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.

Mortality/Morbidity

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.
 

Race

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.
References
  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!

Biological Dysfunctions

Have you ever wondered how a disease gradually develops in your body?

Initially, when your body becomes biochemically or hormonally imbalanced, it sends us warning signs that something is wrong -- long before you find out from your doctor. These warning signs are called Symptoms.

Some of the more common and "innocent" symptoms that we tend to ignore include:
-- Fatigue
-- Headache
-- Upset Stomach
-- Constipation/Diarrhea
-- Irritability
-- Weight Gain
-- Unexplained Weight Loss
-- Loss of Appetite
-- Cravings
-- Brain Fog
-- Memory Loss
-- Sexual Dysfunction (Erectile Dysfunction)
-- Persistent Cough

Unfortunately, most of us ignore these signs unless they are painful or impeding us from going to work or from performing day-to-day activities.

As depicted in the diagram, these symptoms, if ignored, gradually develop into more serious symptoms, which can lead to cellular dysfunction; and, then, a major Biological Dysfunction; and, finally, a full-blown Disease.

Unfortunately, your doctor doesn't really know what blood tests to perform for any of these biological dysfunctions. Why? Because there is no drug that your doctor can prescribe -- until you develop a full blown disease or a health condition that your doctor can measure, e.g. high blood pressure, high cholesterol, high blood sugar, microalbumin.

Most of these diseases and health conditions are fueled by one or more of the following 7 biological dysfunctions, which are the pre-cursors to most of these diseases:
-- Chronic Inflammation
-- Oxidative Stress
-- Nutritional Deficiencies, Impaired Digestion/Absorption
-- Biochemical/Hormonal Imbalances
-- Toxicity
-- Protein Glycation
-- Impaired Immunity (Impaired Repair/Healing, Frequent Infections)

There are hundreds of other biological dysfunctions, but these are the key ones that fuel most diseases and that we will be discussing during the next several posts.

Note: If your doctor measured and tested these biological dysfunctions, we could easily prevent 90% of these diseases from becoming fully developed and wreaking severe damage to our cells, tissues and organs that leads to heart disease, cancer, heart attacks, strokes, hospital stays, surgeries, etc..

If I had to select one of these biological dysfunctions as the Number 1 Health Problem, I would probably select Inflammation (or Nutritional Deficiencies). Why? Because Inflammation (and Nutritional Deficiencies) are interdependent and connected to all of the other biological dysfunctions.

Because these biological dysfunctions are interdependent and inter-related, some of them trigger other dysfunctions and create a feedback loop that causes one dysfunction to fuel another, which, in turn, fuels the previous dysfunction, creating a continuous loop of cellular and tissue damage that eventually leads to a major disease.

As depicted in the diagrams, a disease develops when your body goes through the following stages: Biological Changes, 1-2 Symptoms, Multiple Symptoms, Increased Severity of Symptoms, Organ/System Dysfunction, Health Conditions, Health Impairment, Stages of Decline (Mild, Moderate, Severe), Disease, Multiple Diseases, Levels of Debilitation; and, if these is no intervention, the final stage is Death.

The good news is that all of these biological dysfunctions can be prevented, interrupted or reversed -- long before you develop a full-blown disease or health condition that lands you in the hospital!

In addition, if you have already been diagnosed with a disease, most of these biological dysfunctions can be reversed -- long before the disease becomes more serious and lands you in the hospital!

What to Do
And, yet, despite this information and the overwhelming statistics, most of us don't expect to end up in the hospital or die anytime soon. As a result, most of us won't make any changes until we have a health crisis.

However, for those of you who want to be proactive and prevent a health crisis, there are some simple things that you can do.

Proactive Steps
Here are some of the proactive steps to take to address this before it develops into a more serious problem.
-- Educate yourself about nutrition, disease, drugs, etc. -- don't expect your doctor to have all the answers.
-- Pay attention to your body and be aware of your symptoms, especially if they persist or become more severe.
-- Get an annual physical exam, plus additional tests for hormone levels, inflammation markers, vitamin/mineral deficiencies, heavy metals, etc.
-- Start eating a healthier diet that is rich in vegetables, fruits, plant oils, fish, beans, nuts and seeds.
But, don't deprive yourself of your favorite foods -- treat yourself every once in a while. This will allow you to stick with your dietary changes.
-- Take a brisk 20-30-minute walk 5 days a week.
-- Work with a naturopath, homeopath, health coach or other healthcare professional that is versed in nutritional science and has the skills to perform a nutrient gap analysis. This is critical step, because this will help to determine what is really going on inside your body.
-- Use wholefood supplementation to close nutritional gaps. Avoid synthetic supplements at all cost.
-- Try to avoid depending on medications to manage your disease.



Thursday, May 26, 2016

Greg McCulley: Fighting and Overcoming Depression

Views & Voices MagazineJune 2009

Fighting Depression
by Greg McCulley of Sharon, PA
 
     IF I HAVE LEARNED ANYTHING, IT’S THAT DEPRESSION HAS NO FACE, COLOR, OR GENDER; IT COULD HAPPEN TO ANYONE,  AND IT HAPPENED TO ME.

     Since October 31, 2007, I am happy to say that I have been free from all prescription drugs, clinical depression and a battle with insomnia. I am grateful to God that I made it. And, I am grateful to so many people who helped me during my journey to a full recovery. Now I can share my story with others to let them know that they can be free to live again.

     I have had a lot of losses in my life that have left me feeling hopeless and in much despair, and I felt that I was in the valley of the shadows of death after losing my family – the people who matter the most to me.

     Starting on October 5, 1959, I had my first great loss with the death of my 5-year-old sister, who died of bronchial pneumonia. The losses continued in March 1986 with my father passing due to massive heart attack. January 1996 brought the accidental death of one of my brothers, followed by the deaths of my baby brother, and another brother inn 2000, just 87 days apart from each other.

     Then in January 2005, my 10-year marriage ended in divorce. It was a very hard time emotionally for me, and I felt that, one by one, I was losing the people that mattered most to me.

     My eating and sleeping habits changed, I lost weight and my lacking job performance led to my wages being reduced. It wasn’t long until I found myself filing for Chapter 7 bankruptcy and I had a hard time holding it all together. I was suffering from emotional trauma and there were many nights of painful tears.

     By June 2006, I found myself with seven nights of no sleep at all and I knew something was definitely wrong. Though I tried to cover it up at work, the owner knew my behavior and weight loss were not normal and told me not to mess around with this serious problem. I could no longer hide that I was battling with depression and we discussed my getting help.

    I visited my family doctor and he immediately sent me to a psychiatrist for help. I was placed on a variety of drugs over the next couple of months, including an antidepressant that treats clinical depression; a sleep aid to treat the insomnia; a drug to treat panic disorders; and, another which didn’t work for me. I remained under my doctor’s care all during this time and I also attended general counseling with the Catholic Charities of Sharon, PA twice a month until February 2008.

   Thanksgiving Day 2006 brought upon more devastating deaths, with the loss of my mother to a massive heart attack.



“Yea, though I walk through the valley of the shadow of death …” Psalm 23:4




    

      Just five months later, my baby sister was diagnosed, with colon cancer, given six months to live and passed in August 2007.

     With just one brother and one sister still living, I hit rock bottom and the sleep aids no longer worked.

     I called my ex-wife at 6 one morning in mid-September and she began to read the Word of God to me, which states, “I was more than a conqueror through Christ Jesus my Lord.” She also told me I would need to address my medication issues as I had come to a place where I couldn’t sleep without prescription drugs. My psychiatrist told me that because of all the emotional stress I was under it would not be wise to put me on any more drugs and I would just need to give myself some time to heal.

    With the help of my ex-wife, a neighbor, my co-worker, and a good friend, I finally found the strength to overcome. They all gave me advice, including that if I spoke at least three good things that God has done every day that it would change things around for me. He also suggested exercising every day. A friend also brought me a calming herbal drink, which I used twice a day.

     With all of these changes, my mind became renewed and I slowly was able to get back to normal sleeping patterns within a month, thanks to God.

     Praise the Lord.
Story UpdateGreg, a business graduate of Pennsylvania State University, is currently working for Reyers, a well-known shoe store center in Sharon, PA.

In his free time, Greg speaks at various events to share his story so that he can help others who are suffering from depression, insomnia, and other similar ailments that are difficult for people to talk about and find real help.

Greg has been featured in the newspaper (Views and Voices), on the Internet, and on the radio (for interviews).

Greg's hope is that he will be able to help people the way he was helped when he needed it.

For interviews, conferences, health fairs, and other events, Greg can be contacted (via phone or email) to share his story.

Contact Information

Email: Greg's Email Address

Phone: 724-347-3322

Residence: Sharon, PA 16146

Greg's Web Sites

Defeat Depression (Webs.com)

Greg McCulley
 (Webs.com)

Beat Depression (Webs.com)

Greg McCulley (Google)
“No weapon that is formed against me shall prosper.” Isaiah 54:17

---------------------------------------
TV Interview on Denny/Marge Hazen Christian Show


Near-Death Experience: DeWayne McCulley

In March 2002 I went into a diabetic coma with a blood glucose level of 1337-- more than twelve hundred points above normal. Despite a set of complications that included severe hyperglycemia, dehydration, two blood clots, pneumonia and four insulin shots a day, I awoke from the coma and shocked the doctors.

According to everything I've read or heard about NDEs, I didn't have any of the classic Near-Death Experience (NDE) signs such as seeing any bright light or having an "out of body" experience.
 
While I was in the coma, the doctors had told my daughter to begin making arrangements -- that things didn't look good, my body was shutting down, there wasn't much time left ... When, I awoke from the coma, my daughter shrieked and the doctors were shocked. I heard one doctor say: "I can't believe it. He's alive. He's actually alive. He should be dead." Another doctor said, "He should be dead 10 times over. What do we do now?"

One of the doctors approached me and said "Mr. McCulley, we got some good news, and we got some bad news. The good news is that you're alive. The bad news is that we may need to amputate both your legs." I discuss this event during one of my lectures now on YouTube.

So I was "driven" to find the answer to why I had been in a near-death coma, and why the doctors felt that they needed to amputate both my legs.  Every time I visited my doctor or stopped by the hospital, all I heard was "Mr. McCulley, you should be dead, 10 times over. You are lucky to be alive."

But, my mother didn't believe in "luck" -- she said it was a blessing from God. She believed that God put me into training for 30 years by Corporate America -- to learn everything I could about engineering, and use that knowledge to beat my diabetes, write the book, and then help other diabetics.
 But there were events, that as a scientist, I can't explain logically. For example, after I came out of the coma, I was familiar with my condition, known as a  "non-ketotic hyperglycemic hyperosomolar coma". My daughter said that one of the doctors in the hospital used that term while they were discussing my coma in another room. It's not clear how I was able to "recall" such a complicated medical phrase since I had never been in that room ...
 
I didn't experience the classic NDE signs, but I remember the dreams, the nightmares about the graveyard scene while I was in the coma -- but that was just a dream, not an NDE.
I also remember when I came out of the coma that I had been traveling and I was in a large room (like in a hotel) with my daughter (I could hear her voice, but I couldn't see her). There was a birthday cake and candles. There were people praying. I could hear other voices asking me questions, and I would answer the questions. People were laughing and applauding.

I didn't think about it anymore until a few years later, I was invited to speak at a health/wellness forum. It turned out that I was in a large room (in a hotel) with my daughter. We were standing in front of an audience of diabetics answering their questions -- some of this discussion is now on Youtube in a couple different videos. There are photos here on the website of me and my daughter speaking at this event.

Another memory I had was of a doctor introducing me to speak, and a woman doing the same thing -- I couldn't see their faces, but I could hear them talking about my recovery from a near-death diabetic coma, and people applauding. This came to pass a few years later, and is part of a couple of YouTube videos.

There were other images/memories I had while I was in the coma, but at the time they didn't make any sense...

And, there are so many 'accidents' that have happened to me since the coma event, but as I mentioned, my mother says there are no accidents -- she believes 'it was meant to be' ...

I also had a dream at that time about being dead or, at least I thought I was dead. In the dream, I could see myself walking towards a grave. As I got closer to the grave, I could see that the first letter of the name on the gravestone was "D" which is the first letter of my name. So, I thought that I was dead, and I would panic and wake up in a cold sweat -- realizing it was just a dream and that I wasn't dead.

When I told my mother about the dream (actually a nightmare, since I don't like graveyards), she said that because of the diabetic coma, God was trying to speak to me. So I said "So is God trying to tell me that I'm dead or going to die in the hospital?"

My mother said: "No, God is trying to tell you something, but you can't wake up from the dream out of fear that you are dead. You must have faith and follow through with the rest of the dream." 
It took a couple nights, but I was finally able to watch myself during the entire dream sequence. When I finally got closer to the headstone on the grave site, I could see that the word on the gravestone did start with the letter "D", but the "D" was not for "DeWayne". The name on the headstone was "Diabetes"! But, at that time, I didn't really understand the power of that symbolism.  I was just glad that my name was not on the headstone!

Later on, after my recovery, my mother told me that God spared my life, and that I should write a book about my experience with diabetes, the coma, the doctors, the hospital, the insulin shots, and more importantly how I recovered from the diabetic coma and the diabetes episode to get healthy and wean myself off the insulin -- even though the doctors said I would be on insulin for the rest of my life.

