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Monday, October 5, 2015
Health / Nutrition ... Medicine ...

Like many, many other people, I come from a family with a history of Type 2 diabetes. One study estimates that about 30% of Americans have a family history of diabetes. My grandfather was diabetic, my mother was diagnosed in her elderly years, and her brother (my uncle) developed diabetes at age 50. I’ve reached 62 and so far I’m still OK (my recent physical included both a fasting glucose test and a hemoglobin A1C test, and both came back in the normal range — thank goodness!). But diabetes is something that I’ve been aware of most of my life (when I was a kid, my mother would sometimes make me test my urine for blood sugar with some kind of yellow strips — not a very accurate way to test for diabetes, but perhaps the best that was available to the common person back in 1965). My recent tests inspired me to do some further research on the topic. I thought that I’d share some observations here from my readings. [WITH THE USUAL CAVEAT — I AM NOT A DOCTOR OR MEDICAL EXPERT, JUST AN INTERESTED LAYPERSON WHO HAS DONE SOME RESEARCH]

First off, type 2 diabetes is not one simple, easily defined condition. There are a variety of “flavors” to it. Each version, though, involves the process by which glucose enters the bloodstream from the stomach and intestines after food ingestion, and by which glucose exits, either through conversion into ATP to fuel the muscles and organs which do the body’s work (i.e., cellular respiration); or by being pushed into the fat cells as a storehouse for future ATP conversion if needed (e.g. if there is a famine — something that was once very common for many humans, up thru the 18th Century). Insulin from the pancreas helps to kick start and regulate that process, allowing glucose to enter the cells of muscles and organs in the right amounts. When there is more than enough glucose to cover the current cellular respiration needs, insulin does the dirty work of pushing the excess glucose into the fat cells (i.e., making you fatter, at least temporarily), and signalling the liver to cut back on production. If the glucose stays in the blood for too long and reaches high concentrations, it can start gumming up the works in sensitive places like the heart, eyes and kidneys, causing damage.

Diabetes type 2 occurs when insulin and its regulation mechanisms aren’t doing the job properly; either too much glucose builds up in the blood, or too much glucose is pushed aside by it and there isn’t enough to support the level of cellular respiration needed
to keep the body running at 100%. This is basically what type 2 diabetes is, in a nutshell (admittedly, this is a crude overview, and misses a lot of important things).

As such, type 2 diabetes can be triggered by a number of factors; and what causes it for one person can be quite different from the circumstances behind another person’s insulin and glucose problems. It could possibly be that the food digestion system (including the liver) pumps out too much glucose too quickly; or it could be that the pancreas doesn’t produce enough insulin. Or perhaps the liver and pancreas are working OK, and there is generally enough insulin for the glucose being introduced; but the control mechanisms which measure the amount of glucose in the blood and which increase insulin when it gets too high (and conversely cuts it back when glucose goes too low) aren’t responding quickly enough. Furthermore, perhaps the insulin that is produced doesn’t work all that well in pumping the glucose out of the blood and into the fat cells. The latter situation might be because of bad insulin, or because of something changed in the fat cells — they might not want to take in any more “glucose refugees”, they might have more than they can already handle (this is called insulin resistance).

Diabetes (type 2) can occur because of any combination of these reasons (and there are even more factors involved; this is just a simplified picture). The medical profession has known for a long time that the factors which cause diabetes are genetic in nature, they depend upon the genes that a person inherits from her or his parents.

But it’s also well known that a person’s habits and lifestyle strongly influence whether, when and how they could become diabetic. It’s hard to get a good estimate on just what the balance is between nature and nurture, between genes and the environment. But some rough estimates that I’ve read say that environmental factors have at least a 50-50 say in whether or not an insulin problem occurs, and perhaps that split is even higher on the side of lifestyle (including eating habits, diet, exercise, stress, etc.). Of course, this also varies from person to person. So, the next question is, can medical science come up with a gene test to tell each of us just how bad our genes are with regard to diabetes? Could a test tell each of us individually whether the genetic cards are stacked against us, or do they favor a healthy insulin system in our bodies?

