As some of you may know (and I've written about it before on this blog), I have been seeing an endocrinologist (hormone/diabetes specialist) for several months for "elevated fasting glucose levels." My numbers were more in the pre-diabetic range for a while, and I had none of the classic diabetes symptoms (excessive thirst and urination, etc.) - but because I was young and otherwise healthy, with a normal BMI (and therefore also without the classic Type 2 "red flags"), my doctor was concerned enough to refer me to an endocrinologist.
It turns out there is a third kind of diabetes besides Type 1 and Type 2 - and it's called Type 1.5, or LADA (Latent Autoimmune Diabetes in Adults). It sometimes masquerades as Type 2, because it starts off gradually and gives plenty of "pre-diabetic" warnings (if you're checking your blood glucose and looking for them), and because it doesn't start until adulthood. But in reality, it's more similar to Type 1.
(What follows is an oversimplified explanation. I'm no medical professional, but I have read a few articles and books on diabetes in the last couple months, and here's the general impression I got of differences between the types.)
The pancreas produces insulin to process glucose in the bloodstream. If there isn't enough insulin produced, or if the insulin cannot do its job properly because a person's cells have become resistant to it, then there will be excess glucose in the blood. This is called hyperglycemia (high blood sugar) and can often go undetected for many years - until it's bad enough or has persisted long enough to cause serious complications, such as impaired vision, sores or loss of feeling in the feet, infections, kidney problems, heart attacks, strokes, or diabetic comas.
In Type 2, this excess in blood glucose is because of insulin resistance. The pancreas still produces insulin normally, but there either isn't enough of it to absorb all the glucose, or the insulin malfunctions. It is often caused or exacerbated by obesity, poor diet, or lack of exercise. Type 2 diabetes can therefore be treated with changes in lifestyle - better eating habits, more exercise - or with oral medications that help insulin work properly or more efficiently. If Type 2 has persisted for too long without being controlled, the pancreas might start to lose its ability to produce insulin; in these instances, Type 2 diabetics might also require insulin injections, to ensure that their body has enough insulin to work with.
Type 1 is different. It is an autoimmune disease, meaning that there are antibodies in the blood (produced by the immune system), which mistakenly believe that the pancreatic beta cells that produce insulin are foreign invading cells which need to be fought. These antibodies prevent the pancreas from being able to produce the insulin it needs to. Without insulin, glucose remains in the blood and causes complications. People with Type 1 therefore can only be treated with insulin injections. Though changes in diet and exercise may decrease the amount of insulin they require (because there will be less glucose in the blood that needs to be processed), some amount of insulin will always be necessary.
Usually, people with Type 1 are children when they are diagnosed. Their symptoms may come on with little or no warning. Their pancreas suddenly no longer produces any insulin, or only produces very little insulin, and for the rest of their life they must inject insulin manually.
In recent decades, while doing studies of Type 2 adult diabetics, scientists discovered another class of diabetics - adults who had some Type 1 antibodies in their blood. They were misdiagnosed as Type 2, and were being treated as if they were Type 2, but the truth was their immune system was destroying the pancreatic beta cells' ability to produce insulin - albeit at a slower rate than what is typically seen in Type 1 diabetics (possibly because they had fewer antibodies, or fewer types of antibodies, than people with classic Type 1). Changes in diet and exercise, or even taking oral medications, did little to help these individuals manage their glucose levels - because what they needed was more insulin, to make up for the insulin their pancreases were no longer producing. There is still some disagreement among medical professionals about this new type (Type 1.5, aka LADA) - whether it is a subtype of Type 1 or a distinct third type all of its own. There is also, therefore, disagreement with what to call it.
Personally, I like Type 1.5 and LADA both. If you know enough about diabetes to be able to discern what "Latent Autoimmune Diabetes in Adults" might mean, the LADA moniker gives a good description of what it looks like (latent = slow moving; adults = found in adults) and what treatments should be used (autoimmune = requiring insulin). But "Type 1.5" is a good description for the layperson who has only heard of Type 1 and Type 2 diabetes, because it really does have characteristics of both. It often manifests like Type 2, but has a cause more similar to Type 1 and therefore should be treated more like Type 1.
Thankfully, my primary doctor and the endocrinologist she referred me to are both up on the latest in diabetes care. Unlike many Type 1.5 diabetics, I was not misdiagnosed at Type 2. As soon as I saw my endocrinologist the first time, he ordered antibody blood testing done, to confirm what he suspected - that I had GAD antibodies, and they were slowly inhibiting my pancreas from producing insulin.
Because my blood glucose was only slightly elevated, I was not started on insulin yet. I made some small changes to my diet, keeping track of the amount of carbs I was eating. I also checked my glucose every day (or almost every day) to keep track of where I was at and if my condition was getting more serious. As long as my numbers stayed only slightly elevated, nothing else would have to be done. We took a "wait and see" approach, and waited for my pancreas to get worse.
For about two years, I saw my endocrinologist every few months or so for an A1C test. The A1C measures an average glucose level over the last three months - a non-diabetic should have an A1C level at 5.7 or below, "pre-diabetics" might have an A1C in the range of 5.7-6.5, and anything above 6.5 is considered a characteristic of diabetes, often prompting a diabetes diagnosis. The American Diabetes Association recommends diabetics try to keep their A1C below 7.0. My A1C was gradually rising (5.7, then 5.8, then 6.0) and my fasting glucose in particular was too, but as long as it didn't get too high, we would continue to "wait and see."