When the American Diabetes Association (ADA) heard about my diabetic coma and recovery, they asked me to share my story and I ended up working as a volunteer, running a diabetic support group for the ADA. In addition, various churches and community groups asked me to speak about my recovery from a diabetic coma and a blood glucose level of over 1300. During these speaking engagements, people would ask me if I planned to write a book. At the time, I said: "No, I have no plans to write a book."

But my daughter teamed up with my mother, and both of them kept after me to write a book about my diabetes experience. Instead, I put together a 10-page pamphlet that I handed out during my speaking engagements and at the ADA diabetic support group meetings. But, the pamphlet only drove more questions. I tried to answer the new questions by expanding the pamphlet, which grew to more than 75 pages.

At this point, my daughter said, "Dad, you gotta write the book!" And, when I tried to give my mother excuses for why I'm not qualified to write a book plus I didn't have the time, she said "Son, remember what your father told you when you were growing up? By the time you come up with all those excuses why you can't do something, you could have had it done by now."

If you knew my mother, you would realize that she wasn't going to give in, and that I had no choice. So, I finally relented to write the book, which I did during 2004 and 2005.
 
But, then, I needed a title for the book. The titles started out looking like this: "How I Beat Diabetes", "Living After a Diabetic Coma", "Surviving Diabetes".
 
Then, the book titles evolved into: "Surviving Death & Diabetes", Recovering From a Near-Death Diabetic Coma", "Recovery from "Death & Diabetes", "Surviving Death and Diabetes" "Surviving Death from Diabetes" ... but none of the titles clicked with me.

Then, one day while I was talking to my mother on the phone, she said: "The wordsdeath and diabetes keep coming up in your titles." My daughter noticed the same thing.

Finally one night, I had the dream again about the graveyard and the headstone with the word "Diabetes" on it. My mother reminded me that God was trying to tell me that "Diabetes" belonged in the graveyard, not the names of the people who are dying and will die from diabetes."

Then, it hit me -- what the title of the book should be. "Death to Diabetes"! In other words, put the disease in the graveyard instead of the people with the disease! Kill the disease instead of kill the people! Death to the disease instead of death to the people! Death to Diabetes! -- it made so much sense!

My mother liked the title -- short and sweet, and to the point. My daughter also liked the title. But, the publishers and the so-called book experts didn't like the title. They said it was too grim and too negative, and it didn't make sense. Plus, the title would mean that the first word in my wellness book would be "Death". Publishers told me that a wellness book with "Death" as the first word and with "Death" in the title of the book, that my book would not sell because it sounded too negative.

To further complicate matters, the publishers didn't like the photograph of a graveyard on the front cover. And, they didn't like the color of the book cover -- black. They felt that I would be sabotaging my own book sales with such a negative cover and negative book title. Also, they said that there were no other nutritional or wellness books with the word "Death" in the title or with a black cover. They said that most nutritional books were bright colors with titles of hope and positivity.

But, for some strange reason, I didn't listen to the experts ... I stuck with the book title, the book cover photo, and the color of the book cover.

UPDATE: 7/29/2009:
And, like they say, the rest is history.

"Death to Diabetes" is now one of the top-selling diabetes books in the United States.

"Death to Diabetes" is gradually becoming the rallying cry of many diabetics who are fed up with the disease, the doctors, and the drugs; and are looking for a better answer. Many of them believe that the answer is "death to diabetes" instead of "death tothem". They see the book "Death to Diabetes" as a way out, a beacon of hope. Many diabetics are encouraged when they hear my story -- because they realize that if I can make it back, maybe they can make it back, too.

Wednesday, May 25, 2016

Neuropathy (Nerve Disease)

About 15 million Americans suffer from neuropathy, a nerve problem that can damage the nervous system and cause unrelenting aches and pains. In particular, 60% of diabetics develop peripheral neuropathy when their blood glucose Nervous Systemreaches and remains at dangerous levels for several years.

When blood glucose levels rise too high and remain too high, the glucose molecule attaches itself to cells permanently and is eventually converted to a poison sugar called sorbitol that destroys nerve cells (nerve death). 

The signs of nerve damage include tingling, burning, and the loss of feeling (touch) in the feet, which lead to a high incidence of foot infections, foot ulcers, and amputations.

If motor or autonomic nerves are damaged, this can lead to the loss of muscle control, bladder control, and bowel control. Eventually, after many years of poor blood glucose control and deterioration of the nervous system, the cells in the brain may also become damaged.

Please Note: Foot care is very important. It is critical for diabetics to pay special attention to their feet, since the feet are very susceptible to sores and cuts that don't heal and can lead to gangrene and amputation.

Peripheral Neuropathy
The peripheral nerves that go to the arms, hands, legs, and feet are responsible for relaying information from the central nervous system (brain and spinal cord) to muscles and other organs. Peripheral nerves also relay information back to the spinal cord and brain from the skin, joints, and other organs. High blood glucose levels create trace chemicals that damage the blood vessels that bring oxygen to some nerves and cause oxidative stress to nerve cells, and the degeneration of nerve fibers and the myelin sheath covering on the nerves.

In addition, the high glucose and insulin levels can cause calcium and other minerals to leech from the synaptic junctions. Synaptic junctions can only retain a limited amount of glucose, insulin, and electrolytes; therefore, when glucose or excess insulin enters, something else must be released. Since there is usually a plentiful supply of calcium and potassium from food, as well as a plentiful supply of oxygen from the lungs, these elements are generally the first to be discharged. However, once the nerve cell becomes shorter, it remains in that condition until it is over stimulated.

The calcium ion pump is responsible for the propagation of the nerve impulse along the myelin sheath. As a result, each time the synaptic junctions and nerve cells lose calcium, they conduct fewer impulses. A similar process is facilitated by the electric fields of tiny electrical charges, which are keyed to potassium levels. Atrophy occurs when any body part is used with less and less frequency.
Similarly, when the electrical signals are not propagating correctly and the body assumes that the nerve is no longer necessary and, to conserve energy, further reduces support for that nerve cell. In turn the nerve cell shrinks in order to function due to a reduced input of fuel and oxygen while still keeping itself viable until the nerve ceases to function.

Consequently untreated diabetes, hypoglycemia or poor glucose control could cause wide variations in the blood calcium, potassium, sugar, insulin, and oxygen levels thereby resulting in oxygen deprivation and loss of nerve integrity. Damaged nerves stop sending messages or send messages too slowly or at the wrong times. This leads to neuropathic symptoms such as tingling or numbness in the feet.

As a result, damage to these peripheral nerves can make the arms, hands, legs, or feet feel numb. Also, you might not be able to feel pain, heat, or cold when you should. You may feel shooting pains, burning or tingling like “pins and needles”. These feelings are often worse at night and make it difficult to sleep. Most of the time these feelings are on both sides of your body, like in both of your feet, but they can be on just one side.
Some of the other symptoms of peripheral neuropathy include prickly or burning pains, tightness of the skin, hypersensitivity to touch, impaired coordination, balance problems, difficulty climbing stairs or difficulty getting up from a sitting position, urinary urgency, erectile dysfunction, acid reflux and lightheadedness. The numbness that typically accompanies neuropathy can be particularly problematic because minor injuries may go unnoticed, turning into health problems that are not minor at all.

Peripheral nerve damage can change the shape of your feet because foot muscles get weak and the tendons in the foot get shorter. In some cases, failure of nerves controlling blood vessels, intestinal function, and other organs results in abnormal blood pressure, digestion, and loss of other basic involuntary processes. Peripheral neuropathy may involve damage to a single nerve or nerve group (mononeuropathy) or may affect multiple nerves (polyneuropathy).

Diabetic Foot Problems

When diabetes is not well controlled, damage to the organs and impairment of the immune system is likely. Foot problems commonly develop in people with diabetes and can quickly become serious.
  • With damage to the nervous system, a person with diabetes may not be able to feel his or her feet properly. Normal sweat secretion and oil production that lubricates the skin of the foot is impaired. These factors together can lead to abnormal pressure on the skin, bones, and joints of the foot during walking and can lead to breakdown of the skin of the foot. Sores may develop.
  • Damage to blood vessels and impairment of the immune system from diabetes make it difficult to heal these wounds. Bacterial infection of the skin, connective tissues, muscles, and bones can then occur. These infections can develop into gangrene. Because of the poor blood flow,  antibiotics cannot get to the site of the infection easily. Often, the only treatment for this is amputation of the foot or leg. If the infection spreads to the bloodstream, this process can be life-threatening.
  • People with diabetes must be fully aware of how to prevent foot problems before they occur, to recognize problems early, and to seek the right treatment when problems do occur. Although treatment for diabetic foot problems has improved, prevention - including good control of blood sugar  level - remains the best way to prevent diabetic complications. 

    • People with diabetes should learn how to examine their own feet and how to recognize the early signs and symptoms of diabetic foot problems.
    • They should also learn what is reasonable to manage routine at home foot care, how to recognize when to call the doctor, and how to recognize when a problem has become serious enough to seek emergency treatment.
Diabetes Foot Care
The Importance of Good Foot Care
There are many things you can do to prevent problems with your feet. Most of them involve good foot care. But start by taking care of your diabetes overall. If you keep your glucose level under control, you are less likely to have foot problems.
The following are good foot care tips:
  • Check your feet every day for cuts, red spots, sores or infected toenails.
  • Wash your feet every day in warm, NOT hot water. Dry your feet well and especially between the toes.
  • Put on a thin coat of lotion or petroleum jelly on the tops and bottoms of your feet. Do not put the lotion between your toes because it can cause an infection.
  • Treat corns and calluses gently. Check with your doctor or podiatrist about how to care for them.
  • Trim your toenails weekly or have a foot doctor do it if you can’t see well or reach your feet.
  • Wear shoes and socks constantly. Never go barefoot because you could step on something and hurt your feet.
  • Always check the insides of your shoes to make sure there are no stones or other objects in them.
  • Wear socks at night if your feet get cold. Check your feet often in cold weather in case of frostbite.
  • Put your feet up when sitting. Wiggle your toes for 5 minutes, two or three times a day.
  • Do not cross your legs for long periods of time.
Diabetic Neuropathy
When you have “peripheral” neuropathy in your feet, it’s very difficult to feel pain, cold, or heat. Because you have loss of feeling, you may not feel a foot injury. If you develop a blister, you may not know it. Often, you won’t notice a foot injury until the skin breaks down and becomes infected.
Because of this lack of sensation in your feet, wearing shoes that don’t fit well can potentially cause this kind of damage to your feet. That’s why it’s so important to wear properly fitted shoes.
Diabetic Shoes
Diabetic shoes are specially fitted for people who have even mild forms of neuropathy. There are companies that specialize in pedorthics, which is the design of footwear and special insoles that can prevent or lessen foot injury and pain.
Diabetic shoes are often made wider and deeper that regular shoes, with a larger “toe box.” This is partly to have room if insoles are needed. The pedorthic insoles are usually custom made for each individual diabetes patient. This ensures the fit and helps with uneven weight distribution or rubbing. The shoes should also allow good air circulation.
Trained Professionals
Diabetics need to have their shoes fitted by a trained professional, like a podiatrist. What you need in a diabetic shoe are:
  • Breathable construction—sandals and fabric shoes are best
  • Deep and wide design—to allow for insoles
  • Designs with no interior seams that could rub
  • Easily adjustable fit—elastic can help
Are Diabetic Shoes Covered by Medicare?
Medicare Part B will cover most of the cost of diabetic shoes, but the doctor treating you must certify that you meet all the following conditions:
  1. You have diabetes
  2. You have at least one of the following conditions:
    • Foot amputation—partial or complete
    • Past foot ulcers
    • Calluses that can become foot ulcers and/or lead to nerve damage
    • Poor circulation
    • Deformed foot
  3. You are being treated under a comprehensive diabetes care plan and need therapeutic shoes and/or inserts because of diabetes.
Medicare also requires the following:
  • A podiatrist of other qualified doctor prescribes the shoes.
  • A doctor or other qualified individual provides the shoes.
  • If you meet the conditions above, you are covered for one of the following per year:
  • One pair of depth-inlay shoes and three sets of inserts
  • One pair of customized shoes that have been molded to your foot (including inserts). These are made if you have a foot deformity and cannot wear deep-inlay shoes.
Medicare-Approved Suppliers
For Original Medicare Part B to cover your diabetic shoes, you must get them from a Medicare-approved supplier.
NOTE: If you have a Medicare Advantage Plan, check with your individual plan to see cover limits.
Take Care of Your Feet
Wearing diabetic shoes and taking good care of your feet will help prevent damage and injury to your feet. Discuss any questions you might have with your primary doctor or podiatrist.

