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Diabetes Protocol

 

GUM DISEASE IN DIABETES

The importance of gum health is confirmed in heart disease, but according to data released from the University at Buffalo (UB) School of Dental Medicine, diabetes can be added to the growing list of systemic diseases and conditions associated with bacteria from infected gums (Baker 1999a). Research has emerged suggesting that the relationship between periodontal disease and diabetes goes both ways, that is, periodontal disease may make it more difficult for people who have diabetes to control their blood sugar and poorly controlled Type II diabetic patients are more likely to develop gum disease.

Researchers from UB studied 11,198 nondiabetic subjects (ages 20-90) from the Third National Health and Nutrition Examination Survey (NHANES III) conducted from 1988 to 1994 for their evaluation. They assessed the degree of gum detachment from bone, along with fasting-insulin and fasting-glucose levels.

Gram-negative periodontal infections were found to be significantly associated with insulin resistance. Gram-negative bacteria appear to produce a very potent toxin called LPS, which probably interferes with the action of insulin and is responsible for maintaining a chronic state of insulin resistance in individuals with gum infections (Baker 1999a).

As insulin resistance increases, the severity of periodontal disease also increases. Results show that those with severe gum detachment (regardless of weight, smoking status, gender, or age) have a higher index of insulin resistance than those with little or no gum disease.

Note: Researchers used a body mass index (BMI) of 27 as the dividing line between acceptable and unacceptable degrees of obesity (Baker 1999a). See the chart relating to BMI in the section How Is Obesity Linked to Hyperinsulinemia and Diabetes?

Another study conducted at the University of Buffalo (involving 168 adults with diabetes) showed that those with severe gum deterioration had the most difficulty controlling blood glucose levels (Millman 2001). Some explain that oral bacteria, fed and nurtured by excesses of sugar, escape from the gums and enter the bloodstream. This summons the immune system into action, and cytokines (proteins that amplify immune reactivity) enter the milieu. In an attempt to kill out the bacteria, cytokines overstep their role and attack pancreatic cells, as well (Reuters Health 2001). An assault on the beta cells compromises their ability to supply insulin, and glucose builds up in the bloodstream. This sequence provides more sugar, perpetuating a classic, vicious cycle.

Note: Poorly controlled diabetics also have more cytokines in the gingival tissue, causing destructive inflammation of the gums. In turn, growth factors are also reduced, interfering with the healing response to infection (Cutler et al. 1999; Strayhorn et al. 1999; AAP 2002)..

In 1997, 113 Pima Indians (having both diabetes and periodontal disease) were treated for their gum conditions. The participants (81 females and 21 males) were divided into 5 groups. All underwent ultrasonic scaling and curettage combined with an antimicrobial regime that consisted of (1) topical water and systemic doxycycline, 100 mg for 2 weeks; (2) topical 0.12% chlorhexidine (CHX) and systemic doxycycline, 100 mg for 2 weeks; (3) topical povidone-iodine and systemic doxycycline, 100 mg for 2 weeks; (4) topical 0.12% CHX and placebo; and (5) topical water and a placebo.

Clinical assessments by probing depth, clinical attachment level, the detection of Porphyromonas gingivalis in subgingival plaque, and the determination of serum glucose and glycated hemoglobin (HbA1c) were performed prior to and at 3 months and 6 months after treatment. All study groups showed clinical and microbial improvement, but the doxycycline-treated groups showed the greatest reduction in probing depth and P. gingivalis infection. All three groups receiving systemic doxycycline showed (at 3 months) significant reductions in mean HbA1c--reaching nearly 10% from the pretreatment value (Grossi 1997).

The control of periodontal infections is essential as a prophylactic against diabetes, as well as for better blood glucose control among confirmed diabetics. If neither a medical nor dental provider has explored the gum disease-diabetes association, a patient should consult a periodontist for an assessment regarding the health of the gums.

Note: A study presented at the International Association for Dental Research concluded that overweight people with the highest levels of insulin resistance were about twice as likely to have severe periodontal disease, compared to overweight people with low insulin resistance. Researchers speculate that bacteria from gum disease may be interfering with fat metabolism, promoting both obesity and hyperlipidemia. The obesity-periodontal disease relationship is particularly significant because both are major factors in Type II diabetes.


How is OBESITY LINKED TO HYPERINSULINEMIA AND DIABETES?

The Centers for Disease Control and Prevention reported that extra pounds and inactivity are to blame for hundreds of thousands of premature deaths in the United States annually. As girth increases, the chance of developing some form of ill health dramatically increases, including the risk for diabetes. At least 10 million overweight Americans could sharply cut their risk of developing diabetes by making relatively simple lifestyle changes, e.g., altering eating habits (restricting calories to 1200-1800 a day) and introducing exercise into their daily regime. Walking should never be discredited as a viable form of exercise; as little as 30 minutes of walking a day can dramatically improve the plight of prediabetic and diabetic patients (Cafazzo 2001; Blake 2002). (Read the section entitled Exercise: Helpful in Blood Glucose Control in this protocol.)

