Fresh from writing The Myth that Sugar Causes Diabetes is a Myth I sought to understand the process whereby being overweight supposedly causes diabetes. You see, where you happen to read statements to the effect that sugar as a cause of diabetes is a myth you also read that being overweight is a primary cause of diabetes. Along with genetics (something I will be addressing soon) and the all inclusive “lifestyle factors”.
I don’t deny that something as complex as the system of systems known as the human body is affected by a multitude of factors. In the context of this article that means I’m not declaring sugar (meaning all the “-oses” like sucrose, fructose, maltose and dextrose) to be the one and only cause of conditions such as diabetes and obesity. If you consume an 8,000 calorie a day diet and don’t move an inch all day long your health is surely going to take a dive.
Did you know that way back in 2001 220 million people are projected to have Diabetes by 2010? Clearly what the authorities are doing is not working. So what I am saying is that I see a distinct official denial of the causal role of sugar in Diabetes. This includes all things that are quickly converted to glucose in the bloodstream by the human body such as fruit juice and starch from processed grains such as wheat and rice.
In fact knowing what some competitive powerlifers do to pack on the weight I would like to see someone “bulk” (i.e. get really big) eating grass fed beef, eggs, broccoli and spinach. In all likelihood you would quickly discover that it is very difficult to eat colossal amounts of this sort of food. There are natural appetite restraints that will stop you. If you’ve watched Sugar: The Bitter Truth you would know that this is not so with modern processed and packaged food and drink jammed full of sugar.
How is it that Eskimos eating their traditional diet of almost exclusively fat and protein do not get diabetes and rarely get cancer? Why is it that the French who consume a traditional diet including lots of butter and cream full of fat do not themselves get fat nor do they get diabetes?
At the same time the recommendation to everyone including the millions of diabetics in the west is to eat large quantities of processed starchy grains. This state of affairs is referred to as a paradox. I see no paradox. No paradox exists if the cookie cutter dietary advice recommended by authorities is flat out wrong.
How is it that I can eat full fat butter, yogurt, whole eggs, grass-fed red meat, organically raised chicken with its skin left on and so forth daily and have a blood cholesterol reading well below the threshold above which is considered unhealthy? How is it that if fat makes you fat that I happen to look like this every day without hours of cardio every week?
In fact I only workout around 3 times a week and most of that is heavy lifting with set of no more than 5 reps and rest breaks up to 5 minutes or more between sets. And it’s not like I’ve always been the healthiest person on the planet. Could it be because dietary cholesterol is not the cause of high bad blood cholesterol? Could it be that healthy natural sources of fat in a diet that doesn’t include modern processed food, starchy grains and sugar will not in fact make you fat?
The Official Line on the Cause of Diabetes
A registered dietician I spoke to said that as a person gains weight their fat cells increase in size and it is this that makes it difficult for the person to use their insulin properly. I found a study from way back in 1968 published in the Journal of Clinical Investigation that found the larger an adipose cell the less insulin sensitive was the tissue. All this says is that the bigger the fat cell the more insulin resistant it is. What it does not say is that large fat cells are the cause of their own insulin resistance, no more than insulin resistant muscle cells are the cause of their own insulin resistance. Again we encounter correlation not necessarily causation.
So this begs the question – What caused the fat cells to become insulin resistant? I asked the registered dietitian if they could explain the process whereby increased fat cell size causes insulin resistance. I have yet to receive a response. So I did my own research. Turns out the size of fat cells doesn’t have anything to do with it.
You’re Not Going to Believe What I found
Well actually, if you read my article The Myth that Sugar Causes Diabetes is a Myth and you’re still here then perhaps what I found won’t be all that shocking. According to a relatively recent article in the European Journal of Clinical Investigation (2008) it just so happens that fat cell size is correlated positively with plasma insulin concentration. That means if you have high levels of insulin in your blood then chances are you have big fat cells. Remember that insulin is released only when glucose enters the bloodstream and that this generally only occurs when you eat carbohydrates.