Diabetic Foot Care Causes

Several risk factors increase a person with diabetes chances of developing foot problems and diabetic infections in the legs and feet.
  • Footwear: Poorly fitting shoes are a common cause of diabetic foot problems.
    • If the patient has red spots, sore spots, blisters, corns, calluses, or consistent pain associated with wearing shoes, new properly fitting footwear must be obtained as soon as possible.
    • If the patient has common foot abnormalities such as flat feet, bunions, or hammertoes, prescription shoes or shoe inserts may be necessary.
  • Nerve damage: People with long-standing or poorly controlled diabetes are at risk for having damage to the nerves in their feet. The medical term for this is peripheral neuropathy.
    • Because of the nerve damage, the patient may be unable to feel their feet normally. Also, they may be unable to sense the position of their feet and toes while walking and balancing. With normal nerves, a person can usually sense if their shoes are rubbing on the feet or if one part of the foot is becoming strained while walking. 
    • A person with diabetes may not properly sense minor injuries (such as cuts, scrapes, blisters), signs of abnormal wear and tear (that turn into calluses and corns), and foot strain. Normally, people can feel if there is a stone in their shoe, then remove it immediately. A person who has diabetes may not be able to perceive a stone. Its constant rubbing can easily create a sore.
  • Poor circulation: Especially when poorly controlled, diabetes can lead to accelerated hardening of the arteries or atherosclerosis. When blood flow to injured tissues is poor, healing does not occur properly.
  • Trauma to the foot: Any trauma to the foot can increase the risk for a more serious problem to develop.
  • Infections

    • Athlete's foot, a fungal infection of the skin or toenails, can lead to more serious bacterial infections and should be treated promptly.
    • Ingrown toenails should be handled right away by a foot specialist. Toenail fungus should also be treated.
  • Smoking: Smoking any form of tobacco causes damage to the small blood vessels in the feet and legs. This damage can disrupt the healing process and is a major risk factor for infections and amputations. The importance of smoking cessation cannot be overemphasized.

Diabetic Foot Care Symptoms

  • Persistent pain can be a symptom of sprain, strain, bruise, overuse, improperly fitting shoes, or underlying infection.
  • Redness can be a sign of infection, especially when surrounding a wound, or of abnormal rubbing of shoes or socks.
  • Swelling of the feet or legs can be a sign of underlying inflammation or infection, improperly fitting shoes, or poor venous circulation. Other signs of poor circulation include the following:

    • Pain in the legs or buttocks that increases with walking but improves with rest (claudication)
    • Hair no longer growing on the lower legs and feet
    • Hard shiny skin on the legs
  • Localized warmth can be a sign of infection or inflammation, perhaps from wounds that won't heal or that heal slowly.
  • Any break in the skin is serious and can result from abnormal wear and tear, injury, or infection. Calluses and corns may be a sign of chronic trauma to the foot. Toenail fungus, athlete's foot, and ingrown toenails may lead to more serious bacterial infections.
  • Drainage of pus from a wound is usually a sign of infection. Persistent bloody drainage is also a sign of a potentially serious foot problem.
  • A limp or difficulty walking can be sign of joint problems, serious infection, or improperly fitting shoes.
  • Fever or chills in association with a wound on the foot can be a sign of a limb-threatening or life-threatening infection.
  • Red streaking away from a wound or redness spreading out from a wound is a sign of a progressively worsening infection.
  • New or lasting numbness in the feet or legs can be a sign of nerve damage from diabetes, which increases a persons risk for leg and foot problems.

Diabetic Foot Care Treatment

Self-Care at Home

A person with diabetes should do the following:
  • Foot examination: Examine your feet daily and also after any trauma, no matter how minor, to your feet. Report any abnormalities to your physician. Use a water-based moisturizer every day (but not between your toes) to prevent dry skin and cracking. Wear cotton or wool socks. Avoid elastic socks and hosiery because they may impair circulation.
  • Eliminate obstacles: Move or remove any items you are likely to trip over or bump your feet on. Keep clutter on the floor picked up. Light the pathways used at night - indoors and outdoors.
  • Toenail trimming: Always cut your nails with a safety clipper, never a scissors. Cut them straight across and leave plenty of room out from the nailbed or quick. If you have difficulty with your vision or using your hands, let your doctor do it for you or train a family member how to do it safely.
  • Footwear: Wear sturdy, comfortable shoes whenever feasible to protect your feet. To be sure your shoes fit properly, see a podiatrist (foot doctor) for fitting recommendations or shop at shoe stores specializing in fitting people with diabetes. Your endocrinologist (diabetes specialist) can provide you with a referral  to a podiatrist or orthopedist who may also be an excellent resource for finding local shoe stores. If you have flat feet, bunions, or hammertoes, you may need prescription shoes or shoe inserts.
  • Exercise: Regular exercise will improve bone and joint health in your feet and legs, improve circulation to your legs, and will also help to stabilize your blood sugar levels. Consult your physician prior to beginning any exercise program.
  • Smoking: If you smoke any form of tobacco, quitting can be one of the best things you can do to prevent problems with your feet. Smoking accelerates damage to blood vessels, especially small blood vessels leading to poor circulation, which is a major risk factor for foot infections and ultimately amputations.
  • Diabetes control: Following a reasonable diet, taking your medications, checking your blood sugar regularly, exercising regularly, and maintaining good communication with your physician are essential in keeping your diabetes under control. Consistent long-term blood sugar control to near normal levels can greatly lower the risk of damage to your nerves, kidneys, eyes, and blood vessels.

Prevention

Prevention of diabetic foot problems involves a combination of factors.
  • Good diabetes control
  • Regular leg and foot self-examinations
  • Knowledge on how to recognize problems
  • Choosing proper footwear
  • Regular exercise, if able
  • Avoiding injury by keeping footpaths clear
  • Having a doctor examine the patient's feet at least once a year using a monofilament, a device made of nylon string that tests sensation

Outlook

  • Age: The older the patient, the more likely they are to have serious problems with the feet and legs. In addition to diabetes, circulatory problems and nerve damage are more common in the elderly person with diabetes. The elderly may also be more prone to sustaining minor trauma to the feet from difficulties with walking and stumbling over obstacles they cannot see.
  • Duration of diabetes: The longer the patient has had diabetes, the more likely they have developed one or more major risk factors for diabetic lower extremity problems.
  • Seriousness of infection: Infections that involve gangrene almost universally go on to amputation and also carry a high risk of death. Ulcers larger than about 1 inch across have a much higher risk of progressing on to limb amputation, even with proper treatment. Infections involving deep tissues and bone carry a much higher risk of amputation.
  • Quality of circulation: If blood flow is poor in the patient's legs as a result of damage to the blood vessels from smoking or diabetes or both, it is much more difficult to heal wounds. The likelihood of more serious infection and amputation is greater.
  • Compliance with the treatment plan: How well the patient follows and participates in the treatment plan developed with doctors and nurses is crucial to the best recovery possible. Ask questions if any aspects of the care or treatment plan are unclear. Let the doctor know if something in the plan doesn't seem to be working.
  • Wound care centers: A wound care center is an excellent resource if available. It brings together many specialists and approaches to aid in the treatment of the diabetic foot problem. These centers will often be able to offer the most up-to-date therapies and even may have experimental protocols available for people who have not responded to traditional therapy.
  • Individual physician and nurse skills: Ask about your doctor or nurse's expertise in dealing with diabetic lower extremity problems. Knowledge about and experience with these problems may lead to earlier diagnosis and more appropriate therapy.

Diabetic Shoes

Due to the fact that diabetes can cause circulation problems and nerve damage, as well as other conditions that can affect the feet, some people with diabetes will want special diabetic shoes or orthotics created especially for their condition.
The foot is especially affected by diabetes because:
  • diabetes damages the nerves (damage can occur to the foot and not be detected) - this is called peripheral neuropathy.
  • diabetes also affect the circulation. Poor circulation can affect the ability of the body to heal when damage occurs.
  • those with diabetes are more prone to infection - the body's processes that normally fight infection respond slower and often have trouble getting to infections due to the poor circulation.
  • diabetes can also affect the joints, making them stiffer
  • other diabetes complications that can also affect the foot, for example, kidney disease (affects proteins that are involved in wound healing) and eye disease (can't see the foot to check for damage).
As a consequence of these factors a number of things can go wrong:
  • the foot may get damaged and you do not know about (for example, your shoe rubs a sore onto a toe that gets infected - you can not feel it because of the peripheral neuropathy - you can not heal very well due to the infection and poor circulation).
  • foot ulcer are common (see below)
  • infections can spread
  • the ultimate of this process is an amputation. Diabetes is the main cause of amputations.
  • Charcot's joints is another complication of diabetes in the foot, especially if peripheral neuropathy is present - the neuropathy cause a numbness (imagine spraining your ankle and not knowing you have done this. You will continue to walk on it - imagine the damage that this would do. 
The Do's and Don'ts of Foot Care
If you have diabetes, there are a lot of things you need to do to prevent the problems from developing in your foot:
1) Wash your feet daily (use a mild soap and lukewarm water). Dry very carefully, especially between the toes. It often helps to use talcum powder to dust the foot to further reduce moisture, however be certain to remove all the powder after dusting, as it should not leave a residue between the toes. If the skin is dry, use a good emollient - BUT, not between the toes).

2) Inspect your foot daily (check sores, cuts, bruises, changes to the toenails; use a mirror to look under the foot if you can not see it).

3) Look after your health (loose weight; stop smoking; exercise; reduce your alcohol consumption)

4) Look after your feet:
  • cut toenails straight across and never cut into the corners; use an emery board or file on sharp corners.
  • do not try to remove corns and callus yourself - see a Podiatrist for this; NEVER use commercial corn cures - this is so important in those with diabetes as it is so easy to damage the skin.
  • avoid going barefoot, even in your own home (this lessens the chance of some accidental damage)
5) Fitting of footwear is very important. Poorly fitted shoes are a common cause of problems in the foot of those with diabetes. Some advice:
  • get your feet measured each time you buy new shoes (foot size and shape change over time).
  • make sure the shoe fitter is experienced.
  • new shoes should be comfortable when purchased and should not need a "break-in" period.
  • they should fit both the length and width of the foot, with plenty of room for the toes.
  • avoid shoes with high heels, pointed toes or tight around the toes (these put too much pressure on parts of the foot and can contribute to ulcers)
6) See a Podiatrist, at least annually.
  • Podiatrists have an extremely important role to play in the prevention and management of complications of the foot in those with diabetes. All those who are at risk for a problem should have that risk status assessed at least annually (more if the risk is greater).
  • The Podiatrist should communicate this risk status to other members of the health care team. Advice should be given on how to reduce the chance of damage happening, what to do to prevent it and what to do if something does go wrong.
  • Regular foot care from a Podiatrist is a key way to prevent problems from developing in those who are at risk.
  • When something does go wrong, see a Podiatrist immediately. Waiting a "few days to see what happens" before seeing someone may be the difference between a good and poor outcome. The sooner treatment is started the better.
Note: For more information about foot care, and neuropathy, get the  Nerve Health & Neuropathy  ebook. If you need diabetic shoes, contact our office for a referral.

Amputation                                                                   

High blood glucose levels are responsible for the biological  processes that impair the neurological, vascular, and immune systems, leading to damaged nerves, damaged blood vessels and a weakened immune system. Damaged nerves and blood vessels lead to circulatory problems in the feet and legs, which leads to sores, ulcers and deformed feet. A compromised circulatory system fails to bring enough fresh oxygenated blood, nutrients, and antibiotics to a traumatic wound, and the (weakened) immune system cannot resolve an infection by fighting bacteria and cleansing the wound site on a cellular level.
More than 80% of diabetics will develop one or more of the major diabetic complications (amputation, blindness, kidney failure, heart attack, or stroke) -- if they live long enough and fail to change their diet and lifestyle while relying solely on diabetic medications. Approximately 67% of people with diabetes will develop a mild to severe form of nervous system damage, which can lead to a toe, foot or lower leg amputation. Worldwide, there are more than 1 million amputation procedures performed each year, at the rate of one every 30 seconds.
The most common reason for an amputation is poor circulation. The lack of circulation is caused by narrowing of the arteries or damage to the arteries from diseases such as diabetes and atherosclerosis. When the blood vessels become damaged and the blood flow is impaired to the extremities, the tissue starts to die and may become infected.
Another reason for an amputation is the damage to the foot’s sensory nerves due to diabetic neuropathy. This contributes to foot deformities and/or ulcers that increase the chance of lower-extremity amputations unless treated.
Factors that predict the need for lower extremity amputation in patients with extremity ischemia include tissue loss, end-stage renal disease, poor functional status and diabetes mellitus. Patients with diabetes have a  10-fold increased risk for lower extremity amputation compared with those who do not have diabetes.
Foot ulcers and nerve disease caused by Type 2 diabetes is the leading cause of amputation of feet, toes, legs, hands and arms among diabetes sufferers. Collectively, the disorders which cause these amputations are called Diabetic Neuropathies. Neuropathies lead to numbness and sometimes pain and weakness in the hands, arms, feet, and legs. Problems may also occur in other areas of the body, including the digestive tract, heart, and sex organs. However, complications with the feet and legs are more common.
Treatments for leg and foot ulcers vary depending on the severity of the wound. In general, the treatment employs methods to remove dead tissues or debris, keep the wound clean, and promote healing. But, if the diabetic fails to change their eating habits and lifestyle, healing will either occur very slowly or will not occur at all.
When the condition results in a severe loss of tissue or a life-threatening infection, an amputation is usually the only option. Unfortunately, when a doctor identifies the need for a (diabetic) amputation because the toe (or leg) is "dead", there is very little that the patient can do -- especially, if there is an infection that could spread leading to further damage and possible death.
For a foot or toe to be considered dead, the blood supply must be so completely impeded that infarction and necrosis (dead tissue) develop. Infarction results in dry gangrene, with nonviable tissue becoming dry and black in color (because of the presence of iron sulfide, a product of the hemoglobin released by lysed erythrocytes).
The method of toe amputation (disarticulation versus osteotomy) and the level of amputation (partial or whole phalanx versus whole digit versus ray) depend on numerous circumstances but are mainly determined by the extent of disease and the anatomy.
A surgeon removes the damaged tissue and preserves as much healthy tissue as possible. After surgery, the patient will be monitored in the hospital for a number of days. It may take four to eight weeks for the wound to heal completely.

