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Exercise and MHCP Combine to
Improve Blood Sugar Levels

Cinnamon extract mimics insulin and offers benefits that drugs do not
By Aaron W. Jensen, Ph.D.

ouldn't it be great if the claims made on those late-night infomercials were really true? For example, who wouldn't like to strap a battery-operated muscle contractor around their ample abdomen and have the inches and pounds melt away, as a sleek new waistline emerged in rippling glory after just a few weeks? It sounds too good to be true, doesn't it? Maybe that's why that nagging little disclaimer, "Individual results may vary," always shows up in fine print somewhere during the message.


MHCP, like exercise, boosts the
glycogen content of muscle and
liver cells. In other words,
MHCP is an insulin mimic.
Furthermore, MHCP and insulin
are synergistic in this regard.


Those TV claims are, of course, too good to be true. There's no substitute for actual physical exercise for toning your body (and your mind too), and there's probably nothing that's as good for your overall health. Just about every organ and functional system in your body - even your skin - benefits from exercise in demonstrable ways. For the maximum benefit, however, exercise should be coupled with good nutrition - and that, of course, includes appropriate supplements to make up for certain deficiencies that become ever more problematic as we grow older.

Insulin Problems Lead to Diabetes

One deficiency that affects a growing number of Americans is that of insulin function, which is absolutely vital for controlling blood sugar (glucose) levels. If the pancreas produces inadequate amounts of insulin - or, more commonly, if insulin resistance develops (a gradual loss of insulin's ability to promote the uptake of glucose by the body's cells) - glucose levels in the blood become chronically high. This is a setup for the onset of type 2, or age-related, diabetes, a dreadful disease that can ravage many of the body's vital functions.

Currently, approximately 15 million Americans have type 2 diabetes, and one-third of them don't even know it, because the symptoms often go undetected during the early stages of the disease. The primary risk factor for diabetes is obesity (see the sidebar "Obesity, Diabetes, and Immune Function"). And since the obesity rate in the United States is climbing rapidly, it's no surprise that the incidence of diabetes is doing the same.

Obesity, Diabetes, and Immune Function

It has been well established that obesity is the main risk factor for diabetes - the greater your excess weight, the greater your chances of getting the disease. Recent research on a very large group (84,941) of women indicates that those who are mildly overweight (BMI between 23.0 and 24.9) increase their risk of diabetes 2.7 times compared with those who have a BMI less than 23, while those who are grossly overweight (BMI greater than 35) increase their risk of diabetes by a whopping 38.8 times.1

But why? Why does carrying around excess weight increase your risk for diabetes? This is a difficult question to answer, but researchers in Japan may be on the right track.2 They have determined that obesity increases the production of a specific molecule called interleukin-1-beta (IL-1b), which is produced by cells of the immune system. It turns out that IL-1b is toxic to the specific pancreatic cells - called islet cells - that produce insulin.

The researchers found that obese individuals, regardless of whether they had diabetes or not, produced significantly higher levels of IL-1b than nonobese individuals. They surmise that this may lead to increased islet-cell death and thus decreased insulin levels overall, a condition that would lead to increased blood glucose levels and ultimately to diabetes.

  1. Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med 2001;345:790-7.
  2. Mito N, Hiyoshi T, Hosoda T, Kitada C, Sato K. Effect of obesity and insulin immunity in non-insulin-dependent diabetes mellitus. Eur J Clin Nutr 2002;56:347-51.

The Good News and the Good News

But there is good news about diabetes. First, it's easily preventable through diet and exercise. The key is simply not to get fat. OK, that is easier said than done, what with the fat-rich Western diet of which most Americans are so enamored.

All the more reason to be grateful for the second bit of good news, namely, that there is a nutritional supplement, recently discovered and newly available, that is remarkably similar to insulin in its action and that may thus be helpful in preventing and combating diabetes. It's called MHCP, and we'll get to it shortly. (For previous articles on MHCP, see the February, March, June, and July issues of Life Enhancement.)

Exercise Reduces Blood Sugar Levels

Physical exercise is well known to improve blood sugar regulation, among many other things. And antidiabetic drugs do so, of course, because they're designed for that purpose. The questions arise: How do exercise and antidiabetic drug therapy interact? Do they complement each other, and if so, to what extent?

Researchers seeking to answer these questions performed a four-week-long experiment with diabetic mice.1 They divided the mice into two groups: one that would receive daily forced exercise (swimming in a tank) and one that would not (the control group). Each of these groups was further divided into three subgroups: one received metformin (a drug that inhibits the production and release of glucose from the liver); one received acarbose (a drug that slows digestion and absorption of glucose in the small intestine); and one received only "vehicle" (the same base substance that the other mice got, but without any drug included). Thus, for 28 days, some of the mice got exercise alone; some got exercise plus one drug or the other; some got one drug or the other, but without exercise; and some got nothing but the inert vehicle.

This scheme allowed the researchers to identify and separate the effects of the various combinations of treatments. They found that exercise, metformin, and acarbose, when used alone, each reduced blood sugar levels by 15 to 25% compared with the controls. When either of the two drugs was combined with exercise, the effects on blood sugar were additive, but not synergistic. In other words, the total effect of exercise plus drug equaled the sum of the individual effects, but did not exceed it. These results suggest that each treatment works by a distinct biological mechanism, and it's reasonable to suppose that similar results would be obtained if exercise were combined with a nondrug treatment, e.g., a glucose-reducing supplement such as MHCP.

