Burden of infection on Insulin Resistance, Metabolic Syndrome, Thyroid, Stress, and Inflammation

In his research he found a number of mycotoxins that demonstrate specific toxicity to the pancreas. In his findings he states that the fusarium toxin fumonisin, T-2 mycotoxin and diacetoxyscripenol, all common in corn and its products, produce pancreatic cell damage. Fumonisin contaminates corn with the greatest frequency and is present in corn in particularly high concentrations. Virtually all corn is contaminated with mycotoxins of one type or another 5 and now we find out that corn oil is contaminated with mercury because of the way it is processed.
Fungi and their mycotoxins manipulate their hosts on the cellular level,
and prevent us from defending ourselves by subverting the immune
system. Fungi perform around 350 different hormone conversions.

It is suspected that this may be a prime reason for the epidemic of diabetes spreading through Latin American countries, due to their use of corn as a major staple in their diets.





Barthelow Classen in The Open Endocrinology Journal shows a 50% reduction of type 2 diabetes occurred in Japanese children following the discontinuation of a single vaccine, a vaccine to prevent tuberculosis. This decline occurred at a time when there is a global epidemic of type 2 diabetes and metabolic syndrome, which includes obesity, altered blood cholesterol levels, high blood pressure, and increased blood glucose resulting from insulin resistance. Classen proposes a new explanation for the epidemic of both insulin dependent diabetes (type 1 diabetes), which has previously been shown to be caused by vaccines and non insulin dependent diabetes (type 2 diabetes). Upon receipt of vaccines or other strong immune stimulants some individuals develop a hyperactive immune system leading to autoimmune destruction of insulin secreting cells. Other individuals produce increased cortisol, an immune suppressing hormone, to suppress the vaccine induced inflammation. The increased cortisol leads to type 2 diabetes and metabolic yndrome

http://uncensored.co.nz/2009/04/09/stealth-virus-bacteria-and-fungi/

http://www.curezone.com/forums/fm.asp?i=1567696#i

An overview of what retroviruses are and how our own retroviruses turn up in disease due to DNA hypomethylation.

http://curezone.com/forums/fm.asp?i=1572475

The talk was about successive infection and how viruses and bacteria can work together to cause an autoimmune disease state.

Over the past few years, thanks to these molecular tools there have been so many microbes discovered in the human body that we now realize that just a fraction of these microbes can be succesfully cultured if we used standard laboratory methods. ... most of these have yet to be named.

https://www.youtube.com/watch?v=hO2YXh0ajnk&feature=player_embedded#!

crincrin wrote:ar, could just as easily be that insulin resistance leads to flare-ups of infection.

insulin resistance => immune suppression. this is the default hypothesis.

action<reaction wrote:because where is the proof

The proof is over plenty of studies and personal trial and error, just like everything else on this site.



for starters,

1) rife is nothing other than pseudo-medicine

For the purposes of this thread forget Rife, its besides the point to the understanding of these studies.

Forget rife because it's impossible to justify? It's relevant because thats how you're insinuating you'd treat these darn critters? If not please excuse me. Rife threads have been running rampant which I find rather amusing seeing as they are nothing other than pseudo-medicine.

2) that these infections are the cause of insulin resistance, all I see is correlation which Is not surprising.

People with pathogenic load ---> Much more insulin resistance than people without. Coupled with the information regarding pathogenic upregulation of DKK-1, what more do you need to get interested in this?

If your conclusion of pathogens => insulin resistance, we would see much a higher occurrence of insulin resistance

: Epidemiological studies have suggested a linkage between type 2 diabetes and chronic hepatitis C virus (HCV) infection. However, the presence of additional factors such as obesity, aging, or cirrhosis prevents the establishment of a definite relationship between these 2 conditions. : A mouse model transgenic for the HCV core gene was used. : In the glucose tolerance test, plasma glucose levels were higher at all time points including in the fasting state in the core gene transgenic mice than in control mice, although the difference was not statistically significant. In contrast, the transgenic mice exhibited a marked insulin resistance as revealed by the insulin tolerance test, as well as significantly higher basal serum insulin levels. Feeding with a high-fat diet led to the development of overt diabetes in the transgenic mice but not in control mice. A high level of tumor necrosis factor-α, which has been also observed in human chronic hepatitis C patients, was considered to be one of the bases of insulin resistance in the transgenic mice, which acts by disturbing tyrosine phosphorylation of insulin receptor substrate-1. Moreover, administration of an anti-tumor necrosis factor-α antibody restored insulin sensitivity. : The ability of insulin to lower the plasma glucose level in the HCV transgenic mice was impaired, as observed in chronic hepatitis C patients. These results provide a direct experimental evidence for the contribution of HCV in the development of insulin resistance in human HCV infection, which finally leads to the development of type 2 diabetes.

