Sunday, May 29, 2016

Root Causes 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.

However, there is more to diabetes than the insulin resistance and 
ß-cell dysfunction. There are other biochemical and hormonal imbalances  or root causes that fuel diabetes, including cellular inflammation, excess oxidation, adrenal fatigue, toxicity, and  insufficient nutrient absorption by the gastrointestinalsystem. All of these biochemical and hormonal imbalances must be addressed in order to properly treat diabetes and provide the opportunity to reverse the disease.

Insulin resistance due to the high levels of insulin cause all fat burning hormones in your body like growth hormone, testosterone, glucagon to become inactive, making it very difficult to burn fat and lose weight. Consequently, one of the keys to defeating diabetes is to reduce the insulin levels and insulin resistance.

People who cannot lose weight or have diabetes, have a high degree of cellular inflammation. Consequently, another key to defeating diabetes is to reduce the cellular inflammation.

Adrenal fatigue is another major contributor to diabetes. One of the major keys to chronic inflammation is adrenal fatigue. When the adrenals are stressed, they secrete hormones that cause insulin resistance and also stress the rest of the body.

Another major contributor to diabetes that is commonly overlooked is the insufficient digestion and absorption of nutrients by the gastrointestinal system -- this leads to cellular starvation and severe nutrient deficiencies.

Not many people realize  that 90 percent of what your pancreas produces are digestive enzymes. Insulin and the opposing hormone, glucagon, are only 10 percent of what the pancreas produces. When your digestion is poor, your pancreas will get very stressed. This will eventually cause problems with insulin.

Toxins (poisons) are also a major contributor to diabetes today (that did not exist in the past). Toxins exist in the environment and in the foods we eat today. Ingredients like high fructose corn syrup, alloxan and MSG have all been proven to cause insulin resistance and alloxan also has been proven to destroy the insulin producing cells on your pancreas.

Consequently, other keys to defeating diabetes include enabling better digestion and absorption of nutrients and the removal of excess toxins from the body (i.e. detoxification).

All of these plus a consistent exercise program that causes more oxygen to get into your cells must be part of a comprehensive diabetes program in order to control and reverse your diabetes.

If you've done any research on the Internet, you have discovered that most  diabetes sites discuss insulin resistance, but most of them fail to mention these other biochemical/hormonal issues.

Consequently, it only makes sense that if diabetes is primarily fueled by insulin resistance, cellular inflammation, excess oxidation, adrenal fatigue, toxicity, and gastrointestinal/digestive issues, then, a effective diabetes wellness program must address each of these areas. The Death to Diabetes Wellness Program may be the only program that addresses all of these issues -- that's why the program is so effective.

Diabetic Complications
If Type 2 diabetes goes untreated, the excess insulin and excess blood glucose (hyperglycemia) damages the body's blood vessels and can lead to thicker blood, high blood pressure, high cholesterol, high homocysteine, high c-reactive protein, arterial plaque formation, and low levels of chromium, magnesium, calcium, Vitamin C, and Vitamin E.
These complications affect nearly every organ in the body, leading to kidney failure, diabetic retinopathy and blindness, peripheral neuropathy and amputation, serious skin infections, gangrene, cardiovascular disease, stroke, disability, osteoporosis, Alzheimer's disease, hearing damage, nonketotichyperglycemic hyperosmolar syndrome, and death.
Note: These biological changes and biochemical imbalances can be corrected  and these complications prevented with a superior nutrition, a proper exercise regimen,  spiritual healthand less stress in your life.

The ß-cell Dysfunction

ß-Cell dysfunction is one of the root causes of Type 2 diabetes and is initially characterized by an impairment in the first phase of insulin secretion during glucose stimulation and 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 restoringstrict 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 families with 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 progression of ß-cell failure, obviating or delaying the need for insulin therapy. Superior nutritional therapy may provide the best solution for this disease.
Insulin ResistanceThe presence of hyperinsulinism in type 2 diabetes, insulin resistance is one of the root causes of Type 2 diabetes and has been considered to play an integral role in the pathogenesis of the disease.

