lease anotherpancreatic hormone, glucagon, which will "instruct"her liver and muscles to begin converting glycogen to glucose, to raise bloodsugar.
When sheeats again, herstore of glycogen will be replen ished.
This pattern of basal, phaseI, then phaseII insulinsecretion is per fect for keeping Jane's bloodglucose levels in a safe range.
Her bodyis nourished, and things work according to design.
Her mixed meal is handled beautifully.
This is not, however, how things work for either the type 1 or type 2 diabetic.
The Type 1 Diabetic Let's look at what would happen to me, a type 1 diabetic, if I had the same breakfast as Jane, our nondiabetic.
UnlikeJane,because of a condition peculiar to diabetics,if I take a long-acting insulin at bedtime, I might awaken with a normal blood sugar, but if I spendsometimeawake before breakfast, mybloodsugar may rise, even if I haven't had anything to eat.
Ordinarily, the liver is constantly removing some insulin from the bloodstream, but during the first few hours after waking from a full night's sleep, it clears in sulinout of the bloodat an accelerated rate.
Thisdip in the level of my previously injectedinsulin is called the dawn phenomenon (seeChap ter 6,"StrangeBiology").
Because of it, myblood glucose can rise even though I haven't eaten.A nondiabeticjust makes more insulin to off set the increased insulin clearance.
Those of us who are severely dia betic have to track the dawn phenomenon carefully by monitoring
46 BeforeYou Start
blood glucose levels, and canlearn how to use injectedinsulin to pre vent its effect upon blood sugar.
As with Jane, the minute the meal hits my mouth, the enzymes in my saliva begin to breakdown the sugars in the toast and juice,and al most immediately my blood sugar would begin to rise.
Even if the toast had no jelly, the enzymes in my saliva and intestines and acid in my stomachwould begin to transform the toast rapidly into glucose shortly after ingestion.
Since my beta cells no longer produce detectable amounts of in sulin, there is no stored insulin to be released by my pancreas, so I have no phase I insulin response.
My blood sugar (in the absence of in jected insulin) will rise while I digest my meal.
None of the glucose will be converted to fat, nor will anybe converted to glycogen.
Eventu ally much will be filtered out by my kidneys and passed out through the urine,but not beforemy body hasendureddamagingly high blood sugar levels , which won't kill me on the spot but will do so over a period of days if I don't inject insulin.
The natural question is, wouldn't injectedinsulin"cover" the carbohydrate in such a breakfast?
Not adequately!
This is a common misconception , even by those in the health care professions.
Injected insulin , even with an insulin pump , doesn't work the same as insulin created naturally in the body.
Conventional insulin/diettherapyresulting in high blood sugar after meals is a guaranteed slow, incremental,"silent" death from the ravages of diabetic complications.
Normal phase I insulin is almost instantly in the bloodstream.
Rapidlyit beginsto hustleblood sugar offto whereit's needed.Injected insulin, on the other hand, is injected either into fat or muscle (not usu allyinto a vein) and absorbed slowly.
The fastest insulin we have starts to work in about 20 minutes, but its full effect is drawn out over a num ber of hours, not nearly fast enough to prevent a damaging upswing in blood sugars if fast-acting carbohydrate, like bread,is consumed.
This is the central problem fortype 1 diabetics , the carbohydrate andthe drastic surge it causes in bloodsugar.
Because I know my body produces essentially no insulin, I have a shot of insulin before every meal.
But I no longer eat mealswith fast-acting or large amounts of carbohydrate, because the blood sugar swingsthey causedwere what brought about my long-term complications.
Eveninjection by means of an insulin pump (see discussion near the end of Chapter 19) can not automaticallyfine-tune the levelof glucose in my blood the way a nondiabetic's body does naturally.
Diabetes:TheBasics 47
Now, if I ate only the protein portion of the meal, my blood sugar wouldn't have the huge, and potentially toxic, surge that carbohydrates cause.
It would rise less rapidly, and a smalldose of insulin could act quickly enough tocover the glucose that's slowly derived from the pro tein.
My body would not have to endure wide swings in blood sugar levels. (Dietary fat, bythe way, has noeffect on blood sugar levels, ex cept that it canslightly slow thedigestion ofcarbohydrate.) In a sense, youcould lookat myinsulin shotbefore eating onlythe protein portion of the meal as mimicking the nondiabetic's phase II response.
This is much easier to accomplish than trying to mimic phase I, because of the much lower levels of dietary carbohydrate (only the slow-acting kind) and injected insulin that I use.
The Type 2 Diabetic Let's say Jim, a type 2 diabetic, is 6 feet tall and weighs 300 pounds, much of which is centered around his midsection.
Remember, at least 80 percent of type 2 diabetics are overweight.
If Jim weighed only 170 pounds, he might well be nondiabetic, but because he's insulin- resistant, Jim's bodyno longer produces enough excess insulin to keep his blood sugar levels normal.