SLET-CELL ANTIBODIES AND INSULIN AUTOANTIBODIES IN ASSOCIATION WITH COMMON VIRAL INFECTIONS

Abstract
The appearance of islet-cell antibodies (ICA) and insulin autoantibodies (IAA) was sought in a prospective study of subjects with acute infections (mumps, rubella, chickenpox, and measles) followed for 6 months. IAA appeared in many patients' serum samples after these acute infections, IgM-IAA being more prevalent than IgG-IAA; there was a particularly high incidence (81%) after chickenpox. ICA were detected in 2 subjects—in 1 after rubella and in the other after measles, but this patient had evidence of previous rubella and a strong autoimmune family history. ICA did not appear after mumps. It is postulated that viral infections may trigger the production of IgM-IAA by a common mechanism involving polyclonal immunocyte activation.

abc123 wrote:Ok, we'll leave rife out of this conversation, despite your conviction to use it being absolutely insane.

: Epidemiological studies have suggested a linkage between type 2 diabetes and chronic hepatitis C virus (HCV) infection. However, the presence of additional factors such as obesity, aging, or cirrhosis prevents the establishment of a definite relationship between these 2 conditions. : A mouse model transgenic for the HCV core gene was used. : In the glucose tolerance test, plasma glucose levels were higher at all time points including in the fasting state in the core gene transgenic mice than in control mice, although the difference was not statistically significant. In contrast, the transgenic mice exhibited a marked insulin resistance as revealed by the insulin tolerance test, as well as significantly higher basal serum insulin levels. Feeding with a high-fat diet led to the development of overt diabetes in the transgenic mice but not in control mice. A high level of tumor necrosis factor-α, which has been also observed in human chronic hepatitis C patients, was considered to be one of the bases of insulin resistance in the transgenic mice, which acts by disturbing tyrosine phosphorylation of insulin receptor substrate-1. Moreover, administration of an anti-tumor necrosis factor-α antibody restored insulin sensitivity. : The ability of insulin to lower the plasma glucose level in the HCV transgenic mice was impaired, as observed in chronic hepatitis C patients. These results provide a direct experimental evidence for the contribution of HCV in the development of insulin resistance in human HCV infection, which finally leads to the development of type 2 diabetes.

Two extremely important points you glazed over.

Rats being studied in a lab with one virus is not the same as what I'm trying to convey in this thread abc, the point being that its a long process that started long before we were born. As for the second bold in that line, you left out something as well, the control mice on a high fat diet... were fine.

I

SLET-CELL ANTIBODIES AND INSULIN AUTOANTIBODIES IN ASSOCIATION WITH COMMON VIRAL INFECTIONS

Abstract
The appearance of islet-cell antibodies (ICA) and insulin autoantibodies (IAA) was sought in a prospective study of subjects with acute infections (mumps, rubella, chickenpox, and measles) followed for 6 months. IAA appeared in many patients' serum samples after these acute infections, IgM-IAA being more prevalent than IgG-IAA; there was a particularly high incidence (81%) after chickenpox. ICA were detected in 2 subjects—in 1 after rubella and in the other after measles, but this patient had evidence of previous rubella and a strong autoimmune family history. ICA did not appear after mumps. It is postulated that viral infections may trigger the production of IgM-IAA by a common mechanism involving polyclonal immunocyte activation.

Whats the point of this? So 81% of people who get chicken pox develop type 1 diabetes? This does not appear to be the conclusion, seeing the full study would be nice...
Type 1 diabetes not the same as insulin resistance regardless.

I didn't say it was, I'm merely pointing out that there are commonalities happening here, and that we don't fully understand all the mechanisms here. I didn't have access to the full study, I can hunt it down if you like.

And a question for you: If you think insulin resistance/diabetes is caused by these infections, how is it possible people are going on diets to restore their insulin sensitivity and losing weight? Surely their infection load, which made them insulin resistant in the first place according to you, would of prevented them from losing weight regardless of diet.

action<reaction wrote:

abc123 wrote:Ok, we'll leave rife out of this conversation, despite your conviction to use it being absolutely insane.

