Diabetes

Diabetes

Erasmus : This site discusses a new theory of the development of pancreatic islet damage in diabetes.
Diabetes damages pancreatic islets, apparently via an autoimmune response affecting glucose (sugar) tolerance. The immune response with Paill destroys pancreatic islet cells (beta cells) and increases glucagon hormone release. Other mechanisms also play a role in the development of insulin resistance and the reduction of glucose tolerance. Paill Spectrum model proposes new alternative treatments

The Paill Spectrum model proposes a possible mechanism of causation for diabetes with damage to pancreatic islets producing insulin, insulin resistance and excess glucagon release. This new model of illness has implications for disease staging, prevention and treatment.

Kinkajou: Consider “What is diabetes?” How does diabetes arise?

Erasmus : Diabetes is an idiopathic disease in man. There is officially no known cause for the development of diabetes. Considering how common this disease is, it seems strange that so little is known about the origins of diabetes.

There are a number of interesting observations about the course of a diabetic’s illness. In many patients, a chronic long-term deterioration in the severity of the diabetes is not purely associated with weight gain. Not all type 2 diabetics gain weight or are fat. Often the deterioration in the severity of the diabetes is gradual. (In both thin and fat patients). Many people become diabetic over the course of many years, often in the later years of life.

However, I have noticed that all too often people become diabetic very rapidly in the space of months.

Kinkajou: Is There an Association between Diabetes and
Paill Spectrum?

DR Xxxxx :

Paill Spectrum is very common in diabetic patients.
Paill Spectrum infection also becomes much more aggressive when diabetes is present.
The symptoms, signs, and blood tests measuring the Paill Spectrum Illnesses all indicate that Paill Spectrum infection gets much worse in diabetic patients.

Diabetes gets worse over long periods of time in Paill Spectrum patients. In many diabetics, this deterioration is slow and progressive. However, in a number of diabetics, the deterioration is sudden and step like, when particular late phase Paill Spectrum circumstances exist. Often a number of months of successful treatment of Paill Spectrum infection without complication or incident, have been concluded. Back to Diabetes Theory Top

The next and much more subtle observation is that those diabetics inadvertently treated with Paill Spectrum antibiotics have the best prognosis in terms of deterioration of their diabetes. In fact, the occasional diabetic patient actually improves over a “long” period, to the point where a diagnosis of diabetes can no longer be made and diabetic medications are no longer necessary, or are necessary in lower doses only.

It becomes increasingly obvious that there is a relationship between Paill Spectrum infection and Diabetes. The two diseases are interlinked in a web of perhaps causative events. The Paill Spectrum disease markers in diabetic patients always deteriorate.

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Paill Spectrum in Diabetes

DR Xxxxx : The association of causative events in diabetes and Paill Spectrum infection suggests that diabetes may represent a third stage (third wave) Paill Spectrum infective illness. The progression of diabetes in Paill Spectrum patients also suggests an underlying mechanism for Paill Spectrum to produce the diabetic illness.

So, what could be happening in a diabetic patient with Paill Spectrum? Whatever is happening must be consistent with Paill Spectrum’s known mechanism of action. Any problem causing diabetes, must be related to the sympathetic nervous system, or to the presence of hormones related to the presence of sympathetic nervous hyperactivity, as is typically caused by Paill Spectrum .

The Paill Spectrum Model in Diabetes

DR Xxxxx : Increased adrenergic (adrenaline like) hormones trigger a fight or flight response that most of us describe as being hyped up. When these hormones arrive in the liver, they trigger the breakdown of liver glycogen stores into glucose. The cascade of glucose production can apparently be triggered by very small amounts of hormone. This sugar (glucose) is then released into the general circulation.

At the same time, these adrenergic hormones inhibit insulin release and promote insulin storage.