Since this past November, however, my fasting numbers were getting noticeably worse. Instead of being occasionally in the 120-130 range, they were creeping into the 150s. ("Normal" fasting glucose is supposed to be between 70-100.) At first I thought it was just because of stress or trouble sleeping (since I hadn't made any changes to my diet that might account for the change), but as the fasting numbers continued to be in the 150s on more than just an occasional basis, it became clearer that it was just going to gradually worsen, no matter what I tried to do.
Now, having numbers in the 150s is still not super high; undiagnosed diabetics may often get into the 300s or 400s without even noticing. But the push in diabetes treatment lately has been all about prevention - which is why they try to screen people early, to find them when their numbers are still "pre-diabetic" and start treatment early. The earlier it is caught and treatment is started, the less serious the complications will be in the future. Some recent studies with Type 1.5 diabetics have also indicated that starting insulin sooner rather than later might be better in the long run - because it might preserve the remaining insulin production the pancreas has for longer.
In February, my A1C was 6.2. Again, not super high; in fact, not yet in the range considered "diabetic." But the trajectory was clear - it kept rising, and would continue to rise toward that 6.5 cut-off. My endocrinologist said the "wait and see" approach might finally be over. Because I'm young (28 years old) and have a long life of trying to avoid diabetes complications ahead of me, it might be best to start the insulin sooner rather than later. Furthermore, keeping blood glucose levels as close to normal (non-diabetic levels) as possible is extra important during pregnancy - especially during the first trimester - and now that my husband and I are approaching the time in our lives when we want to expand our family, it would be better to be on insulin and keep careful track of my glucose levels for the sake of any potential babies, even if it wasn't yet required for my own health. Before, my endocrinologist was saying I would probably have to be on insulin when I was pregnant; now, he was saying I should start it now, so that when my husband and I want to start trying to conceive, we will 1) be able to (high blood glucose can affect fertility), and 2) the baby will be healthy during the first few weeks of pregnancy (before I might even know I was pregnant yet).
Long story short, I started taking insulin at the end of February.
I am on Levemir, which is a long-lasting basal insulin. I take it at bedtime, and it lasts for 24 hours, keeping my glucose levels as steady as possible throughout the day. I do not (yet) take any bolus insulin, which is the type taken with meals, to account for the amount/type of food being consumed and to prevent after-meal spikes in glucose.
My endocrinologist had me start with 12 units of insulin at night, but that seemed to be a bit much, giving me low blood sugar - a problem I never thought I'd have! Now I do 10 units of Levemir at bedtime, or 6 units if my bedtime glucose level is under 100.
Within three days, my glucose readings improved. My fasting numbers are always less than 100 now, and usually in the 70s or 80s. In fact, my biggest problem so far has been occasional mild hypoglycemia (low blood sugar) overnight or during the day, especially between breakfast and lunch, if I eat lunch late. Low blood sugar is anything under 70; my hypoglycemic episodes are usually just below that, or only very occasionally as low as the low 60s/mid 50s. It wakes me up (if I'm asleep) with fairly obvious symptoms (sweatiness, rapid heartbeat); during the day, though, I find it harder to recognize.
I check my glucose much more often than I used to - several times a day, instead of just once a day (or less). I check at bedtime (to figure out how much insulin to take), and I check my fasting number (which is the number I always checked before). But I also check now before I drive home from work - since it's a 45 minute commute, and if I haven't eaten anything lately, I need to make sure I'm not going to start dipping low while I'm driving. And I often check about 1.5-2 hours after eating a meal, to see how much of a post-meal spike I'm getting.
It is that last category that has been most disappointing lately. My post-meal numbers are sometimes as high as 250 (when they should be less than 180, or, if I was pregnant and trying to be as close to non-diabetic levels as possible, less than 140). I do not remember having this problem before I started taking the insulin - though I also checked my glucose a lot less frequently, so it's possible my levels were that high, but I just didn't realize. More likely, I think, is that despite my insulin injection regime, my personal pancreatic insulin production is still gradually getting worse. I wonder if the next time I see my endocrinologist (in June), he will start me on bolus (mealtime) insulin now, too, to counteract those spikes. I guess we'll just have to see what my A1C level is at in June, to determine how much the insulin is helping and figure out what else can or should be done to make my glucose readings even better.
In the meantime, I should probably try not to obsess over it too much. Part of me worries if I keep track of too much - counting calories and carbs and fiber intake, testing my glucose several times a day - to the point where it's starting to border on obsession. On the other hand, every study about diabetes ever concludes that the more often you check your glucose, the better control you have over your diabetes - and the better the control, the less problems with serious complications. Early detection, self-advocacy, and taking a personal stake in your diabetes treatment are key. So I'm trying to find that good balance - especially since I'm still new to a lot of this, many of my numbers are still in the pre-diabetic range anyway, I've never had a super high glucose reading/landed in the hospital from my blood sugar, my insulin dosage is small, I'm healthy otherwise, and I'm not pregnant.
There is no real need for me to test too often (other than idle curiosity for what my glucose is at any given time), and in fact two pretty good reasons not to:
- The cost of test strips, which are about $1/each and really start to add up if I'm testing 5-6 times a day. (My insurance pays for the insulin, but not the test strips, because my endocrinologist never wrote me a prescription for them.)
- My poor fingertips, which have to be stabbed with a lancet anytime I want to test. (In case you're curious - finger pricks for blood testing hurt more than my Levemir insulin shots, which go into the abdomen and usually don't hurt at all.)
But despite this, I do like knowing what my numbers are. I figure as long as frequent testing doesn't cause extreme financial hardship or too many unnecessary finger calluses - or make me too anxious, tying my mood to whether or not I get a "good" glucose reading - then knowing how my body reacts to different things (different types of food, exercise, etc.) can only help me in learning how to care for and manage my diabetes.
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