Interesting Study on Insulin Resistance

J Hepatol. 2009 Apr;50(4):712-718.

Insulin resistance predicts response to peginterferon-alpha/ribavirin combination therapy in chronic hepatitis C patients.

Dai CY, Huang JF, Hsieh MY, Hou NJ, Lin ZY, Chen SC, Hsieh MY, Wang LY, Chang WY, Chuang WL, Yu ML.
Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, No. 100, Tzyou 1st Rd, Kaohsiung 807, Taiwan; Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Occupational and Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

BACKGROUND/AIMS: Insulin resistance (IR) might be associated with hepatitis C virus (HCV) infection. This study aimed to elucidate impact of IR and beta-cell function on the response to peginterferon-alpha (PEG-IFN)/ribavirin combination therapy in chronic hepatitis C (CHC) patients.

METHODS: Three hundred and thirty patients without overt diabetes were treated with combination therapy with (PEG-IFN)/ribavirin for 24 weeks. The IR and beta-cell function were evaluated by homeostasis model assessment of IR (HOMA-IR) and homeostasis model assessment of beta-cell function (HOMA-beta) before treatment.

RESULTS: HCV genotype, pretreatment HCV RNA level and pretreatment HOMA-IR, but not HOMA-beta, were independent factors associated with sustained virologic response (SVR). In 150 patients with genotype 1b infection, pretreatment HCV RNA level, HOMA-IR and age were independent predictors for SVR. The significantly lower SVR rate in high HOMA-IR patients was observed in 76 patients with high HCV RNA levels (400,000IU/mL) who were defined as 'difficult-to-treat' patients. The mean HOMA-IR of 'difficult-to-treat' patients was significantly lower in 42 sustained responders than in 34 non-responders.

CONCLUSIONS: IR was associated with SVR to (PEG-IFN)/ribavirin therapy for CHC, especially among 'difficult-to-treat' patients. These findings suggested clinical application of pretreatment HOMA-IR could enable treatment outcome to be predicted and treatment regimens to be determined.

[geterdone]

Treatment may not be in vain for those who may not know that they are IR or boarder line diabetic and to be tested before starting treatment will give more information for a better outcome rather than finding out that the past 48 weeks was a waste.
jasper

[Trinity4]

Thank you Max

[Trinity4]

Just a matter to time wasn't it.......

[Trinity4]

Correction:  matter OF time

[bandman54]

Wish I had read something about IR before I treated and failed.

Still fighting it.. just got my labs today.
HOMA = 4.48  ... uggghh.

Jacked up the metormin , hopefully that will help.
Took me a long time to become IR and it will probably take awhile to get back to "normal".

My dad was a type II diabetic, so was his mother.
If you have a family history of diabetes , it is worth looking in to.

IR's are 7 years from progressing to type II diabetes if not treated.
Wish they had known about IR (many doctors are still not aware, mine wasn't) when my dad was alive.  He eventually progressed to renal disease and diaylisis (sp?).
they always said the kidney problem caused the diabetes... but I am convinced that the diabetes caused his kidney problems.



bandman

[Trinity4]

It would have been fine if the case in point was just IR awareness but we know it goes a whole lot deeper than that.  
Let sleeping dogs lie

[GreatBird]

My understanding is that diabetes type 1 involves underproducing insulin. Type 2 is with overproduction. Do you know whether the diabetics who cleared were type 1 or type 2?

[Bill1954]

I am a type 2 diabetic that SVRrd. Although I had a slow response during the first treatment, the second time I cleared relatively early, and went on to achieve sustained viral response. I think part of the misunderstanding here is that some members on this board have become obsessed by insulin resistance, and look at it as if it were a panacea to HCV treatment; but it doesn’t *preclude* SVR; it’s only another hurdle to jump on the path. I’m not suggesting it be ignored either; but a balance needs to be found.

Type 1 diabetes typically involves underproduction of insulin from the beta cells in the pancreas. Type 2, on the other hand, can be a combination of factors; underproduction of insulin, coupled with insulin resistance that prevents cells from absorbing or utilizing the insulin that *is* produced. A type 1diabetic typically requires very little exogenous insulin; they can get by with injecting small amounts. I, on the other hand, at times require very large amounts of insulin because my body is unable to ‘accept’ either my own insulin (endogenous), or the insulin we inject (exogenous). It’s common for type 2 diabetics such as myself to require both oral insulin sensitizers (metformin) as well as insulin injections to maintain firm blood sugar control.

Take care—

Bill

[Max60]

My original post asked for clarification. . . which was not given.

What were the viral loads? What were the ages of the successful and unsuccessful participants?  Who do the terms 'difficult to treat' mean precisely in the context of this study?

Is there some reason you can not post the full text?

[jdwithhcv]

Google this and you will get the articles.  

J Hepatol. 2009 Apr;50(4):712-718.

[geterdone]

did you know the first time around that your IR would play a part in your not being successful in treatment? Just curious, thanks!
jasper

[Bill1954]

Actually, both treatments occurred prior to current studies showing any correlation between insulin resistance and SVR; any attempts at challenging IR were in the interest of blood glucose control only.