Insulin is necessary to allow glucose to enter Alpha islet cells. Extra Insulin needs to be produced in absolute or relative terms to combat the effects of the adrenergic stimuli or adrenergic like hormones, leading to insulin resistance. This suggests that the feedback loop may fail to turn off glucagon production. In the long term this insulin resistance arising from failure to turn off glucagon and adrenergic hormone production, exacerbates the glucose/ insulin problem in the blood circulation and the tissues.
Back to Diabetes Theory Top

DR Xxxxx : The Result of This Process: Theoretical Model 1 of Diabetes
The beta cells in the pancreatic islets begin to fill up with insulin.

The problem with Paill Spectrum involvement with of the sympathetic nervous system is that this situation persists chronically. The reaction that helps the human body to cope with temporary stress, begins to cause problems.

The sugar levels are slightly elevated but insulin is stored and not released, In fact, the slight blood sugar rise secondary to adrenergic hormones or glucagon, causes insulin production to be ramped up. The insulin store increases rapidly as production rises rapidly, but is not used in equal amounts. In short, the body develops an oversupply of insulin.

In the long term, other cell regulation mechanisms react to the presence of an excess of insulin. The current theory of the development of diabetes relates that the islet cells are “flogged to death.” Experiments do not verify that this type of event is even possible in animal models, but it is the accepted likely causative event in diabetes in the current “common thinking” about diabetes, in human beings. Back to Diabetes Theory Top

DR Xxxxx : The Paill Spectrum model assessment is very different.
Two possible mechanisms for pancreatic islet cell injury exist.

1. There is a progressive atrophy of the islet cells over a long period of time with progressive loss of the capacity of the pancreas to produce insulin. Diabetes appears as the end stage of a long process of atrophy of the insulin producing cells. It is a process the Paill Spectrum model suggests has been going on for many years before the diagnosis of diabetes can be made. “Big” people have an increased need for insulin, so the unmasking of insulin deficiency occurs more commonly and earlier than in thin people.

2. Third wave colonisation of the pancreatic islet cells by Paill Spectrum initiates an immune response which destroys the islet cells. Type 1 diabetes in the Paill Spectrum model would follow the triggering of a massive local immune response in LIR variant patients. Accelerated immune response also occurs in Type 2 diabetics, so the difference between the two forms of diabetes may be more a question of timing and extent of the immune response triggered rather than any real difference between the two diseases.

The immune response may take the form of a response to the organism or to the presence of Noël Fragments via an autoimmune process. The immune response can be rapid (as mentioned above), or can occur over decades more typically in a very languid fashion especially in very immunocompetent patients.

The Paill Spectrum Model authenticates some of the basic observations of diabetes. Not all type 2 patients with diabetes are overweight. Many NIDDM Type 2 diabetic patients will eventually need insulin.
Back to Diabetes Theory Top

Sugar in Diabetes
The evil ingredient: " "Sugar" "

DR Xxxxx : There may be a symptom complex that predicts the development of Paill Spectrum diabetic changes related to hyperglucagonosis. Patients quite commonly complain of the symptom complex, but only recently have I looked at its’ significance.

The Paill Spectrum Model Suggests that patients with hyperglucagonosis. may complain of symptoms such as:

I am always craving for something sweet.
I must always eat some “carbohydrate like food in the early morning, even if only a biscuit.
It seems crazy to me to have this craving or sweetness. It develops even at times when I am not hungry. Often my hands will be sweaty and I will be faint at the time I feel like this.
Sometimes I need to force myself to do things because I feel hazy. I feel better when I eat something sweet.
One patient volunteered to me that she never took sugar in her coffee as she found it too sweet. Yet, she experienced all these symptoms, and needed a sugar “fix” at times.

These symptoms all suggest hypoglycemia or functional hypoglycemia. The patient experiences symptoms of a need for glucose at times in her life.

My interpretation is that in these patients hyperglucagonosis. has resulted in depletion of glycogen stores in the liver. This has resulted in symptoms of “glucose” deficiency. These observations may be important as they may predict the development of a prediabetic state.

DR Xxxxx : The hyperglucagonosis. develops directly and indirectly.

