Update: I just came across an excellent article linking diabetes with thiamine deficiency. Check out the article here.
(Can anyone get this information to Larry H. Miller?)
A patient recently came into my office for a consultation. She was in her early 50s, overweight, and was struggling with constant tiredness and a sense of being overwhelmed. She had tried multiple diets, with little to no success, and when she succeeded in dropping a couple of pounds, they came right back on. She was sick and tired of being sick and tired. She, like countless other baby boomers, is dealing with a physical condition that is nearly epidemic in proportion. If untreated, it has the potential to lead to full blown diabetes. This condition is called insulin resistance.
As I have treated numerous patients who have been diagnosed with diabetes, over and over again the thought occurs to me that the diagnosis of diabetes does not magically happen overnight. It is a process that the body goes through as it compensates for an unhealthy state.
Diabetes and Insulin Resistance
At the outset, we must differentiate between Diabetes Mellitus Type I and Type II. Diabetes Mellitus Type I occurs when the immune system attacks the insulin-producing cells of the pancreas (beta cells) so that an inadequate amount of insulin is secreted and blood sugar rises, with subsequent life threatening ketoacidosis. Type II Diabetes, on the other hand, is a product of our Western society’s habit of overeating carbohydrates, especially refined carbohydrates (sugar). It is preceded by the condition I described earlier, called insulin resistance.
Before moving on to what procedures I use in my practice to treat diabetes and insulin resistance, let’s look at where this whole problem with diabetes began. This requires us to do some elementary biochemistry. All carbohydrates eventually break down in the body into glucose. As the blood glucose, or sugar, rises, insulin is released from the beta cells in the pancreas. Insulin takes the glucose to insulin receptors on each cell in the body, so that glucose can enter the cell. On the average, 50% of this glucose will be burned as energy, 10% will be stored as glycogen, and 40% is stored as triglycerides. [ii] Glycogen is the storage form of glucose which can be immediately released when the body needs more sugar. Most of the glucose is stored in muscle, and the rest is stored in the liver. Triglycerides are a specific type of fat (lipid) molecule that can be burned as energy in the body; however, they are not as easily accessible as glycogen.
When refined carbohydrates (sugar) are ingested (cookies, candies, cakes, Twinkies, PopTarts), especially when taken without fiber, blood glucose levels rise rapidly. This rapid rise in blood sugar is followed by an overshooting of the amount of insulin released from the pancreas, causing the blood sugar to drop or fall below normal. The body does not like the sugar levels to be low, so it triggers a stress response in the adrenal gland. The adrenal gland will release adrenalin, which stimulates the breakdown of glycogen in the liver, slowly causing the glucose levels to rise in the blood.
Another way to relieve the symptoms of hypoglycemia triggered by this overshooting is by the ingestion of another refined carbohydrate. These two corrective mechanisms may cause the blood sugar to overcorrect (that is, the blood sugar’s too high again), with another overcorrection by insulin, and the cycle repeats itself over and over and over …
Effects of Diabetes on the Body
After years of these glucose swings, the cell wall thickens (there are approximately 30 trillion cells in our body), insulin receptors become less efficient at glucose delivery into cells, and insulin resistance results. By definition, insulin resistance is seen as high fasting levels of glucose and insulin. Normal healthy fasting level of glucose is between 75-80, although any number in the 80s is acceptable. A healthy level of insulin in the fasting state is 0-5, while 5-10 is borderline. Anything above 10 is cause for concern. A diagnosis of Diabetes Mellitus Type II is made when the fasting glucose level is greater than 140 on two separate occasions.
To understand the effects of high glucose levels to the body, we need to understand a principle called glycosylation [iii] . This is a fancy term for the binding of glucose to proteins. Glycosylated LDL (“bad” cholesterol) molecules do not bind to LDL receptors, nor shut off cholesterol synthesis. Glycosylated red blood cells do not carry as much oxygen, are more sticky, and clump together more. Glycosylation of the lens of the eye may lead to cararacts. Glycosylation of the myelin sheath around nerves leads to loss of nerve function, tingling, pain, and numbness called neuropathy. Atherosclerosis (plaque buildup in the blood vessels) is the single biggest complication of diabetes. It may be due to platelet stickiness, glycosylated LDL, glycosylated red blood cells, or glycosylation of proteins in the blood vessel wall.
Atherosclerosis causes a reduction in blood flow, with subsequent organ damage, hypertension, cyanotic feet (with possible gangrene and amputation), retinopathy, and even kidney dysfunction and failure. Poor healing of skin from infection or trauma leads to chronic ulcers or sepsis (bacteria spreading throughout the body through the blood stream). [iv]
High insulin levels affect the body differently. They increase fat formation and storage, while inhibiting fat breakdown to be used as energy. This makes it easy to gain weight, and VERY difficult to lose weight. High insulin also enhances sodium (salt) reabsorption from the kidney, thus promoting water retention and hypertension. High insulin levels also stimulate certain ovarian hormones that result in elevations in free testosterone, with subsequent androgen effects. [v]
Treatment for Insulin Resistance and Diabetes
Diet is the reason we got into this mess and diet is the key to getting out of it! Since all carbohydrates break down into sugar, we must decrease the total amount of carbohydrates coming into the body. This translates into no more than 60-100 grams of carbohydrates per day — the less, the better. We need to look at those foods that are high and low in carbohydrates. As a start, all sugar must be eliminated. The next highest source of carbohydrates comes from potatoes (look out, Idaho!) and grains such as wheat (bread and pasta) and rice. Fruits are the next highest source of carbohydrates; their mostly fructose sugar is converted in the body into glucose. Certainly, whole fruit, with its fiber, and whole grains (rather than refined flour or wheat) for breads and pasta, and whole brown rice are much better tolerated than the refined, processed white foods and low fiber juices.
