Optimizing Insulin Sensitivity and Body Composition Through Diet and Exercise By Jason Feldman
For Precision Nutrition. America is growing; that's a fact. So are its citizens, though, with 17.1% of children being overweight in 2004 and 31.1% of adults being overweight. This is compared to 13.9% and 27.5% respectively in 2000 (16), catalyzing the so-called obesity epidemic.
Obesity can lead to many problems later in life, such as an increased risk for type II diabetes, high blood pressure, and escalating health care costs. It's clear that something needs to be done. The most obvious first step is caloric control and to balance the first law of thermodynamics. This can be simplified by stating that one needs to balance their consumption of calories versus their expenditure to reach their goals. |
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This is not always enough, though, as evidenced by the myriad of diets that have popped up over the years focusing on both macro and micronutrients, and often fruitless supplementation.
The truth is that there is no"magic pill," or a two-day weight loss cure. One needs to eat properly, exercise regularly, and manage their insulin through normal, non-pharmaceutical means. The role insulin plays becomes exponentially important in athletes and anyone looking to improve their body composition.
The role of insulin in the body and diabetes
Insulin is often called the most anabolic hormone in the body. Its role is to shuttle nutrients into tissues, primarily adipose, liver, and muscle tissue. It is released by the beta cells of the pancreas in response to an increase in glucose, amino acids, and free fatty acids. Within the liver it promotes anabolism increasing the uptake and storage of glucose as glycogen. At the same time it prevents catabolism by inhibiting glycogenolysis and the Cori Cycle. In muscle cells it promotes anabolism by stimulating protein synthesis through an increased uptake of amino acids while concurrently increasing the uptake of glucose to form glycogen and inhibiting phosphorylase to prevent its breakdown. Adipose tissue is subject to similar mechanisms; glucose and triglyceride storage are increased while the production of Hormone-Sensitive Lipase (HSL) is inhibited. HSL prevents the re-esterification of triglycerides, promoting their breakdown.
The release of insulin and its cellular response are critically integrated within the body. Under normal conditions blood sugar levels stay between 70 and 110 mg/dl controlled by a complicated network of hormones including but not limited to insulin, glucagon, and growth hormone (GH). Glucagon and GH both work to raise plasma blood sugar levels. Unfortunately this network is not always properly maintained leading to diabetes.
There are two types of diabetes: Type 1 and Type II. Type I is referred to as insulin-dependent diabetes. It is characterized by the body lacking the ability to produce insulin and results in sustained hyperglycemia. Treatment for it generally includes insulin injections and constant monitoring of blood glucose levels.
Diabetics need to carry around sugary snacks because their constant insulin injections rob them of blood sugar. Since the brain can only function on carbohydrates (or ketones) a hypoglycemic state is not a good one to be in.
90% of diabetics have Type II Diabetes which is characterized by either a decreased ability to secrete insulin or a decrease in insulin sensitivity.
The glycemic index and its link to diabetes
Two critical ways to control and manage both diabetes and insulin are through diet and exercise. With respect to ones diet it is important to pay heed to the glycemic index (GI). The glycemic index is a ranking of carbohydrates (CHOs) on a scale of 0 to 100 in relation to the rate at which they raise blood sugar levels after eating.
Foods with a high GI rapidly raise blood sugar levels and generally spike insulin levels; whereas foods with a low GI slowly raise blood sugar levels and have a more blunted and sustained insulin response. To measure the GI, 10 subjects fast overnight and are fed 10-50 grams of CHO containing foods and then finger-prick blood sugar samples are taken at 15-30 minute intervals for the next two hours. A blood sugar response curve is then constructed from this data and the area under the curve is used to calculate the GI compared to a base food (an equal amount of glucose). The area under the curve is divided by the area under the curve for glucose and then multiplied by 100 to achieve the GI rating. Generally foods with a low GI are preferential because it will cause a smaller insulin burst.
Chronically elevated insulin levels are not to be viewed as optimal. According to the University of Syndey Human Nutrition Unit recent studies from Harvard have indicated that diets rich in high GI foods increase the risk for type II diabetes and heart disease. This led the World Health Organization (WHO) in 1999 to recommend that people in industrialized countries base their diets on low-GI foods.
