Monday, October 4, 2010

Meal Planning & Meal Preparation to Help Reverse Your Diabetes

Meal planning is one of the key enablers for diabetics to be successful with controlling and reversing their diabetes. Unfortunately, many diabetics don't perform meal planning because they think it's boring, they think it's time-consuming, or they don't know how to properly meal plan -- especially to improve their diabetes and their overall health.

Consequently, the author expanded his Death to Diabetes cookbook to demonstrate that meal planning is not boring and it's not time-consuming. In fact, proper meal planning will save time and will save money, and can even be enjoyable.

Key aspects of proper meal planning include:

  • How to shop for groceries
  • How to read food labels
  • How to select the proper foods
  • When to shop for groceries and why
  • How to save time and money when grocery-shopping
Another key enabler is meal preparation. Once you purchase the proper foods, it's very important that you know how to prepare the meals such that you obtain maximum nutrition from the meals. For example, if you overcook the vegetables, then, you destroy many of the key nutrients that your body needs to fight the diabetes.

Key aspects of proper meal preparation include:

  • The best oils for salads, cooking, etc.
  • How to prepare super meals
  • How to prepare quick meals that are healthy
  • How to prepare snacks that are healthy
  • How to prepare quick lunches
  • How to prepare vegetables
  • How to prepare vegetable soups
  • How to prepare stir-frys
  • What herbs/spices to use with what foods
  • How to transform comfort foods into healthier foods
  • How to transform your favorite meals and desserts into healthier meals
  • How to reduce the fat and sugar in your meals but keep the meals tasty
For more details about meal planning, grocery-shopping, and meal preparation, get the Death to Diabetes cookbook, the Grocery Shopping PDF, or the 90-Day Meal Planner PDF.

Saturday, September 4, 2010

Should We Take Nutritional Supplements?


An estimated 40 percent of the U.S. population uses nutritional and dietary supplements on a regular basis while 70 per cent uses supplements occasionally. Vitamin E and Vitamin C are among the most commonly used supplements.

So, are nutritional supplements really necessary?
In today’s fast-paced, hectic world, it is very difficult to eat nutritiously all day long every day. So, the short answer is “yes”. If you are relatively healthy and you are eating four to six super meals/snacks with primarily raw organic foods and superfoods every day, you may not need any nutritional supplementation until you get older.

On the other hand, if you are ill with a disease like diabetes, this should tell you that you are not consuming and absorbing enough of the proper nutrients. Because your body is very depleted in terms of nutrients, you need to supplement the super foods that you’ve begun to consume with some food-based nutritional supplements to help accelerate the body’s healing process.

You may find it difficult to obtain all the necessary nutrients from the food you eat due to the loss of soil quality, water quality, picking vegetables/fruits in unripened state, and how animals are fed and raised. But, as long as you are predominantly eating the “live” (raw) foods instead of the “dead” foods, you will be successful.

If finances are not an issue, you can buy organic food to ensure you are receiving the best quality foods, but for the most part this is not necessary. I did not eat organic food during my recovery. The reduction and elimination of eating the “dead” processed foods will have a more dramatic positive effect on your health, more so than any other single factor.

Because it may be difficult to eat four to six super meals consistently each day due to your work life, family, or lifestyle, some type of nutritional supplementation is necessary. In fact, medical institutions, such as the American Medical Association (AMA), agree that nutritional supplementation is necessary today.

Note: For more information about nutritional supplements, get the Nutritional Supplements PDF.

Wednesday, July 21, 2010

Benefits of the "Death to Diabetes" Wellness Program



Death to Diabetes (ISBN 0977360741), now one of the top-selling diabetes books in the U.S, is one of the few diabetes books that looks at diabetes at the cellular level and from several aspects of medical science, including pathology, etiology, and epidemiology. The book also looks at diabetes from the aspect of several engineering sciences including reverse engineering, failure modes & effects analysis, root cause analysis, statistical analysis, meta analysis, and process engineering. The book identifies more than 200 clinical studies that support the nutritional recommendations of the author.

As a result, the book provides a concise and easy-to-read set of procedures for a Type 2 diabetic to customize to his/her needs and get their diabetes under control within three months. As a result, many diabetics have been able to reverse their diabetes and beat the disease.

The key benefits to following the “Death to Diabetes” wellness program include:
  • Lower your blood glucose level to the normal range within days.
  • Increase your energy level, and avoid the cravings and highs and lows associated with eating processed foods.
  • Begin reversing and beating your diabetes within 30 days.
  • Lose weight (fat) by turning your body into a fat-burning machine.
  • Reduce the belly fat, which is hard to get rid of following conventional diets.
  • Save thousands of dollars from drugs, more drugs, surgeries, hospital stays, and high healthcare insurance premiums.
  • Save hundreds of dollars from grocery-shopping and food bills.
  • Learn how to transform your favorite foods into healthier foods, so that you can enjoy eating without the anxiety.
  • Enjoy weddings, picnics, birthday parties, and other social events – because the book teaches you how to eat before and after these events to limit the damage to your health.
  • Enjoy a better sex life, because the wellness program addresses circulatory issues that have proven to be one of the primary problems associated with sexual dysfunction.
  • Look younger and so much better that your friends think that you have had a facelift or liposuction!
  • Prevent the complications of diabetes, including heart attack, stroke, blindness, amputation, gum disease, and kidney failure.
  • Reverse your diabetes and its complications in 3 to 6 months
  • Lifetime subscription to the Death to Diabetes Newsletter (valued at more than $839)
More than 91% of Type 2 diabetics who followed this program have achieved some improvement in their diabetes and overall health, including lower blood pressure, lower A1C and lower BMI.

