“You know you’re going to become a diabetic, don’t you?” Said my doctor as we went over my blood work.
I suppose I know this – I just thought that I could keep it at bay a bit longer.
I just had my blood work done, and although my numbers are pretty good, my glucose was 106 mg/dL. This is the indicator that I’m on the path my father, mother, sister, and brother have trod before me – the path to full-blown type 2 diabetes.
I told him my family history, and for him, there was a certitude in his pronouncement – it was just a matter of time – you can run, but you can’t hide.
Now, here I am in the home stretch to year 5 of a low carb lifestyle (with numerous little transgressions into high-carb territory) and part of me thinks: low carb failed me – I was hoping it would prevent this.
Another part says: your glucose 2 years ago was 98 – perhaps you have slowed the progression of a disease that struck your parents and siblings with a vengeance. And – don’t forget – you’ve kept off 60-65 lbs. My doctor expressed surprise at this, saying that the long-term weight-loss chances are about the same for low-carb and low calorie dieting, which, with a moment’s reflection, doesn’t make a bit of sense: if the weight-loss chances were less for low carb, there should be surprise on his part.
He’s a nice fellow, but I suspect he’s not at all convinced that this low carb stuff is valid.
Anyhow, his main recommendation was to exercise more, which for me, is easy: since my current time exercising is zero, anything resembling exercise is a plus.
Partly because of his recommendation, when I got home, I took my daughter and our bikes and cycled along the Raritan Canal, which was fun (though I didn’t like the exercise part).
So now I begin my research into insulin resistance. As this condition is a big part of low carb science, I am not unfamiliar with it, but when it doesn’t impact you directly, it’s somewhat academic – like frog biology.
So here I am reading about it with a deeper, more renewed interest. So first, it’s off to Wikipedia – the freewheeling, anyone-can-contribute encyclopedia that proves the old about an infinite number of monkeys with typewriters would produce all the works of Shakespeare – or at least an online encyclopedia.
Wikipedia says, and I quote:
Insulin resistance is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin. Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma. Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells reduces storage of glycogen, making it unavailable for release into the blood when blood insulin levels fall (normally only when blood glucose levels are low). Both cause elevated blood glucose levels. High plasma levels of insulin and glucose due to insulin resistance often lead to metabolic syndrome and type 2 diabetes, including its complications.
Which, frankly, becomes this as I read it:
Insulin resistance is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells reduces the effects of insulin and results in blah blah of stored triglycerides in the absence of blah which either increase blah blah or which provide blah blah. Increased mobilization of stored lipids in these cells elevates blah blah acids in the blah blah. Blah blah in blah blah reduces blah blah (blah blah blah blah blah blah), whereas blah blah in blah blah reduces blah blah, making it unavailable for blah blah when blah blah levels fall (normally only when blah blah). Both cause blah blah. High blah blah of blah blah due to blah blah often lead to metabolic syndrome and type 2 diabetes, including its complications.
So the result, once I’ve trudged my way through the blah blah, is:
Insulin resistance is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Higher levels of insulin are needed to control glucose levels in the blood, which often leads to metabolic syndrome and type 2 diabetes, including its complications.
Ok – next up are the symptoms – again from Wikipedia:
- Brain fogginess and inability to focus. Sometimes the fatigue is physical, but often it is mental.
- Low blood sugar. Mild, brief periods of low blood sugar are normal during the day, especially if meals are not eaten on a regular schedule; they are normally raised by mobilization of glucose into the blood from stored glycogen made from blood glucose previously taken by liver cells. But prolonged hypoglycemia, with some of the symptoms listed here, especially physical and mental fatigue, is not normal. Feeling agitated, jittery, moody, nauseous, or having a headache is common in insulin resistance, commonly with rapid relief once food is eaten.
- Intestinal bloating. Most intestinal gas is produced from carbohydrates in the diet. Insulin resistance sufferers who eat carbohydrates sometimes suffer from gas.
- Sleepiness. Many people with insulin resistance get sleepy immediately after eating a meal containing more than 20% or 30% carbohydrates.
- Weight gain, fat storage, difficulty losing weight. For most people, too much weight is too much fat. The fat in IR is generally stored in and around abdominal organs in both males and females. It is currently suspected that hormonal effects from such fat are a precipitating cause of insulin resistance.
- Increased blood triglyceride levels.