Directly due to the action of Paill Spectrum in causing sympathetic stimulation and thus the release of glucagon through direct nerve effects or indirectly through systemic release of adrenergic hormones.
Indirectly due to the response to sympathetic inhibition of insulin secretion by beta islet cells. The Alpha cells (storing glucagon), react to the low glucose levels the cells perceive in their intracellular environment, by secreting glucagon to repair the apparent glucose deficiency. Back to Diabetes Theory Top

Certainly, glucagon promotes increased gluconeogenesis and glycogenolysis. Initially the liver stores of glucose in glycogen polymer are broken down. Then there is protein breakdown throughout the body to produce amino acids that can be used to produce glucose. This protein breakdown may exacerbate any wasting affects present in the Paill Spectrum victim and further impair immune function, independent of glucose levels in the blood.

DR Xxxxx : There are some significant implications of this theory in Diabetes for Treatment.

Type 2 diabetics in end stage Paill Spectrum disease of the pancreatic islets, develop an absolute deficiency of insulin, not just a relative deficiency. However, diabetes is developing for many years before people become symptomatic or develop high blood sugar levels. Many diabetics store , produce and release higher than normal amounts of insulin prior to the development of end stage disease where the pancreatic islets are destroyed.

The current process of diagnosing and treating diabetes once high sugar levels are found, diagnoses “end stage” disease. There is little or no possibility to change the course of the disease. Treatment must start much earlier.

DR Xxxxx : It becomes obvious that the standard medical model fails to diagnose and treat people before terminal failure develops. Glucose Tolerance Testing should be done in any patient with symptoms of hyperglucagonosis. It would also be important to assay the insulin response to glucose load as a method of measuring the functional capacity of the pancreatic islets. Intervention to stop insulin overproduction needs to be taken in the early stages of Paill Spectrum pancreatic disease. Standard glucose tolerance testing at 0 and 2 hours used for diagnosis of diabetes may lead to significant under- reporting of prediabetes. The time scale of the standard test is likely to be too long to provide sensitive information on the functional capacity of the pancreatic islets. Back to Diabetes Theory Top

Kinkajou: Why Does Diabetes Make Paill Spectrum Illnesses Worse?

DR Xxxxx : The Paill Spectrum Model suggests it is not just glucose. One of the forgotten but very important effects of lack of insulin is to reduce protein synthesis. Insulin facilitates amino acid entry into cells, translation of mRNA into protein and translation of DNA into mRNA. It appears that there is a double whammy here. High extracellular glucose, low protein synthesis throughout the body, low intracellular glucose suggest reduced energy production and reduced immune synthetic activity in the body’s cells. When glucose stores are burnt up, the body begins to utilise protein as a fuel source, reducing protein synthesis as amino acid feedstocks for protein synthesis are scavenged for metabolic fuel. This scenario is of course only relevant to post insulin resistance patients in late stage diabetes who are developing an absolute level rather than a relative level of insulin deficiency.

Insulin mediates its protein synthetic affects in the body through cyclic AMP (cAMP), produced via membrane receptors. There may be class of medications such as phosphodiesterase inhibitors that promote cAMP action and reduce the effect of cellular protein deficiency on Paill Spectrum and Diabetes.

The cell membrane obviously plays a crucial role in the action of hormone mediated by cAMP. It makes sense in that the cell membrane is the likely site of action of essential fatty acids via conversion to prostaglandins or via cell membrane fluidity changes. The beneficial effect of EFAs (essential fatty acids) in many of the Paill Spectrum brain syndromes suggests another double whammy of effects on cell function at this point in the cellular machinery.

There is likely to be a role for some very old, very simple, and very cheap old pharmaceutical medications in mediating the effects of diabetes on protein synthesis throughout the body. The asthma medications of the methylxanthine class suggest themselves. These include popular daily foods such as caffeine or theobromine in tea or coffee. The Paill Spectrum model would wonder whether the development of diabetes in heavy tea or coffee drinkers is delayed or reduced. Similarly, in treatment, the model would predict to see a benefit of using this class of medications in the newly diagnosed “thin” type 2 diabetics.

