The big secret that pharmaceutical industry who doesn't want you to know !

Never heard of 'inflamed pancreas' at a diagnosis of type two.

Interesting, but neither of these articles states that 95% of type 2 diabetes is caused by bacteria and viruses.
Maybe a small minority of type 2 is possibly caused by bacteria and viruses, but nowhere near 95%!!

Khaled1972 said:

" inflamed pancreas "

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Interesting and not something I'd heard of although well aware of pancreatic cancer, maybe there's a connection there. In the University of Iowa paper I noted a few things.

.......found that prolonged exposure to a toxin produced by Staphylococcus aureus (staph) bacteria causes rabbits to develop the hallmark symptoms of Type 2 diabetes, including insulin resistance, glucose intolerance, and systemic inflammation.

International standards established regarding the species suitable for testing state that dogs, sheep, goat, pigs, or rabbits are suitable. It doesn't make rabbits the best, there's a lot of debate over which is the best, but I'm splitting hares, I mean hairs.

.....obesity also alters a person’s microbiome—the ecosystem of bacteria that colonize our bodies and affect our health.

Here we go again. No doubt what we eats affects the microbiome, but there's a lot of research, especially with twins eating the same diet, to suggest that the microbiome affects weight, rather than the other way round. Personally, I have found that my microbiome is radically changed after taking antibiotics, for obvious reasons and yes I've sent my poo off to be analyzed, mainly because it's something I've been investigating with the help of a nutritional therapist.

The second link was possibly more interesting, baring in mind:

Infection with a common virus may increase the risk of Type 2 diabetes in older adults, a new study from the Netherlands suggests.


In the study, adults ages 85 and over who were infected with cytomegalovirus were about twice as likely to have Type 2 diabetes compared with those not infected.

On the other hand and no disrespect to octogenarians, it's only a slice of the overall population, 2.5 million in the UK.

In my mind, type 2 diabetes is simply hyperinsulinemia brought about through excess glucose in the body. Remove the glucose and the problem goes away (credit largely to Jason Fung). Not sure it needs to be any more complicated than that, with these studies popping up from time to time claiming a cure is on the horizon. The cure is don’t eat carbohydrate. The prevention is don’t eat too much of it.

Jim Lahey said:

In my mind, type 2 diabetes is simply hyperinsulinemia brought about through excess glucose in the body. Remove the glucose and the problem goes away (credit largely to Jason Fung). Not sure it needs to be any more complicated than that, with these studies popping up from time to time claiming a cure is on the horizon. The cure is don’t eat carbohydrate. The prevention is don’t eat too much of it.

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Doesn’t that go against what usually expressed for type 2? We are constantly told we have hyperinsulinema because it is ineffective, and despite being high it still isn’t working (insulin resistant) and that’s why we have high glucose. Removing carbs removes the need for as much insulin so that inefficiency is less of a problem ie a management tool rather than a cure of the inefficiency

HSSS said:

Doesn’t that go against what usually expressed for type 2? We are constantly told we have hyperinsulinema because it is ineffective, and despite being high it still isn’t working (insulin resistant) and that’s why we have high glucose. Removing carbs removes the need for as much insulin so that inefficiency is less of a problem ie a management tool rather than a cure of the inefficiency

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That depends whether you subscribe to the older key & lock insulin hypothesis, or the new overflow theory, where the insulin would be effective if the body weren’t already stuffed to bursting point with glucose.

In either case the prevention and cure is to remove the glucose. It’s free and effective

Jim Lahey said:

, or the new overflow theory, where the insulin would be effective if the body weren’t already stuffed to bursting point with glucose.

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So in this theory type 2 have a lower “stuffed to bursting” point than none diabetics? Or else how to explain some non diabetics eating even higher than the average carb levels type 2s fail to manage without problems ? Can’t quite get my head around this idea - more reading required maybe.

HSSS said:

So in this theory type 2 have a lower “stuffed to bursting” point than none diabetics? Or else how to explain some non diabetics eating even higher than the average carb levels type 2s fail to manage without problems ? Can’t quite get my head around this idea - more reading required maybe.

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The theory is that some people have a bulletproof pancreas that is able to continue pumping out huge quantities of insulin without ever failing. It’s very possible that the people who live on carbohydrate and never get diabetes do in fact have high blood insulin concentrations that will never become an issue because their pancreas can handle it with one hand on the wheel. This explains why some people get obese, through elevated insulin, but do not become diabetic.

Additionally, in complete contradiction to orthodox beliefs, obesity is actually a protective mechanism for diabetes. Some people are genetically unable to lay down much fat. In these cases denovo lipogenesis is unable to create huge fat reserves in which to safely store the unused glucose. There is simply nowhere to put it. This explains why there are many type 2 diabetics who are not obese. Obesity simply delays the onset, when the body runs out of places to stash the glucose and it begins to accumulate in the blood.