To understand how type II diabetes is manifested in the body it is first necessary to understand the hormonal and physiological mechanisms in place. It all begins with the ingestion of food. Food enters the gastro-intestinal tract and through various enzyme-linked reactions is broken down into simpler molecules. In the case of CHOs there are three primary types: monosaccharides, disaccharides, and polysaccharides.
A monosaccharide is a simple sugar that is not further broken down before it enters the blood stream such as glucose of fructose. Its molecular formula is C6H12O6. A disaccharide is also a sugar but is broken down into two different sugars; such as sucrose which is a combination of fructose and glucose, or lactose which is a combination of glucose and galactose.
Polysaccharides are multiple (greater than two) molecules of sugar linked together such as starch found in vegetables and grains. They are then broken down into simple sugars once they enter the body.
In general (since there are many exceptions) the speed of digestion and GI is linked to the type of saccharide one ingests with the rates being: monosaccharide (highest GI) > disaccharide (moderate GI) > polysaccharide (lowest GI). If one eats a diet rich in monosaccharides they can have chronically elevated insulin levels in response to this. This will cause a myriad of things to happen. For one this may cause subjects to eat more due to rapid blood sugar fluctuations. Primarily though it can lead to insulin resistance.
With the advent of processed foods, sweets, and foods loaded with high fructose corn syrup, sugar consumption has significantly increased. In 1980 the average person ate 39 pounds of fructose and 84 pounds of sucrose; by 1994 the average person ate 66 pounds of sucrose and 83 pounds of fructose. As of 2001 25% of caloric intake was coming from sugars (6).
So, not only is sugar consumption increasing; but so is fructose consumption. While fructose is generally considered a"better" sugar being predominantly found it fruits, its processed form is not so great. For example, according to Dr. Nancy Appleton, fructose is not metabolized the same as other sugars and does not cause the pancreas to release insulin normally and leads to higher fat gain. It can also lead to mineral deficits such as in copper and magnesium since in its purified state it contains no enzymes, vitamins or minerals.
The take home message is that fructose should come from natural sources such as fruit where these co-factors are present. In a 1983 study by Hallfrisch et. al. fructose was found to decrease the affinity of insulin receptors for insulin. This is the classic benchmark for Type II diabetes. This increase in sugar consumption causes the body to pump out more insulin. Since insulin is chronically elevated insulin receptors in turn down-regulate, or"desensitize." This makes it more difficult for the body to remove sugar from the blood leading to many other various problems such as blood clots, potential blindness, potential need for amputations, etc. Also it increases the risk for fat gain since insulin is primarily a storage hormone.
Enhancing insulin sensitivity through weight loss and the role of adiponectin
Adiponectin is protein produced by adipocytes. It promotes insulin sensitivity. In contrast to other adipokines it has been shown to have smaller total circulating levels in obese individuals.
In an August 2005 study by Abbasi et. al. 24 insulin-resistant non-diabetic subjects were recruited and either put on a weight-loss protocol based on caloric restriction or treated with rosiglitazone. The subjects all had a BMI of 30-35 (which is considered significantly overweight or obese). In the study the rosiglitazone group increased their adiponectin concentrations by 30% and enhanced their insulin sensitivity.
The weight-loss group though did not have any changes in adiponectin levels but they had the same 30% increase in insulin sensitivity. This suggests that factors other than adiponectin concentrations play a significant role in insulin sensitivity and that even mild weight loss can help one improve their insulin sensitivity thus supporting the hypothesis that exercise, weight loss, and a proper diet play major roles in promoting general health and maintaining proper functioning of the body.
In contrast a 2003 study by Faraj et. al. showed conflicting results regarding adiponectin on patients that underwent gastric bypass surgery. In almost all subjects adiponectin increased in response to weight loss and their insulin sensitivity increased. It is important to note though that this group lost significantly more weight than the group in the Abbasi study.
Based on these two studies, the jury is still out on the correlation between adiponectin and enhanced insulin sensitivity. Something else is extremely clear though from the two studies: fat loss in obese individuals is a major catalyst to enhance insulin sensitivity.
It is interesting to note something though from the Faraj study that should have been explored in greater depth; in the results section it reads"subjects who were receiving medical treatment for diabetes before the surgery (six women and four men) had discontinued all hypoglycemic agents."
This is the most striking part of the paper; diabetes was self-corrected through weight loss! Granted gastric bypass surgery is a drastic measure but similar if not the same results can be achieved through a proper calorie-controlled diet and exercise. This method also happens to be a lot safer and less expensive than surgery.