Chronic hyperinsulinemia inhibits both insulin secretion and action, and hyperglycemia can impair both the insulin secretory response to glucose as well as cellular insulin sensitivity.

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 adipose tissue 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.
Prospective studies have demonstrated the presence of either insulin deficiency or insulin resistance before the onset of type 2 diabetes.
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 fasting and 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 ofinsulin. 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.


United States/International Scope

In 2007, the estimated prevalence of diabetes in the United States was 7.8% (23.6 million people); almost one third of cases were undiagnosed. More than 90% of cases of diabetes are type 2 diabetes mellitus. With increasing obesity in the population, an older population, and an increase in the population of higher-risk minority groups, prevalence is increasing.

Type 2 diabetes mellitus is less common in non-Western countries where the diet contains fewer calories and caloric expenditure on a daily basis is higher. However, as people in these countries adopt Western lifestyles, weight gain and type 2 diabetes mellitus are becoming virtually epidemic.


Diabetes mellitus is one of the leading causes of morbidity and mortality in the United States because of its role in the development of optic, renal, neuropathic, and cardiovascular disease. These complications, particularly cardiovascular disease (~50-75% of medical expenditures), are the major sources of expenses for patients with diabetes mellitus. Approximately two thirds of people with diabetes die from heart disease or stroke. Men with diabetes face a 2-fold increased risk for coronary heart disease, and women have a 3- to 4-fold increased risk. In 1994, 1 of every 7 health care dollars in the United States was spent on patients with diabetes mellitus. The 2002 estimate for direct medical costs due to diabetes in the United States was $92 billion, with another $40 billion in indirect costs. Approximately 20% of Medicare funds are spent on these patients.
  • Diabetes mellitus is the leading cause of blindness in working-age adults in the United States; diabetic retinopathy accounts for 12,000-24,000 newly blind persons every year.The National Eye Institute estimates that laser surgery and appropriate follow-up care can reduce the risk of blindness from diabetic retinopathy by 90%.
  • Diabetes mellitus is the leading cause of end-stage renal disease (ESRD), accounting for 44% of new cases, according to the Centers for Disease Control and Prevention (CDC).In 2005, 46,739 people in the United States and Puerto Rico began renal replacement therapy, and 178,689 people with diabetes were on dialysis or had received a kidney transplant.
  • Diabetes mellitus is the leading cause of non-traumatic lower limb amputations in the United States, with a 15- to 40-fold increase in risk over that of the non-diabetic population. In 2004, about 71,000 non-traumatic lower limb amputations were performed related to neuropathy and vasculopathy.


The prevalence of type 2 diabetes mellitus varies widely among various racial and ethnic groups. Type 2 diabetes mellitus is becoming virtually pandemic in some groups of Native Americans and Hispanic people. The risk of retinopathy and nephropathy appears to be greater in blacks, Native Americans, and Hispanics.


The Root Causes of Type 2 Diabetes

The Biochemical Pathology of Insulin Resistance and the Metabolic SyndromeOver 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.

Insulin 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.
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.
Leptin, resistin, and adiponectin
The hormone leptin may be important in this fat ectopia/lipotoxicity scenario. Leptin is a 167-amino-acid polypeptide with a molecular mass of about 16 kDa that is produced by adipose tissue. It is known to regulate body adipose tissue. The ob/ob mouse is genetically deficient in leptin production, while the db/db mouse or the fa/fa (ZDF) rat have mutations in the leptin receptor. In these animal models, there is either a deficiency of leptin or there is a nonfunctional leptin receptor. These animals display hyperphagia and obesity as well as steatosis liver, skeletal muscle, and pancreatic islets.  Leptin is believed to reduce appetite and control thermogenesis via actions on the hypothalamus.