I’m not asserting any of this as fact. It’s just my understanding

Staph, Strep, and a host of nasties have always lived on our skin. That’s why we have skin. To keep the nasties out side of our bodies. My question, in the first study, would be
- do rabbits normally have Staph within their normal skin flora? If not, then it would be equivalent to the studies that fed meats to herbivores and then said meats were bad for people.
- What Is the normal Staph. Count on human skin,
- is it different for diabetics,
- if so, when does this occur? keep in mind that the hyperinsulinemia leadinTo T2 starts 10 or more years before diagnosis, as shown in Dr Kraft’s studies.
- Could the hyperinsulinemia with associated abnormal glucose metabolism encourage Staph proliferation? Please, just ask someone with a foot ulcer

This study may work for rabbits, but there are way too many unanswered questions for you to be extrapolating the data, applying it to humans, and then crying coverup!

The second study clearly states they see an association, not causation, between a herpes virus and some age groups who develop T2 diabetes. Association is basically meaningless outside of being interestingly.

I do not feel either of these articles constitute some great medical cover up.

There is the theory that with central obesity, the body starts filling up the liver with fat and then starts filling up the pancreas. When the pancreas get fatty, it blocks insulin release, exacerbating the effects of insulin resistance. In other words, the pancreas is blocked and cannot release the insulin, so now the blood glucose goes up. This is when a diagnosis of T2 would occur. Since a fatty pancreas is probably inflamed, you could associate the inflammation with the diagnosis, but you could not say causation

Sorry for punctuation and grammer. My laptop is crazy today’s.

Big Pharma are really not doing very much by way of research into new antibiotics, far more emphasis is given over to the developement of treatments for chronic diseases and vaccines because this is where the big bucks are. As to antivirals, I have no idea. The papers you cite are little more than speculation and as such pose a mildly interesting hypothesis but to suggest cover up is over egging conspiracy.

I too would like to know where the figure of 95% comes from and I wonder about the remaining 5%.

Staph infections are a major consequence of our propensity to demand and overuse antibiotics and MRSA is also a major cause rampant wound infections in all patients, not just diabetics
https://familydoctor.org/condition/methicillin-resistant-staphylococcus-aureus-mrsa/
Medics are running out of options when it comes to developing new antibiotics and many “ second generalion” ones are based on the chemical formula of penicillin causing adverse / allergic reactions in some of us with allergies to penicillin

Kailee56 said:

Staph, Strep, and a host of nasties have always lived on our skin. That’s why we have skin. To keep the nasties out side of our bodies. My question, in the first study, would be
- do rabbits normally have Staph within their normal skin flora? If not, then it would be equivalent to the studies that fed meats to herbivores and then said meats were bad for people.
- What Is the normal Staph. Count on human skin,
- is it different for diabetics,
- if so, when does this occur? keep in mind that the hyperinsulinemia leadinTo T2 starts 10 or more years before diagnosis, as shown in Dr Kraft’s studies.
- Could the hyperinsulinemia with associated abnormal glucose metabolism encourage Staph proliferation? Please, just ask someone with a foot ulcer

This study may work for rabbits, but there are way too many unanswered questions for you to be extrapolating the data, applying it to humans, and then crying coverup!

The second study clearly states they see an association, not causation, between a herpes virus and some age groups who develop T2 diabetes. Association is basically meaningless outside of being interestingly.

I do not feel either of these articles constitute some great medical cover up.

There is the theory that with central obesity, the body starts filling up the liver with fat and then starts filling up the pancreas. When the pancreas get fatty, it blocks insulin release, exacerbating the effects of insulin resistance. In other words, the pancreas is blocked and cannot release the insulin, so now the blood glucose goes up. This is when a diagnosis of T2 would occur. Since a fatty pancreas is probably inflamed, you could associate the inflammation with the diagnosis, but you could not say causation

Sorry for punctuation and grammer. My laptop is crazy today’s.

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I acquired MRSA in a surgical foot wound while Inwas in hospital - the main cause I could see was the “double dipping” of doctors ties into the various wounds they examined on the ward round

Jim Lahey said:

The theory is that some people have a bulletproof pancreas that is able to continue pumping out huge quantities of insulin without ever failing. It’s very possible that the people who live on carbohydrate and never get diabetes do in fact have high blood insulin concentrations that will never become an issue because their pancreas can handle it with one hand on the wheel. This explains why some people get obese, through elevated insulin, but do not become diabetic.

Click to expand...

Well, given the huge variation in carbs:insulin ratio for those on insulin, could it be that some people don't reach this point because the absolute insulin level is low so therefore within the normal capacity of a typical pancreas?

Additionally, in complete contradiction to orthodox beliefs, obesity is actually a protective mechanism for diabetes. Some people are genetically unable to lay down much fat. In these cases denovo lipogenesis is unable to create huge fat reserves in which to safely store the unused glucose. There is simply nowhere to put it. This explains why there are many type 2 diabetics who are not obese. Obesity simply delays the onset, when the body runs out of places to stash the glucose and it begins to accumulate in the blood.

I’m not asserting any of this as fact. It’s just my understanding

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In my naive ignorance of T2, I've often wondered if insulin resistance could be a kind of protective response for when the reserves are full. I've no illusions there's more to it that that...