Note: For more information about diabetic amputations, read the Death to Diabetes blog posts about amputation and prevention.

What if amputation is the only option?

Treatments for foot ulcers vary depending on the severity of the wound. In general, the treatment employs methods to remove dead tissues or debris, keep the wound clean, and promote healing. When the condition results in a severe loss of tissue or a life-threatening infection, an amputation may be the only option.
A surgeon removes the damaged tissue and preserves as much healthy tissue as possible. After surgery, you'll be monitored in the hospital for a number of days. It may take four to eight weeks for your wound to heal completely.
In addition to your primary care doctor and surgeon, other medical professionals involved in your treatment plan may include:
  • Endocrinologist, a physician who specializes in the treatment of diabetes or other hormone-related disorders
  • Physical therapist, who will help you regain strength, balance and coordination and teach you how to use an artificial (prosthetic) limb, wheelchair or other devices to improve your mobility
  • Occupational therapist, who specializes in therapy to improve everyday skills and to use adaptive products that help with everyday activities
  • Mental health provider, such as a psychologist or psychiatrist, who can help you address your own feelings or expectations related to the amputation or to cope with the reaction of other people
  • Social worker, who can assist with accessing services and planning for changes in care
Even after amputation, it's important to follow your diabetes treatment plan -- especially if you don't want to lose the other foot!. Eating healthy foods, exercising regularly, controlling your blood sugar level and avoiding tobacco can help you prevent additional diabetes complications.

Note: Refer to the Death to Diabetes Blog for more information about amputations.


Health Problems Associated with Neuropathy         

Damage to Autonomic Nervous System & Brain

After a period of years, diabetes can damage the nerves of the autonomic nervous system, and eventually, even affect the nerve cells of the brain. Damage to the autonomic nervous system causes one or more of the following:
  • Difficulty in feeling the symptoms of hypoglycemia (low blood sugar).
  • Gastroparesis due to damage to the autonomic nerves that go to the stomach, intestines, and other parts of the digestive system, making food pass through the digestive system too slowly or too quickly. This may also cause nausea, vomiting, constipation, or diarrhea.
  • Erectile dysfunction or impotence due to the damage to the autonomic nerves going to the man’s penis nerves.
  • Prevention of a woman’s vagina from getting wet when she wants to have sex or having less feeling around her vagina.
  • A faster beating of the heart or the heart beating at different speeds.
  • Difficulty in knowing when to go to the bathroom due to damage to the autonomic nerves that go to the bladder. The damage can also make it hard to feel when your bladder is empty. Both problems can cause you to hold urine for too long, which can lead to bladder infections.
  • Slow movement of your blood to keep your blood pressure steady when you change position due to damage to the autonomic nerves going to the blood vessels that keep your blood pressure steady. When you go from lying down to standing up or when you exercise a lot, the sudden changes in blood pressure can make you dizzy.
  • Double vision due to damage to the autonomic nerves going to the cranial nerves that control the eye muscles. Damage to these nerves usually happens in one eye. This problem happens all of a sudden and usually lasts for a short time.
  • A side of the face hangs lower or sags due to damage to the autonomic nerves going to the cranial nerves that control the sides of the face. Damage to these nerves usually happens on only one side of the face. This nerve damage causes that side of the face to hang lower or sag. Usually the lower eyelid and lips sag. This problem, which is called Bell’s palsy, happens all of a sudden and tends to correct itself most of the time.
Diagnosis & TestsThe diagnosis of diabetic neuropathy is made on the basis of symptoms and a physical exam. During the exam, the doctor may check blood pressure and heart rate, muscle strength, reflexes, and sensitivity to position, vibration, temperature, or a light touch.

The doctor may also perform other tests to help determine the type and extent of nerve damage including a foot exam, nerve conduction test, electromyography test, sensory testing, heart rate variability check, ultrasound, and a nerve or skin biopsy.

A comprehensive foot exam assesses skin, circulation, and sensation. The test can be done during a routine office visit. To assess protective sensation or feeling in the foot, a nylon monofilament (similar to a bristle on a hairbrush) attached to a wand is used to touch the foot. Those who cannot sense pressure from the monofilament have lost protective sensation and are at risk for developing foot sores that may not heal properly. Other tests include checking reflexes and assessing vibration perception, which is more sensitive than touch pressure.

A nerve conduction test checks the transmission of electrical current through a nerve. With this test, an image of the nerve conducting an electrical signal is projected onto a screen. Nerve impulses that seem slower or weaker than usual indicate possible damage. This test allows the doctor to assess the condition of all the nerves in the arms and legs.

An electromyography (EMG) test shows how well muscles respond to electrical signals transmitted by nearby nerves. The electrical activity of the muscle is displayed on a screen. A response that is slower or weaker than usual suggests damage to the nerve or muscle. This test is often done at the same time as nerve conduction tests.

An ultrasound test uses sound waves to produce an image of internal organs. An ultrasound of the bladder and other parts of the urinary tract, for example, can show how these organs preserve a normal structure and whether the bladder empties completely after urination.

Brain DamageCurrent research indicates a connection between diabetes and Alzheimer’s disease. Since diabetes damages the nerves of the peripheral and autonomic nervous systems, it would follow that, eventually, it would affect the nerve cells of the brain itself.

The average human brain, which weighs about 3 pounds, is comprised of billions of neurons (brain cells), water, and phospholipids, namely arachidonic acid and docosahexaenoic acid. The brain produces electrical signals, which, together with chemical reactions, lets the parts of the body communicate.
Although the brain is only 2% of the body’s weight, it uses 20% of the oxygen supply, more than 50% of the glucose, and gets 20% of the blood flow. Blood vessels (arteries, capillaries, veins) supply the brain with oxygen and nourishment, and take away waste. More subtly, the blood-brain barrier protects the brain from chemical intrusion from the rest of the body. Blood flowing into the brain is filtered so that many harmful chemicals cannot enter the brain.

When a part of the brain (e.g. brain cells, blood vessels, neuro-transmitters) becomes damaged due to a combination of consistently high blood glucose levels and other factors, after a period of years, a diabetic may develop Alzheimer’s or some other brain-related ailment. These other factors may include exposure to aluminum (e.g. sodas, aluminum utensils) and other chemicals and toxins that have gradually built up in the body, and some accumulating in the brain.
This can lead to a formation of a sticky plaque that inhibits the transmission of brain signals. This decrease in signal transmission causes atrophy and death of the brain cells, which leads to further decreased signal transmission, and decreased neural transmission, which leads to further deterioration of the brain’s function. This decrease in brain function may be exhibited in many ways, including a significant increase in memory loss, e.g. confusion, forgetfulness, or a major change in behavioral and personality such as unprovoked anger or loss of social skills.

Note: Neurotransmitters are small molecules whose function is to transmit nerve signals (impulses) from one nerve cell to another. Neurotransmitters are chemical messengers that neurons use to tell other neurons that they have received an impulse. There are many different neurotransmitters - some trigger the receiving neuron to send an impulse and some stop it from doing so.
Neurotransmitters include: acetylcholine, serotonin, histamine, glutamate, gamma aminobutyric acid glycine, aspartate, histamine, norepinephrine, epinephrine (adrenalin), endorphins, dopamine, adenosine triphosphate (ATP), and nitric oxide.

Because of the amount of time that it may take for the brain to begin deterioration, the diabetic will experience problems with one or more of the other organs long before a disease like Alzheimer’s settles in. Consequently, there is time to nourish, protect, and exercise the brain to prevent these types of complications.
    Leg Ulcers
    Ulcers are wounds or open sores that will not heal or keep returning.
    Ulcers may or may not be painful. The patient generally has a swollen leg and may feel burning or itching. There may also be a rash, redness, brown discoloration or dry, scaly skin. 