Growing evidence suggests that leptin can also act directly on adipose tissue and that this may well be a major site of its action. It has been proposed that, in this setting, leptin normally prevents steatosis in non-adipose tissue--it blocks the ectopic deposition of fat and thus prevents lipotoxicity. In leptin-deficient or leptin-resistant animals, this control is absent and ectopic fat deposition (steatosis) with consequent lipotoxicity continues unabated.  A similar situation is found in individuals with congenital lipodystrophies. In the latter case, the lack of adipose tissue is responsible for the leptin deficiency. In human diet-induced obesity, leptin levels initially are high, preventing ectopic fat deposition. Resistance to leptin ultimately occurs, however, and control over the ectopic deposition of fat is lost.
How does leptin exert its action to prevent steatosis? It enhances fatty-acid oxidation by tissues, leading to the generation of both ATP and heat.  It also reduces de novo fatty acid biosynthesis and reduces synthesis of triglycerides. In the absence of leptin, these processes are blocked and triglycerides accumulate in non-adipose tissue.

Furthermore, these metabolic studies have shed light on the lipotoxicity of ectopic fat deposition. In the absence of leptin, and when intracellular triglycerides accumulate, fatty acids enter a pathway of non-oxidative metabolism.  This leads to increased ceramide formation. Ceramide is a sphingolipid, derived from sphingosine (an amino alcohol) joined to a fatty acid. Ceramide promotes apoptosis (programmed cell death).
Recent studies in adipose tissue biology have lead to the discovery of a another new hormone (termed resistin) that (like leptin) is produced by adipose tissue. Initial evidence pointed to resistin playing a major role in the pathogenesis of insulin resistance by virtue of its ability to oppose certain actions of insulin. This was supported by the observation that thiazolidinedione drugs that activate the transcription factor PPAR-gamma decrease adipose tissue resistin secretion and, therefore, help to reverse insulin resistance. Since its initial description, the role of resistin has been somewhat less clear cut with conflicting reports in the literature.

A study published in 2002 showed, however, that the removal of visceral fat from Zucker diabetic rats prevented the development of insulin resistance, and that resistin expression in visceral fat was much higher than subcutaneous fat. The role of resistin in human biology however, remains rather uncertain.
Adiponectin is yet another adipose tissue-derived protein with endocrine effects.  Adiponectin is a 244-amino-acid protein (30 kDa) with a collagen-like domain. Part of the molecule shares structural similarities with the cytokine tumor necrosis factor-alpha (TNF- alpha). Plasma concentrations of adiponectin are lowered in obesity and insulin resistance, in contrast to many other adipose-derived cytokines. Adiponectin production is associated with insulin sensitivity; conversely, low adiponection concentrations produce insulin resistance. Adiponectin also stimulates fatty-acid oxidation and lowers plasma triglycerides.

In addition, adiponectin appears to have antiatherogenic effects. When adiponectin "knock-out" mice were given high-fat, high-sucrose diets, they developed insulin resistance. Of relevance to the metabolic syndrome, visceral fat accumulation is associated with lowered adiponectin concentrations. TNF-a, which is also known to be associated with insulin resistance, inhibits adiponectin gene expression.
Islet amyloid
Another development in the field of type 2 diabetes has been the identification of islet amyloid and its relationship to beta-cell failure. The standard model of type 2 diabetes, as described above, raises the question: Is the beta-cell failure that occurs as the disease advances simply a result of cell exhaustion? Is it due to the lipotoxicity described above? There is evidence that islet amyloid may be important, too, although it is probably not the only factor.

Amyloid is a proteinaceous fibrillary deposit that is seen in tissues during certain pathologic processes and that can fold into beta-pleated sheets. Amyloid has a characteristic electron-microscopic appearance, as well as a green birefingence in polarizing light microscopy when stained with Congo Red. Islet amyloid is a form of local amyloidosis, since it is confined to the islets of Langerhans.
Islet amyloidosis is frequently observed in individuals with type 2 diabetes mellitus. The amyloid appears to promote beta-cell damage and death. Is there any connection with insulin resistance? There may well be. A major component of islet amyloid is a 37-amino-acid polypeptide termed islet amyloid polypeptide (IAPP) or amylin, produced and secreted by the islet beta cells.

