merryBe, that's sweet. But I wouldn't have it any other way. It will make a great book!
"She came out of nowhere and inundated the forums with insulin resistance stuff"
oh wow, so a medically trained person brought in new info...wow...
and out of nowwhere....well Houston, I think we have a problem...
"Also, preliminary data suggest that insulin resistance may lose its inhibitory effect when the investigational HCV protease inhibitor telaprevir is added to the standard regimen of pegylated interferon and ribavirin, Dr. Serfaty’s team points out in the Journal of Hepatology posted online April 13th"
it MAY lose some effect, or, as I suspect, the VEVR that some get immediately lowers the IR.
meaning basically absent the hcv virus the insulin level corrects itself. Insulin resistance occurs because our natural interfeon cancels out insulin, requiring more to be produced. The cells then become awash in all the extra insulin the body must produce, and the insulin resistance commences...
however, at treatments inception even a 10-20 increase in fasting insulin is linked to drops in rates of SVR.
here is a good primer to get folks started if they wish to increase their chances.
opps almost forgot...the other issue is once you start treating you are going to have high Interferon no matter what...therefore your pancreas with work harder, and regulation will be more difficult. The trend toward higher blood sugars in the treatment enviornment is therefore of concern as long as the INF level is being artificially raised.
The cells themselves may begin to fair better for a variety of reasons unrelated directly to the insulin however, chiefly because metabolism is far more complex than simply insulin resistance.
It's also been show that pituitary function increases absent the virus which also increases cell response, and obviously lowering liver enzymes and hence cell death and waste products all improve cell health...however those metabolic gains can be offset by other unfortunate events in tx....such as thyroid dysfunctions, or full blown type 1 diebetes, also possible outcomes of the tx regime.
The real truth is that every patient should be monitored by an endocrinologist to help avoid all the pitfalls, just my opinion.
Excellent information. Thanks.
Since being IR effects odds of SVR by ... up to apx 20% .. especially in P/R Tx, which has only recently come to be accepted by some doctors in the medical community ..
It's unfortunate that many "Docs" don't routinely check fasting insulin/glucose HOMA scores before starting P/R Tx .... especially if the patients BMI is normal ..
Some countries like England, apparently it's hard to get a fasting insulin test if fasting glucose is normal ...
My fasting glucose during Tx has stayed normal over 37 wks of Tx so far - 85-90 , but fasting insulin has increased during Tx, but still got a cEVR with a HOMA of 3.5 at Wk12 ... BMI 23.3 ...
It just goes to show , none of this is written in stone ...
And, still several months to go before my EOT + the 1, 3 , 6 & 12 month EOT PCR tests ... long way to go ...
Time will tell the impact of the PI's on IR .. hopefully they prove to desensitize insulin resistance .
Don't you mean Diabetes Mellitus type 2 developing as a result of Tx ... not Diabetes type 1 ?
Interferon-Ribavirin Combo May Boost Type 1 Diabetes Risk
By David Douglas
NEW YORK (Reuters Health) Aug 01 - Use of pegylated interferon plus ribavirin seemed to accelerate the development of type 1 diabetes in Japanese patients, researchers there report.
"Monitoring of anti-islet autoantibodies and blood glucose before and during interferon therapy would definitely help for the prediction and prevention of interferon-induced type 1 diabetes," lead author Dr. Eiji Kawasaki of Nagasaki University Hospital told Reuters Health by email.
Dr. Kawasaki and colleagues studied 91 patients who developed type 1 diabetes during or shortly after interferon therapy, including 14 who already had type 2 diabetes.
They developed type 1 disease at a median age of 56 years. The median time from treatment to onset was slightly more than half a year, suggesting rapid beta-cell destruction. Onset was significantly faster in patients on pegylated interferon and ribavirin than in those on nonpegylated interferon monotherapy, according to a July 20th online paper in Diabetes Care.
Ninety-five percent of patients had anti-islet autoantibodies when their type 1 diabetes was diagnosed.
The authors say stronger antiviral treatments may contribute to patients' risk of autoimmune diabetes. They note that pegylation extends the half-life of interferon and ribavirin may alter the immune response.
Genetic susceptibility also plays a role.
"Type 1 diabetes susceptibility HLA-DRs in the Japanese population, DR4 and DR9, were also associated with interferon treatment-related type 1 diabetes," the authors say.
The HLA-DR13 allele was present in 15.4% of interferon-related type 1 diabetics but only in 7.8% of classical type 1 diabetic patients, a significant difference. The frequency of HLA-DR14 was also significantly higher.
Diabetes Care 2011.
"end game....diet, activity and monitoring blood sugars are part of the equation whether we like it or not"
Sounds great , I was already doing that before I knew of my HCV.
Propably why I was not IR (Homa 1.4) before tx and halfway thru tx it
went down to 1.3 .
