Diabetes- What I Wish I Knew a Few Years Ago When My Brother in Law Was Sick

This began as my way to explain everything I was learning about Diabetes to my family (of whom a few are Diabetic), and it evolved to be something I wanted to include on my blog because from what I can tell, this info really isn’t out there unless you know what to look for.  So I’m going to focus on Type 2 here, for now, then I edited it and added stuff about Type I.  The epiphany for me in studying Diabetes can when I realized that Diabetes is as much  disorder of fat metabolism as it is of glucose metabolism.  Did you hear that?  Crazy.  My grandfather is 87 and has had Diabetes for decades, and had no idea it had anything to do with fat.  My epiphany expanded as I realized that insulin does way more than lower blood glucose.  That’s right.  So what’s going on?

Insulin is a hormone secreted by the Pancreas.  As we grow and change (and gain weight for many) our body adjusts how much insulin it produces according to our needs.  Problems begin to arise when our cells start to ignore insulin, this is called “insulin resistance,” (essentially insulin at normal levels does not exert its normal effects) and the pancreas has to start pumping out more insulin.  Some people can flood their cells with enough insulin to compensate for the resistance, and do not have Diabetes.  If someone cannot produce insulin at high enough quantities to overcome their own resistance (and keep their glucose level at 126 after a 24 hour fast) they are diagnosed with Diabetes Mellitus 2.   It’s a combination of insulin resistance with the pancreas unable increase the quantity of insulin to compensate.  It’s important to note that people with Type 2 Diabetes do secrete some insulin.  The insulin isn’t enough to overcome the resistance but insulin does so much more than that, and thus this small quantity of insulin secreted does make a positive difference.

Let’s talk about what insulin actually does.  We know that it “lowers blood glucose.”  How does it do that?  Insulin binds to cells, and signals the cells to suck in glucose that’s floating around the blood from that bowl of ice cream you just ate.  The muscle cells, fat cells, and liver cells take in large quantities of glucose (the most being in the muscles).  Someone with Diabetes has insulin resistance, so their receptors ignore the insulin, unless there is a large enough quantity of insulin that the cell says “ok FINE” and takes in the glucose.  It’s like peer pressure.  You don’t cave until everyone in the class tells you to do it.  This is where most people, including my understanding (until a few weeks ago) of Diabetes stops.  Let’s get into the cool stuff.

Say you just ate dinner, so you’re not exercising, starving, anything abnormal right now.  Glucose from your meal is now floating around your blood, and the pancreas releases insulin in response.  Insulin tells the body to “build and store fuels.”  Part of that is taking in glucose, but it is also other things.  Insulin tells muscle cells to store glucose for later (like when you exercise later, or tonight when you go to sleep and you are “fasting,” your muscles will have the energy they need to function).  It also tells the liver to store glucose, so that tonight when you are sleeping, it can release that stored glucose into the blood to keep the body’s blood glucose level normal, and make glucose available for cells that need it.  Build and store.  Here’s where it gets interesting.  Insulin tells fat cells to build and store fats.  They do this by taking in fats from the blood (the ice cream, AND fats that the liver has secreted).  It tells fat cells “do not release fats into the blood stream, store them, and take any excess glucose and turn it into fat too for storage.”  It also tells liver cells to store fats and cholesterol too.  So insulin not only lowers blood glucose, it lowers fats (triglycerides) in the blood.   Now think what’s going on in a Diabetic patient- they are insulin resistant, so their fat cells are not storing the fats, they are sending them out into the blood.  This is why people with Diabetes also tend to have high blood triglycerides (fats).

Let’s talk about the liver for a minute.  The liver stores glucose and fats to meet energy needs later.  So let’s go back to our example, you ate dinner, and then you go to sleep.  Your blood sugar level starts to go down, you’re not eating anything while you’re asleep, and your insulin level goes down.  Insulin’s opposite partner, a hormone called glucagon is secreted because blood sugar level is starting to get lower (recap- insulin secreted when sugar is HIGH, glucagon secreted when sugar is LOW).  Your body cells use their stored glucose for energy, and once that starts to run out, the liver MAKES GLUCOSE and secretes it into the blood.  Cells that are running low on fuel take in glucose and use it for energy.  This is called “gluconeogenesis”- making glucose.  Your body will make glucose to power the brain until you eat again (breakfast, in our example), insulin is released, and that glucose is absorbed.  Simultaneously the insulin tells the liver to stop making glucose (store and build, remember?) because you just ate and have a ready supply.   So now let’s look at what’s going on in the Diabetic liver- because the liver cells are resistant to insulin, the liver will continue to make glucose and secrete it into the blood, even though the person just ate.  So they don’t just have high blood sugar because of what they ate, it’s also because the liver isn’t listening to the insulin, and continues to secrete glucose into the blood.  This is why people can have such high blood glucose levels, even when their diet is well controlled.  This is where the drug metformin acts- one of the things it does is tell the liver to stop making glucose.