Here are several of the hundreds of testimonials from diabetics and non-diabetics:

“My doctor told me that all signs of my diabetes were gone! And, the pain in my foot from the neuropathy is gone.” D. Carter, ex-diabetic

“I got this book “Death to Diabetes” for a relative and she loved it so much she got one for her doctor! Her doctor loves “Death to Diabetes” too! Her glucose readings have been steadily returning to normal ranges and she is off oral diabetic meds and is no longer on daily insulin injections. All this within 6 months of reeducating herself to the truth. This is truly DEATH to DIABETES!!! Follow it, don’t question it, and see the results for yourself!!” V. Koehler

“My husband has diabetes and up until recently it has been uncontrollable, so we've been reading book after book on the subject. When I purchased "Death to Diabetes", it was like none other in scope … This is the one book that every diabetic should read.” G. Martin (Houston, TX)

“My daughter sent me two books and while I refer to the other occasionally, this book “Death to Diabetes” set me in the direction of getting off my meds and reversing my diabetic condition. A MUST READ for all diabetics, newly diagnosed or long term. I loved it.” Janeice Pennington (Hawaii)

“I recommend this book (“Death to Diabetes”) not only to all diabetics but to anyone who is suffering from his or her unhealthy lifestyle. Although McCulley's theories are not strictly in line with current medical thinking, his advice for changing our lives for the better is right on. Over half of all Type 2 diabetics who strictly follow his advice will be cured of their diabetes problem, as well as lowering their cholesterol and blood pressure. Don't miss out on this book.” Dr. William Bayer, MD (Rochester, NY)

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Notes:
This book has coined several new phrases that are spreading across America, e.g. ex-diabetic, the 5 super foods, the 5 dead foods, The Super Meal Model, The Death to Diabetes Diet, super carbs, super fats, the 7 diabetes wellness factors, victor of wellness vs. victim of illness, diabetes engineer, engineer1337, 6-stage diabetes program, etc.

McCulley’s workshops and seminars have been well-received because of the thoroughness of his lectures and his ability to use humor and his personal stories to bring hope and connect with other diabetics.

McCulley states during his lectures: “You can beat your diabetes, and you can reverse the complications of Type 2 diabetes – if you are armed with the knowledge and the drive to want to live a healthier life. Just follow the Super Breakfast protocol on my website.”

McCulley says emphatically: “You can become a victor of knowledge & wellness, and stop being a victim of ignorance & illness – it’s all up to you.”

Web Site Reference: Diabetes Abstract (with supporting data from diabetics who followed the program)

Tuesday, July 20, 2010

Death to Diabetes Book (ISBN 09773607412)

The Death to Diabetes book (Version 3.0)  is available in the online store.
Note: Don't forget that when you order the book from the online store, you get the latest version, plus a free CD, subscription to the newsletter, and a 30-minute health consultation.

Thursday, July 15, 2010

Diabetic Drugs

Western Medicine uses diabetic drugs such as metformin (Glucophage), glyburide (Micronase, DiaBeta) and glipizide (Glucotrol) to "treat" your diabetes.

So, do these drugs work? It depends on your point of view.

These drugs help to lower your blood glucose level, but they do absolutely nothing to help your body get rid of the disease!
In fact, these drugs cause long-term side damage that leads to gastrointestinal problems, kidney failure, liver failure, and other health issues that your doctor may not mention to you.

In addition, these drugs do not stop the development of diabetic complications such as amputation, kidney failure or heart attack.

If you find this hard to believe, just visit any of the pharmaceutical websites or google on "diabetic drug expenses" or "diabetic drug side effects" to verify for yourself. Or, if you know someone with diabetes who's taking any of these diabetic medications, you will see that their health is not improving. In fact, they're probably taking more and more medications as their diabetes worsens.

Because of the damage that some drugs can cause to your liver and kidneys, ensure that you get the critical blood tests to determine your current state of health, and also to ensure your health is not being damaged by the drugs. Don't assume that your doctor is getting all the right tests done for you. Some people have died suddenly because they didn't get a complete set of blood tests and, therefore, were not diagnosed properly.

If you want to know more about the drug companies and their kickback payments to the doctors, go to this link on the web site: Drug Companies and Kickbacks

For more information about the dangers of high blood pressure and cholesterol drugs, go to this link on the web site: High Blood Pressure and Cholesterol Drugs

Note!: Just because you don't feel any discomfort such as an upset stomach or headache, does not mean that your body is not experiencing any side effects!! Most side effects such as liver/kidney damage go undetected for years!

Health Impact of Drugs
Just like any other drug, these diabetic drugs create biochemical and hormonal dependencies within your body that can lead to
long-term damage to your cells and organs.

If you are taking one of these drugs, it may be difficult to believe this, because you feel fine, you do not feel any discomfort or side effects.

However, many of the side effects will not be felt for several years, maybe even longer. But, eventually the following scenario will occur:
  1. The drug loses its effectiveness and your blood glucose level starts to rise.
  2. Your doctor increases the dosage to bring your blood glucose level back to the normal range.
  3. If this doesn't work, your doctor adds a new drug.
  4. Eventually when the oral drugs lose their effectiveness to lower your blood glucose level, your doctor will put you on insulin.
I know that you're probably thinking that if you keep taking the oral drugs and watch what you eat, you won't have to go on insulin.