Still was not enough for RVR (170 wk4) , incl. pre/highdose Riba and Alinia.
as best I can tell there is no controversy over the fact that in-range BMI can play a role in improving SVR odds and that a good diet and exercise always make sense, whether pre, during or post tx. Nor about the existence of a dangerous connection between diabetes and accelerated fibrosis progression. Nor about the fact that monitoring blood sugar levels should be part of routine health checks.
However failure to incorporate the HOMA IR scale into clinical practice seems well justified: as an index it's simply not reliable. The HOMA-1 scale originally proposed by Matthews in '85 was replaced by a recalibrated model in '98 (HOMA-2) which improved acknowledged deficiencies in the original model. HOMA1 and HOMA2 scores calculated from the same patient glucose/insulin data can be quite different. See
Notwithstanding the shortcomings of HOMA1, all research has continued to use it because it is expressed as a simple formula whereas HOMA2 requires more elaborate interpolation buried inside the software binary distributed by the authors rather than as a published algorithm.
More importantly, unlike say BMI, there are no clear guidelines for the expected distribution of values among healthy subjects : how do you know there's a problem?
One can't do science without reliable measurement and the HOMA-1 IR index isn't much to build on. This of course doesn't mean the underlying issues aren't real, only that the yardstick is not reliable.
M , not saying that type one could not be brought on by Inf Tx .... however type 2 seems more prevalent and commonly associated with HCV Tx ..
"Type 1 diabetes is usually diagnosed in children and young adults, and was previously known as juvenile diabetes. In type 1 diabetes, the body does not produce insulin.
Insulin is a hormone that is needed to convert sugar, starches and other food into energy needed for daily life.
Only 5% of people with diabetes have this form of the disease."
Type 2 association with Inf Tx:
"It is now clear that hepatitis C conveys a risk to develop diabetes mellitus, in particular type 2: in a cross sectional national survey on 9841 adults, the prevalence of diabetes and hepatitis C were 8.4 and 2.1 %, respectively ...
Persons with age over 40 and hepatitis C had a 3.8 increased risk to have diabetes in this study."
Finally a confirmation! I've been suggesting this since 2003. I felt my husband's attempt at inf/rib tx (3 mos only) had something to do with his onset of Type 2 DM shortly thereafter. Did a little research back then and found some hints that "maybe".
Wow! tks for some added light!
Peg INF+Riba can cause diabetes (listed on the package insert),
HCV can cause diabetes,
genetics can cause diabetes,
modern day diet can cause diabetes
as MerryBe said:
"....diet, activity and monitoring blood sugars are part of the equation whether we like it or not"
sorry to be so long in answering, been gone most of the summer...
it could be either type diebetes, the tx can cause either and or both, says so right in the literature and warnings.
IR, type 2 occurs when the body is awash in too much insulin, caused by higher interferon, which uses up the insulin forcing the body to make more, and the cells finally shut down and become resistant to protect themselves, which then backfires and harms them,
Or type 1,when the organ itself shuts down and can't make the insulin as a result of all this overwork or an autoimmune attack.
either evene tis possible, it is also possible to have BOTH type 1 and type 2 diebetes simutaneously, regardless of whether you are treating or not.
I'm not sure which is the more accurate so don't wish to speak out of turn here, but it does bear repeating that at least during treatment the HOMA is more reliable. WHY?
The A1C is reliant on the red blood count, and since that is thrown off entirely by the chemo, A!C is not a reliable diagnostic during the chemo.
One can't loose 1/3 of their red blood cells, like I did, and then not expect a test relying on RBC to be accuracte. The proof was that I was normal on A1C and highly IR on the HOMA at the same time.
All that really proves is that something was askew...but how many times around the elephant before someone figures out it's an elephant? That's for bigger minds than mine,
As to which is better outside the treatment landscape, I'm sure there is sound reasoning on both sides of the pond, and I'd be hard pressed to say which group knows more. Bet ya in about another hundred years they'll figure it out!! : ) Meanwhile, pass the stevia...: )
Type 2 diabetes is caused by a dysfunctional pancreas. It still functions but does not produce enough insulin. I have never known a Type 2 diabetic to be awash with insulin.
As I understand it one can produce adequate insulin levels and be a type 2 diabetic because the insulin doesn't work right, And type 2 diabetics can also not produce sufficient amounts of insulin.
"...With type 2 diabetes, your body either resists the effects of insulin — a hormone that regulates the movement of sugar into your cells — or doesn't produce enough insulin to maintain a normal glucose level...."
Yes, it is possible for a T2 diabetic to be "awash with insulin". Weight plays a significant role here.
I have T1 diabetes and it is an autoimmune disease. The pancreas doesn't "shut down", though. My pancreas is still alive and kicking. If it wasn't, I imagine someone would have suggested removing it in the past few decades. ;)
The islet cells are what is destroyed in T1 diabetes, not the organ. :D
Thank you all very much for this informative thread, this forum has helped me so much I will always be grateful