And now for the main attraction- what I think was going on when my brother in law got sick, wasn’t eating, and his wife was calling me about him having high “ketones” in his urine.  When a normal person is starving (not eating because they’re sick,. Or they’re deserted in the desert,..etc) their liver can make glucose for the brain, can break down proteins from muscles to make glucose, or it can power the brain with Ketones, a byproduct of fats.  They can survive this way (for a while) because the glucose they make can be used (they don’t have resistance to insulin, and their body can release insulin as necessary to tell the cells to absorb the glucose).  He wasn’t eating because he was feeling sick, and was worried about taking his insulin because it might make him hypoglycemic (send his blood sugar too low).  Fair enough, that’s what I thought too, until I learned about everything else insulin does.  Without glucose from foods, the liver will make glucose (remember?) and will use fatty acids for fuel.  By not taking his insulin, his body could not absorb the glucose his liver was making (his brain could, but not the rest of his body).  Second, without insulin, his fat cells were dumping fats into the blood, which were then converted to lots of ketones in the liver.  (remember? Insulin tells the body to store fats, without insulin, fats are released into the blood).  The brain can survive on ketones like I said, but too many ketones can make the blood acidic, which is dangerous.  Now here’s an important point (and since I don’t know how insulin resistant Matt is, or how much insulin he’s making on his own, I don’t know the extent of this in his body, but these facts are true) people with Type II diabetes do secrete SOME insulin, usually enough to prevent what’s called “ketoacidosis” (too many ketones) so most literature and scholars would say that Ketoacidosis in Type II diabetics is rare, while it is a big risk in people with Type I.    However, he was sick, which is a risk factor for ketoacidosis because he was under metabolic distress.  Plus, his urine ketone test was high, so he was headed in that direction.

What I should have said then, that I know now is that he should have taken his insulin, even though he wasn’t eating.  At that point, he needed to be able to absorb the glucose that his liver was making, and tell his fat cells to STOP SECRETING FATS INTO THE BLOOD, which the liver was converting to lots of ketones.  The only thing that signals these things is INSULIN.  He was headed down the spiral of more glucose in the blood, no insulin, more fats, more ketones,.. and around and around.  The recommended treatment is fluids and insulin.  So instead of worrying about making him hypoglycemic, stand by with a glass of OJ, or oral glucose gel.  Take the insulin, monitor the blood sugar, and if it makes a dive, stick some oral glucose gel under the tongue, or if tolerable, drink some OJ.  The worry here is not hypoglycemia, it’s stopping the fat breakdown to ketones, and getting glucose to the cells.  Insulin is what does that.  Hypoglycemia is almost immediately reversed.  (be afraid of hypoglycemia when you’re out in the desert with no access to food!)  As soon as that insulin is introduced, it immediately starts to signal cells to store fat not release it, signals the liver to store glucose not secrete it into the blood, and signals all the cells to take in glucose from the blood.

I’m not saying that going to the hospital was totally avoidable, there’s no way I could venture to guess that.  But based on logic, it would seem that as soon as a diabetic patient is sick enough that they can’t eat foods, call the doctor’s office to inform them of the sickness, keep taking the medications (unless the doctor specifies otherwise of course!) and try to tolerate juices (or if vomiting, at least try oral glucose gel under the tongue where it readily absorbs).  We even studied a case study where the patient, a child, had to go to the hospital because her mom halved her insulin dose because she was sick, afraid to make her hypoglycemic.  Well she didn’t have enough insulin and her body started pumping out the ketones!  And that was half dose!  So,.. very interesting.