In the setting of insulin resistance, not only does insulin secretion by the beta cell increase, IAPP production follows suit. Although the IAPP sequence is normal, the high polypeptide concentrations promote amyloid fibril formation, leading to localized islet amyloidosis. This ultimately may contribute to beta-cell failure. Thus, insulin resistance leads to islet amyloid, which, in turn, promotes insulin lack of.
In the course of a normal physiologic response to starvation, free fatty acids or FFA have a carbohydrate-sparing effect so that glucose can be preserved for oxidation by the central nervous system. Fatty acids are also elevated in obese individuals, and these have direct effects on carbohydrate metabolism. Fatty acids decrease glucose uptake, glycogen synthesis, and glycolysis, effects normally promoted by insulin. The evidence from the original studies suggested the effect of fatty acids to be at the level of glucose transport or phosphorylation. (18) Furthermore, fatty acids inhibit insulin suppression of hepatic glucose production, leading to increased hepatic glucose production.

Pathogenesis of Type 2 Diabetes
The pathological sequence for type 2 diabetes is complex and entails many different elements that act in concert to cause that disease. One of the flow charts (below) proposes a sequence of events and how the disease progresses in the human body.

A genetic predisposition must exist, although to date very little is known about specific genetic defects in this disease. Whether the diabetes phenotype will occur depends on many environmental factors that share an ability to stress the glucose homeostasis system, with the current explosion of obesity and sedentary lifestyle being a major cause of the worldwide diabetes epidemic.

We also propose that a lowered beta-cell mass either through genetic and/or beta-cell cytotoxic factors predisposes for glucose intolerance. As the blood glucose level rises even a small amount above normal, then acquired defects in the glucose homeostasis system occur -- initially to impair the beta cell's glucose responsiveness to meals by impairing the first phase insulin response -- and cause the blood glucose level to rise into the range of impaired glucose tolerance (IGT).

This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, cause additional deterioration in beta-cell function along with further insulin resistance, and the blood glucose levels rise to full-blown diabetes. This sequence also provides insight into how to better prevent or treat type 2 diabetes, by studying the molecular basis for the early defects, and developing targeted therapies against them.

Candida Problems and Diabetes

If you have diabetes, chances are good you will also have problems with a bacteria known as candida. Why? Because every living human has candida in his or her system. Usually the "friendly bacteria" keep the non-friendly candida at bay, but certain factors can allow the candida to flourish -- factors that are often brought on by diabetes.
For example, candida is a cause of vaginal yeast infections in women, and while yeast infections are very common, they are even more common among women with diabetes.This is because diabetes impairs the body's immune system and its ability to fight infections. Candida growths that would be taken care of naturally in non-diabetic people become problematic in people with diabetes.
In addition, a high blood sugar level makes the mucous membranes more sugary, which is a perfect environment for yeasts to grow in.
Foods that can trigger candida include sugar, flour, alcohol, corn, potatoes, pasta, rice, bread and other processed foods that contain sugar or flour. By eliminating these foods, most people can get rid of their candida. Ironically, these are the same foods that diabetics need to avoid to better control their blood glucose levels. Focus on periodic detox and eating more yogurt and vegetables, especially those that inhibit the growth of candida, i.e. cabbage, raw garlic, onions, broccoli, turnip, kale.