Improved Lifestyle Beats Drugs

A paper published in the New England Journal of Medicine earlier this year convincingly demonstrates that wise lifestyle choices, particularly in terms of diet and exercise, can dramatically reduce the incidence of diabetes in at-risk adults.1 The study was performed with 3234 nondiabetic individuals who had elevated glucose levels and were thus at high risk of getting diabetes. Importantly, the participants were afflicted with the dominant risk factor for diabetes: obesity. Their average body mass index (BMI) was 34, which borders on gross obesity.

The goal of this study was to determine whether lifestyle intervention, such as a 7% decrease in body weight and a minimum of 150 minutes of exercise per week, was an effective weapon against the onset of diabetes. Serving as counterpoint for this group was a similar group of participants who underwent no changes in lifestyle but who were given the antidiabetic drug metformin.

The average follow-up period for the participants was 2.8 years, and the results of the study were striking, and gratifying. The lifestyle intervention consisting of modest weight loss and modest exercise reduced the incidence of diabetes by 58%, whereas taking the drug reduced it by only 31%.

  1. Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New Engl J Med 2002;346:393-403.

Exercise Boosts Glycogen Storage

In another aspect of the study, however - namely, the measurement of glycogen levels in the muscles and liver of the mice - the results of the exercise and drug treatments were distinctly different. Glycogen is a polymeric form of glucose that's produced and stored primarily in the liver and muscle tissues. This process is under the control of insulin. When the body needs more glucose than is currently available, such as during vigorous exercise, the glycogen is converted back to glucose for quick energy.

In the experimental mice, the exercise regimen increased the glycogen content of the muscles by 30% and of the liver by 155%. By contrast, the two drug treatments had no effect on the glycogen content of muscles or liver.*


*A further bonus from the exercise regimen was that it largely prevented a decline in serum insulin levels during the course of the study. Insulin levels in the control mice declined by 30 to 40%, as part of the progression of their disease. By contrast with the exercise regimen, neither of the two drugs had any effect on insulin levels.


MHCP Boosts Glycogen Storage Too

Well, so what? The drugs still performed their primary function of controlling blood sugar, didn't they? Yes, they did. But here's what: MHCP does that too, and, like exercise, it boosts the glycogen content of muscle and liver cells. In other words, MHCP acts as though it were insulin - it is an insulin mimic. Furthermore, MHCP and insulin are synergistic in this regard, meaning that the total effect when they are both at work is greater than the sum of their individual effects. This is true not only of their action in boosting glycogen levels in muscle and liver tissue, but also of their primary action in regulating blood sugar levels - the key objective of every therapy for diabetes.


MHCP reduces blood glucose
levels not just in the presence of insulin
but also in its complete
absence - and it does so almost
as well as insulin itself.


MHCP Is Almost as Effective as Insulin

Our knowledge of MHCP's actions comes from experiments not with living mice, but with cultured mouse cells called adipocytes, which are the cells of adipose (fat-storage) tissue. The pioneering work in this field has been done by Dr. Richard Anderson and his colleagues at Iowa State University and the U.S. Department of Agriculture.2 In searching for a natural substance that could mimic the effects of insulin, they found it in a most unlikely place: apple pie.

Narrowing the search through analyses of the pie's ingredients, they homed in first on the spices, then on cinnamon in particular, and finally on a compound in cinnamon called methylhydroxychalcone polymer (MHCP). They discovered that MHCP reduces blood glucose levels not just in the presence of insulin but also in its complete absence - and it does so almost as well as insulin itself.

Exercise + MHCP = A Winning Formula

Is the action of MHCP related in any way to the benefits of exercise? Indirectly it is, because what they have in common is an improvement in insulin function. Exercise is believed to enhance insulin sensitivity (i.e., to decrease insulin resistance) throughout the body, which would explain its ability to reduce blood glucose levels. In other words, exercise makes it possible for insulin to do its appointed job more effectively, all else being equal. But all else need not be equal, because one can supplement with MHCP, which also (in laboratory experiments, anyway) improves insulin function and boosts cellular glycogen levels, as exercise does.

The benefits of exercise and of MHCP are likely to be additive, as in the mouse experiment described above, so it makes sense to avail oneself of both of these approaches to the control of blood sugar levels. The benefits of exercise in this and many other aspects of human physiology are indisputable, and it is exciting to contemplate the possibility that a compound extracted from cinnamon may become a powerful ally to regular exercise and good nutrition in the battle against diabetes.

References

  1. Tang T, Reed MJ. Exercise adds to metformin and acarbose efficacy in db/db mice. Metabolism 2001;50(9):1049-53.
  2. Jarvill-Taylor KJ, Anderson RA, Graves DJ. A hydroxychalcone derived from cinnamon functions as a mimetic for insulin 3T3-L1 adipocytes. J Am Coll Nutr 2001;20(4):327-36.


Dr. Jensen is a cell biologist who has conducted research in England, Germany, and the United States. He has taught college courses in biology and nutrition and has written extensively on medical and scientific topics.


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