But, that's not true. Why? Because while you were taking the drugs, the diabetes continued to progress (silently) and cause damage to more and more cells in your body. Eventually, the damage becomes so widespread that your doctor has to either increase your dosage, add another drug, or put you on insulin.

Read Chapters 3, 12, 14 and 15 of Death to Diabetes to learn how to decrease the damage caused by the long-term use of these drugs.

Sidebar:
The author has nothing against drugs -- in fact, drugs saved his life! He believes that drugs are important and especially critical in acute life-threatening situations, such as what he experienced.

However, long-term use of these drugs causes too much damage to the organs and tissues.
Consequently, a non-drug solution would provide the best opportunity for optimum health.

Oral Diabetes Medications (Diabetes Pills)
Oral diabetes medications -- diabetes pills -- help control blood sugar levels in people whose bodies still produce some insulin (the majority of people with type 2 diabetes).

These diabetes drugs are usually prescribed to people with type 2 diabetes along with recommendations for making specific dietary changes and getting regular exercise.
However, most people do not make the dietary changes! And, for the people who do make the dietary changes, the drugs cancel out the benefits of eating healthy!

Diabetes pills work in one of three ways:
1. Stimulate the pancreas to release more insulin (causing you to gain weight)
2. Increase the body's sensitivity to the insulin that is already present (but causes damage to the liver/kidneys)
3. Slow the breakdown of foods (especially starches) into glucose (but doesn't really work that well).

Diabetes pills are grouped into the following categories:

Sulfonylureas:
These diabetes pills lower blood sugar by stimulating the pancreas to release more insulin. The first drugs of this type that were developed -- Dymelor, Diabinese, Orinase and Tolinase -- are not as widely used since they tend to be less potent and shorter-acting drugs than the newer sulfonylureas.
Second generation sulfonylureas include Glucotrol (glipizide), as well as Micronase, Diabeta, and Glynase (all contain glyburide).
A third generation called Amaryl (glimepiride) is also available.

Sulfonylureas work best when taken at the same time each day. Glyburide and glipizide are shorter-acting versions. Glyburide (Micronase and Diabeta), and glipizide (Glucotrol) are usually taken twice a day, half before breakfast and half before dinner. Sustained-release versions called Glynase or Glucotrol XL are also available.

Glucotrol (glipizide): Glucotrol controls diabetes by stimulating the pancreas to secrete more insulin. Treatment with Glucotrol may increase the risk of death from cardiovascular disease.

Glimepiride (Amaryl): Amaryl lowers blood sugar by stimulating the pancreas to produce more insulin. Amaryl is often prescribed along with the insulin-boosting drug Glucophage. It may also be used in conjunction with insulin and other diabetes drugs.

Glyburide + Metformin (Glucovance): is a combination of 2 drugs —glyburide and metformin — that attack high blood sugar levels in several ways. The glyburide component stimulates the pancreas to produce more insulin and helps the body use it properly. The metformin component also encourages proper insulin utilization, and in addition works to decrease sugar production and absorption.

WARNING: Glucovance has been known to cause a dangerous condition called lactic acidosis, a buildup of lactic acid in the blood. Lactic acidosis is a medical emergency that requires immediate treatment in the hospital. Notify your doctor without delay if you experience any of the following symptoms:
A slow or irregular heartbeat; a cold, dizzy, or light-headed feeling; a weak, tired, or uncomfortable feeling; stomach discomfort; trouble breathing; unusual muscle pain

Side Effects:
Hypoglycemia (low blood sugar)
Upset stomach
Skin rash or itching
Weight gain

Biguanides: These diabetes pills improve insulin's ability to move sugar into cells especially into the muscle cells. They also prevent the liver from releasing stored sugar. Biguanides should not be used in people who have kidney damage or heart failure because of the risk of precipitating a severe build up of acid (called lactic acidosis) in these patients. An example includes metformin (Glucophage, Glucophage XR, Riomet, Fortamet and Glumetza).

Two drugs from the biguanide class, metformin and phenformin, were developed in 1957. Unfortunately, phenformin reached the U.S. market first and resulted in several deaths from lactic acidosis. When this risk surfaced, phenformin was pulled from drugstore shelves worldwide. Metformin was eventually found to be 20 times less likely to cause lactic acidosis, but it was tainted by the history of its cousin. Metformin first became available in France in 1979 and has been widely used in Europe since then, but it was not cleared for use in Type 2 diabetes in the U.S. until 1994.
Dosage Range: 500 - 2550 mg, 2-3 times a day

WARNING: Metformin can rarely cause a serious (sometimes fatal) condition called lactic acidosis. Stop taking metformin and seek immediate medical attention if you develop any of the following symptoms of lactic acidosis: unusual tiredness, severe drowsiness, chills, blue/cold skin, muscle pain, fast/difficult breathing, unusually slow/irregular heartbeat.

Lactic acidosis is more likely to occur in patients who have certain medical conditions, including kidney or liver disease, conditions that may cause a low oxygen blood level or poor circulation (e.g., severe congestive heart failure, recent heart attack, recent stroke), heavy alcohol use, a severe loss of body fluids (dehydration), X-ray or scanning procedures that require an injectable iodinated contrast drug, recent surgery, or a serious infection. Tell your doctor immediately if any of these conditions occur or if you notice a big change in your overall health. You may need to stop taking metformin temporarily. The elderly are also at higher risk, especially those older than 80 years who have not had kidney tests.