The legumes, which include beans, peas and soy, have about 1/3 carbohydrates, 1/3 protein, and 1/3 fats. Generally nuts and seeds have that same ratio. (This is a highly simplified version of these ratios.) Vegetables have the least amount of carbohydrates, although corn, tomatoes and carrots (the ones we tend to like the most) are the highest of the vegetables in the carbohydrate category. There are no carbohydrates in meats, cheese, or eggs.
So, the recommendation is: eat less of the breads, potatoes, rice, pasta, and fruit categories, and eat more of the legumes, nuts, seeds, vegetables, eggs, cheese and meat (sparingly) categories.
There are nutritional substances that reduce insulin resistance in the body. These include chromium [vi] , vanadium, biotin and alpha-lipoic acid. There is mixed success in reducing carbohydrate cravings with Gymnema or L-Glutamine, but these are certainly worth a try if sugar cravings persist. Vitamin E at 900 IU/day improves insulin action and may prevent many long-term complications. It also plays a significant role in the prevention of diabetes [vii] (the recent vitamin E scare is incorrect).
Magnesium plays an important role in glucose management, through its effect on insulin. Magnesium levels are lowest in those patients with diabetic complications. Vitamin C is needed for collagen formation, which is at the core of all repair in the body. It also improves insulin sensitivity and is a potent antioxidant. It inhibits glycosylation of proteins. [viii] Vitamin B6 protects against diabetic neuropathy, probably because it also inhibits glycosylation. Some studies indicate it may even resolve gestational diabetes. [ix] Omega 6 fatty acids offer protection against diabetic neuropathy, and omega 3 fatty acids protect against atherosclerosis and augment insulin secretion. Niacinamide may prevent development of Type I Diabetes Mellitus. If taken early enough after onset, it may help restore beta cell function, or slow down their destruction in Type I Diabetes Mellitus. [x]
Exercise enhances insulin sensitivity, perhaps through increasing levels of chromium. Lowered triglycerides and improved weight loss are other beneficial effects of exercise. I’ll be addressing the benefits of exercise more fully in a future article.
1. Low carbohydrate diet (no more than 60-100 grams per day)–the less the better, for the most part
2. Chromium (200-400 micrograms/day)
3. Vanadium (100-125 milligrams/day long term or 5-10 grams/day, short term)
4. General supplements include:
a) Vitamin C (2000 mg/day)
b) Vitamin B6 (150-200 mg/day)
c) Vitamin E (900 IU/day)
d) Magnesium )600-1000 mg/day)
5. If insulin resistance is still present with the above recommendations, add Biotin (9-16 mg/day), Glucophage (500-1700 mg/day). Glucophage needs a prescription.
6. For Type I Diabetes Mellitus, Niacinamide 1000-2000 mg/day and insulin
This approach puts a much heavier emphasis on treating insulin resistance, the underlying cause of diabetes, rather than treating the symptoms of high blood sugar with sulfonylureas that push the beta cells toward increasing insulin release. More insulin is not what is needed. Less insulin resistance is needed. With this approach, we get away from the problems associated with high insulin levels. We also avoid the potential exhaustion of beta cells because of their chronic high production to handle insulin.
Diabetes is the end result of problems in the body that can be addressed with nutrition. The positive results I have seen in my practice are incredibly successful! It is critical to begin addressing your health issues at the cause level, rather than the end organ damage level.
Although a more complete description of eating concepts will be included in another article, I felt it wise to place an outline of some critical concepts of eating that should be included in this article:
1) Eat only when hungry
2) Stop eating when not hungry (don’t eat until you are full)
3) Chew until liquid
4) Savor each bite (or better yet, each chew)
5) Relax and be cheerful during a meal
6) Focus on eating (so that you can savor each bite and chew until liquid, and so you will sense when your body no longer needs nutrients—this means no talking or watching television during meals)
The advantages of this approach are many, but for now I’ll just list two of them:
1) You will never go hungry, so your body will never perceive that you are in a starvation state. (If your body thinks it is starving, it will reduce your metabolic rate and store fat instead of burn energy).
2) There will be less stress on the body. When you are hungry, your body needs nutrients and is ready to receive them. If you are not hungry, eating is a stress on your body, and more of the food will be converted to storage (fat) instead of being burned as needed energy.
[i] Cecil Textbook of Medicine 19th Edition pp. 1296-1302.
[ii] Principles of Anatomy and Physiology, Tortora, Grabowski. 10th Edition pp. 928-9
[iii] Textbook of Natural Medicine, Joseph E. Pizzoni Jr, Michael T Murray p. 1200.
[iv] Ibid pp. 1200-2.
[v] Lukaczer, Dan. “Nutritional Support for Insulin Resistance.” Applied Nutritional Science Reports, 2001.
[vi] Anderson R et al. “Beneficial effects of chromium for people with Type II Diabetes.” Diabetes 1996; 45: 124A/454.
[vii] Salonen JT, Jyyssonen K, Tuomainen TP. “Increased risk of non-insulin diabetes mellitus at low plasma Vitamin E concentrations. A four-year follow-up study in men.” Br Med J 1995; 311: 1124-27.
[viii] White JR, Campbell RK. “Magnesium and Diabetes. A Review.” Ann Pharmacother 1993; 27: 775-80.
[ix] Solomon LR, Cohen K. “Erythrocyte O2 transport and metabolism and effects of vitamin B6 therapy in Type II diabetes mellitus.” Diabetes 1989; 38: 881-886.
[x] Pocoit F, Reimers JI, Anderson HW. “Nicotinamide-biological actions and therapeutic potential in diabetes prevention.” Diabeto Logia 1993; 36: 574-76.