I sleepwalk a lot. This seems off-topic, and it is. Last night I dreamed that I was scaling a building wall to cure diabetes. What woke me up was me trying to climb my dresser by lodging a microphone stand into the drawers. It made a lot of noise. Turns out I didn't cure diabetes at all. I refuse to let this failure get the best of me however, and instead of quitting, I altered my cure-approach (this) with high hopes of a greater impact.
And a greater impact is certainly needed as the prevalence of diabetes continues to climb every year. When I was little, fewer people had tons of diabetes. I was certainly not offended by this. Even so, I still had several diabetes'd people to pick from, and my favorite by far was Joyce. She would keep candy in strategic places all over her house in case she needed it to remedy her low blood sugar. Because I was 7, I routinely ate all of that candy and felt great about it as a person. In retrospect, that probably wasn't helpful. Nonetheless, she would also let me inject her insulin for her. In retrospect, that probably wasn't helpful either. Plus it was super creepy and I hated doing it. Even so, I would still be willing to commit to primary-injection-administrator status while simultaneously leaving her candy alone if it could somehow conjure up a vivify spell.
Alas, in real life, probably not. The take home message here is this: people with diabetes are usually and/or sometimes fantastic, and the diabetes itself really doesn't have to be all that bad. Or it does and it will kill you. But there's no reason it has to. If you have the attentive-diligence to actually make it through this article, we'll explain how to cure diabetes, or at least drastically diminish its damage on your body.
Before we get into anything diabetes-related however, we have to first set up non-diabetes. Understanding the endocrine system of someone without diabetes will help lay a foundation that we can address diabetes from in a much more meaningful way.
So here goes: when a person without diabetes ingests carbohydrates, the carbs are pulled from the small intestine into the blood and converted to glucose. This causes total blood sugar to go up. When blood sugar goes up, your body releases the hormone, insulin. Insulin is made by the beta cells in your pancreas and its primary function is to force your energy substrates into storage. It just pushes your carbs, fat, and protein out of the blood and into their natural storage sites. It's pretty simple. Carbohydrates are insulin's main concern however, considering blood sugar levels actually dictate its release. This should all be pretty logical and obvious so far.
The actual process of taking carbohydrates from the blood and moving it into the cells is a little more tricky. It works through a process called translocation. What happens is this: the glucose is hanging around in your blood just outside of the cells that need it. In order for the glucose to actually enter those cells, insulin receptors need to be activated. When you activate the insulin receptors, a glucose transporter comes to the cell wall and pulls the glucose in. That's how translocation works, and in its entirety, it's referred to as "insulin stimulated glucose uptake."
This is exactly what a biologist will tell you is the only major concern for a diabetic. And knowing only what I've discussed so far makes this statement seem justifiable. But it's not. And the fact that it's not implies that there are methods to treat diabetes with less regard for insulin. That's not to say that biologists are being equivocal, they're just adhering specifically to biology, which studies the body at rest. And when your body's at rest, insulin stimulated glucose uptake actually is
the only major consideration. But in real life, you don't have to lay motionless for eternity, and lucky for you, physiology studies the non-motionless you, offering up several other important diabetes-relieving considerations.
Before looking at those considerations however, we now have enough information to understand the biological differences between type I and type II diabetes.
In type I diabetes, your beta cells are destroyed, so you lack the ability to produce insulin at all. This is a genetic disorder that seems to cause the adapting immune system during early teen years (ballpark age) to be the culprit. Not only is the timing right, but if you harvest pancreatic stem cells and administer them, you can cure type I diabetes for a matter weeks- and then the immune system destroys those cells. So it would appear that it's a matter of genetic immune system dysfunction. Regardless, what we're looking at is no insulin production, so it has to be injected.
In type II diabetes, it's onset by controllable physical conditions as opposed to genetics. Furthermore, insulin availability isn't the problem. Your beta cells are fine and insulin is being released in generally appropriate quantities. The problem is that your insulin receptors don't care. For whatever reason, they've lost sensitivity to the presence of insulin (we'll cover the reasons), so as a result, your carbs and insulin both just hang out in the blood stream and sit there all stagnant-like.