Side Effects of Glucophage:
Nausea, stomach upset, diarrhea, or a metallic taste in the mouth may occur at first as your body adjusts to the medication. If any of these effects persist or worsen, tell your doctor or pharmacist promptly. If stomach symptoms return later (after you are on the same dose for several days or weeks), tell your doctor immediately. Stomach symptoms that occur after the first days of your treatment may be a sign of lactic acidosis.

Precautions:
This medication should not be used if you have certain medical conditions. Before using this medicine, consult your doctor or pharmacist if you have: kidney disease, liver disease, conditions that may cause a low level of oxygen in the blood or poor circulation (e.g., severe congestive heart failure, recent heart attack, recent stroke), metabolic acidosis (e.g., diabetic ketoacidosis), serious infection, severe loss of body fluids (dehydration).
Before using this medication, tell your doctor or pharmacist your medical history, especially of: adrenal/pituitary gland problems, severe breathing problems (e.g., obstructive lung disease, severe asthma), blood problems (e.g., anemia, vitamin B12 deficiency), fertility problems (e.g., ovulation problems), alcohol use.

Thiazolidinediones: These diabetes pills improve insulin's effectiveness (improving insulin resistance) in muscle and in fat tissue. They lower the amount of sugar released by the liver and make fat cells more sensitive to the effects of insulin. Actos and Avandia are the two drugs of this class. These drugs may take a few weeks before they have an effect in lowering blood sugar. They should be used with caution in people with heart failure. Your doctor will do periodic blood testing of your liver function when using this diabetes medicine.

These drugs include Actos (pioglitazone), Avandia (rosiglitazone), and Avandamet (rosiglitazone and metformin).

Side Effects:
Elevated liver enzymes (liver damage)
Liver failure
Respiratory infections and sinusitis
Headache
Fluid retention (This may lead to heart failure)
Mild anemia
Increased risk for upper arm or foot fractures (women)

WARNING: The thiazolidinedione medication troglitazone (Rezulin) has been removed from the market in the United States and some European countries. Troglitazone has been shown to cause severe liver problems in a small number of people who take it.

Alpha-glucosidase inhibitors: include Precose and Glyset. These drugs block enzymes that help digest starches, slowing the rise in blood sugar. These diabetes pills may cause diarrhea or gas. They can lower hemoglobin A1c by 0.5%-1%.
Side Effects:
Stomach upset (gas, diarrhea, nausea, cramps)

Meglitinides: include Prandin and Starlix. These diabetes medicines lower blood sugar by stimulating the pancreas to release more insulin. The effects of these diabetes pills depend on the level of glucose. They are said to be glucose dependent. High sugars make this class of diabetes medicines release insulin. This is unlike the sulfonylureas that cause an increase in insulin release, regardless of glucose levels, and can lead to hypoglycemia.
Side Effects:
Hypoglycemia (low blood sugar)
Stomach upset
Sore throat

Dipeptidyl peptidase IV (DPP-IV) inhibitors: include Januvia. The DPP-IV inhibitors (Januvia) work to lower blood sugar in patients with type 2 diabetes by increasing insulin secretion from the pancreas and reducing sugar production. These diabetes pills increase insulin secretion when blood sugars are high. They also signal the liver to stop producing excess amounts of sugar. DPP-IV inhibitors control sugar without causing weight gain. The medication may be taken alone or with other medications such as metformin.

Combination therapy: There are several combination diabetes pills that combine two medications into one tablet. One example of this is Glucovance, which combines glyburide (a sulfonylurea) and metformin. Others include Metaglip, which combines glipizide (a sulfonylurea) and metformin, and Avandamet which utilizes both metformin and rosiglitazone (Avandia) in one pill.

Studies have been done showing that some diabetes pills may fuel the diabetes and its complications. Both metformin and Precose have been shown to increase a person's risk of developing type 2 diabetic complications, particularly when lifestyle changes of a proper diet and regular exercise are not implemented. Actos has been shown to increase the risk of heart attack, stroke, and premature death in those with type 2 diabetes.

PLEASE NOTE:
This list is not complete as there may be other drugs that can interact with Januvia and can potentially lower blood sugar, such as:
probenecid (Benemid);
nonsteroidal anti-inflammatory drugs (NSAIDs);
aspirin or other salicylates (including Pepto-Bismol);
sulfa drugs (Bactrim and others);
a monoamine oxidase inhibitor (MAOI);or
beta-blockers (Tenormin and others).

Note: Go to the following web pages for more information about the dangers of prescription drugs:


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Insulin

Background Information about Insulin
When we eat, our bodies break food down into organic compounds, one of which is glucose. The cells of our bodies use glucose as a source of energy for movement, growth, repair, and other functions. But before the cells can use glucose, it must move from the bloodstream into the individual cells. This process requires insulin.

Insulin is produced by the beta cells in the islets of Langerhans in the pancreas. When glucose enters our blood, the pancreas should automatically produce the right amount of insulin to move glucose into our cells. People with type 1 diabetes produce no insulin. People with type 2 diabetes do not always produce enough insulin.