Insulin sensitivity and exercise and the role of glucose gransporters
Exercise also plays a crucial role in helping improve insulin sensitivity, especially resistance training. It's myriad of benefits include elevating GH and testosterone (TEST) levels and increasing ones metabolic rate through an elevated post exercise oxygen consumption (EPOC). It also blunts the insulin response and the contraction of skeletal muscle causes glucose-transport-protein-4 (GLUT-4) to propagate to cell surfaces.
GLUT-4 is an insulin sensitive glucose transporter present in skeletal muscle. It is necessary for sugar transport into cells and may facilitate the transport of glucose into muscle fiber. To quantify this Ren et. al. performed a study to examine the effect of GLUT-4 protein expression on fat and whole body glucose metabolism. The euglycemic hyperinsulinemic clamp technique was used on conscious mice. The rate of glucose disposal was significantly higher (70%) in the transgenic mice (who had over-expression of GLUT-4) than in normal mice in both fed and unfed states. According to the study"the results suggest that skeletal muscle glucose transport is rate-limiting for whole body glucose disposal."
This combined response of a blunted insulin response and up-regulation of GLUT-4 allows more glucose to selectively enter muscle cells while bypassing fat cells. This also results in an increased action of HSL (which is suppressed by insulin) which in conjunction with an increase in catecholamine concentration helps to catalyze the breakdown of adipose tissue.
To demonstrate this a December 2005 study by Polak et. al. placed 12 obese men (as determined by BMI) on a three-month dynamic strength-training protocol. Not surprisingly at the end of the protocol fasting glucose decreased by 20% and fasting insulin by almost 50%. Insulin resistance markers also were cut in half. It appears that dynamic strength straining improves whole body insulin sensitivity and improves lipid mobilization in subcutaneous adipose tissue in obese subjects.
Aerobic training also enhances insulin sensitivity. A 1999 study by Cox, Cortright, Dohm, and Houmard compared the effects of short-term exercise training on GLUT-4 concentrations and insulin sensitivity in older and younger individuals. They found that with exercise training at the same relative intensity quantified by VO2 max there was a similar increase in GLUT-4 concentration and similar enhancements in insulin sensitivity between both groups.
Other studies though refute this data such as 2005 study by Goulet, Melancon, Leheudre, and Dionne that found no increases in insulin sensitivity in older women 96-120 hours post workout. This study though measured insulin sensitivity 3-5 days after the last exercise session. It can be suggested that insulin sensitivity in older subjects might only improve for a briefer expanse of time post-exercise; possibly for less than 24 hours.
Even if increases in insulin sensitivity are more short-lived in older subjects there is still some benefit; the older subjects still saw improvements in body composition. It just follows that older subjects just might need to exercise more frequently to enhance their insulin sensitivity. Then again most people would benefit from an increase in their activity level.
Taking advantage of this data
There is now a plethora of data regarding nutrient timing and what to eat pre and post-workout. General recommendations from authors such as Dr. John Berardi in his Massive Eating series are to concentrate most of your intake around your workout period when your body is most insulin sensitive. This is recommended because the post-workout period"is marked by a dramatic increase in insulin sensitivity, glucose tolerance, and glycogenic activity; this means that muscle glycogen re-synthesis rates are dramatically elevated during the immediate post-exercise period." (17)
A 2000 study by Rasmussen, Tipton, Miller, Wolf, and Wolfe was"designed to determine the response of muscle protein to the bolus ingestion of a drink containing essential amino acids and carbohydrate after resistance exercise."
The study found that the combination of amino acids and carbohydrates in a beverage taken either one or three hours post-workout had a synergistic effect in promoting anabolism. They theorized that the timing was not as important because previous studies done by them had demonstrated that muscle fractional synthetic rate is elevated for at least 48 hours after heavy resistance training.
It is clear that exercise and proper dietary intake play pivotal roles in helping the body to function optimally. It is also clear than many major health problems plaguing today's modern American society can easily be offset if one chooses to exercise and consumer lower GI carbohydrates throughout most of the day; though higher GI CHOs have been found to beneficial when centered around an exercise period.
Even diabetic symptoms can be controlled or reversed through modest weight loss and exercise. The problem is that"bad habits;" e.g. eating high GI CHOs, processed foods, and driving everywhere instead of walking have become cultural and everywhere one turns there is seemingly a donut or fast-food set of French fries within a few steps.