    Warning! Ulcers should not be ignored! See your doctor immediately! Untreated ulcers can eventually lead to gangrene and leg or foot amputation! Have your doctor review your blood test results to determine the root cause of your ulcer. Unfortunately, some doctors only treat the ulcer externally with salves and with drugs such as antibiotics and steroids.
    The wounds, in the context of diabetes, are notoriously difficult to resolve. Healing resistance is thus a well-recognized element of frustration in their clinical care.
    In most of the above conditions, multiple factors play into healing resistance. Among them are circulatory impairments, neurological deficits, tissue injury, and immunological compromise. A central factor is the proliferation of infectious microorganisms that, by the variety of their families, their toxin-producing capacities, and their resistance to antibiotics, offer daunting obstacles to standard treatment regimens.Diabetic Leg Ulcer
    Approximately 15% of the estimated 24 million Americans afflicted with diabetes mellitus develop lower leg skin ulcers and foot ulcers. Of those patients, 20% will eventually require amputations. Diabetes mellitus is the leading cause of nont-raumatic lower extremity amputation in the United States (LeRoith 2003).
    In addition, people with pre-diabetes who develop lower leg/foot ulcers are also in danger of facing amputation. Why? Because they assume that just because they have not been diagnosed as a diabetic, they underestimate the danger of the leg ulcers!
    Factors contributing to skin lesions in diabetes:
    Circulatory impairment
    Arteries and arterioles in chronic diabetes are prone to plaque buildup (Tesfaye 2005). The precise reason for this phenomenon is still elusive, yet it is well documented that Type II non-insulin dependent diabetes is linked to abnormal blood lipid profiles known as diabetic dyslipidemia (Goldberg 2004). Low-density lipoproteins particles are smaller in size and thus more apt to adhere to vessel walls, resulting in progressive vascular occlusion (Beckman 2002; Renard 2004). Lowered oxygen and nutrient supplies stress tissue resilience and impair recovery from injury (Chapnick 1996).
    Neuropathy
    Poorly controlled diabetes is correlated with peripheral nerve dysfunction. The mechanisms of diabetic injury to neurons are poorly understood. Higher blood glucose level seem to promote oxidative stress in neurons, but much more complex mechanisms are implicated (Tomlinson 2002).Diabetic neuropathy can involve motor, sensory, and autonomic system neurons. Sensory neuron malfunction is translated as loss of feeling, reflex loss, problems with limb position sense, tingling (paresthesias) and pain. 
    Motor impairment shows as muscle weakness. Autonomic neuropathy alters local circulation (Boulton 2004, Bensal 2006).
    Mechanical stress
    Chronic and repeating pressure on the skin compresses dermal arterioles, inhibiting tissue perfusion. Tissue weakness leads to ulceration. Ulcers are fertile ground for pathogenic microorganisms, and surrounding tissues become prone to cellulitis. At times, the ulcer crater reaches the underlying bone, initiating osteomyelitis (Boulton 2000). 
    The good news is that diabetic ulcers can be prevented and treated by following a superior nutritional program such as the Death to Diabetes wellness program.
    Types of Leg and Foot Ulcers
    The three most common types of leg and foot ulcers include:
    • Venous stasis ulcers
    • Arterial (ischemic ulcers)
    • Neurotrophic (diabetic)
    Ulcers are typically defined by the appearance of the ulcer, the ulcer location, and the way the borders and surrounding skin of the ulcer look.
    1. Venous stasis ulcers
    Venous ulcers are located below the knee and are primarily found on the inner part of the leg, just above the ankle.
    The base of a venous ulcer is usually red. It may also be covered with yellow fibrous tissue or there may be a green or yellow discharge if the ulcer is infected. Fluid drainage can be significant with this type of ulcer.
    The borders of a venous ulcer are usually irregularly shaped and the surrounding skin is often discolored and swollen. It may even feel warm or hot. The skin may appear shiny and tight, depending on the amount of edema (swelling).
    Venous stasis ulcers are common in patients who have a history of leg swelling, varicose veins, or a history of blood clots in either the superficial or the deep veins of the legs. Ulcers may affect one or both legs.
    Venous ulcers affect 500,000 to 600,000 people in the United States every year and account for 80 to 90% of all leg ulcers.
    2. Arterial (ischemic)
    Arterial ulcers are usually located on the feet and often occur on the heels, tips of toes, between the toes where the toes rub against one another or anywhere the bones may protrude and rub against bed sheets, socks or shoes. Arterial ulcers also occur commonly in the nail bed if the toenail cuts into the skin or if the patient has had recent aggressive toe nail trimming or an ingrown toenail removed.
    The base of an arterial or ischemic ulcer usually does not bleed. It has a yellow, brown, grey, or black color. The borders and surrounding skin usually appear as though they have been punched out. If irritation or infection are present, there may or may not be swelling and redness around the ulcer base. There may also be redness on the entire foot when the leg is dangled; this redness often turns to a pale white/yellow color when the leg is elevated.
    Arterial ulcers are typically very painful, especially at night. The patient may instinctively dangle his/her foot over the side of the bed to get pain relief. The patient usually has prior knowledge of poor circulation in the legs and may have an accompanying disorder, such as those listed in the section, "What causes leg ulcers?"
    3. Neurotrophic (diabetic)
    Neurotrophic ulcers are usually located at increased pressure points on the bottom of the feet. However, neurotrophic ulcers related to trauma can occur anywhere on the foot. They occur primarily in people with diabetes, although they can affect anyone who has an impaired sensation of the feet.
    The base of the ulcer is variable, depending on the patient's circulation. It may appear pink/red or brown/black. The borders of the ulcer are punched out, while the surrounding skin is often calloused.
    Neuropathy and peripheral artery disease often occur together in people who have diabetes. Nerve damage (neuropathy) in the feet can result in a loss of foot sensation and changes in the sweat-producing glands, increasing the risk of being unaware of foot calluses or cracks, injury or risk of infection. Symptoms of neuropathy include tingling, numbness, burning or pain.
    It is easy to understand why people with diabetes are more prone to foot ulcers than other patients. This is why people with diabetes need to inspect their feet and their shoes daily and wear appropriate footwear. People with diabetes should never walk barefoot.
    What causes leg ulcers?
    Leg ulcers may be caused by medical conditions such as:
    • Poor circulation, often caused by arteriosclerosis
    • Venous insufficiency (a failure of the valves in the veins of the leg that causes congestion and slowing of blood circulation in the veins)
    • Other disorders of clotting and circulation that may or may not be related to atherosclerosis
    • Diabetes
    • Renal (kidney) failure
    • Hypertension (treated or untreated)
    • Lymphedema (a buildup of fluid that causes swelling in the legs or feet)
    • Inflammatory diseases including vasculitis, lupus, scleroderma or other rheumatological conditions
    • Other medical conditions such as high cholesterol, heart disease, high blood pressure, sickle cell anemia, bowel disorders
    • History of smoking (either current or past)
    • Pressure caused by lying in one position for too long
    • Genetics (ulcers may be hereditary)
    • A malignancy (tumor or cancerous mass)
    • Infections
    • Certain medications
    How are leg ulcers diagnosed?
    First, the patient's medical history is evaluated. A wound specialist will examine the wound thoroughly and may perform tests such as X-rays, MRIs, CT scans and noninvasive vascular studies to help develop a treatment plan.
    How are leg ulcers treated?
    At the Cleveland Clinic, patients are treated by a team of world-class experts in the Lower Extremity Wound Clinic in the Tomsich Family Department of Cardiovascular Medicine. This Clinic includes doctors, nurses and other medical specialists. These experts work together to determine the cause of the problem and develop an individualized treatment program.
    The goals of treatment are to relieve pain, speed recovery and heal the wound. Each patient's treatment plan is individualized, based on the patient's health, medical condition and ability to care for the wound.
    Treatment options for all ulcers may include:
    • Antibiotics, if an infection is present
    • Anti-platelet or anti-clotting medications to prevent a blood clot
    • Topical wound care therapies
    • Compression garments
    • Prosthetics or orthotics, available to restore or enhance normal lifestyle function
    Venous ulcers are treated with compression of the leg to minimize edema or swelling. Compression treatments include wearing compression stockings, multilayered compression wraps, or wrapping an ACE bandage or dressing from the toes or foot to the area below the knee. The type of compression treatment prescribed is determined by the physician, based on the characteristics of the ulcer base and amount of drainage from the ulcer.
    The type of dressing prescribed for ulcers is determined by the type of ulcer and the appearance at the base of the ulcer. Types of dressings include:
    • Moist to moist dressings
    • Hydrogels/hydrocolloids
    • Alginate dressings
    • Collagen wound dressings
    • Debriding agents
    • Antimicrobial dressings
    • Composite dressings
    • Synthetic skin substitutes
    Arterial ulcer treatments vary, depending on the severity of the arterial disease. Non-invasive vascular tests provide the physician with the diagnostic tools to assess the potential for wound healing. Depending on the patient's condition, the physician may recommend invasive testing, endovascular therapy or bypass surgery to restore circulation to the affected leg.
    The goals for arterial ulcer treatment include:
    • Providing adequate protection of the surface of the skin
    • Preventing new ulcers
    • Removing contact irritation to the existing ulcer
    • Monitoring signs and symptoms of infection that may involve the soft tissues or bone
    Treatment for neurotrophic ulcers includes avoiding pressure and weight-bearing on the affected leg. Regular debridement (the removal of infected tissue) is usually necessary before a neurotrophic ulcer can heal. Frequently, special shoes or orthotic devices must be worn.
    Wound care at home
    Patients are given instructions to care for their wounds at home. These instructions include:
    • Keeping the wound clean
    • Changing the dressing as directed
    • Taking prescribed medications as directed
    • Drinking plenty of fluids
    • Keeping blood glucose levels in the normal range by following a wellness program such as the Death to Diabetes program (get the Death to Diabetes book)
    • Following a healthy diet, such as the Death to Diabetes plant-based diet, including eating plenty of vegetables and fruits; and, get the Power of Juicing ebook
    • Avoidance of alcohol, tobacco, drugs
    • Avoidance of processed foods, trans fats, flour, sugar, most grains, etc.
    • Exercising regularly, as directed by a physician
    • Wearing appropriate shoes
    • Wearing compression wraps, if appropriate, as directed
    The treatment of all ulcers begins with careful skin and foot care, and a proper diet.
    Foot and skin care guidelines
    Inspecting your skin and feet is very important, especially for people with diabetes. Detecting and treating foot and skin sores early can help you prevent infection and prevent the sore from getting worse.
    Here are some guidelines:
    • Gently wash the affected area on your leg and your feet every day with mild soap (Ivory Snow or Dreft) and lukewarm water. Washing helps loosen and remove dead skin and other debris or drainage from the ulcer. Gently and thoroughly dry your skin and feet, including between the toes. Do not rub your skin or area between the toes.
    • Every day, examine your legs as well as the tops and bottoms of your feet and the areas between your toes. Look for any blisters, cuts, cracks, scratches or other sores. Also check for redness, increased warmth, ingrown toenails, corns and calluses. Use a mirror to view the leg or foot if necessary, or have a family member look at the area for you.
    • Once or twice a day, apply a lanolin-based cream to your legs and soles and top of your feet to prevent dry skin and cracking. Do not apply lotion between your toes or on areas where there is an open sore or cut. If the skin is extremely dry, use the moisturizing cream more often.
    • Care for your toenails regularly. Cut your toenails after bathing, when they are soft. Cut toenails straight across and smooth with an emery board.
    • Do not self-treat corns, calluses or other foot problems. Go to a podiatrist to treat these conditions.
    • Don't wait to treat a minor foot or skin problem. Follow your doctor's guidelines.
    How can ulcers be prevented?
    Controlling risk factors can help you prevent ulcers from developing or getting worse. Here are some ways to reduce your risk factors:
    • Quit smoking
    • Manage your blood pressure
    • Control your blood cholesterol and triglyceride levels by making dietary changes and avoid taking medications if possible
    • Limit your intake of sodium
    • Manage your diabetes and other health conditions, if applicable
    • Exercise - start a walking program after speaking with your doctor
    • Lose weight if you are overweight
    • Ask your doctor about aspirin therapy to prevent blood clots
    • Follow a wellness program like the Death to Diabetes program
    Foot Ulcers
    Diabetic foot complications are the most common cause of nontraumatic lower extremity amputations in the industrialized world. The risk of lower extremity amputation is 15 to 46 times higher in diabetics than in persons who do not have diabetes mellitus. Furthermore, foot complications are the most frequent reason for hospitalization in patients with diabetes, accounting for up to 25 percent of all diabetic admissions in the United States and Great Britain.Diabetic Foot Ulcer

    The vast majority of diabetic foot complications resulting in amputation begin with the formation of skin ulcers. Early detection and appropriate treatment of these ulcers may prevent up to 85 percent of amputations. 

    Indeed, one of the disease prevention objectives outlined in the "Healthy People 2000" project of the U.S. Department of Health and Human Services is a 40 percent reduction in the amputation rate for diabetic patients. Family physicians have an integral role in ensuring that patients with diabetes receive early and optimal care for skin ulcers.

    Unfortunately, several studies have found that primary care physicians infrequently perform foot examinations in diabetic patients during routine office visits. The feet of hospitalized diabetics may also be inadequately evaluated.

    Careful inspection of the diabetic foot on a regular basis is one of the easiest, least expensive and most effective measures for preventing foot complications. Appropriate care of the diabetic foot requires recognition of the most common risk factors for limb loss. Many of these risk factors can be identified based on specific aspects of the history and a brief but systematic examination of the foot.

    Ulceration
    Despite the best intentions and careful attention to foot care, many diabetic patients eventually develop foot ulcers. These wounds are the principal portal of entry for infection in patients with diabetes. Frequently, the ulcers are covered by callus or fibrotic tissue. This makes the trimming of hyperkeratotic tissue important for comprehensive wound evaluation.

    Because these ulcers almost always form in patients with neuropathy, they are typically painless. Even in the presence of severe infection, many patients have few subjective complaints and are often more concerned with soiled footwear and stockings than with the penetrating wound.

    Adequate debridement is the first step in the evaluation of a foot ulcer. Debridement should remove all necrotic tissue and surrounding callus until a healthy bleeding edge is revealed. Patients (and physicians) often underestimate the need for debridement and may be surprised by the appearance of the newly debrided ulcer. Topical debriding enzymes are expensive and have not been conclusively shown to be beneficial.

    After debridement, the ulcer should be probed with a sterile blunt instrument to determine the involvement of underlying structures, such as tendon, joint capsule or bone. Probing to bone is a simple and specific test for osteomyelitis, but it has low sensitivity. Plain-film radiographs should be obtained to look for soft tissue gas and foreign bodies and to evaluate the ulcer for bone involvement.

    Recognition of risk factors, preventive foot maintenance and regular foot examinations are essential in preventing foot ulcers in patients with diabetes. When foot ulcers develop despite preventive measures, a systematically applied regimen of diagnosis and classification, coupled with early and appropriate treatment, should help to reduce the tremendous personal and societal burden of diabetes-related amputations.

    Nutritional Program for Good Nerve Health               

    To support good nerve health and prevent further damage, patients should adhere to a sound nutritional and wellness program that includes the following:
    • Following a comprehensive diabetes management program such as theDeath to Diabetes 6-Stage Wellness Program that keeps blood glucose levels in the normal range (refer to the Death to Diabetes book)
    • Following a healthy plant-based diet, eating plenty of vegetables and some fruits, i.e. the Death to Diabetes diet
    • Drinking raw vegetable juices (refer to the Power of Juicing ebook)
    • Drinking plenty of fluids, especially filtered water 
    • Taking wholefood nutritional supplements, with a focus on B-complex vitamins, especially B1, B6, B12 to help nerve regeneration; plus supplements such as alpha lipoic acid, evening primrose oil, turmeric, gingko, Omega-3 EFAs.
    • Avoidance of alcohol, tobacco, drugs
    • Avoidance of processed foods, flour, sugar, pork, excess animal meat
    • Exercising regularly, as directed by a physician
    • Note: Acupuncture can help relieve the pain of peripheral neuropathy. Additionally, a practitioner of Chinese medicine can provide you with herbs that may speed recovery. 
    • Note: Reflexology for neuropathy of the legs, feet and toes may help. If a toxic exposure is the cause, time is your greatest ally - injured nerves will slowly recover, as long as the exposure has stopped.

    Nerve Cell Regeneration                                             

    It is known that injured neurons in the central nervous system (CNS) do notregenerate, but it is not clear why. Adult CNS neurons may lack an intrinsic capacity for rapid regeneration, and CNS glia create an inhibitory environment for growth after injury. However, neurons of the peripheral nervous system (PNS) can regenerate provided that the nerves have not been completely destroyed.
    Current strategies being investigated and studied for nerve cell regeneration (or neurogeneration) include autografting, stem cells, and nanotechnology. But, unfortunately, progress in any of these areas has been very slow.
    Studies show that usually, when the gap between the severed nerve endings is larger than a few millimeters, the nerve does not regenerate on its own. If left untreated, the end result is permanent sensory and motor paralysis. A few hundred thousand people suffer from this debilitating condition annually in the U.S.

    However, if the nerve cell damage (to the myelin) associated with the PNS due to biochemical problems instead of physical problems with the CNS, there may be hope for nerve cell regeneration, i.e. diabetics with diabetic neuropathy.

    Note: Myelin is a lipoprotein that is found in the body of vertebrates and which covers the stem of the neurons or nerve cells, so its function is being the transmission and routing of electrical nerve impulses or send and receive messages of any kind to the body. 
    When myelin is lost or damaged, nerve impulses are slowed down (slows down the process of the nervous system) or fail to be transmitted, can cause a short circuit in the conduction of nerve impulses that can cause nervous system dysfunction creating sensory deficits as blurred vision, poor coordination and identification of handedness, difficulty walking, go to the bathroom very often (due to insufficient control of sphincters), paralysis, etc.

    When problems arise in nerves of the PNS, neuropathy might result, and when injury affects the nerves of the CNS, multiple sclerosis is often diagnosed.
    Multiple sclerosis (MS) is the more common example of a demyelinating disease.  This disease attacks the central nervous system and myelin generating phases of remission (or shoots), and whose symptoms include any combination of partial blindness (blurring or gray vision), spastic paraparesis, unsteady gait, dizziness, diplopia, and incontinence.
    To care, prevent and heal the smooth transmission and conduction of the nervous system, it is essential that myelin gets produced properly, and for this, is essential to maintain a plant-based diet with those nutrients required for good production and regeneration.