Types of Insulin
The following is a list of some of the more common insulin preparations available today.
-- Rapid-acting
-- Short-acting (Regular)
-- Intermediate-acting (NPH)
-- Intermediate and short-acting mixtures
-- Long-acting

Rapid-acting Insulin
-- Humalog (lispro)
-- Eli Lilly
-- NovoLog (aspart)
-- Novo Nordisk

Short-acting (Regular) Insulin
-- Humulin R
-- Eli Lilly
-- Novolin R
-- Novo Nordisk

Intermediate-acting (NPH) Insulin
-- Humulin N, L
-- Eli Lilly
-- Novolin N, L
-- Novo Nordisk

Intermediate and short-acting mixtures Insulin
-- Humulin 50/50
-- Humulin 70/30
-- Humalog Mix 75/25
-- Humalog Mix 50/50
-- Eli Lilly
-- Novolin 70/30
-- Novolog Mix 70/30
-- Novo Nordisk

Long-acting Insulin
-- Ultralente
-- Eli Lilly
-- Lantus (glargine)
-- Aventis


Go to the following web site pages for more information about the dangers of prescription drugs:

The Epidemiology of Type 2 Diabetes

Starting in the second half of the twentieth century, the prevalence of non-insulin-dependent (type 2) diabetes increased substantially in many populations and ethnic groups, including African Americans, Native Americans, Mexicans Americans, and Pacific Islanders.

Diabetes is a metabolic disorder characterized by an inability to regulate blood sugar. The increase in this disease is clearly related to shifts in diet and lifestyle. While some researchers have proposed that it is related to genetic factors, other researchers point to stressful and challenging life conditions resulting from poverty and social inequality.

More than 90 percent of all diabetics have type 2 diabetes. Unlike the more rare form of the disease, type 1 diabetes, people with type 2 diabetes produce insulin and therefore seldom need therapeutic insulin at the initial onset of the disease.

Type 2 diabetes is considered a late-onset chronic disease and is associated with risk factors such as increased obesity, dietary fat intake, smoking, and low physical activity. Racism, stress, and socioeconomic status have also been implicated in the development of diabetes. Diabetes is diagnosed by measuring the percentage of red blood cells that are bound with glucose. There is no cure for diabetes, but the traditional treatment includes alterations in diet, exercise, and drug therapies to control glucose metabolism.

Prevalence rates follow a strikingly similar pattern in varied populations. For First Nations Canadian men and women, age-adjusted prevalence rates are 3.6 and 5.5 times higher, respectively, than among the general Canadian population. Among Indigenous Australians, the prevalence rates are almost four times higher than the rate for the non-Indigenous population. Researchers comparing age-adjusted prevalence rates for Nigerians and people of African origin living elsewhere found diabetes rates were

2.5 to 5 times higher for those living in the Caribbean and United Kingdom. In the United States, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) estimates that at least 8 to 10 percent of all Latinos, African Americans, and Native Americans aged twenty years or older have diabetes. The comparable prevalence rates for non-Hispanic whites is 4.8 percent.

According to the U.S. Centers for Disease Control and Prevention (CDC), diabetes is the seventh leading cause of death in the United States. The World Health Organization (WHO) has called diabetes an emerging epidemic, with more than 24 million people affected in the United States and millions more in the rapidly urbanizing Southern Hemisphere and China.

According to the WHO, approximately 366 million people worldwide will have diabetes by 2025. The very similar epidemiological patterns that exist for U.S. minorities, First Nations Canadians, Indigenous Australians, peoples of the African diaspora, and peoples of the Pacific Islands strongly indicate that diabetes disproportionately affects subordinated groups around the world.

Diabetes as a Biocultural Disease
As a racializing practice, gene-based approaches to diabetes advance the myth that biology can explain social phenomena. In fact, considerable evidence suggests that biology and social phenomena are co-produced, that biological and social phenomena develop in mutually interdependent ways. In its most crude form, this is evident when genetic researchers use social labels to describe human groups, which renders their findings both biological and social in origin. Similarly, researchers using evolutionary models for complex diseases require genetic samples of the populations most impacted by diabetes. They are thus investigating the physiological impact of social stratification and the radical lifestyle transformation required of advanced capitalism.

Viewing complex disease through a genetic lens is a long-established sociocultural phenomenon, one that has been applied to diseases such as sickle-cell anemia, hypertension, and diabetes. For diabetes, the alleged metabolic adaptation within the thrifty genotype hypothesis presumes that hunter-gatherers experienced severe episodes of feast and famine. Selective evolutionary pressures would therefore favor those whose metabolism would best convert glucose to fat for use during periods of food scarcity.

Contemporary human groups impacted by diabetes are viewed as genetically predisposed to the disease by virtue of their current similarity to the lifeways of earlier humans. However, both the extent of the feast-and-famine cycles of hunter-gatherers and the association of contemporary human groups with early human life-ways are unsubstantiated premises, relying on presumed rather than empirically supported benefits of modernity. The widespread adherence to the evolutionary hypothesis of diabetes (and the considerable resources directed toward such studies) is another iteration of a race theory that advances the cultural notion that diabetes affects human groups differently because of innate genetic differences.

Examining diabetes as an evolutionary trait denies the impact of the social dislocation, dispossession, colonization, slavery, racism, and other sociohistorical impact on those groups affected by diabetes. For example, the groups most disproportionately impacted by diabetes, Native Americans, experienced extreme deprivations during the violent dispossession of their lands and subsequent attempts by white settlers to eradicate them. It is the children and grandchildren of those born during this period who now suffer disproportionately from diabetes.

These conditions support the fetal origins hypotheses and do not require the logical leap that such recent experiences could have evolutionary significance, and thus result in genotypic human variation. Thus, the widespread adherence to the genetic predisposition thesis for diabetes reflects a dominant cultural way of making sense of relations between groups impacted by the disease.

In order to understand the causes of diabetes, its evolutionary hypothesis must be seen as fitting not the natural history of the disease, but rather the ideological premise of a subordinating majority whose scientists refuse to seriously account for the social history of those peoples most impacted by the disease. Researchers seriously interested in preventing diabetes would greatly benefit by approaching the disease in ethnoracial groups as a biocultural phenomenon.