What you should be wondering now, is why this is bad. What makes glucose in the blood stream a detrimental thing? And the answer, is that you have blood vessels that don't like it. Left unaddressed, you'll experience all sorts of peripheral neuropathies (blood vessel problems). Everyone hears about diabetics having kidney problems, so we'll cover that one first. The capillary beds in your kidneys are critical for renal function and urine production. When you destroy them, you get in stage renal disease and end up on dialysis because capillaries are basically too small to deal with and consequently, it's impossible by all medical measures to restore adequate blood flow.
Your kidneys aren't the only area with capillary beds though. There are extensive capillary networks in your eyes, and when diabetes causes them to bulge and leak blood, you get retinopathy: the death of your rods and cones (the structures that give you vision). Neuropathies like this in untreated diabetics are virtually endless. Worst case scenario: you cut your toe and die. In order to heal anything, it takes blood flow. If you destroy the vessels supplying blood somewhere, that structure loses its ability to heal. If you cut your toe and it gets infected, you have to remove the toe. Since you can't heal the wound from where your toe was removed, it'll get infected and you have to have your whole foot cut off. Because you can't heal that, you cut off the lower leg, upper leg, and so on. Piece by piece until you're just a head. That's the worst case scenario.
Best case scenario? Depends. Type I diabetics can vastly reduce their reliance on insulin and type II diabetics can cure their diabetes completely.
This is a pretty good deal for type II diabetics considering they experience even worse side effects than the type I's. Not only do they experience all the neuropathies to a horrendous degree, but they also have tons of insulin floating around in their system. Type I diabetics don't have that. They only have what they inject, which is usually an appropriate amount. Type II diabetics have tons of insulin, and just because it's not triggering translocation of the glucose transporters doesn't mean its other functions are halted as well. As long as insulin is hanging around in the system, it will encouraging your carbohydrates to be converted into fat for storage and preventing you from actually using your stored bodyfat as energy.
Notice how type I diabetics (they don't have insulin) are usually all skinny while type II diabetics (they have insulin) are usually quasi-huge with fat heft. The insulin in their system really helps them achieve this fat heft, and that gives them a slew of other problems. Things like cardiovascular disease. So if type II diabetics aren't careful, they'll be getting triple bypasses while on dialysis without limbs. But at least they won't be able to see any of it.
Now that I hope you're appropriately terrified, we're ready to talk about cures. And lucky for you, a complete medical cure is no more than 5 years away.
I'm just kidding. It's totally not. That's a sales pitch for you to donate money to various funds that are nowhere near a cure. They've been following the 5-year-promise plan since the Civil Rights Act. It's not coming.
This means in real life, you have to monitor your diet and activity levels. I realize this sounds a lot like "diet and exercise." That's what it is. I also realize that this is the most challenging cure ever and usually if someone says "diet and exercise," they're just dodging the obligation to provide real advice because they don't know anything. In this one instance, that's not the case. But I applaud your criticism. Keep reading.
When the body is not at rest, inslulin is no longer the sole regulator of your blood sugar. The first (huge) contributing factor is the relationship between your muscle tissue and nervous system. Your nervous system's contribution happens through sympathetically mediated nerves called hepatic efferents. These are nerves that go from your brain to your liver and when called upon, stimulate hepatic glucose production. What this means, is that any time you start an activity, you use muscles, and this triggers your liver to produce glucose and dumps it into the blood.
This would be a bad thing, except that the muscle cells can take in the glucose in the absence of insulin through "non insulin dependent glucose uptake." Every time a muscle flexes, this happens. That's your basic muscle metabolism while not at rest.
So think about it. During complete inactivity, maintaining blood sugar levels is accomplished by food and insulin. You increase blood sugar with carbohydrate ingestion, and decrease via insulin letting that sugar into the cells. While not at rest, however, the primary system to get glucose out of the blood is your muscle, and your liver helps to regulate blood sugar as well by adding more to the blood if you need it. This little nervous system-muscle partnership is called "pseudo insulin resistance." And as long as you're not at rest, it's the primary regulator of your blood sugar.
Additionally, what little amount of regulation is left over falls into the wonderful hands of the wonderful catecholamines. Your catecholamines are epinephrine and norepinephrine. They're released in response to muscle activity and can fairly well take the reigns in the absence of insulin.