Shiba Park said:

Well, given the huge variation in carbs:insulin ratio for those on insulin, could it be that some people don't reach this point because the absolute insulin level is low so therefore within the normal capacity of a typical pancreas?



In my naive ignorance of T2, I've often wondered if insulin resistance could be a kind of protective response for when the reserves are full. I've no illusions there's more to it that that...

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You point on insulin resistance possibly being a protective measure (at the outset) is being researched and is a salient point.

I did read about that somewhere. Insulin resistance certainly ensures that de novo lipogenesis keeps sucking glucose out of the blood and safely storing it away as fat tissue.

Isn’t the human body a gloriously complicated and wonderous biological machine?

Boo1979 said:

I acquired MRSA in a surgical foot wound while Inwas in hospital - the main cause I could see was the “double dipping” of doctors ties into the various wounds they examined on the ward round

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I wasn’t there, but I am so sorry. I hate MRSA and what I consider criminal arrogance. About 25-30 years ago the Open Heart Unit nurses traced a MRSA outbreak in their unit to a surgeon who didn’t wash his hands between patients when doing post-op checks. Criminal! The nurses were furious, since they were the ones who kept “reminding” and then tracked him.

However, at one point about 13 years ago, I assisted the infection control practitioner who monitors all cultures that go through the hospital lab. I was shocked at the number of healthy children who had mosquito or spider bites infected with MRSA. One was just 2 years old. MRSA is now part of the normal flora within the healthy population. There is actually some sort of in depth testing that can be done to further subdivide MRSA and there are now subsets differentiating hospital vs community acquired. Your body doesn’t care, but it’s disheartening to realize MRSA is so ingrained into our culture. 50 years ago it was Pseudomonas plaguing hospitals. Now it’s all drug resistant “bugs”.

A weird one was a study that determined the “dirtiest” item in hospitals. Guess what was at or near the top.......the patient’s individual wash basin! People would keep rinsing the wash cloths in the basin, it would remove the soap, but deposit bacteria leading to cross contamination. Yes, my patients think I am crazy when I come at them with a huge pile of washcloths and disinfect their basin. As I tell them, I am not doing the laundry and once a cloth touches their body it does NOT go back to the basin! No exceptions.! Then I explain why.

I also tell them from the start, they need to be proactive. You do not let anyone touch you if you are not sure their hands or other items are clean. Doubly so if you have a wound or central line. This includes visitors and stethoscopes. It is not an insult to tell someone you want to see them wash or disinfect their hands or shared equipment before they touch you or item s in your room. I’m thankful. We all try, but we are human and can get distracted At least today we now have alcohol gel, easier on the hands, and disinfecting wipes in every room.

Khaled1972 said:

The answer to the question of inflamed pancreas and other body's organ comes from Medical researcher Finley Schofieldz : https://www.quora.com/Is-there-a-natural-way-to-cure-diabetes-and-high-blood-pressure

"Researchers from the University of Michigan and the University of California have just made an interesting discovery that reveals a natural cure for type 2 diabetes.

They were interested in medication that could treat type 2 diabetes, so they tested a common drug called Amlexanox.

But this led them down a rabbit hole that we, natural health researchers, have been preaching for years.

Amlexanox is mostly used to treat inflammation of all sorts.

For example, canker sores, Behçet’s disease (an inflammatory condition that causes ulcers, sores and arthritis), asthma (inflammation of the lungs), rhinitis (inflammation of the nasal mucous membrane) and conjunctivitis (inflammation of the eye).

The scientists recruited 42 obese people with type 2 diabetes and tested this drug on them.

In addition to lowering inflammation, study subjects also experienced a significant drop in blood sugar level and decreased fat storage level in their livers.

Simply put, lowering inflammation treated the major onsets of type 2 diabetes.

Now, it might not be such a great idea to take the drug, as it can cause nausea, diarrhea and stomach pain. In fact, it is not even manufactured in the United States at the moment.

But the real revelation of the study is that it proves inflammation is the underlying cause of type 2 diabetes and by decreasing it, you can cure the disease.

I hate to say, “I told you so!” But the fact is, I’ve helped thousands of people (including my own mother) to reverse their type 2 diabetes completely by fighting inflammation. "

So there's no doubt that sugar inside human body is an inflammation factor which actually creates the appropriate environment for bacteria and viruses to grow,and high sugar level in blood will eventually lead to organs inflammation including exhausted pancreas in case of T2D.
I'm putting here another link for the same study : https://labblog.uofmhealth.org/roun...-blood-sugar-improvement-among-some-diabetics

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The link to Quora flies in the face of my own experience, I'm afraid. It advocates exotic fruit calling it naturally sweet and inferring that there is a beneficial difference between a sweet carb and a savoury one. In my opinion this is not true, fructose can only worsen an already fatty liver and (again, in my opinion) should be avoided or at the very least eaten as a great treat.

I must admit to not having read the whole piece as tbh I'm sorely tired of such misinformation and refuse to waste time on said.

Isn't it weird my diabetes was caused by taking prednisolone an anti-inflammatory.