    Foods that Damage the Myelin and Nervous System

    Processed foods, Dental fillings: Reduce chemical and heavy metal toxins in your body. Lower the amount of mercury in the body from seafood sources as well as dental fillings. Limit your exposure to x-rays, insecticides and organic solvents. Detox on a regular basis.

    HFCS, Refined sugar, Refined flour: Avoid HFCS, aspartame, etc. at all cost -- these chemicals are some of the strongest irritants of the nervous system. They deteriorate and eventually produce a host of health conditions. Do all your effort to avoid sodas, pastries and sweets, breads, gluten, ketchup, fast foods, and other processed foods. 

    Trans fats
    , Saturated animal fats: Avoid at all costs partially hydrogenated oils (trans fats), fried foods, fried sausages; and, reduce red meat, cow's milk and derivatives.

    Foods and Vitamins that Nourish and Repair the Myelin

    Nerve damage occurs when the myelin sheath that covers and protects nerves---much like the rubber encasing surrounding electrical wires---deteriorates. The nerves misfire, triggering other nerve cells, which in turn contribute to further excessive nerve cell activity.

    Nerve foods that actually repair and feed the nervous system are non-active yeast flakes, spirulina, essential fatty acids, whole-grains, particularly organic oats and wheat germs, which are very rich in Vitamin B. Vitamin B is vital because the immune system 'eats up' the acetycholine receptors which are neurotransmitters and the B vitamins are able to remake them.

    Spirulina and non-active yeast flakes enter the bloodstream very quickly and need little to no digestion. Soya foods naturally containing lecithin, which is an excellent nerve building food, will also help.

    Celery, courgettes, avocados, lettuce, carrots, and pumpkin are supreme nerve foods and can be juiced, steamed or used raw in salads. Almonds and sesame seeds are rich in calcium and will feed the nervous system. Herbs and spices such as mint, rose petals, marjoram, rosemary, basil and aniseed will also help.

    Vitamin B12 foods can help heal damaged nerves. Foods with vitamin B12 contribute to the repair and maintenance of nerve cells, and particularly the myelin sheath. Foods that contain high levels of vitamin B12 include calf's liver, sardines, snapper, venison, Chinook salmon, lean beef tenderloin, lamb loin, scallops, shrimp and halibut.

    Antioxidant Foods
    Nerve damage occurs when atoms, often called free radicals, interact with cell tissues and cause deterioration of the cells. Free radicals that are synthesized from oxygen are especially egregious. They not only interact with cells tissues, but also create more radicals. Antioxidants are compounds that neutralize free radicals. Various "superfoods" contain high levels of antioxidants. These foods not only heal damaged nerves, but also may help reduce the risk of cancer and immune diseases, and slow the effects of aging. Foods that contain high levels of antioxidants include blueberries, raspberries, blackberries, tomatoes, broccoli, red grapes, garlic, spinach, carrots, pomegranates, dark chocolate and green tea, according to Clemson University Cooperative Extension, located in Clemson, South Carolina.

    Anti-Inflammatory Foods
    Inflammation results when the body's immune system attempts to protect itself against invading foreign organisms such as bacteria and viruses. White blood cells and other chemicals attack the invaders and destroy them. Sometimes, however, the body's immune response is misguided, and the immune system attacks and destroys its own tissues. Inflammation causes damage to nerves and causes pain to you. Certain foods reduce inflammation. Foods high in omega-3 fatty acids have anti-inflammatory properties. High omega-3 foods include flaxseeds, walnuts, soybeans, shrimp and tofu as well as coldwater fish such as snapper, sardines, salmon, trout, halibut, tuna and cod.

    Vitamins & Minerals
    The most important nutrients for nerve cell growth and regeneration are: vitamins B6, B12, calcium, magnesium, alpha lipoic acid and acetyl-L-carnitine.  Gentle massage, yoga, mineral salt baths, and acupuncture are other modalities that might help. Remember, the nervous system takes the longest of any system to heal so patience is very important.

    Acetyl-l-Carnitine: 
    In a study published in 2004 in the journal Diabetes Care conducted by A.F. Sima, MD, PhD, Menotti Calvani, MD, Munish Mehra, PhD and Antonino Amato, MD from the Department of Pathology at Wayne State University School of Medicine, it was found that Acetyl-l-Carnitine supplementation helps reduce pain associated with nerve regeneration in diabetic patients. The group of researchers found that after taking Acetyl-l-Carnitine, patients illustrated an improvement in fiber cluster regeneration, and there was significant pain reduction in those individuals taking more than 1000 milligrams of Acetyl-l-Carnitine daily. Acetyl-l-Carnitine can be consumed in capsule form by taking 1 to 4 588 milligram capsules daily with or without food.
    Alpha lipoic acid (ALA): ALA is an organic molecule produced by the body, and it is soluble in both fat and water. It occurs in all cells, and plays a role in the metabolism of glucose. Alpha-lipoic acid also serves as an antioxidant that can work to neutralize harmful free radicals throughout the body, according to the University of Maryland Medical Center. Its antioxidant activity may be responsible for its ability to alleviate the tingling, burning and numbness in people who have experienced the nerve damage associated with peripheral neuropathy.
    Intravenous Treatment with ALA: In the February 2004 issue of "Diabetic Medicine," researchers describe their meta-analysis of clinical data on the intravenous treatment of diabetic neuropathy with alpha-lipoic acid. Their analysis indicates that a treatment regimen consisting of an intravenous dose of 600 mg of alpha-lipoic acid per day for three weeks significantly alleviates the symptoms of diabetic neuropathy. In addition, patients receiving this therapy did not experience any serious side effects.
    Oral Treatment with ALA: In the November 2006 issue of "Diabetes Care," researchers describe a clinical trial of orally administered alpha-lipoic acid. The trial was multicentered and conducted in Russia and Israel. The scientists studied doses of 600 mg, 1200 mg and 1800 mg separately in three groups of patients. After five weeks of once-a-day treatment, it was clear that the 600 mg dose alleviated neuropathy symptoms and kept side effects of nausea, vomiting and vertigo at acceptable levels. Higher doses increased the incidence of these side effects.

    Patients should be aware that oral formulations of alpha-lipoic acid for the treatment of diabetic neuropathy are available in Germany but not in the United States. In the United States, alpha-lipoic acid is approved only for use as an over-the-counter dietary supplement.
    Note: If you are healthy, your body makes enough alpha-lipoic acid. It is also found in red meat, organ meats (such as liver), and yeast, particularly brewer's yeast.

    Vitamin B-6:
     Vitamin B-6 helps your body make chemicals that carry messages between cells, known as neurotransmitters. It's one of the eight-member vitamin-B family, which is essential for the proper functioning of your nervous system. Vitamin B-6 is crucial for brain development, growth and function. Whole-grain breads and cereals, wheat germ, beans, lentils, lean meat, fish, nuts, seeds and dark greens, such as spinach, are excellent dietary sources of vitamin B-6. The recommended daily allowance for adults 19 to 50 years of age is 1.3 milligrams.

    Vitamin B-12: Your body's nerves -- including those in the spinal cord and brain -- are surrounded by an insulating layer, known as the myelin sheath. This layer, made up of protein and fatty substances, helps nerve signals travel quickly and efficiently. Vitamin B-12 helps maintain the myelin sheath's structure and is essential for regenerating nerve cells and the growth of new cells. Fortified cereals, trout, tuna, low-fat milk and yogurt are good sources of this essential vitamin. The recommended daily allowance for adults 14 years and older is 2.4 micrograms.

    Vitamin B-1 (thiamine): Vitamin B-1 is essential to the growth and development of the protective myelin sheath surrounding your body's nerves. It helps metabolize carbohydrates, providing glucose for your nervous system. According to Oregon State University's Linus Pauling Institute, thiamine is necessary for maintenance of nerve membranes and for conducting nerve impulses. Whole grains, fortified cereals, wheat germ, bran, legumes, organ meats, brewer's yeast and black-strap molasses are good dietary sources. The recommended daily allowance for male adults 19 years and older is 1.2 milligrams, and for female adults 19 years and older, it 1.1 milligrams per day.

    Vitamin C: it is a great debugger, inflammatory and potent antioxidant; it is certainly recommended to keep the body with an immune system in good condition, free of body fat and toxins to help reduce inflammation. All this is necessary to make the nervous system work properly and the myelin gets well protected. Vitamin C can be found in foods such as citrus fruits (oranges, lemons, etc.), broccoli, seaweed, guava, etc.

    Green tea and anti-inflammatory herbs and vegetables
    to protect the myelin sheath, is necessary to reduce inflammation in the body, which is the mainstay of treatment for multiple sclerosis. Green tea, white willow, lemon tea or citrus, devil's claw, as well as vitamin C and D, should not miss in your diet.

    Folic acid:
     essential for the proper functioning of the nervous system. Foods that contain it are whole grains.

    Omega-3 & Omega-6 Essential fatty acids: should be included in the daily diet; they are essential for the production and maintenance of myelin sheaths, which are composed mainly of oleic acid.

    Dietary fats are broken down into fatty acid molecules and then used for brain cell growth and development. The myelin sheath that covers and protects neurons is 70 percent fat and 30 percent protein. By including foods such as avocados, olive oil and oils from almonds, pecans, macadamia and peanuts, you help provide your body with sufficient omega-3 fatty acids as well as protein for proper nerve growth and regeneration.

    Oleic acid: Olives are a rich source of this essential amino acid, an omega-6 is also found in fish, chicken, walnuts, extra virgin olive oil and seeds.

    Omega-3: deep-sea fish contain good amounts of omega 3 fatty acids, which are involved in brain function by improving nerve impulse transmission, as well as to help reduce inflammation in the body.

    Vitamin A and D: are extra supports for the immune system to be in good condition and assist in recovery of myelin damage in case of demyelinating diseases. Orange vegetables such as papaya, oranges, carrots, etc., are rich in vitamin A, and cod liver oil is a good source of vitamin A, D and essential fatty acids. Vitamin D has been one of the best options to reduce the risk of demyelination and multiple sclerosis significantly.

    Amino Acids: are essential for the transmission of brain messages; they are the bricks with which proteins are constructed to improve communication skills within the brain. We recommend you include in your diet amaranth (contains all essential amino acids your body needs), brewer's yeast, seaweed and spirulina (which is also rich in minerals and vitamins).

    Fruits: fruit sugar is an elixir for the brain. Consume 3 or 4 pieces of fruit a day, but avoid combining them with other foods. Blueberries and grapes are great to eat between meals instead of candy.

    Supplements and vitamins: you should take food supplements rich in folic acid and vitamin B12, vitamin essential for the protection of the nervous system and adequate repair of myelin, as well as help prevent damage. Research has confirmed that people with multiple sclerosis and who included folic acid treatment in their diets with significantly improved both the symptoms and the repair of myelin.

    Additional Lifestyle Changes:

    You need to balance your blood glucose, including in your diet foods high in carbohydrates of slowly release as whole grains, vegetables, etc. These are the best fuel for the brain and nervous system, are not toxic substances in the body and release their energy in a slow and steady way.

    Drink plenty of water: Did you know that water is a better conductor of electrical impulse? So your diet should include at least 4-6 cups of filtered water per day.

    Avoid cooking too much rich foods: as they lose many of their natural nutrients. Try to eat raw as much as possible.

    Seeds: Seeds are a super food for all functions of the nervous system.

    St. John's Wort: St. John's Wort can be used as a holistic treatment for nerve regeneration pain. St. John's Wort can be consumed in capsule form by taking three 300-mg capsules a day with or without meals.

    Do not forget to exercise: which stimulates a strong influence in general body functions, helps the brain to be well oxygenated and releases tension. Try to choose an activity you enjoy a lot, because when you enjoy your brain secretes hormones that cause joy and welfare states, which helps greatly to stimulate the neural connections.

    Acupuncture: Acupuncture is a form of Chinese alternative medicine that uses micro-needles placed at different points of the body in order to alter one's body energies. The needles help to stimulate the nerve fibers, which send certain signals to the spinal column and brain which, in turn, activates your body's nervous system. Then, your body begins to produce needed hormones for diminishing pain, improving circulatory processes, regulating body temperature, and enhancing the functioning of white blood cells.

    In a study released in the American Journal of Chinese Medicine conducted by Yueh-Sheng Chen, Jaung-Geng Lin, Chih-Jui Lao from the Institute of Chinese Medical Science, China Medical College in Taiwan along with colleagues Ter-Hsin Chen, Ching-Liang Hsieh, Chun-Ching Lin, Chih-Jui Lao, and Chin-Chuan Tsai revealed that acupuncture offers positive effects in terms of nerve regeneration.

    The researchers found that electroneedling treatment helped enhance the ultrastructural nerve organization, increases nerve axon density, and improves the condition of blood vessels. Similar studies were conducted by S Schröder, J Liepert, A Remppis, and JH Greten from the Heidelberg School of Chinese Medicine in Germany. The latter researchers studied the effects of acupuncture in the treatment of peripheral neuropathy; the study revealed that those patients that received acupuncture illustrated improvements in terms of the painful symptoms associated with their condition.

    Science Outlook for Nerve Regeneration 
    Scientists used to think that nerve cells were incapable of regeneration if they were damaged.  This means that when you are born, you would have all the neurons that you would ever have in your life--take care of them because if they die they don't come back.