: Epidemiological studies have suggested a linkage between type 2 diabetes and chronic hepatitis C virus (HCV) infection. However, the presence of additional factors such as obesity, aging, or cirrhosis prevents the establishment of a definite relationship between these 2 conditions. : A mouse model transgenic for the HCV core gene was used. : In the glucose tolerance test, plasma glucose levels were higher at all time points including in the fasting state in the core gene transgenic mice than in control mice, although the difference was not statistically significant. In contrast, the transgenic mice exhibited a marked insulin resistance as revealed by the insulin tolerance test, as well as significantly higher basal serum insulin levels. Feeding with a high-fat diet led to the development of overt diabetes in the transgenic mice but not in control mice. A high level of tumor necrosis factor-α, which has been also observed in human chronic hepatitis C patients, was considered to be one of the bases of insulin resistance in the transgenic mice, which acts by disturbing tyrosine phosphorylation of insulin receptor substrate-1. Moreover, administration of an anti-tumor necrosis factor-α antibody restored insulin sensitivity. : The ability of insulin to lower the plasma glucose level in the HCV transgenic mice was impaired, as observed in chronic hepatitis C patients. These results provide a direct experimental evidence for the contribution of HCV in the development of insulin resistance in human HCV infection, which finally leads to the development of type 2 diabetes.

Two extremely important points you glazed over.

Rats being studied in a lab with one virus is not the same as what I'm trying to convey in this thread abc, the point being that its a long process that started long before we were born. As for the second bold in that line, you left out something as well, the control mice on a high fat diet... were fine.

Hmm I didn't want to expand on my point further but since you dont get it:

A High fat diet can mean many things, trans fats, saturated fats, etc. Scientists are often not very specific on what "A high-fat diet means".

What time frame did this study cover? Who's to say that the control rat's wouldn't of developed disease in a 6month study vs 2 year study. I have seen many studies where control rodents have been fed poorly and developed diseases. Maybe the transgenic rats would not of developed type two if fed a clean diet. At best HCV is a contributing factor but not a cause.

And the statistical significance still stands


I

SLET-CELL ANTIBODIES AND INSULIN AUTOANTIBODIES IN ASSOCIATION WITH COMMON VIRAL INFECTIONS

Abstract
The appearance of islet-cell antibodies (ICA) and insulin autoantibodies (IAA) was sought in a prospective study of subjects with acute infections (mumps, rubella, chickenpox, and measles) followed for 6 months. IAA appeared in many patients' serum samples after these acute infections, IgM-IAA being more prevalent than IgG-IAA; there was a particularly high incidence (81%) after chickenpox. ICA were detected in 2 subjects—in 1 after rubella and in the other after measles, but this patient had evidence of previous rubella and a strong autoimmune family history. ICA did not appear after mumps. It is postulated that viral infections may trigger the production of IgM-IAA by a common mechanism involving polyclonal immunocyte activation.

Whats the point of this? So 81% of people who get chicken pox develop type 1 diabetes? This does not appear to be the conclusion, seeing the full study would be nice...
Type 1 diabetes not the same as insulin resistance regardless.

I didn't say it was, I'm merely pointing out that there are commonalities happening here, and that we don't fully understand all the mechanisms here. I didn't have access to the full study, I can hunt it down if you like.

Well if you dont know what you're trying to say dont throw studies at me which dont reinforce any point.



And a question for you: If you think insulin resistance/diabetes is caused by these infections, how is it possible people are going on diets to restore their insulin sensitivity and losing weight? Surely their infection load, which made them insulin resistant in the first place according to you, would of prevented them from losing weight regardless of diet.

There's an abundance of ways to manipulates the outcome of a chain of events, to answer the first question I would say: is your mode of altering the outcome of that chain of events the cause or a correlated factor?

Second question, I don't see how you can really say that, it would change between each person, which to me is what we see daily. And besides, I know plenty of people who can't lose weight regardless of diet, and some who can't keep weight on, I don't have all the answers here abc but we must scrutinize and scrutinize until we get them. Point of this thread.

action<reaction wrote:abc, What's the point of me posting all this? I'm not trying to convince you of anything... its for discussion and progress, I don't want this to get heated.

action<reaction wrote:...jdp is it as crazy to you as it is to me that this information is getting such little attention? maybe it's just me.

abc123 wrote:

actionabc, What's the point of me posting all this? I'm not trying to convince you of anything... its for discussion and progress, I don't want this to get heated.

Fair enough, I'll stop posting. Saw the thread a few days ago and was planning to stay out of it but:

action...jdp is it as crazy to you as it is to me that this information is getting such little attention? maybe it's just me.

This forum is a great resource for hair. Too much pseudo-science as of late making it now deserve it's previously undeserved reputation at many hair loss sites.

action What's the point of me posting all this? I'm not trying to convince you of anything...