- Increased blood pressure. Many people with hypertension are either diabetic or pre-diabetic and have elevated insulin levels due to insulin resistance. One of insulin’s effects is on arterial walls throughout the body.
- Depression. Because of the deranged metabolism resulting from insulin resistance, psychological effects are not uncommon. Depression is said to be the prevalent psychological symptom.
Some of these are great symptoms for the hypochondriac – they are so vague, and can be caused by so many other factors, that each of us can cuddle our symptoms in their embrace and claim our fatigue is from Insulin resistance, when it could also be from a dozen other things.
I do notice that I feel a bit sick after eating too many carbs – and I do feel a sense of swelling up. Those do fit the symptom set above, so maybe we’re on the right track.
So next up – what causes this?
The cause of the vast majority of cases of insulin resistance remains unknown. There is clearly an inherited component, as sharply increased rates of insulin resistance and Type 2 diabetes are found in those with close relatives who have developed Type 2 diabetes. However, there are some grounds for suspecting that insulin resistance is related to a high-carbohydrate diet. An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance. Insulin resistance has also been linked to PCOS (polycystic ovary syndrome) as either causing it or being caused by it. Further studies are in progress. Other studies have also linked to the increased amounts of fructose (e.g., in HFCS – high fructose corn syrup, currently the least expensive nutritive sweetener available in industrial quantities), its fructose causing changes in blood lipid profiles, among other things. The high amounts of ordinary sucrose (i.e., table sugar) in the typical developed-world diet is also suspected of having some causative effect on the development of insulin resistance (sucrose is 1/2 fructose, which may account for the effect, if any). IR has certainly risen in step with the increase in sugar consumption and the addition of HFCS (since its invention in the last few decades).
At the cellular level, down-regulation of insulin receptors occurs due to high circulating insulin levels, apparently independently of insulin resistance. Inflammation also contributes to insulin resistance. Mice without JNK1-signaling do not develop insulin resistance under dietary conditions that normally produce it.
Some research has shed light on a complex interaction between elevated free fatty acids and inflammatory cytokines seen in obesity activating Protein Kinase C isoform theta. PKC Theta inhibits Insulin Receptor Substrate (IRS) activation and hence prevents glucose up-take in response to insulin.
Finally recent research and experimentation has uncovered a non-obesity related connection to insulin resistance and Type 2 diabetes. It has long been observed that patients who have had some kinds of bariatric surgery have increased insulin sensitivity and even remission of Type 2 diabetes. It was discovered that diabetic / insulin resistant non obese rats whose proximal small intestine and duodenum has been surgically removed also experienced increased insulin sensitivity and remission of Type 2 diabetes. This suggested similar surgery in humans and early reports in prominent medical journals are that the same effect is seen in humans, at least the small number who have participated in the experimental surgical program. The speculation is that some substance is produced in that portion of the small intestine which signals body cells to become insulin resistant. If the producing tissue is removed, the signal ceases and body cells go back to normal insulin sensitive behavior. No such substance has been found as yet, so this remains speculation.
I got the blah blah thing going on again. Translated so people who don’t feel the need to pretend they are smart can understand:
- They don’t know what causes insulin resistance in most cases
- It tends to run in families
- High carb diets might cause it
- Glucosamine might cause it
- PCOS is somehow linked to it, but they don’t know how
- Eating sugar, especially that monster from Japan, high fructose corn syrup (HFCS)
- Bariatric surgery sometimes reverses it, and docs don’t know why.
So what to make of all this?
- First – quit whining. There are people who would love to say their blood sugar is 106. And there’s a lot of people who’d see this number only on medication.
- It’s been caught early – the whole point of getting bloodwork. It gives you the opportunity to do something about it.
- It gives further impetus to maintaining my low carb lifestyle, losing a bit more weight and continuing the battle to work some exercise into my life. Each of these can help to get that number on the low side of 100.
I think I had a mental rationalization that said that, as long as I could keep the scale from going up, eating junk wouldn’t harm me. I had focused on weight alone as my indicator of health. I also have my wife, who thinks at 200 lbs., I’m just fine in the weight department.
Now I can’t hide behind these rationalizations. A reduction in weight will help in insulin response. Exercise helps here, too.
Maybe the silver lining here is I have fewer rationalizations to hide behind. I think a big part of attaining optimal health is a mind game – it’s not only what you eat, but what you think.
Oh, and there’s one other motivation I have: I want to prove my doctor wrong.