    More recently, biologists have discovered that nerve cells probably can regenerate. They just don't do it very much or very fast. This has been a problem for people who injure their nerves or nervous system. Damage to the nervous system can often cause a person to be paralyzed.  These broken nerves can't regenerate their neurons to fix themselves.  Without these neurons, it becomes difficult or impossible to move arms or legs or even to breathe.

    New research shows that stem cells might be able to help this problem by becoming neurons themselves. What are stem cells?  Well, each cell in your body has a purpose.  Muscle cells contract and make your muscles move your body.  Skin cells form a barrier between the inside of your body and the outside world.  Nerve cells send information and tell your body what to do. 

    Stem cells don't have a purpose.  Well, not yet at least.

    All cells start out without a purpose.  They have no job.  But all cells go through a process called differentiation.  Differentiation turns them from a cell without a job into a specific type of cell that has a specific purpose--like a muscle cell or a neuron.

    You might ask, "So what?"  Remember how neurons don't regenerate, or at least do it very slowly?  Scientists think that if they can tell stem cells to turn into neurons, then they might be able to help paralyzed people move again.  They can make neurons from stem cells and then put those neurons into the person's body.  They might even be able to grow new organs (like kidneys or hearts) for people who need those too by using stem cells.

    Unfortunately, stem cell research is being held back by due to politics and morality issues associated with embryonic tissue and pro-life issues.

    Wellness Protocols to Prevent Diabetic Complications       The Death to Diabetes Wellness Program consists of 10 steps, 6 stages, and 3 levels of discipline that includes a detailed set of wellness protocols that can stop the rot and reverse many of these diabetic complications -- as long as you don't wait too long to start the program.

    If you are experiencing one or more of the major diabetic complications, you should follow a very strict program that requires you to use Level 3 of the program and implement all 10 steps of the program [Ref: Chapter 16, Page 329]. This is mandatory if you want to protect your eyes, kidneys, legs, and other organs from further damage!

    Implementing Level 3 and all 10 steps includes increasing your intake of raw foods, adding high quality nutritional supplements such as CoQ10, alpha lipoic acid, evening primrose oil, and Omega-3 EFAs; and, adding super foods such as flaxseed, wheat grass, and chlorella. Also, you must eliminate your intake of the 5 "dead" foods, including wheat, flour, sugar, vegetable oils, processed foods, and animal meat.

    You should also go through a major detox/cleanse and, if necessary, use organic herbal tinctures for your eyes, kidneys, and nerves to complement your raw food nutritional program. If you don't know where to purchase herbal tinctures and high quality supplements, contact our office or get theNutritional Supplements Brand Names ebook.

    In addition, it is imperative that you work with a knowledgeable diabetes health coach and gradually wean off as many of the toxic diabetic drugs and other drugs as soon as possible -- to prevent further damage to your eyes, kidneys, nerves, heart, etc.

    Refer to Chapter 15 of the Death to Diabetes book, which provides a detailed step-by-step procedure that addresses each of the major diabetic complications; and, identifies the key foods, nutrients and supplements for each diabetic complication.

    Prescription Drugs -- The Answer?

    Prescription drugs help to (artificially) lower your blood pressure, blood glucose, and cholesterol -- but, are they really the answer to you improving your health? Go to the following web pages for more information about the danger of prescription drugs:
    Note: If you want to safely wean off these dangerous drugs, start a sound nutritional program and get the How to Wean Off Drugs Safely ebook.

    --------------------------------------------------------------------------------------------------------

    Eczema         Unrecognized Guid format.                                                                            

    Eczema is a skin disease caused by inflammation of the skin that itches and can cause a reddish rash. Eczema can occur on almost any part of the body but is most common on the face, scalp, inside of elbows, knees, ankles, and hands. Atopic dermatitis is the most common of the many types of eczema. Approximately 15 million Americans suffer from eczema, with 85% to 90% being infants, many of whom outgrow it before adulthood. People with eczema have a higher risk of developing allergic conditions like asthma or hay fever.

    Typically, eczema causes skin to become itchy, red, and dry -- even cracked and leathery. Eczema can appear on any part of the body. Eczema is a chronic problem that is most common in.

    When you have eczema, your skin is dry and damaged. And because of this damage, your skin has little protection from allergens like pollen and dust, or other environmental triggers that can cause skin to react. These triggers can easily enter through the skin's surface, initiating a flare. That's where the real problem begins... the itching.

    Once the itch starts, the scratching follows. That scratching leads to more itching which leads to even more scratching, which is the very definition of the Itch-Scratch Cycle. As the scratching continues, your skin becomes more irritated, and there's more itching.

    It's unpredictable how eczema is going to affect you or when it will occur. Eczema, by its very nature, is a disease of episodes with many experiencing extended "normal" periods between "flares". During these times, it is important to take special note of your surroundings like temperatures, allergens, soaps, foods, and more that may impact your skin and its reaction.

    What Causes Eczema?

    The cause of eczema is unknown but is presumed to be a combination of genetic and environmental factors. Eczema appears to run in families. Certain genes can make some people have extra-sensitive skin. An overactive immune system is thought to be a factor as well. Also, it's thought that defects in the skin barrier contribute to eczema. These defects can allow moisture out through the skin and let germs in.

    Factors that may trigger eczema include:
    -- Stress
    -- Insomnia
    -- Contact with irritating substances such as woolen and synthetic fabrics and soap
    -- Heat and sweat
    -- Cold, dry climates
    -- Dry skin
    -- Nutrient deficiencies

    The hygiene hypothesis postulates that the cause of asthma, eczema, and other allergic diseases is an unusually clean environment. It is supported by epidemiologic studies for asthma. The hypothesis states that exposure to bacteria and other immune system modulators is important during development, and missing out on this exposure increases risk for asthma and allergy.

    While it has been suggested that eczema may sometimes be an allergic reaction to the excrement from house dust mites, with up to 5% of people showing antibodies to the mites, the overall role this plays awaits further corroboration.

    Researchers have compared the prevalence of eczema in people who also suffer from celiac disease to eczema prevalence in control subjects, and have found that eczema occurs about three times more frequently in celiac disease patients and about two times more frequently in relatives of celiac patients, potentially indicating a genetic link between the two conditions.

    The failure of the body to metabolize linoleic acid into y-linoleic acid (GLA) may be a cause of eczema, and administration of GLAs (i.e. evening primrose oil) has been demonstrated to alleviate symptoms. Eczema may be in some cases caused by an inherited abnormality of essential fatty accid metabolism.

    Diet
    Recent studies provide hints that food allergy may trigger atopic dermatitis. For these people, identifying the allergens could lead to an avoidance diet to help minimize symptoms, although this approach is still in an experimental stage.

    Dietary elements that have been reported to trigger eczema include dairy products, coffee (both caffeinated and decaffeinated), soybean products, eggs, nuts, wheat and maize (sweet corn), though food allergies may vary from person to person. However, in 2009, researchers at National Jewish Medical and Research Center found that eczema patients were especially prone to misdiagnosis of food allergies.

    Food Triggers
    To learn if food can trigger a reaction, dermatologists recommend that the patient (or parent) keep a food diary. If a certain food seems to trigger a flare-up, conduct your own research. Remove the food from the diet and see what happens. Does the eczema subside? Does the eczema flare when the patient again eats the food?

    Foods that can potentially trigger atopic dermatitis, especially in children, include nuts, milk, eggs, soy, and wheat. It is important to realize that these foods do not trigger eczema for everyone.

    If a food triggers eczema and needs to be removed from the patient’s diet, dermatologists recommend that a healthcare provider carefully monitor the diet. Children can suffer from severe protein and calorie deficiencies when placed on an elimination diet, such as one that substitutes rice milk for milk.

    Note:
     Sweat can act as a trigger or exacerbate eczema. So avoid sweating whenever possible or shower immediately afterward sweating.
    Conventional Treatment for Eczema
    Conventional doctors often recommend a combination of self-care techniques and medical therapies to treat eczema. First, people with eczema should avoid any potential triggers that appear to make symptoms worse. Take warm, not hot, showers or baths. Use soap as sparingly as possible, and apply a soothing, hypoallergenic moisturizer immediately after bathing. Physicians may also suggest using over-the-counter anti-itch lotions or low-potency steroid creams.
    When these measures don’t alleviate eczema, the doctor may prescribe one or more of the following treatments:
    • Steroids. Prescription steroid creams and ointments - and, in severe cases, oral steroid medications - can relieve the itching and inflammation of eczema, but they can have side effects such as skin thinning and are not recommended for long-term use.
    • Immunomodulators. Newer prescription creams called calcineurin inhibitors (such as pimecrolimus and tacrolimus) work by modulating the body’s immune response. Although these drugs don’t have the same side effects as steroids, their long-term safety isn’t yet clear.
    Alternative Therapies
    A number of alternative therapies that can be used for eczema include the following:
    • Plant-based anti-inflammatory diet with lots of greens, salads, Omega-3s, GLA (evening primrose oil); plus, the avoidance of inflammatory foods including grains, so-called "natural" cereals, milk, cheese, other dairy, wheat, soy, flour, gluten, some nuts, chemically sprayed vegetables and fruits, vegetable oils, canola oil, processed foods, fast foods, junk foods, sugars, HFCS, PHO (trans fats), soda, diet soda, lunch meats, red meat, artificial sweeteners.
    • Probiotics are live microorganisms taken orally, such as the Lactobacillus bacteria found in yogurt. They are not effective for treating eczema in older populations, but some research points to some strains of beneficial microorganisms having the ability to prevent the triad of allergies, eczema and asthma, although in rare cases some species of probiotic bacteria have a very small risk of infection in those with poor immune system response. Exposure to probiotics in infancy may shape the immune system to resist eczema. Certain strains of probiotics are more effectual than others, and the timing of administration is also important.
    • Evening primrose oil/Borage oil/Black currant seed oil contains gamma-linolenic acid (GLA) which has anti-inflammatory properties and has been used in other inflammatory diseases. A meta-analysis of 26 studies of evening primrose oil found improvement in itch, crusting, and redness at one of two months of treatment (Morse, 2006). Adding to that literature, last year a randomized, placebo-controlled trial determined that the 96 percent of the patients who received evening primrose oil by mouth showed improvement versus only 32 percent of those in the placebo group (Senapati, 2008).
    • Omega-3 EFAs in avocados, wild salmon and tuna from unpolluted waters, organic eggs, organic raw nuts, organic hemp, chia or flax seeds.
    • Vitamin D (via sunlight) may be helpful for eczema. One small study performed in Boston suggested that Vitamin D3 supplementation can improve eczema in patients who report that they are worse during the winter and better during the summer, with 80 percent of the vitamin D group improving versus only 17 percent of the control group (Sidbury, 2008). Though exciting, the effect was fairly modest and not universal; it is possible that vitamin D-responsive eczema represents a subset of patients.
    • Behavior modification (incl. quality sleep, eating healthier, helping others, yoga, exercise, support group participation, etc.) may help eczema patients by reducing stress. The areas of stress reduction and behavior modification are promising and deserve further exploration as a means to complement traditional medical therapies.
    • Other supplements that may help but may also make the eczema worse  include:Flaxseed oil, Vitamin B6, herbal teas, Chinese herbal medicine, zinc.
      Consequently, a lot more research is needed.
    • Topical treatments: aloe vera gel, calendula lotion or cream, Witch Hazel extract, and chaparral lotion on irritated skin.
    • Acupuncture can be very relaxing, and patients frequently report feeling energized and renewed after treatment. The traditional explanation for how acupuncture works is based on the idea that there are energy channels running through the body that can become blocked or unregulated and that by stimulating these channels with needles, energy flow can be restored. It is possible, however, that modulation of stress via the nervous system, with subsequent immune system alteration may explain some or all of the effects of acupuncture. There are very few studies of acupuncture for eczema. One study, however, found that when paired with Chinese herbal therapy, 100 percent of the patients improved at the end of 12 weeks; they were on average 63 percent better than when they started (Salameh, 2008). Because most of the data is anecdotal, more work needs to be done in this area.
    • Sulfur has been used for many years as a topical treatment in the alleviation of eczema, although this could be suppressive. However, there is currently no scientific evidence for the claim that sulfur treatment relieves eczema.
    • Other remedies include nutritional therapy, hypnotherapy, chiropractic spinal manipulation and acupuncture.
    Patients can also wear clothing designed specifically to manage the itching, scratching and peeling associated with eczema.

    Note: Eczema vs. Psoriasis
    It is very important to correctly diagnose a skin condition as eczema or psoriasis and treat it accordingly. With eczema, the skin is hot, dry, itchy and scaly. In severe outbreaks the skin may become raw, red and bleeding. Eczema is thought to be a reaction to environmental irritants or allergies, and symptoms are worsened by stress and hormonal fluctuations.

    Psoriasis is a different inflammatory skin condition. It is marked by patches of raised reddish skin, covered with a whitish silver layer. The most common form (plaque psoriasis) is common on the knees, elbows, scalp and the lower back.

    Eczema is generally a response to environmental factors like exposure to products containing harsh chemicals; while psoriasis usually has a genetic link and is the response to factors inside of the body.