A lot of research has been done on that. By now, over 120 testable gene variants have been identified that contribute to whether or not someone becomes a diabetic. And today, genes can be tested for a reasonable price. But still, the medical profession is not ready yet to use such testing to tell patients just how bad their diabetes risk is. Some studies (e.g., here and here) conclude that a DNA test based on current knowledge about gene variants and diabetes would not significantly add to what can be known by a traditional diabetes risk assessment (which mostly looks at lifestyle habits, but indirectly accounts for genetics by assessing family history of diabetes). But other experts indicate that gene tests might improve risk assessment for many people. Most doctors aren’t ordering gene tests for type 2 diabetes yet, but that could change in the near future.

Still, that doesn’t mean that some members of the public aren’t looking into their genes anyway. Until 2013, 23andme.com offered a $99 gene test for both ancestry and health risk assessment purposes. I took advantage of that offer. In late 2013, the US FDA told 23andme to stop doing the health assessment, although it could continue to offer the family genealogy services. However, someone really interested in finding out how their gene variants might match up with what is presently known (or hinted at) through genetic research studies can take their results from 23andme (or from the other popular genetic genealogy sites like ancestry.com and ftdna.com) and upload them on the promethease.com site. For a $5 fee, they can find out how their tested gene segments matched up against the thousands of gene studies that are summarized and classified on the snpedia.com “public wiki” site.

As to my own type 2 diabetes risk results on 23andme.com, I would call them “mixed”. 23andme tested 11 gene sites relevant to diabetes (a small fraction of the known DNA points that relate to diabetes), and it put those results thru a formula to assess my overall risk (as compared to the overall male European-ancestry population). That formula indicates that I have a slightly lower than average chance of getting diabetes (when genetic factors alone are considered — obviously if I subside on Twinkies and Mountain Dew and get little exercise, my chances go up regardless of my genes). My overall classification, though, was “average risk”; only those conditions where the formula came out more than 20% higher or 20% lower than average are classified “above average” or “below average”.

OK, that’s reasonable enough, but just how much can be known through only 11 genes, relative to such a complex disease as type 2 diabetes? Of the 11 genes tested, my results showed 6 “bad” ones and 5 “good” ones. But the formula that 23andme uses said that the good ones had stronger effects than the bad ones. Hey, sounds good to me, but can this really be trusted? These estimates are based on just a handful of studies, usually with just a couple of hundred people each. It becomes obvious that this is not really ready for prime time yet. The promethease site will supposedly test a larger number of gene sites, but still . . . this has the feel of the home computer world of 1988. Remember the Tandy 1000 that you bought in Radio Shack, or the Commodore 64, with their floppy disk drives and Windows 2.0? Or the Apple II, if you wanted to go another route?

So, the nature versus nurture issue is still very fuzzy with regard to type 2 diabetes (and the role of genetics is weaker still with regard to Type 1 diabetes, which is an autoimmune syndrome often contracted at a young age). Most experts make it quite clear, though, that lifestyle and diet do play a significant role in delaying or even preventing the onset of type 2 diabetes in many if not most people with genetic pre-dispositions. (And it might also be possible that very bad diet and exercise habits could cause even those with generally good genes and family histories to become diabetic). It’s no surprise that diet and exercise are critical in this disease, since insulin is entirely concerned with regulating what goes into the blood and body cells from the food you consume, and how it us used to create body energy.

One of the big diabetes issues regards eating too much, and thus causing a person to become overweight and eventually obesity. In general, having too much fat in your body increases the risk of diabetes, especially (but not exclusively) the insulin resistance factor. Body fat, or at least certain kinds of body fat, seem to have hormonal effects which decrease the effectiveness of insulin in removing glucose from the blood. Some research indicates that this is especially so for “visceral fat” and “white fat”. Such fat usually accumulates deep inside the core of the body, and above the belly. “Brown fat” and “hip fat” are felt to not be as bad. Preliminary research indicates that people with a lot of fat above the belt (the “apple” shape body) tend to be more prone to insulin resistance and diabetes, whereby people with fat accumulations in the hips (the “pear” shape body) are more likely to remain healthy.