To avoid merely reproducing another unprovable evolutionary genetic predisposition claim, researchers must carefully investigate diabetes as the biological impact of economic and sociocultural changes for human life. This requires uncommon multi-disciplinary methods spanning the biological and social sciences and humanities. More importantly, researchers must actively counter the racialized hypothesis of genetic predisposition, especially in research into health inequalities among minority and emerging majority groups in parts of the world with high levels of ethnoracial stratification and an unequal distribution of resources.

In short, researchers must recognize the link between diabetes and institutional racism.

Note: For more information about the science of Type 2 diabetes, go to the following links:
-- The
Pathophysiology
-- More Facts & Figures
-- Overview of Diabetes

-- Medical Sciences
-- Nutritional Science

Body Fat and Insulin Resistance

How does body-fat content produce insulin resistance? First, it appears that it is particularly intra-abdominal fat (also termed visceral fat) that is the culprit here. Intra-abdominal fat is adipose tissue associated with the abdominal viscera. Subcutaneous fat is much less of a problem. One hypothesis suggests that a process that is central to the pathogenesis of insulin resistance is fat ectopia. In the simplest terms, adipose tissue can only hold a certain amount of fat, and if excessively loaded with fat, there is a spillover or redistribution of lipid to ectopic sites, including liver and skeletal muscle.

In support of this, hepatic steatosis is frequently observed in individuals with the metabolic syndrome. Nonalcoholic fatty liver disease has a prevalence of 57% to 74% in obese individuals. It is the most common cause of abnormal liver function tests in the United States. The ectopic triglyceride deposition in non-adipose tissue, such as liver and skeletal muscle, has deleterious effects. There is both tissue damage (lipotoxicity) and the development of insulin resistance.

Another aspect of the lipid ectopia hypothesis is that the beta cells themselves are damaged by the deposition of the fat. This results in a gradual failure to produce sufficient insulin, making the insulinopenia worse. The evidence that this hypothesis has some validity comes from rare cases of lipodystrophic diabetes. Congenital lipodystrophies are conditions where body fat is significantly reduced or almost absent. The dearth of normal fat-storage capacity leads to early fat ectopia with deposition of fat (triglycerides) in skeletal muscle and liver and the development of insulin resistance despite the absence of obesity.

Conversely, in the Prader-Willi syndrome, where significant obesity is a major feature, insulin resistance is uncommon. These individuals appear to have an expanded capacity to store fat, so their risk of fat ectopia and type 2 diabetes is less than average. Additional support of this hypothesis derives from studies of low-birth-weight infants. As adults, these individuals are predisposed to insulin resistance. It appears that they have reduced amounts of adipose tissue and, therefore, a reduced capacity to store fat. They are more likely to experience spillover or fat ectopia, according to the hypothesis outlined above.

Further evidence comes from the use of a class of drugs termed PPAR-gamma agonists (thiazolidinediones). These compounds stimulate the development of new adipose tissue, allowing the redistribution or normalization of fat stores. Fat leaves the ectopic tissues and re-enters the new adipose tissue. Thiazolidinediones are known to be effective in treating type 2 diabetes.

The Biochemical Pathology of Insulin Resistance and the Metabolic Syndrome

Over the past decade the metabolic syndrome has become prominent in the literature in addition to emerging as a major public health concern. The metabolic syndrome presents many diagnostic problems for clinicians and laboratorians alike. The metabolic syndrome is a constellation of symptoms and signs that include central obesity, insulin resistance, dysglycemia, dyslipidemia, and hypertension. The definition has many subtleties and clinically, there are a multitude of presentations. Included in the current understanding of the metabolic syndrome is a subtext of a pro-inflammatory and a pro-thrombotic state.

There is certainly no agreement on any single causative agent; however, it is clear that the modern calorie-rich Western diet in the setting of little or no regular exercise plays a central role. A recent concise review on metabolic syndrome was published in this journal. The current review addresses the biology of insulin resistance, viz., what is it and how does it present? The insulin resistance of the metabolic syndrome remains somewhat of an enigma, but a number of plausible models have come to light in recent years.

Here we review: (a) the many metabolic actions of insulin, (b) the pathogenesis of type 2 diabetes mellitus, (c) insulin resistance (in general), (d) the ectopic fat hypothesis of insulin resistance, (e) the possible role of the hormones leptin, resistin, and adiponectin, and (f) the connection between insulin resistance and islet amyloid.

Insulin and insulin resistance
Insulin is an essential polypeptide hormone produced under conditions of feeding by the beta cells of the pancreatic islets of Langerhans. Insulin is critical for entry of glucose into multiple tissues, including skeletal muscle and adipose tissue (via activation of the glucose transporter molecule [GLUT4]), but is not necessary for glucose entry into erythrocytes, liver, or brain. Insulin promotes the oxidation of glucose to carbon dioxide and water by tissues and also blocks "new" glucose biosynthesis (i.e., gluconeogenesis) by hepatic tissue. I

nsulin is also very important in promoting the storage of glucose in the form of glycogen by liver and muscle. The drive of glucose into the cells with its subsequent oxidation is the basis for the glucose-lowering effect of insulin. Insulin also has major effects on lipid metabolism. It blocks the breakdown of triacylglycerols (triglycerides) by adipose tissue and promotes the biosynthesis of fatty acids and triacylglycerols by liver and adipose tissue. In short, insulin promotes fat storage.