    Eczema usually occurs in childhood, while psoriasis generally is a disease of adults.
    References
    1. Lavery LA, Ashry HR, van Houtum W, Pugh JA, Harkless LB, Basu S. Variation in the incidence and proportion of diabetes-related amputations in minorities. Diabetes Care 1996;19:48-52.
    2. Armstrong DG, Lavery LA, Quebedeaux TL, Walker SC. Surgical morbidity and the risk of amputation due to infected puncture wounds in diabetic versus nondiabetic adults. South Med J 1997;90:384-9.
    3. Gibbons G, Eliopoulos GM. Infection of the diabetic foot. In: Kozak GP, et al., eds. Management of diabetic foot problems. Philadelphia: Saunders, 1984:97-102.
    4. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care 1990;13:513-21.
    5. Reiber GE, Pecoraro RE, Koepsell TD. Risk factors for amputation in patients with diabetes mellitus. A case-control study. Ann Intern Med 1992;117:97-105.
    6. United States National Diabetes Advisory Board. The national long-range plan to combat diabetes. Bethesda, Md.: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, 1987; NIH publication number 88-1587.
    7. Edmonds ME. Experience in a multidisciplinary diabetic foot clinic. In: Connor H, Boulton AJ, Ward JD, eds. The foot in diabetes: proceedings of the 1st National Conference on the Diabetic Foot, Malvern, May 1986. Chichester, N.Y.: Wiley, 1987:121-31.
    8. Wylie-Rosset J, Walker EA, Shamoon H, Engel S, Basch C, Zybert P. Assessment of documented foot examinations for patients with diabetes in inner-city primary care clinics. Arch Fam Med 1995;4:46-50.
    9. Bailey TS, Yu HM, Rayfield EJ. Patterns of foot examination in a diabetes clinic. Am J Med 1985; 78:371-4.
    10. Edelson GW, Armstrong DG, Lavery LA, Caicco G. The acutely infected diabetic foot is not adequately evaluated in an inpatient setting. Arch Intern Med 1996;156:2373-8.
    11. Kannel WB, McGee DL. Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study. Diabetes Care 1979;2:120-6.
    12. LoGerfo FW, Coffman JD. Vascular and microvascular disease of the foot in diabetes. Implications for foot care. N Engl J Med 1984;311:1615-9.
    13. Lee JS, Lu M, Lee VS, Russell D, Bahr C, Lee ET. Lower-extremity amputation. Incidence, risk factors, and mortality in the Oklahoma Indian Diabetes Study. Diabetes 1993;42:876-82.
    14. Kannel WB, McGee DL. Update on some epidemiologic features of intermittent claudication: the Framingham study. J Am Geriatr Soc 1985;33:13-8.
    15. Bacharach JM, Rooke TW, Osmundson PJ, Gloviczki P. Predictive value of transcutaneous oxygen pressure and amputation success by use of supine and elevation measurements. J Vasc Surg 1992;15:558-63.
    16. Apelqvist J, Castenfors J, Larsson J, Strenstrom A, Agardh CD. Prognostic value of systolic ankle and toe blood pressure levels in outcome of diabetic foot ulcer. Diabetes Care 1989;12:373-8.
    17. Orchard TJ, Strandness DE Jr. Assessment of peripheral vascular disease in diabetes. Report and recommendation of an international workshop sponsored by the American Heart Association and the American Diabetes Association 18­20 September 1992, New Orleans, Louisiana. J Am Podiatr Med Assoc 1993;83:685-95.
    18. Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW, Karchmer AW. Assessment and management of foot disease in patients with diabetes. N Engl J Med 1994;331:854-60.
    19. Harati Y. Diabetic peripheral neuropathy. In: Kominsky SJ, ed. Medical and surgical management of the diabetic foot. St. Louis: Mosby, 1994:73-85.
    20. Brand PW. The insensitive foot (including leprosy). In: Jahss MH, ed. Disorders of the foot & ankle: medical and surgical management. 2d ed. Philadelphia: Saunders, 1991:2173-5.
    21. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot's arthropathy in a diabetic foot specialty clinic. Diabet Med 1997;14:357-63.
    22. Edmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ. Increased uptake of bone radiopharmaceutical in diabetic neuropathy. Q J Med 1985;57: 843-55.
    23. Brower AC, Allman RM. The neuropathic joint: a neurovascular bone disorder. Radiol Clin North Am 1981;19:571-80.
    24. Birke JA, Sims DS. Plantar sensory threshold in the ulcerative foot. Lepr Rev 1986;57:261-7.
    25. Armstrong DG, Lavery LA, Vela SA, Quebedeaux TL, Fleischli JG. Choosing a practical screening instrument to identify patients at risk for diabetic foot ulceration. Arch Intern Med (In press).
    26. Fernando DJ, Masson EA, Veves A, Boulton AJ. Relationship of limited joint mobility to abnormal foot pressures and diabetic foot ulceration. Diabetes Care 1991;14:8-11.
    27. Rosenbloom AL, Silverstein JH, Lezotte DC, Richardson K, McCallum M. Limited joint mobility in childhood diabetes mellitus indicates increased risk for microvascular disease. N Engl J Med 1981; 305:191-4.
    28. Bild DE, Selby JV, Sinnock P, Browner WS, Braveman P, Showstack JA. Lower-extremity amputation in people with diabetes. Epidemiology and prevention. Diabetes Care 1989;12:24-31.
    29. Lavery LA, Armstrong DG, Quebedeaux TL, Walker SC. Puncture wounds: normal laboratory values in the face of severe infection in diabetics and non-diabetics. Am J Med 1996;101:521-5.
    30. Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW. Probing to bone in infected pedal ulcers. A clinical sign of underlying osteomyelitis in diabetic patients. JAMA 1995;273:721-3.
    31. Sutter CW, Shelton DK. Three-phase bone scan in osteomyelitis and other musculoskeletal disorders. Am Fam Physician 1996;54:1639-47.
    32. Lavery LA, Armstrong DG, Harkless LB. Classification of diabetic foot wounds. J Foot Ankle Surg 1996;35:528-31.
    33. Armstrong DG, Lavery LA, Harkless LB. Treatment-based classification system for assessment and care of diabetic feet. J Am Podiatr Med Assoc 1996;86: 311-6.
    34. Lavery LA, Armstrong DG, Vela SA, Quebedeaux TL, Fleischli JG. Identifying high risk patients for diabetic foot ulceration: practical criteria for screening. Arch Intern Med
    35. ^ Foot Complications, from the American Diabetes Association; first published no later than November 4, 2009 (as per archive.org); retrieved September 6, 2011.
    36. ^ Diabetic Foot Care at ePodiatry; published 2003; retrieved September 6 2011.
    37. ^ Frykberg RG, Armstrong DG, Giurini J, et al. (2000). "Diabetic foot disorders: a clinical practice guideline. American College of Foot and Ankle Surgeons"J Foot Ankle Surg 39 (5 Suppl): S1–60. PMID 11280471.http://ukpmc.ac.uk/abstract/MED/11280471/reload=0;jsessionid=C38C571D5D1CB95F188AC5E80A9D6B05.jvm1.
    38. ^ Brem Harold, Tomic-Canic Marjana (2007). "Cellular and Molecular basis of wound healing in diabetes"JCI 117 (5): 1219–1222. doi:10.1172/JCI32169PMC 1857239.PMID 17476353http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1857239.
    39. ^ Arad Y, Fonseca V, Peters A, Vinik A (2011). "Beyond the Monofilament for the Insensate Diabetic Foot: A systematic review of randomized trials to prevent the occurrence of plantar foot ulcers in patients with diabetes"Diabetes Care 34 (4): 1041–6. doi:10.2337/dc10-1666PMC 3064020PMID 21447666
    References (for Nerve Regeneration)
    1. ^ Principles of Neural Science; Kandel, Schwartz; McGraw-Hill Medical; 4 edition (January 5, 2000); Chapter 55
    2. ^ Stabenfeldt, S.E., A.J. Garcia, and M.C. LaPlaca, Thermoreversible laminin-functionalized hydrogel for neural tissue engineering. Journal of Biomedical Materials Research. Part A, 2006. 77: p. 718-725
    3. ^ Prang, P., et al., The promotion of oriented axonal regrowth in the injured spinal cord by alginate-based anisotropic capillary hydrogels. Biomaterials, 2006. 27: p. 3560-3569.
    4. ^ a b c d e Recknor, J.B. and S.K. Mallapragada, Nerve Regeneration: Tissue Engineering Strategies, in The Biomedical Engineering Handbook: Tissue Engineering and Artificial Organs, J.D. Bronzino, Editor. 2006, Taylor & Francis: New York
    5. ^ a b c d YIU, G. & ZHIGANG, H. (2006). Glial inhibition of CNS axon regeneration. Nature Reviews Neuroscience, 7, 617-627
    6. ^ BRADBURY, E.J., MCMAHON, S.B. (2006). Spinal cord repair strategies: why do they work? Nature Reviews Neuroscience, 7, 644-653
    7. ^ KARNEZIS, T., MANDEMAKERS, W., MCQUALTER, J.L., ZHENG, B., HO, P.P., JORDAN, K.A., MURRAY, B.M., BARRES, B., TESSIER-LAVINGE, M., BERNARD, C.C.A. (2004). The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination. Nature Neuroscience, 7, 736-744
    8. ^ REGMAN, B.S., KUNKEL-BAGDEN, E., SCHNELL, L., DAI, H.N., GAO, D., SCHWAB, M.E. (1995). Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors. Nature, 378, 498-501
    9. ^ a b Zhang HQ, Uchimura K, Kadomatsu K. Brain keratan sulfate and glial scar formation. ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1086: 81-90 2006.
    10. ^ Gilbert RJ, McKeon RJ, Darr A, et al. CS-4,6 is differentially upregulated in glial scar and is a potent inhibitor of neurite extension. MOLECULAR AND CELLULAR NEUROSCIENCE 29 (4): 545-558 AUG 2005
    11. ^ Wang H, Katagiri Y, McCann TE, et al. Chondroitin-4-sulfation negatively regulates axonal guidance and growth. JOURNAL OF CELL SCIENCE 15 (12): 3083-91 2008
    12. ^ YIU, G. & ZHIGANG, H. (2006). Glial inhibition of CNS axon regeneration. Nature Reviews Neuroscience, 7, 617-62
    13. ^ KARNEZIS, T., MANDEMAKERS, W., MCQUALTER, J.L., ZHENG, B., HO, P.P., JORDAN, K.A., MURRAY, B.M., BARRES, B., TESSIER-LAVINGE, M., BERNARD, C.C.A. (2004). The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination. Nature Neuroscience, 7, 736-744
    14. ^ De Winter F, Oudega M, Lankhorst AJ, Hamers FP, Blits B, Ruitenberg MJ, Pasterkamp RJ, Gispen WH, Verhaagen J. Exp Neurol. 2002 May;175(1):61-75.
    15. ^ Tannemaat MR, Korecka J, Ehlert EM, Mason MR, van Duinen SG, Boer GJ, Malessy MJ, Verhaagen J. J Neurosci. 2007 Dec 26;27(52):14260-4.
    16. ^ a b c d e f The Southern Orthopaedic Association > Patient Education: Nerve Repair and Grafting in the Upper Extremity 2006. Retrieved on Jan 12, 2009
    17. ^ Kalantarian B, Rice DC, Tiangco DA, Terzis JK. Gains and losses of the XII-VII component of the "baby-sitter" procedure: a morphometric analysis. J Reconstr Microsurg. 1998;14:459-471.
    18. ^ Tiangco DA, Papakonstantinou KC, Mullinax KA, Terzis JK. IGF-I and end-to-side nerve repair: a dose-response study. J Reconstr Microsurg. 2001;17:247-256.
    19. ^ Fansa H, Schneider W, Wolf G, Keilhoff G. Influence of insulin-like growth factor-I (IGF-I) on nerve autografts and tissue-engineered nerve grafts. Muscle Nerve. 2002;26:87-93.
    20. ^ Shiotani A, O'Malley BW Jr, Coleman ME, Alila HW, Flint PW. Reinnervation of motor endplates and increased muscle fiber size after human insulin-like growth factor I gene transfer into the paralyzed larynx. Hum Gene Ther. 1998;9:2039-2047.
    21. ^ Flint PW, Shiotani A, O'Malley BW Jr. IGF-1 gene transfer into denervated rat laryngeal muscle. Arch Otolaryngol Head Neck Surg. 1999;125:274-279.
    22. ^ Phillips, J.B., et al., Neural Tissue Engineering: A self-organizing collagen guidance conduit. Tissue Engineering, 2005. 11(9/10): p. 1611-1617.
    23. ^ KARNEZIS, T., MANDEMAKERS, W., MCQUALTER, J.L., ZHENG, B., HO, P.P., JORDAN, K.A., MURRAY, B.M., BARRES, B., TESSIER-LAVINGE, M., BERNARD, C.C.A. (2004). The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination. Nature Neuroscience, 7, 736-744.
    24. ^ Application of Neutralizing Antibodies against NI-35/250 Myelin-Associated Neurite Growth Inhibitory Proteins to the Adult Rat Cerebellum Induces Sprouting of Uninjured Purkinje Cell Axons; Annalisa Buffo1, Marta Zagrebelsky1, Andrea B. Huber2, Arne Skerra3, Martin E. Schwab2, Piergiorgio Strata1, and Ferdinando Rossi1; The Journal of Neuroscience, March 15, 2000, 20(6):2275-2286