Another major issue regards the “starch versus sugar” question, i.e. which is worse (in terms of causing diabetes — which is usually but not always the same question as to which is better or worse for someone who is a diabetic). Much of the current literature and web site guides to diabetes today pin much of the blame for T2 diabetes onset and its worsening to consumption of starchy, refined high-carbohydrate foods such as bread (and anything else made with milled white flour), potatoes and white rice. These foods are said to be highly “glycemic”, i.e. they are converted rapidly by your stomach and liver into blood glucose, raising glucose levels very quickly after consumption. Rapid glucose elevation stresses the pancreas in its attempt to put out enough insulin to avoid high, potentially damaging levels of sugar in the blood.

If there is a genetic impairment of this response mechanism, or if insulin resistance is developing, a “glycemic” food might raise insulin to damaging levels for a period of time. Some of the damage might be to the liver and pancreas themselves, making the control or insulin resistance situations even worse, spiraling the body towards full-blown diabetes. So, certainly those with T2 diabetes need to track the glycemic load of what they eat, as to avoid further bodily damage. But some authorities and studies go so far as to suggest that eating a lot of glycemic foods is also a cause of diabetes.

There seems to be another school of thought which feels that starchy carbs and glycemic ratings aren’t quite as important as they once seemed. Sure, a diabetic who is known to have insulin response problems will need to eat carefully so as to avoid glucose spikes, which their body cannot respond to quickly enough. But the really damaging element is felt by many to be consumption of concentrated sources of fructose — i.e., table sugar, soda, honey, fruit juice, anything which packs a lot of natural sweetness from fructose into a small volume of food or liquid. Fructose and glucose are the two components of table sugar (sucrose), but are metabolized differently in the body. Glucose can be used up by a wide variety of tissues and organs, whereas fructose can only be processed in the liver. Too much fructose leads to high triglycerides, fatty liver, insulin resistance and poor insulin response to glucose (e.g., when the liver accumulates too much fat, it doesn’t detect changes in blood glucose as well, and therefore doesn’t cut back on pumping glucose into the blood when levels are high). All of these factors speed up the onset of T2 diabetes.

Fructose may also interfere with the natural processes of controlling appetite, such that a person who chugs down a Coke or a glass of apple cider or a coffee with two sugars is still hungry and ready for a big meal, even though they have just ingested a huge dose of calories. It thus also promotes obesity, which in itself contributes to insulin resistance and diabetes. (High-fructose foods are more prevalent than you might think — many yogarts have a lot of added sugar, as do canned spaghetti sauce, catsup, salad dressings, cereals, ice cream, even pickles; and most cakes, pies and cookies are little sugar bombs). But one recent study suggests that even thin people who chug down a lot of fructose sweetener are at increased risk of becoming diabetic. This may help to explain the seemingly paradoxical phenomenon of thin people with type 2 diabetes.

There have been a number of studies and papers favoring this point of view over the past 5 years or so. However, other experts have argued that fructose is being unfairly picked out, and that all sources of low-fiber “fast carbs” (bread, potatoes, pasta, rice) are equally to blame for increased obesity and diabetes onset. Nonetheless, a recent study which was published by the Mayo Clinic is entitled “Added Fructose – Principal Driver of Type 2 Diabetes Mellitus and Its Consequences“. Obviously the “fructose as the bigger enemy” viewpoint is now picking up mainstream support in the medical establishment. The sugar and soft industry obviously doesn’t like this development, including the Corn Refiners Association and the American Beverage Association. The latter group promotes “balanced calories” dietary reductions, implying that fructose is no worse than any other source of calorie. Obviously, there is a vested financial interest behind this advice.

I would conclude that anyone who might be concerned about diabetes and is trying to eat and live healthy so as to avoid getting it should take a “both roads” approach. I.e., keep the “high glycemic” carbs under control, don’t pig out on bread and potatoes and rice or any other high glycemic food. And ditto for fats, especially saturated fats — eat them in moderation and in combination with other foods, especially the more fibrous foods. But the more serious concern should be with fructose. Starchy foods can be consumed in small amounts with other less glycemic foods such as vegetables and fats (preferably healthy fats like olive oil), so as to slow down their metabolization.