The Good News!
These biochemical and hormonal imbalances fueling your diabetes can be corrected  and the complications of diabetes can be prevented and reversed with a comprehensive diabetes wellness program that includes a superior nutritional program, a proper exercise regimen,  spiritual health,cleanse/detox, less chronic fatigueand less stress in your life.
For more information about the science of Type 2 diabetes, go to the following links:-- The Epidemiology
-- More Facts & Figures
-- The Etiology
-- Overview of Diabetes
Medical Sciences
-- Nutritional Science

Note: If you concerned about what the drugs are doing to you, follow these steps to get started today on your journey to wellness.

Note: If you want to to learn more about diabetes and if you're serious about defeating your diabetes, request a free copy of the author's research paper titled The 7 Mistakes That Diabetics  Make.
  1. Hoefner DM. The ruthless malady: Metabolic Syndrome. Medical Laboratory Observer 2003;35:(10):12-23.
  2. Grundy SM, Brewer Jr HB, Cleeman JI, Smith Jr SC, Lenfant C. Definition of Metabolic Syndrome. Report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition. Circulation 2004;109:433-438.
  3. Williams RH, Foster DW, Kronenberg HM, Larsen PR, Wilson J Md. Williams Textbook of Endocrinology, 10th ed. W B Saunders; Copyright [c] January 2003 Elsevier.
  4. Baron AD. Insulin resistance and vascular function. J Diabet Complications. 2002;16:92-102.
  5. Wheatcroft SB, Williams I L, Shah AM, Kearney MT. Pathophysiological implications of insulin resistance on vascular endothelial function. Diabetic Med. 2003;20:255-268.
  6. Unger RH. The Physiology of Cellular Liporegulation. Annu Rev Physiol 2003;65:333-347.
  7. Unger RH. Lipotoxic Diseases. Annu Rev Med. 2002;53:319-336.
  8. Angulo P. Nonalcoholic fatty Liver Disease. N Engl J Med. 2002;346:1221-1231.
  9. Garg A. Acquired and Inherited Lipodystrophies N Engl J Med. 2004;350:1220-1234.Rea R, Donnelly R. Resistin: an adipocyte-derived hormone. Has it a role in diabetes and obesity? Diabetes Obes Metab. 2004;6:163-170.
  10. Gabriely I, Ma XH, Yang XM, Atzmon G, et al. Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process? Diabetes. 2002;51(10):2951-2958.
  11. Ukkola O, Santaniemi M. Adiponectin: a link between excess adiposity and associated comorbidities? J Mol Med. 2002;80(11):696-702.
  12. Beltowski J. Adiponectin & Resistin--new hormones of white adipose tissue. Med Sci Monit. 2003;9(2):RA55-61.
  13. Matsuzawa Y, Funahashi T, Kihara S, Shimomura I. Adiponectin and metabolic syndrome. Arterioscler Thromb Vasc Biol. 2004;24(1):29-33.
  14. Hoppener JWM, Nieuwenhuis MG, Vroom TM, Ahren B, Lips CJM. Role of islet amyloid in type 2 diabetes mellitus: consequences or cause? Mol Cell Endocrinol. 2002;197:205-212.
  15. Hull RL, Westermark G, Westermark P, Kahn SE. Islet Amyloid: a critical entity in the pathogenesis of type 2 diabetes. J Clin Endocrinol Metab. 2004;89(8):3629-3643.
  16. Boden G. Effects of free fatty acids (FFA) on glucose metabolism: significance for insulin resistance and type 2 diabetes. Exp Clin Endocrinol Diabetes. 2003;111(3):121-124.
  17. Boden G, Chen X. Effects of fat on glucose uptake and utilization in patients with non-insulin-dependent diabetes. J Clin Invest. 1995;96(3):1261-1268.
BG-Insulin Graph: Beat, Reverse & Cure Your Diabetes!

Diabetes Pathology at Celular Level: Beat, Reverse & Cure Your Diabetes!
Diabetes Pathology -- Cellular Level: Beat, Reverse & Cure Your Diabetes!

The Pathogenesis of Type 2 Diabetes
Pathogenesis: Beat, Reverse & Cure Your Diabetes!

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