That’s all well and good but what about some causal proof that high insulin levels cause fat cells to be insulin resistant? As I’ve said correlation is not causation. Well, according to an article in the Journal of Nutritional Biochemistry (2005) plasma insulin concentrations appeared as one of the main determinants of adipose tissue lipoprotein lipase (LPL) activity. According to a study published in the Proceedings of the National Academy of Sciences of the United States of America (2001) tissue specific over-expression of LPL causes tissue specific insulin resistance. And at least everyone generally agrees that long term insulin resistance results consequently in the development of Type 2 Diabetes. If you didn’t get all that you seriously may want to read this paragraph again.
What it all means is this. If you have high insulin from eating or drinking lots of sugar or starch with little to no fiber LPL activity in your fat tissue increases. Too much LPL activity in your fat cells causes your fat cells to become insulin resistant. Long-term insulin resistance causes Diabetes. Therefore, once again it is high levels of insulin that causes insulin resistance and consuming sugar or starch and no fiber is the easiest way to get high insulin. Therefore, sugar has a powerful causal role in the occurrence of Diabetes.
Really though, did you honestly need a bunch of researchers fractionating rat brains to tell you this?
Fat is the third and last place insulin tries to deposit glucose circulating in the bloodstream for storage. The first location is cells in the liver and the second are your muscle cells. So for glucose to be going into your fat cells you had to consume more than you required for your immediate energy needs and more than what can fit into your short term storage.
If you look up the many things insulin does you’ll find that insulin happens to also be a growth hormone. This may be one of the reasons why high blood insulin levels are associated with several types of cancer. High circulating levels of insulin in your blood also happens to increase your appetite.
If you consume high starch or sugar food or drink with little fiber often (i.e. this is you dietary habit) you will have high circulating levels of insulin and subsequently as a result because of the insulin (as mentioned above) your appetite will increase. When your appetite increases you’ll logically consume more of the foods and drink that form your dietary habit. Since this constituted high sugar and/or high starch and low fiber soon the continuing high level of insulin in your bloodstream will result in insulin resistance. Remain insulin resistant for a number of years and you’ll develop diabetes.
If you’re meal or drink (drink water damn it!) is relatively low in sugar or high in fiber as it would be if you ate an apple or broccoli then the release of sugar is slow and gradual and the insulin response is far less extreme. Recall that just a moment ago we learned about the three locations insulin stores glucose in sequential order – liver first, muscle second, and then finally fat. So if you’re eating lots of sugar or starch without fiber and you don’t exercise like a maniac your liver and muscle stores are probably already full and insulin resistant anyway. Thus all this extra energy you’re consuming will go to your fat stores and you’ll get fat.
Thus, I point out again that the same thing that is causing people to gain weight is causing their diabetes. It is not the fact that they are overweight that is causing their diabetes.
Wrapping it Up
What gets me really is that it apparently takes years of insulin resistance caused by self-abuse to become type 2 diabetic. If this describes you – Snap out of it and take some positive action. As a practical, simple and easy way to get started in my next article I will provide you with step-by-step guide to making a delicious and inexpensive substitute for mashed potatoes (remember high starch foods like potatoes equals sugar in your bloodstream) that is healthy beyond belief. You just wait until you taste it! I also recommend you incorporate resistance exercise such as kettlebells into your workout if a medical professional clears you to do so. If you’re not already subscribed to Balanced Existence now would be the time. It’s free and you sure don’t want to miss this next article.
Lipoprotein lipase is an enzyme produced in fat cells. It breaks down triglycerides into free fatty acids and glycerol, which can enter cells for storage or energy production.
‘The role of adipose cell size and adipose tissue insulin sensitivity in the carbohydrate intolerance of human obesity’, 1968, Journal of Clinical Investigation, Vol. 47, Issue 1, pp. 153 – 165
‘The glucose uptake of human adipose tissue in obesity’, 2008, European Journal of Clinical Investigation, Vol. 1, Issue 6, pp. 480 – 485
‘Tissue leptin and plasma insulin are associated with lipoprotein lipase activity in severely obese patients’, 2005, Journal of Nutritional Biochemistry, Vol. 16, Issue 5, pp. 279 – 285
‘Tissue-specific overexpression of lipoprotein lipase causes tissue-specific insulin resistance’, 2001, Proceedings of the National Academy of Sciences of the United States of America, Vol. 97, Issue 13, pp. 7522 – 7527,
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