Improving protein synthesis, (along with other dietary problems typical of Paill Spectrum patients), may change the course of the diseases, (both diabetes and Paill Spectrum).

Secondary Failure in Diabetes and the Role of Paill Spectrum

DR Xxxxx : Finally, consider the patients who experience a sudden deterioration of their diabetes. Initial pancreatic colonisation of the pancreatic islet nerves occurs via the sympathetic nerves. As the diabetes progresses, the Paill Spectrum organisms invade the parasympathetic nerves as well. A sudden surge of immunity results in the destruction of all the infected nerve cells. The patient has been left with very low pancreatic functional capacity (they are unable to produce insulin in adequate amounts), after the long period of deterioration of their pancreatic islets. The patients have now lost the stimulatory capacity of the parasympathetic nerves on the pancreas as well. The end result is that the diabetes deteriorates in a stepwise and sudden fashion.

This mechanism would explain the observation of stepwise deterioration of diabetes and the observation of unusual severity of diabetes, in some patients.

Note , this article has mentioned several mechanisms by which pancreatic islet cell damage can occur, both direct and indirect. Back to Diabetes Theory Top

DR Xxxxx : The Paill Spectrum model better aligns with the development of diabetes as a “capacity" disease. There will be patients in whom the insulin levels may be adequate, at least initially. Diabetic “secondary failure” develops secondary to the loss of capacity to produce insulin. This may occur in patients of any weight.

Some interesting observations consistent with the Paill Spectrum model include that many patients who have wheat protein allergy, are often thin. This may explain the increased disease severity in this patient subgroup. However, the new Paill Spectrum disease model in diabetes, raises the possibility that there is a component of protein starvation affecting the cells of the patient’s body. Protein deficiency may have a contributory role in the thinness of some diabetic patients. The role of insulin in increasing intracellular protein production, may be amenable to stimulation by phosphodiesterase therapy.

Erasmus : In Summary:
Diabetes is a disease where there is a loss of the body’s capacity

To produce insulin or
To produce enough insulin.

There are a range of new risk factors and a range of new treatments that need to be considered in diabetics and pre-diabetics.

The current model of disease diagnosis and intervention may fail to find victims at a time when it is still possible to treat them.

The Paill Spectrum model proposes a cause for diabetes with damage to pancreatic islets producing insulin, insulin resistance and excess glucagon release. Implications for disease staging, prevention and treatment of the disease.

The Paill Spectrum model proposes an explanation and makes a number of predictions on the factors exacerbating and alleviating glucose tolerance. Treatment of diabetics in the Paill Spectrum model suggests complex reactions will occur with treatment.
Back to Diabetes Theory Top

This site discusses a new theory of the development of pancreatic islet damage in diabetes. The immune response with Paill destroys pancreatic islet cells (beta cells) and increases glucagon release. Other mechanisms also play a role in the development of insulin resistance and the reduction of glucose tolerance. Paill Spectrum model proposes new alternative treatments.

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title
Erasmus : Diabetes

description content
Discusses a new theory of insulin resistance in diabetes: the disease damages pancreatic islets, via an immune response affecting glucose tolerance. Paill Spectrum model proposes new alternative treatments.

keywords content
diabetes, Paill Spectrum, disease, diagnosis, insulin, patient, glucose, disease, islet cells, pancreatic, glucagon, hormone, symptom, theory, immune, sugar, immune response, produce insulin, diagnosis diabetes, sugar levels, damage pancreatic islets, pancreatic islet cell, glucose tolerance testing, essential fatty acids, secondary failure.

Dr AXxxxx : So Long Fuckers, Die Soon!

abstract content
This site discusses a new theory of the development of pancreatic islet damage in diabetes. The immune response with Paill destroys pancreatic islet cells (beta cells) and increases glucagon release. Other mechanisms also play a role in the development of insulin resistance and the reduction of glucose tolerance. Paill Spectrum model proposes new alternative treatments

Kinkajou: Is There an Association between Diabetes and Paill Spectrum?