Last week's Science News directed my attention to a fascinating new study. I could not find the actual study posted online, but I did find this excellent article provided by the UK NHS which gives more information about it than you will find in the abstract when it comes out:
NHS: Diabetes Linked to Virus
This study replicated findings of an earlier study linking the finding of enterovirus on autopsy in human pancreases of people with Type 1 diabetes but not those without it. The enterovirus is a stomach virus that causes vomiting.
This new study went beyond the earlier study in quantifying how frequently this virus was found in people with and without Type 1 diabetes and looking at where the virus was found in the pancreas.
The researchers used sophisticated techniques to hunt for viral proteins in the pancreases of 72 young people diagnosed with diabetes who had died on average 8 months after diagnosis and of 39 children who had died at the same age who did not have diabetes.
They found that 61% of the children recently diagnosed with Type 1 diabetes showed signs of pancreatic infection with the enterovirus. Furthermore, when they looked at where the protein was being expressed, they discovered that it was being expressed almost entirely in the beta cells found in the pancreas islets that further testing showed had been still producing insulin at the time of death. The researchers also found an antiviral protein, PKR in these same islets.
In contrast, only about 8% of the pancreases of children who had died of other causes were found to have viral proteins from enterovirus, and their pancreases did not have any antiviral PKR protein in their islets.
This association of the virus and the anti-viral protein is very interesting, and may suggest an explanation for why, even though we know there is a genetic profile associated with Type 1 diabetes, some people with that profile get Type 1 and others do not. This is true even in identical twins, which has always suggested that there must be some environmental factor that causes someone with a certain genetic make-up to develop Type 1.
But, as they say on the infomercials, That's Not All!
These brilliant researchers went on to use the same techniques to examine the pancreases of a group of adults who had been diagnosed with Type 2 diabetes and then compared them with the pancreases of a group of adult controls who did not have Type 2 diabetes. Here's what they found: Forty percent of the pancreases from adults with type 2 diabetes contained the enterovirus protein. But it was found in only 13% of the normal adult pancreases. The incidence of enterovirus in pancreases of people diagnosed with Type 2 was three times higher than in those without it.
They did not, apparently, check the Type 2 pancreases for the antiviral protein PKR. That is a shame because it would be important to know if the people without Type 2 diabetes who harbored enteroviruses in their pancreases also lacked the PKR that was lacking in those children with enterovirus in their pancreases who did not develop Type 1 diabetes.
The most important thing about this study is that hints very strongly that both Type 1 and Type 2 diabetes may be related to infection with this common gut virus.
Though it is important that the study confirms the earlier finding that the virus is linked to Type 1 diabetes and found that further implication of the PKR anti-viral protein, finding the link between enterovirus and Type 2 strikes me as being the real news here--one that appears to have eluded those writing the reports about this study in the media.
If you've been reading my blog and web site you know that I'm convinced that Type 2 diabetes is no more "caused by obesity" than Type 1 is. There is a huge amount of evidence accumulating that suggests that while "prediabetes" is common among people who are overweight, people, no matter how overweight do not develop full fledged Type 2 diabetes unless they have one of dozens of specific underlying genetic conditions that have been linked in research study after research study with Type 2 diabetes. Even then, as was the case with Type 1 genes, you need some environmental factor to turn the genetic profile into actual diabetes.
We already knew from other research, that these environmental factors may include exposure to pharmaceutical drugs like Zyprexa and some SSRIs, exposure to pesticides or PCBs, and plastics like Bisphenol-A. Now we have found another possible culprit. A common virus your children are likely to bring home from elementary school.
The good news is that it may be possible to create a vaccine against this particular virus and if that happens, it might eliminate one factor that pushes beta cells towards failure.
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3 comments:
VERY interesting! I'll be waiting impatiently for studies that can determine a causal relationship here. Maybe they can infect mice with this virus? I'm sure someone's trying it.
I saw one of the researchers interviewed (briefly) on the BBC. It's long been known that there's an association between the onset of Type 1 and (often mild) infections but this is the first work I've seen to put forward a viable candidate for the infectious agent. The fact that it's also found in Type 2 is interesting as a potential environmental trigger which reacts with the genes to start the pancreatic destruction as the "second insult" to the IR which is primary in many forms.
If they can find the chemical pathways the virus generates there may be potential new treatments. Wouldn't it be ironic if you caught the virus from Healthy Whole Grains?
Interestingly, that a few months ago, nearly the whole family developed novovirus. I know it's not quite the same virus. Anyway, I still didnt come back 100% well so had blood tests taken.It came back with the result of low zoned(no medication yet) type2 diabetes. This is also hereditry in my family, plus I am NOT obese. Cosequently, had always tried to keep healthy and fit. Up until I was violently ill form this virus, I thought I had dodged the bullet. I guess DNA and viruses are possibly going to get you in the end. Who knows...but interesting article.
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