This summary of insulin's many actions helps to clarify the effects of insulin deficiency. In the absence of sufficient insulin, glucose (now unable to enter cells) accumulates in excess within the extracellular fluid. This has two major effects: (a) the cells undergo a functional starvation and (b) the high plasma glucose has many untoward physiologic effects, including osmotic problems and tissue damage from protein glycation.

Cell starvation manifests as increased synthesis of ketone bodies. Furthermore, there is adipose tissue breakdown with production and release of fatty acids. The latter are delivered to the liver in such high quantities that hepatic lipoprotein synthesis is increased and the liver puts out abundant very low-density lipoproteins (VLDLs). Insulin is required for VLDL breakdown in the capillary beds via lipoprotein lipase and so, in cases of insulin deficiency, these large triglyceride-rich lipoproteins persist.

Diabetes is a disease that results from decreased insulin action. Insulin action is a product of insulin concentration and tissue insulin sensitivity. For many decades, researchers have been aware of the essential differences between type 1 and type 2 diabetes. In type 1 diabetes, there is a true deficiency of insulin due to pancreatic beta-cell damage by an autoimmune, cell-mediated response. Insulin concentrations are very low. In type 2 diabetes, insulin concentrations may be normal or even high. In type 2 diabetes, there is an insensitivity of the tissues to the effects of insulin--an effect termed insulin resistance. Insulin is present, but it cannot get its message through to the cells. What has happened? Before addressing this, let us review what normally happens when insulin interacts with a cell.

In order to initiate its many metabolic effects, insulin must interact with a specific cell-surface receptor that belongs to a family of receptor-enzymes known as tyrosine kinases. The binding of insulin to the insulin receptor initiates a complex chain of events that ultimately generates a multitude of intracellular second messengers. The latter eventually produce the characteristic effects of insulin, for example, by promoting the movement of GLUT4 molecules to the cell surface.

Although cases of insulin resistance have been described due to specific mutations in the insulin cell-surface receptor tyrosine kinase, these are rather rare and constitute only a minority of cases. They have, however been extensively studied and have shed much light on the biology of insulin action. The insulin resistance of the common type 2 diabetes is not related to receptor mutations, but is somehow related to the amount of fat in the body.

The standard model of type 2 diabetes is that the body tissues progressively become more insulin resistant, so that ever-higher blood concentrations of the hormone are needed to produce the identical effect. In the early stages of the disease, plasma insulin concentrations tend, therefore, to be higher than normal. The insulin resistance eventually achieves a level where the person is relatively insulinopenic. He has above-normal concentrations of insulin, but the circulating insulin nevertheless is still not sufficient to fully activate the insulin-resistant tissues, such as skeletal muscle and adipose tissue. There is a price to pay for this profligate expenditure of insulin. The beta cells cannot keep up with the demand and begin to fail--an event that may also be promoted by body-fat content. Such individuals enter a stage where they are truly insulinopenic. Indeed, even when the beta cells are still able to secrete large amounts of insulin, the temporal pattern of insulin secretion is no longer normal.

Initially, the insulin resistance is most likely sub-clinical, since insulin is not routinely measured in the clinical laboratory as part of a standard clinical chemistry analysis. As the condition progresses, there will be evidence of pre-diabetes, either impaired fasting glucose and/or impaired glucose tolerance, the latter based upon a standard oral two-hour glucose-tolerance test. Eventually, frank hyperglycemia sets in and the physician can make the diagnosis of diabetes. Interestingly, insulin resistance, besides producing diabetes, may produce other physical signs. One of these is a skin condition termed acanthosis nigricans--a velvety, brown-black skin discoloration, often in skin folds or at the back of the neck.

Insulin resistance has important effects on the vascular bed. It leads to decreased nitric oxide synthesis by endothelial cells with subsequent endothelial dysfunction. Nitric oxide is an important vasodilator that reduces resistance in blood vessels. This may be one of the mechanisms underlying the hypertension of the metabolic syndrome. Hyperinsulinism is also responsible for other phenomena not typically associated with carbohydrate metabolism. It produces hyperandogenism in females; hyperinsulinism is a key feature of the polycystic ovarian syndrome, a close relative of the metabolic syndrome. The polycystic ovarian syndrome is a constellation of signs that include insulin resistance, hyperandrogenism, hirsutism, obesity, infertility, and menstrual irregularities.

Pathophysiology and the Pathogenesis of Type 2 Diabetes


Type 2 diabetes mellitus is a heterogeneous disorder with varying prevalence among different ethnic groups. In the United States the populations most affected are native Americans, particularly in the desert Southwest, Hispanic-Americans, African-Americans, and Asian-Americans. The pathophysiology of type 2 diabetes mellitus is characterized by peripheral insulin resistance, impaired regulation of hepatic glucose production, and declining ß-cell function, eventually leading to ß-cell failure.

The primary events are believed to be an initial deficit ininsulin secretion and, in many patients, relative insulin deficiency in association with peripheral insulin resistance.



The ß-cell Dysfunction
ß-Cell dysfunction is initially characterized by an impairment inthe first phase of insulin secretion during glucose stimulationand may antedate the onset of glucose intolerance in type 2 diabetes.

Initiation of the insulin response depends upon the transmembranous transport of glucose and coupling of glucose to the glucose sensor. The glucose/glucosesensor complex then induces an increase in glucokinase by stabilizing the protein and impairing its degradation. The induction of glucokinase serves as the first step in linking intermediary metabolism with the insulin secretory apparatus. Glucose transport in ß-cells of type 2 diabetes patients appears to be greatly reduced, thus shifting the control point for insulin secretion from glucokinase to the glucose transport system.