The Diabetes Prevention Program (a 3-year study) was the first large-scale study to show that losing weight and exercising can effectively delay diabetes. A study reported in the New England Journal of Medicine, involving 84,041 nondiabetic female nurses tracked from 1980-1996, substantiated earlier findings. During the 16-year follow-up, 3300 new cases of Type II diabetes were documented. Obesity was the single most important predictor of diabetes, but a lack of exercise, poor diet, and current smoking also contributed to the risk. The researchers concluded that the vast majority of cases of Type II diabetes (about 90%) could be prevented by the adoption of a healthier lifestyle (Hu et al. 2001).

It appears not to be a fluke that 50-90% of all people with Type II diabetes are overweight. According to Dan Lukaczer, N.D., obesity and chronic hyperinsulinemia induce insulin resistance in peripheral tissues. Chronic hyperinsulinemia (in turn) is a predictor of obesity. The Tulane National Center for Cardiovascular Health has determined that individuals with consistently elevated insulin levels (versus those with normal insulin levels) had a 36-fold increase in the prevalence of obesity (Bao et al. 1996). Many hormones play a role in fat regulation, among them cortisol, estrogen, androgen, and insulin, but hyperinsulinemia makes weight management particularly difficult.

Hyperglycemia is also involved in obesity. If the body takes in more carbohydrates than needed (glycogen stores are filled and energy requirements are satisfied), the leftovers are broken down (by the liver) to smaller fat molecules. The fat then travels to fatty tissues of the body where it takes up residency. Unlike the liver (which has limited glycogen capacity), fat cells can store unlimited quantities of fat (Whitney 1998). Researchers (addressing the conversion of glucose to fat) make the challenge that one has to be "prepared to play the game" if excessive amounts of carbohydrates are consumed (Hamilton et al. 1988).

Although obesity often parallels Type II diabetes (about 90% of newly diagnosed Type II diabetic patients are overweight), many obese patients do not display insulin resistance, and about 50% of hyperinsulinemic patients (those not yet diagnosed with diabetes) are of normal weight (Bogardus et al. 1985; Zavaroni et al. 1994).

BMI appears to be a valuable tool in assessing the gravity of obesity as a contributor to Type II diabetes. BMI may be calculated as follows:

Determine body weight in pounds and convert to kilograms (1 kg = 2.2 pounds).
Determine height and convert to inches.
Convert height in inches to meters. Divide height in inches by 39.37 (1 meter = 39.37 inches).
Square height in meters by multiplying it by itself.
Divide weight in kilograms by height in meters squared.
Men
Women
BMI >35 = 42-fold increase in diabetes BMI of 25 = 5-fold increase in diabetes
BMI of 30 = 28-fold increase in diabetes
BMI >35 = 93-fold increase in diabetes

As problematic as a few extra pounds are in Type II diabetes, a weight loss can be just as significant. When Type II diabetic patients lost from 1.5-14% of their body weight, all diabetic parameters improved, that is, fasting blood glucose, hemoglobin A1c, plasma insulin, triglycerides, and HDL cholesterol. Those who lost 15% of their body weight were able to discontinue oral diabetic therapy. According to Priscilla Hollander, M.D., consuming 100 extra calories a day can result in a weight gain of approximately 12 pounds over 1 year; the consequence of consuming 200 extra calories a day reflects a 24-pound annual gain.

Certain factors remain constant: a weight loss increases insulin sensitivity and deters the onset and progression of diabetes. Also, when blood insulin levels are reduced, the patient experiences an almost automatic weight loss. If the reader needs help with weight management, please consult the Obesity protocol for direction on suppressing excess insulin levels.


Simple and Complex Carbohydrates: Their Digestion and Absorption
Carbohydrates are probably the largest group of foodstuffs most individuals consume with regularity. It is estimated that 60-90% of the average American diet is composed of carbohydrates, ranging from simple sugars and fast foods to grains and starchy vegetables, such as potatoes, corn, and beans.

The least complex of all carbohydrates are the simple sugars (monosaccharides), which require virtually no digestion to metabolize. This means that after consumption they swiftly flood the bloodstream. If these food factors are eaten, it must be with extreme caution to avoid crowding the bloodstream with unnecessary burdens of glucose and insulin (Whiting 1989).