One little trick that I think MIGHT help is to swallow down some psyillium fiber (most of us mix it with water) before eating a big meal. You would do this anyway if you are concerned about constipation. But even those who don’t need psyllium for that might now want to consider a gulp before chowing down on pasta or a stir fry with rice or a sandwich on a loaf of Italian bread. (But be careful which psyllium product you use — some have sugar added to make them taste better, including certain versions of the popular Metamucil brand; be sure you get the sugar-free stuff). Another idea is to wash down a carb-laden meal with some cinnamon tea, which you can make using cinnamon sticks (available in most supermarkets). It actually tastes pretty good — even without any added honey or sugar! No guarantee that it will help with your blood sugar, but it probably couldn’t hurt.

As to added dietary fructose — you need to just stop ingesting that stuff, as much as possible. (Recall that fructose is 50% of table sugar and 55% of high-fructose corn syrup.) Most diet experts say that you don’t have to worry much about the most natural sources of fructose, e.g. whole fresh fruit. They have enough fiber relative to the fructose they have (which isn’t all that much relative to a processed sweetened food or soft drink like Pepsi or Coke) to keep your body from any damage, if eaten in moderation (but be more careful with dried fruits like raisins and dates, which have become unnaturally sugary). You probably can’t eliminate fructose completely from everything else that you eat — but you can avoid or cut back on the worst and most concentrated sources of it (once again: soda, fruit juices, cookies, coffee or tea with sugar, muffins, cake, flavored yogart, many cereals, on and on).

Do you need other web sites saying the same thing, perhaps even better than I am saying it here? OK, try this one or this one or this one or this one or this one . . .

Oh, and as to the integrity of search engines . . . search on “fructose and diabetes” on Google, and right at the top of the results is a link to the “Fructose Information Center“, an industry group trying to keep you from turning sour on the stuff. As to diabetes, this site suggests that fructose isn’t so bad because of its low glycemic index. That’s like saying that a rattlesnake won’t tear you to shreds like a tiger can. As anti-fructose advocate Dr. Robert Lustig says, “Glycemic index is a canard . . . fructose’s poisonous effects have nothing to do with glycemic index; they are beyond glycemic index.” I mean, really Google — I know that you have stockholders who are hungry for sweet dividends and earnings growth, but . . .

Overall, my two cents is to keep exercising, keep thinking positive, keep eating right, and enjoy life! Hopefully without all the hassle of diabetes. But if it does eventually get you, if the genes were just stacked too heavily against you, well . . . at least you know that you did all you could to stop it. And all that you did do to prevent it (and should continue to do, for the most part) will give you the best chance to fight it and continue to live a good and active life nevertheless.

◊   posted by Jim G @ 7:07 pm      
 
 


  1. Jim, You have a good explanation of diabetes and how it works (or doesn’t work right) in the body.

    It certainly is true that often, for some people, a simple change in diet and some loss in weight can bring sugar levels in the blood down to the normal range.

    What is missing from this explanation, though, is something I doubt too many doctors will readily admit: That under certain circumstances, with some diseases that require steroid use – particularly that of prednisone – prednisone will “always raise blood sugar” (to quote a doctor who told me this personally). For those people who require this medication to maintain good health when they have a certain medical problem, diabetes is all too often a concomitant problem that arises. (One’s damned if one does and damned if one does not.)

    Furthermore, I can see that with a history of diabetes in the family, it is always good to take care that one doesn’t aggravate the situation. But I would also caution that too much worry about whether or not one will get this or that disease is a problem that can ruin quality of life, which is of utmost importance. I have learned through life that when it comes to death, one will die when the appointed time arrives; and nothing will stop it and nothing will bring it on faster. It will come when it comes and not before.

    While it’s always good to be aware of those genes one might carry in one’s body that could be harmful in some way, it’s also important to put things in perspective. Thus, if one has something akin to a 50/50 chance of acquiring some particular medical problem, I’d not give it a great deal of thought beyond using common sense in one’s health care; and I’d make it a point to enjoy life. MCS

    Comment by Mary S. — October 6, 2015 @ 6:10 pm

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