The overweight tend to be insulin-resistant as a group,a condition that's not only hereditary but also directly related to the ratio of vis ceraland total bodyfatto leanbodymass (muscle).
The higherthis ra tio, the more insulin-resistant a person will be.
Whether or not an overweight individual is diabetic, his weight, intakeof carbohydrates, and insulinresistance alltend to makehim produceconsiderably more insulinthan a slenderpersonof similar ageand height (seeFigure 1-3, page 48).
Many athletes, because of their low fat mass and high percentage of muscle, tend as a group to require and make less insulin than non- athletes.
An overweight type 2 diabetic like Jim, on the other hand, typically makes two to three times as much insulin as the slender non diabetic.
In Jim's case, from manyyears of having to overcompensate, his pancreas has partially burned out, his ability to store insulin is di minished or gone, and his phase I insulin responseis attenuated.
De spite his huge output of insulin, he no longer can keep his blood sugars within normal ranges. (In my medical practice, a number of patients come to me for treatment of their obesity, not diabetes.
On examination, however, most of these very obese "nondiabetics" have slight elevations of theirHgbAlc test for average blood sugar.)
48 Before You Start
1 1 ^^ObcscDonnal subjects
w^ Obe* patients wi h diabetes
' fcinn >rraal tubje » ""
V inpatient*' vithdiabcte i Fig. 1-3. Serum insulin response toglucose consump 0 15 30 45 60 90 120 150 1810 tion of individuals withand Time (minutes) without type 2 diabetes.
Let's take another look at that mixed breakfast and see how it affects a type 2 diabetic.
Jimhasthe sametoastand jelly and juiceand boiled egg that Jane, our nondiabetic, and I had.
Jim's blood sugar levels at waking may be normal.* Since he hasabigger appetitethan either Jane or I, he hastwo glasses of juice, four pieces of toast, and two eggs.
As soon asthe toastandjuice hit hismouth, hisblood sugar beginsto rise.
Unlike mine,Jim's pancreas eventually releases insulin, but he hasvery Httle or no stored insulin (his pancreas workshardjust to keep up his basal insulin level), so he has impaired phase I secretion.
His phase II insulin response, however, may be partially intact.
So, very slowly, his pancreas will struggle to produce enough insulin to bring his blood sugar down towardthe normal range.
Eventually it may get there,but not until hours after his meal, and hours after his body has been ex posed to highbloodsugars.
Insulin isnot onlythe major fat-building hormone,it also serves to stimulate thecenters in thebrain responsible for feeding behavior.
Thus, in all likelihood, Jim will groweven more overweight, asdemonstrated by the cycle illustrated in Figure 1-1.
Since he's resistant to insulin, his pancreas has to work that much
*Waking, or fasting, bloodsugars arefrequendy normalin mildtype 2 diabetics. After theyeatcarbohydrate, however, their postprandial blood sugars areusually elevated.
Diabetes: The Basics 49
harder toproduce insulin toenable him toutilize the carbohydrate he consumes.
Because of insulin's fat-building properties, hisbodystores away some of hisblood sugar asfat andglycogen; but hisblood sugar continues to rise, since hiscells areunable to utilize all of the glucose derived from his meal.
Jim, therefore, still feels hungry.
As he eats more, his beta cells work harder to produce more insulin.
The excess insulin and the "hungry" cells in his brain prompt him to want yet more food.
He has just one more piece oftoast with a little more jelly on it, hoping that it will be enough to get him through until lunch.
Meanwhile, his blood sugar goes even higher, his beta cells work harder, and perhaps a few burn out.* Even after all this food, he still may feel many of thesymptoms of hunger.
His blood sugar, however, will probably not goanywhere nearashighasminewould if I took no insulin.
In addition, hisphase II insulin response could even bringhis blood sugardown to normal aftermanyhours without more food.
Postprandial (after-eating) blood sugarlevels that I would call un- acceptably high, 140 mg/dl, or even 200 mg/dl , may be consid ered by other physicians to be unworthy of treatment because the patient still produces adequate insulin to bring them periodically downto normal,or "acceptable," ranges.
IfJim, our type2diabetic, had received intensive medical intervention before the betacells of hispan creas began to burn out, he would have slimmed down, brought his bloodsugars into line,and eased theburden on hispancreas.
Hemight evenhave"cured" his diabetesbyslimmingdown, as I've seen in several patients.
But many doctors might decide such "mildly" abnormal blood sugars are only impaired glucose tolerance (IGT) and do little more than "watch" them.Again, it'smybeliefthat aggressive treatment at an earlystagecan save most patientsconsiderable lost time and per sonalagony by preventing complications that willoccur if blood sugar levels are left unchecked.
Such intervention can make subsequent treatment ofwhat can remain , a mild disease , elegantly simple.
ON THE HORIZON
I include some hopeful forecasts of future treatments in this first chapterbecause asyou're learning howto controlyour diabetes, hope
Betacellburnout can be causedboth byoveractivity of the cells and by the tox icity of high glucose levels.
50 BeforeYou Start