Glucose, a monosaccharide also known as dextrose, is the only sugar that can be utilized by the body. All other forms of starches and sugars must eventually be broken down and converted to glucose. Fructose or levulose (also a monosaccharide) is found in fruits and honey. The concept that fructose, in a concentrated form, is a better choice for the diabetic is erroneous; the release of fructose into the system takes only slightly longer than glucose. Fiber and attending enzymes in fruits assist in metabolizing the sugar, making naturally occurring fructose far less problematic than isolated concentrations. Unfortunately, fruits are not all equally safe for individuals with unstable blood glucose levels. Please consult the Glycemic Index (in this protocol) to read about fruits that are less likely to prompt a rise in blood sugar and an insulin rush.

The more complex sugars in the soluble group are made of double bonds (disaccharides) that are broken down by specialized enzymes within the body. Sucrose, common table sugar (a disaccharide), is one of the sweetest and perhaps the most tempting of all sugars. In order for sucrose to be absorbed, it must be broken down into two simple sugars, such as fructose and glucose. Lactose, also known as milk sugar, is the least sweet of sugars from the disaccharide group because it is less soluble.

The starch group of foods is regarded as insoluble. Starches are classified as insoluble because of the complex process required in breaking down complex starches into disaccharides and eventually to basic sugars or monosaccharides. Of all the carbohydrate groups, polysaccharides (complex carbohydrates) are probably the most beneficial to human metabolism. Types of polysaccharides (often extremely complex with long chains of glucose molecules) are cellulose (the primary constituent of plant cell walls), hemicellulose (the main constituent of cereal fibers), pectin (found in vegetables and fruits), and gums and mucilages (plant secretions). Examples of food sources include wheat, oat bran, and stalks and leaves of vegetables, seeds, and fruits. Raw, unrefined, or unprocessed carbohydrates are surrounded with other valuable food factors, such as protein, fats, vitamins, and minerals.

The time required to break down a complex carbohydrate minimizes the risk of overloading the body with a blast of sugar and a sudden release of insulin from the pancreas. A complex carbohydrate may, in fact, take hours to convert to glucose, rather than the few minutes required for processing a simple sugar.

Note: While complex carbohydrates usually serve diabetic individuals far better than simple sugars, some individuals find carbohydrates (in general) problematic. This likely occurs because of food allergies or exaggerated consumption of carbohydrates in relationship to other macronutrients (fats and protein). Consult the following section to learn the percentage of carbohydrates, proteins, and fats deemed most desirable in a diet to control blood glucose levels and symptoms of Syndrome X.

The Biochemical Nature of Macronutrients (Carbohydrates, Fats, and Protein)
Foods, that is, macronutrients, deliver powerful messages. According to Barry Sears, Ph.D., "Once food is broken down into its basic components (glucose, amino acids, and fatty acids) and sent into the bloodstream, it has a more powerful impact on your body and your health than any drug your doctor could ever prescribe."

The principal function of carbohydrates is to serve as a major source of energy for the body. If insufficient carbohydrates are available, the body will convert protein to glucose in order to supply energy (gluconeogenesis). The energy needs of the body take precedence over all other requirements (Krause et al. 1984). But, if consumed in excess, carbohydrates overwork the pancreas and are an invitation to obesity, diabetes, hypertension, hyperlipidemia, and some types of arrhythmias.

Proteins are the main structural components of cells and the enzymes that keep the cells running. Even our immune systems are essentially composed of protein (Sears 1995). However, proteins, when consumed in excess, create demands for vitamin B6 and calcium, stress the kidneys, and promote a weight gain. There are, however, several opinions regarding the influence protein has on insulin levels:

According to various researchers, protein blunts a glucose rise and insulin response in normal glucose-tolerant individuals (Wang et al. 1991; Garg et al. 1994).
Proteins primarily stimulate glucagon (a hormone that releases stored carbohydrates in the form of glucose from the liver); if too much protein is taken in at a meal, insulin levels will increase (Sears 1995).
Dr. Gerald Reaven (head of endocrinology, gerontology, and metabolism at Stanford University) challenges: "Why trade one insulin-raising nutrient for another? It is far safer, and just as nutritious, to decrease carbohydrates and maintain protein at a reasonable level, while increasing your intake of the `good' unsaturated fats" (Reaven et al. 2000).
According to information in the American Journal of Clinical Nutrition, protein induces an increase in insulin concentrations when ingested in combination with carbohydrate. A mixture of wheat protein hydrolysate, free leucine, phenylalanine, and carbohydrate can be applied as a nutritional supplement to strongly elevate insulin concentrations (van Loon 2000).
Poorly selected fats produce a harvest of undesirable (even destructive) hormone-like substances such as PGE2, a prostaglandin produced from arachidonic acid. It appears, however, that fats (saturated or unsaturated) neither increase nor decrease insulin levels. It is only when fats replace carbohydrates that insulin levels drop and the clusters of symptoms associated with Syndrome X become less apparent (Reaven 2000).

Diabetes Protocol Pg (1) (2) (3) (4) (5) (6) (7) (8) (9) (10)

 

 

 

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