Crazy sidenote: people on the Atkins diet, and other high protein, low carbohydrate diets put themselves intentionally in ketosis, where their body doesn’t have enough glucose (carbohydrates, by definition, are glucose) so it survives on fat breakdown- ketones.  They’re losing weight because their body is breaking down fats for fuel but how crazy is that?!  I’m sorry, I don’t want my brain running on its emergency plan B fuel- ketones.  That is supposed to be for when you are starving and need enough energy to make it to the oasis!  Not for daily life!  They avoid keto-acidosis (too much ketones) by overworking their liver and kidneys to keep their ketones at an ok level, and because they do make insulin and can absorb glucose made by the liver, or by what little glucose they do eat.  Whether or not living in a state of ketosis is bad for you is a hotly contended scientific debate.  I just think it’s unnatural, and there are so many more healthy ways to lose weight.  Plus, my professor did it one time just to see how it felt to be running on ketones, she said she felt weird, not herself,. Awful,.. so you kind of wonder how social and behavioral problems from atkins diet-related ketosis play out in our society..

I am adding this additional info once I was kindly informed that in fact, another family member has Type I, and I didn’t really address Type I.  So, Type I is more extreme, in that it’s an autoimmune disease in which the body attacks and destroys the cells in the Pancreas that make insulin (scientists at this point do not know why this occurs). Interestingly enough, there is a stronger genetic tie between family members getting Type II than Type I.  There are some similarities, and some differences between type I and II that I’ll try to clarify from what I wrote about earlier.  So once all those cells (Pancreatic β cells in the Islets of Langerhans if you’re curious,) are destroyed, yes, the patient must replace all of their lost insulin with injections.  Big sad face!

OK- so someone with Type II has insulin resistance for sure, but someone with  Type I can also have insulin resistance (and would need extra insulin-the docs have to figure that one out with insulin resistance testing.)  Without insulin injections, a patient with Type I not only can’t absorb glucose (that’s the basic thing everybody knows..) but remember all that fat stuff I was talking about?  Their fat cells are releasing fats into the blood at a completely uncontrolled rate.  The liver is also making glucose (from amino acids broken down from muscles) at a completely uncontrolled rate.  You want the liver to make glucose like a normal person- at night, or during exercise, not all the time.  And you certainly don’t want your muscles wasting away in the process.  The liver is also desperately trying to fuel the body and will turn a lot of those fatty acids into ketones (by the way- we are making ketones all the time, that’s not unusual, bad, or dangerous.  In fact, around 8% of our normal energy needs are supplied by ketones, it’s only dangerous when it builds up to massive amounts, and I think it’s weird with the Atkins stuff).  So with untreated type I, there is this wasting away of muscle tissues and body fats going on.  Ketoacidosis IS a risk for this patient, because they aren’t secreting ANY of their own insulin, and eventually their blood becomes too acidic that they begin to experience has neurologic effects (and eventually death, without insulin).

I just wanted to mention a few details about the long term complications associated with Diabetes.  And, scientists cannot completely explain everything.  But, just by understanding how much fat is floating around in the blood, it’s easy to understand why there is a big increased risk in cardiovascular problems.  Hardening of arteries is common, and cardiovascular disease is the most common cause of death.  Problems with eyes, kidneys, and circulation also are related.  High levels of glucose, however, also are a problem.  Glucose is a reactive molecule- which basically means that it messes around with things it runs into, in ways that we don’t necessarily want it to.  Scientists are studying “glucosylation” and hopefully we’ll know more specifics of “how” in the future.  We do know that one of the biggest problems is circulation issues, basically with uncontrolled Diabetes, people lose adequate circulation to their limbs, get infections, can’t heal, and that’s how people have to have amputations.  These are the long term problems associated with long-term high blood glucose.

Moral of the Story:

Don’t forget the insulin!  Even when they’re sick, they must have insulin!  Exercise and diet control are soooo important, not just for the here and now, but to prevent long term complications.  It is sooo important to avoid obesity, because obesity frequently increases insulin resistance, and exacerbates lots of aspects of Diabetes.  Avoid things that contribute to cardiovascular disease- like too many fats (increase Omega 3 fatty acids in the diet- cook with canola oil, for example).  And finally, when you’re having to restrict the amounts of carbohydrates in the diet, make sure that the carbs that are being eaten are “nutrient dense.”  In other words- I could eat a snickers bar or a giant salad with the same number of carbs.  Opt for the carbs that provide the most additional nutrients-the most bang for your buck.  You don’t want to be nutritionally deficient in things found IN high carbohydrates foods (veggies, fruits, grains) like vitamins and minerals.  Carbohydrates are not the devil, they are glucose by definition, or other monosaccharides that break down in the same metabolic pathway as glucose.  J  That’s why it kills me when I overhear women say things like,.. “Oh I’m on a low carb diet,. I’ll just have a salad.  Carbs make me fat!”  Well guess what, genius, salads ARE carbs!  You probably just eat more calories than you need!  Oy.  I digress…


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