounts of synthetic glucocorticoids [to control any of a variety of diseases that will be discussed later in the book] they have succumbed to “steroid diabetes.”)
Why is this stress-induced insulin resistance bad for someone with juvenile diabetes? They have everything nice and balanced, with a healthy diet, a good sensitivity to their body’s signals as to when a little insulin needs to be injected, and so on. But throw in some chronic stress, and suddenly insulin doesn’t work quite as well, causing people to feel terrible until they figure out that they need to inject more of the stuff…which can make cells even more resistant to insulin, spiraling the insulin requirements upward…until the period of stress is over with, at which point it’s not clear when to start getting the insulin dose down…because different parts of the body regain their insulin sensitivity at different rates…. The perfectly balanced system is completely upended.
Stress, including psychological stress, can wreak havoc with metabolic control in a juvenile diabetic. In one demonstration of this, diabetics were exposed to an experimental stressor (speaking in public) and their glucocorticoid secretion was monitored. Those who tended to have the largest stress-response under those circumstances were the ones least likely to have their diabetes well controlled. Moreover, in related studies, those who had the strongest emotional reactions to an experimental stressor tended to have the highest blood glucose levels.
Stress may sneak in another way. Some careful studies have shown higher rates of major stressors suffered by people during the three years before the onset of their juvenile diabetes than would be expected by chance. Does this mean that stress can make the immune system more likely to attack the pancreas? There is a little bit of evidence for this, which will be discussed in chapter 8 on immunity. A more likely explanation is built around the fact that once the immune system begins to attack the pancreas (that is, once the diabetes has started), it takes a while before the symptoms become apparent. By having all the adverse effects just talked about, stress can speed up the whole process, making the person notice sooner that he or she is just not feeling right.
Thus, frequent stress and/or big stress-responses might increase the odds of getting juvenile diabetes, accelerate the development of the diabetes, and, once it is established, cause major complications in this life-shortening disease.* Therefore, this is a population in which successful stress management is critical.
Adult-Onset Diabetes In adult-onset diabetes (type 2, non-insulin-dependent diabetes), the trouble is not too little insulin, but the failure of the cells to respond to insulin. Another name for the disorder is thus insulin-resistant diabetes. The problem here arises with the tendency of many people to put on weight as they age. (However, if people do not put on weight as they age, they show no increased risk of this disease. This is the case among people in non-westernized populations. The disease is not, therefore, a normal feature of aging; instead, it is a disease of inactivity and fat surplus, conditions that just happen to be more common with age in some societies.) With enough fat stored away, the fat cells essentially get full; once you are an adolescent, the number of fat cells you have is fixed, so if you put on weight, the individual fat cells are distended. Yet another heavy meal, a burst of insulin trying to promote more fat storage by the fat cells, and the fat cells refuse—“Tough luck, I don’t care if you are insulin; we’re completely full.” No room at the inn. The fat cells become less responsive to insulin trying to promote more fat storage, and less glucose is taken up by these cells.* The overstuffed fat cells even release hormones that trigger other fat cells and muscle into becoming insulin resistant. Do the cells now starve? Of course not, the abundant amounts of fat stored in them was the source of the trouble in the first place. The body gets into trouble because of all that circulating glucose and fatty acids, damaging blood vessels. Same old problem. And if the adult-onset diabetes goes on for a while, an additional, miserable development can occur. Your body has become insulin-resistant. Your pancreas responds by secreting even more insulin than usual. You’re still resistant. So the pancreas secretes even more. Back and forth, your pancreas pumping out ever higher levels of insulin, trying to be heard. Eventually, this burns out the insulin-secreting cells in the pancreas, actually destroying them. So you finally get your adult-onset diabetes under control, thanks to losing weight and exercising, and you discover you’ve now got juvenile diabetes, thanks to that damage to your pancreas.
Photomicrograph of bloated fat cells. How does chronic stress affect adult-onset diabetes? Once again, constantly mobilizing glucose and fatty acids into the bloodstream adds to the atherosclerotic glomming. And there’s that problem of the stress-response involving your fat cells being instructed to become less responsive to insulin. Suppose that you’re in your sixties, overweight, and just on the edge of insulin resistance. Along comes a period of chronic stress with those stress hormones repeatedly telling your cells what a great idea it is to be insulin-resistant. Enough of this and you pass the threshold for becoming overtly diabetic.