Later in the course of the disease, the second phase release of newly synthesized insulin is impaired, an effect that can be reversed, in part at least in some patients, by restoring strict control of glycemia. This secondary phenomenon, termed desensitization or ß-cell glucotoxicity, is the result of a paradoxical inhibitory effect of glucose upon insulin release and may be attributable to the accumulation of glycogen within the ß-cell as a result of sustained hyperglycemia. Other candidates that have been proposed are sorbitol accumulation in the ß-cell or the non-enzymatic glycation of ß-cell proteins.

Other defects in ß-cell function in type 2 diabetes mellitus include defective glucose potentiation in response to non-glucose insulin secretagogues, asynchronous insulin release, and a decreased conversion of proinsulin to insulin.

An impairment in first phase insulin secretion may serve as a marker of risk for type 2 diabetes mellitus in family members of individuals with type 2 diabetes mellitus and may be seen in patients with prior gestational diabetes. However, impaired first phase insulin secretion alone will not cause impaired glucose tolerance.

Autoimmune destruction of pancreatic ß-cells may be a factor in a small subset of type 2 diabetic patients and has been termed the syndrome of latent autoimmune diabetes in adults.This group may represent as many as 10% of Scandinavian patients with type 2 diabetes and has been identified in the recent United Kingdom study, but has not been well characterized in other populations.

Glucokinase is absent within the ß-cell in some familieswith maturity-onset diabetes of young . However, deficienciesof glucokinase have not been found in other forms of type 2diabetes.

In summary, the delay in the first phase of insulin secretion, although of some diagnostic import, does not appear to act independently in the pathogenesis of type 2 diabetes. In some early-onset patients with type 2 diabetes (perhaps as many as 20%), there may be a deficiency in insulin secretion that may or may not be due to autoimmune destruction of the ß-cell and is not due to a deficiency in the glucokinase gene. In the great majority of patients with type 2 diabetes (±80%), the delay in immediate insulin response is accompanied by a secondary hypersecretory phase of insulin release as a result of either an inherited or acquired defect within the ß-cell or a compensatory response to peripheral insulin resistance.

Over a prolonged period of time, perhaps years, insulin secretion gradually declines, possibly as a result of intra-islet accumulation of glucose intermediary metabolites. In view of the decline in ß-cell mass, sulfonylureas appear to serve a diminishing role in the long term management of type 2 diabetes. Unanswered is whether amelioration of insulin resistance with earlier detection or newer insulin-sensitizing drugs will retard the progressionof ß-cell failure, obviating or delaying the need for insulin therapy. Superior nutritional therapy may provide the best solution for this disease.

Insulin Resistance
The presence of hyperinsulinism in type 2 diabetes, insulin resistance has been considered to play an integral role in the pathogenesis of the disease. Recent critical reviews, however, have questioned the primacy, specificity, and contribution ofinsulin resistance to the disease state. As chronic hyperinsulinemia inhibits both insulin secretion and action, and hyperglycemia can impair both the insulin secretoryresponse to glucose as well as cellular insulin sensitivity, the precise relation between glucose and insulin level as a surrogate measure of insulin resistance has been questioned. Lean type 2 diabetic patients over 65 years of age have been found to be as insulin sensitive as their age-matched non-diabetic controls.

Moreover, in the majority of type 2 diabetic patients who are insulin resistant, obesity is almost invariably present. As obesity or an increase in intra-abdominal adiposetissue is associated with insulin resistance in the absence of diabetes, it is believed by some that insulin resistance in type 2 diabetes is entirely due to the coexistence of increased adiposity. Additionally, insulin resistance is found in hypertension, hyperlipidemia, and ischemic heart disease, entities commonly found in association with diabetes, again raising the question as to whether insulin resistance results from different pathogenetic disease processes or is unique to the presence of type 2 diabetes.

Prospective studies have demonstrated the presence of either insulin deficiency or insulin resistance before the onset of type 2 diabetes. Two studies have reported the presence of insulin resistance in non-diabetic relatives of diabetic patients at a time when their glucose tolerance was still normal. In addition, first degree relatives of patients with type 2 diabetes have been found to have impaired insulin action upon skeletal muscle glycogen synthesis due to both decreased stimulation of tyrosine kinase activity of the insulin receptor and reduced glycogen synthase activity.

Other studies in this high risk group have failed to demonstrate insulin resistance, and in the same group, impaired early phase insulin release and loss of normal oscillatory pattern of insulin release have been described. Based upon these divergent studies, it is still impossible to dissociate insulin resistance from insulin deficiency in the pathogenesis of type 2 diabetes. However,both entities unequivocally contribute to the fully established disease.

The Liver
The ability of insulin to suppress hepatic glucose production both in the fasting state and postprandially is normal in first degree relatives of type 2 diabetic patients . It is the increase in the rate of postprandial glucose production that heralds the evolution of IGT. Eventually, both fastingand postprandial glucose production increase as type 2 diabetes progresses.

Hepatic insulin resistance is characterized by a marked decrease in glucokinase activity and a catalytic increased conversion of substrates to glucose despite the presence of insulin. Thus, the liver in type 2 diabetes is programmed to both overproduce and under-use glucose. The elevated free fatty acid levels found in type 2 diabetes may also play a role in increased hepatic glucose production. In addition, recent evidence suggests an important role for the kidney in glucose production via gluconeogenesis, which is unrestrained in the presence of type 2 diabetes.

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