In conclusion the solution to obesity and type II diabetes is simple and not even pharmaceutical and certainly non-surgical; it's about changing ones lifestyle to incorporate better foods in proper quantities while simultaneously becoming more active.
About the Author
Jason Feldman is currently a senior studying kinesiology at Arizona State University and applying to medical school at the end of the semester. His area of interests include but are not limited too: endocrinology, nutrition, physiology, and supplementation. His true passion though is the integration of all of the above to export science from the lab and convert it to progress.
Works Cited
1.Cataldo, Donna (March 2006). Fuel Mobilization Presented at ASU in Exercise Endocrinology KIN 443
2. glycemicindex.com
3. Beatrice Trum Hunter, Confusing Consumers About Sugar Intake, Consumer's Research 78, no 1 (January 1995): 14-17.
4. Fallon, Sally and Mary Enig, Nourishing Traditions, New Trends Publishing, Washington DC, 2001, p. 23.
5. Appleton, Nancy Ph.D., Fructose is No Answer For a Sweetener
6. Sanda, Bill. "The Double Danger Of High Fructose corn syrup" 2 May 2006 (westonaprice.org)
7. Beradi, John, and Rob Wilkins. "The Anabolic Power of Insulin." (2001). 2 May 2006
8. Faraj, May, Peter J. Havel, Steve Phelis, David Blank, Allan D. Sniderman, and Katherine Cianflone. "Plasma Acylation-Stimulating Protein, Adiponectin, Leptin, and Ghrelin Before and After Weight Loss Induced by Gastric Bypass Surgery in Morbidly Obese Subjects." The Journal of Clinical Endocrinology & Metabolism 88 (2003): 1594-1602. 1 May 2006.
9. Abbasi, Fahim, Sang-Ah Chang, James W. Chu, Theodore P. Ciaraldi, Cindy Lamendola, Tracey McLaughlin, Gerald M. Reaven, and Peter D. Reaven. "Improvements in Insulin Resistance with Weight Loss, in Contrast to Rosiglitazone, are Not Associated with Changes in Plasma Adiponectin or Adiponectin Multimeric Complexes." Am J Physiol Regul Integr Comp Physiol 290 (2005): 139-144. 1 May 2006.
10. Polak, J., C. Moro, E. Klimcakova, J. Hejnova, M. Majercik, N. Viguerie, D. Langin, M. Lafontan, V. Stitch, and M. Berlan. "Dynamic Strength Training Improves Insulin Sensitivity and Functional Balance Between Adrenergic Alpha 2A and Beta Pathways in Subcutaneous Adipose Tissue of Obese Subjects." Diabetologia 48 (2005): 2631-2640. 2 May 2006.
12. Ren, Jm, Ba Marshall, Mm Mueckler, M McCaleb, Jm Amatruda, and Gi Shulman. "Overexpression of Glut4 Protein in Muscle Increases Basal and Insulin-Stimulated Whole Body Glucose Disposal in Conscious Mice." J. Clin Invest (1995): 429-432. 2 May 2006.
13. Goulet, Eric D. B., Micheal O. Melancon, Mylene A. Leuhudre, and Isabelle J. Dionne. "Aerobic Training Improves Insulin Sensitivity 72–120 H After the Last Exercise Session in Younger But Not in Older Women." European Journal of Applied Physiology (2005). 2 May 2006.
14. Cox, Julie H., Ronald N. Cortright, G, L. Dohm, and Joseph A. Houmard. "Effect of Aging on Response to Exercise Training in Humans: Skeletal Muscle GLUT-4 and Insulin Sensitivity." Journal of Applied Physiology 86 (1999): 2019-2025. 2 May 2006.
15. Rasmussen, Blake B., Kevin D. Tipton, Sharon L. Miller, Steven E. Wolf, and Robert R. Wolfe. "An Oral Essential Amino Acid-Carbohydrate Supplement Enhances Muscle Protein Anabolism After Resistance Exercise." Journal of Applied Physiology 88 (2000): 386-392. 2 May 2006.
16. "Americans Getting Even Fatter." 2 May 2006 (forbes.com)
17. Beradi, John. "Massive Eating Reloaded, Part II." (2004). 2 May 2006
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