Between the catecholamines and the muscle-nervous system blood sugar balance, while you're not at rest, insulin is effectively rendered useless regardless of whether you're type I or II. That's why insulin actually leaves your system during workouts.
Do you see why working out is a good thing? This alone should be plenty enough incentive to work out. This is what will diminish the reliance on insulin in type I diabetics.
And remember how I said type II diabetics could actually cure their diabetes entirely through exercise? Here's why. Their problem is insulin sensitivity. In addition to the body not even needing insulin during moderate to vigorous activity, insulin sensitivity improves following that workout for a period of an hour or two.
If this was the only benefit, you would have to workout a good half dozen times daily to cure your diabetes. On the contrary, growing fat cells release proteins called inter leukin 6, tumor necrosis factor-alpha, and resistin. Shrinking fat cells don't. When these proteins are being released, they shut down your insulin receptors. Conversely, if your fat cells shrink, you no longer have this problem. When you no longer have this problem, your insulin sensitivity goes up.
Because insulin sensitivity is not only the actual problem with diabetes, but also the largest determinant of the rate of your fat loss or gain, sensitivity improvements will create a self-perpetuating cycle of sweet, sweet, whimsical goodness. You losing weight causes your insulin sensitivity to increase, which causes you to lose more fat, which causes your insulin sensitivity to increase, which causes you to lose more fat, and so on.
So to recap for you type II's, insulin sensitivity is the most influential modifiable determinant of adiposity. The less insulin sensitivity you have, the fatter you will become. When you exercise, you temporarily improve sensitivity, and thus increase the rate of fat loss. This causes heightened effects of non-insulin dependent glucose uptake. Cumulative effects of these last two phenomena allow you to reach lower bodyweight more quickly. The lower your bodyweight gets, the more your inter leukin 6, tumor necrosis factor-alpha, and resistin levels all cause your insulin sensitivity to return to a healthy level even faster. When you reach that healthy level, you no longer have diabetes do you? 100% cured. It's practically guaranteed and it doesn't take all that long.
If this doesn't motivate you, literally nothing in the world ever will and you have my full blessing to just give up now and breathe your last little diabetes'ed breath.
And because I'm not only genuinely compassionate, but also exceedingly thorough, I'll explain to you what actually makes it challenging to maintain your status as a post-diabetic cured sexy wonk.
When your fat cells grow, they release more than what we talked about earlier. They also release a hormone called leptin. When they shrink, they stop releasing it. Leptin counters the release of neuropeptide tyrosine and anandamine (both of these increase appetite), and promotes the release of alpha-MSH (appetite suppressant). So if you're fatter, leptin is in your system making you less hungry. If you're leaner, it's not in your system and that makes you more hungry.
There are a couple other hormones and peptides like grehlin and orexins which are involved with insulin sensitivity and appetite both- mainly affecting you in the same way that leptin does. So your natural endocrine function makes you hungrier as you get leaner, and when people are all hungry, they tend to lose motivation.
This is where that diet component I was talking about earlier plays in. If you eat right, you'll feel less intestinally unfulfilled, and this will greatly eradicate the de-motivation of it all. At this point, you could continue to take advantage of the insulin sensitivity link that those substances offer while not wanting to quit. Do this and your diabetes is cured 100 times over.
In conclusion, if you can't pull yourself together and be consistent with diet and exercise, clearly knowing the benefits if you do, and the consequences if you don't, you're a useless bundle of fleshy, diabetes'd flesh-mass. And you could otherwise be a fantastic person who doesn't die all young and in a state of vast, cosmic, bulky unhappiness.
Providing I read this right, if I start working out consistently, my blood sugar should be maintained at better levels. I'm a type I diabetic, so I understand there's very little chance in getting off insulin injections altogether, but could I improve to the effect that I don't have to test my blood sugar as often?
You read it right, and yes. But don't rush it. You really have to be practical with how you keep tabs on your blood sugar. Waiting for your body to give you cues on what to eat or when to test won't always work. These cues would be coming from your central nervous system, and sent to notify you that you have unordinary blood glucose levels. But your central nervous system needs glucose to function properly- that's part of the problem. So you can't really depend on it with that much confidence. You can, but it would be fairly dangerous. But you can
get to that point, just don't rush it. You have to be a little more careful with how you approach type I. Type II's can fully cure their diabetes, but both types have to address it like adults still.