Why is any of this worth paying attention to? Because there is a worldwide epidemic of adult-onset diabetes going on, especially in our country. As of 1990, about 15 percent of Americans over age sixty-five had adult-onset diabetes. That was considered a health disaster then. As of a decade later, there’s been a 33 percent increase above that, and among middle-aged adults as well. And this disease of aging is suddenly hitting far younger people as well—in the last decade, there’s been a 70 percent increase in its incidence among thirty-year-olds. In addition, something like 20 million Americans are “pre-diabetic”—barreling toward a formal diagnosis. Adult-onset diabetes has even become more prevalent among kids than juvenile diabetes, which is pretty horrifying. Moreover, as people in the developing world are first being exposed to westernized diets, not only do they develop diabetes, they develop it at a faster rate than do westerners, for reasons that are probably both cultural and genetic. This once nonexistent disease afflicts an estimated 300 million people worldwide and killed 200,000 Americans last year.
What’s this about? It’s obvious. Despite the impression that everyone spends their days eating low-fat/carb/cholesterol/cardboard diets and power walking uphill while loudly reciting the writings of Atkins or Ornish, with each passing year, we are eating more food—more junk food—and exercising less. Twenty percent of Americans are now technically “obese” (versus 12 percent in 1990), and 54 percent are “overweight” (versus 44 percent then). To paraphrase the allostasis theorist Joseph Eyer, prosperity has become a cause of death.*
Metabolic Syndrome/Syndrome X In the well-entrenched tradition of medical compartmentalizing, there’s a whole set of things that can go wrong in you that would get you sent to a cardiologist, whereas a bunch of different problems would get you turfed to an internal medicine doc who specializes in diabetes. With any luck, they’d even confer with each other now and then. What should be obvious over the last two chapters is that your metabolic and cardiovascular systems are intimately interconnected. “Metabolic syndrome” (also known as Syndrome X) is a new term recognizing this interconnection. It’s actually not so new, having been formalized in the late 1980s by Gerald Reaven of Stanford University. It’s just become tremendously trendy in the past few years (so trendy that it’s even been described in a population of wild baboons who forage through the desserts in a garbage dump at a tourist lodge in East Africa).
Make a list of some of the things that can go wrong from the last two chapters: elevated insulin levels in the blood. Elevated glucose levels. Elevated systolic and diastolic blood pressure. Insulin resistance. Too much LDL-cholesterol. Too little HDL. Too much fat or cholesterol in the blood. Suffer from a subset of these, and you’ve got Metabolic syndrome (the formal diagnosis involves “one or more” from a list of some of these problems, and “two or more” from a list of the others).* The syndrome-ness is a way of stating that if you have a subset of those symptoms, you’re probably heading toward the rest of them, since they’re all one or two steps away from each other. Have elevated insulin levels, low HDL, and abdominal obesity and the chances are pretty good you’re going to get insulin resistance. Elevated LDL-cholesterol, high blood pressure, and insulin resistance, and you’re likely to be obese soon. Another bunch and they predict hypertension.
Subsets of these clusters of traits not only predict each other, they collectively predict major disease outcomes, like heart attacks or stroke, and mortality rates. This was shown with particular subtlety in an impressive study carried out by a team headed by Teresa Seeman of UCLA. Medicine normally works in diagnostic categories: have glucose levels above X, and it’s official, you have hyperglycemia. Have blood pressure levels above Z, you’re hypertensive. But how about if your glucose levels, blood pressure, HDL-cholesterol, and so on, are all in the normal range, but all of them are getting near the edge of where you have to start worrying? In other words, no measure is abnormal, but there’s an abnormally large number of measures that are almost abnormal. Technically, nothing is wrong, amid it being obvious that things are not right. Take more than a thousand study subjects, all over age seventy, none of whom are certifiably sick—that is to say, where none of those measures are technically abnormal. Now, see how they’re doing on all those Metabolic syndrome measures. Throw in some other measures as well—including resting levels of glucocorticoids, epinephrine, norepinephrine. Combine the insights into these measures mathematically and, collectively, this information was significantly predictive of who was going to have heart disease, a decline in cognitive or physical functioning, and mortality, far more predictive than subsets of those variables alone.
This is the essence of that “allostasis” concept, of keeping things in balance through interactions among different, far-flung systems in the body. This is also the essence of the wear-and-tear concept of allostatic “load,” a formal demonstration that even if there’s no single measure that’s certifiably wrong, if there are enough things that are not quite right, you’re in trouble. And, as the final, obvious point, this is also the essence of what stress does. No single disastrous effect, no lone gunman. Instead, kicking and poking and impeding, here and there, make this a bit worse, that a bit less effective. Thus making it more likely for the roof to cave in at some point.
Sapolsky, Robert M. (2004-09-15). Why Zebras Don't Get Ulcers, Third Edition: The Acclaimed Guide to Stress, Stress-Related Diseases, and Coping - Now Revised and Updated (pp. 69-70). Macmillan. Kindle Edition.
by roundcoconut » Fri May 27, 2016 9:50 pm
Maer wrote:Do a search for KensCircus posts. He's a type 1 diabetic and has posted a slew of really helpful notes on his experience doing this very successfully. He also posts on the website Starch Smart under the name Ken Thomas.
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