Bill

[geterdone]

Thanks! I don’t know what could or can be done to ease these obstacles to those who have IR problems or are db1 or 2 and starting to look at treatment but it is better to be aware than not and am sure it will come up again.

jasper

[Deb_c430]

  

Diabetes is a serious disease, so is treating,  Bill as always your words are clear and honest!  maybe a sidebar like  the Occult Hep C? trihep is great about posting new articles,  

[jmjm530]

Max: Is there some reason you can not post the full text?
--------------
Can't speak for the original poster, but I hear you.

A very quick search shows that  full-text is not available for free online as is the case with many studies.

For anyone who would like to read full-text, here's a link to the study and note the "full-text" box to the right.

http://www.ncbi.nlm.nih.gov/pubmed/19231011

That will take you to one or two sites where you can download the full-text for a fee. Alternatively, some of you with professional or university access may be able to get it that way. Also, full-text is generally available for free in some public medical libraries.

When I was treating, I always ordered full-text for any study I was going to base an important treatment decision on. Abstracts often leave as many question unanswered as answered.

-- Jim

[jmjm530]

For further interested, here is a collection of HCV/IR/Diabetes articles from the HIVandHepatitis.com web site:

http://www.hivandhepatitis.com/hep_c/hepc_news_insulin.html

"CoWriter" has also compiled a list along with commentary here:
http://www.medhelp.org/user_journals/index/568322?personal_page_id=450
--------------------------
IR and HCV tx is definitely an evolving subject and hopefully anyone with HCV, and especially about to treat, will first get tested for IR including a fasting serum glucose and serum insulin test. The fasting glucose is commonly a part of a normal HealthScreen but really don't see why a doc would refuse a serum insulin test if requested, mine didn't even though my fasting glucose values were normal.

Beyond that, study up as much as you feel comfortable with, and discuss with your medical team where relevant. Diet and exercise are the first line defense for IR but they may not work in all cases.

With tests in hand (and perhaps some supplied studies) hopefully your medical team can put your IR status in a clinical context and come up with a plan where needed. And again, if you're not seeing a hepatolgoist, I highly recommend you switch over to one if feasible. They tend to be more on top of HCV and related topics and would be best to help pull your HCV strategy together.

-- Jim

[CoWriter]

"I am a type 2 diabetic that SVRrd. Although I had a slow response during the first treatment, the second time I cleared relatively early, and went on to achieve sustained viral response."
--------------------
I am going to take a wild guess and say that perhaps your blood sugar control was better the second time?


"Type 1 diabetes typically involves underproduction of insulin from the beta cells in the pancreas."
--------------

Actually Bill, Type 1 means that you don't produce ANY insulin at all.  


" A type 1diabetic typically requires very little exogenous insulin; they can get by with injecting small amounts."
----------------

Think about it.  They don't produce any insulin at all.


"but it doesn’t *preclude* SVR"
------------------
I disagree with that, however, I do agree that IR is only one of many hurdles.



"some members on this board have become obsessed by insulin resistance"
-------------------

You can't be talking about me.  I didn't just become.  I've been obssessed with it for years...LOL

I find your case incredibly interesting and wish I could see what the difference was between the two times you treated (same with FlGuy) since high levels of insulin make interferon ineffective and that includes injected insulin...and you were on quite a bit of Lantus insulin.

It's fascinating.  I would love it if you share more details.

Co  


Dig Dis Sci. 2009 Jan 16.

Diabetes Mellitus Is Associated with Impaired Response to Antiviral Therapy in Chronic Hepatitis C Infection.

Elgouhari HM, Zein CO, Hanouneh I, Feldstein AE, Zein NN.
Avera Center for Liver Disease, Transplant Institute, Sanford School of Medicine, University of South Dakota, 1001 East 21st Street, Suite 303, Sioux Falls, 57105, South Dakota, USA

Insulin resistance may promote hepatic fibrosis in chronic hepatitis C (HCV) and has emerged as a cofactor in failure to achieve sustained viral response (SVR). Aims (1) To assess the association of diabetes mellitus (DM) in HCV patients to the severity of hepatic fibrosis and to the response to antiviral treatment. (2) To assess the safety of pegylated interferon and ribavirin combination therapy (Peg IFN/RBV) in diabetic HCV patients. Methods HCV diabetics (n = 61) were identified. A 2:1 matching control group was used to identify independent factors of advanced fibrosis and treatment failure. Results Compared to HCV non-diabetics, HCV diabetics were more likely to have steatosis (P < 0.0001) and advanced fibrosis (P = 0.003). Patients' age, Caucasian ethnicity, obesity, and histologic activity index were independently associated with advanced fibrosis (P < 0.05). Only 23% of HCV diabetics achieved SVR compared to 46% of HCV non-diabetics (P = 0.003). DM, genotype 1, high baseline viral load, and African-American ethnicity were independently associated with less SVR (P < 0.05). Significant adverse events were more common in HCV diabetics compared to HCV non-diabetics (P = 0.001). Side effects did not increase in patients receiving PEG IFN/RBV and insulin sensitizers. Conclusion DM was associated with impaired virologic response to PEG IFN/RBV in HCV patients. Adverse events during therapy were more frequent in diabetic compared to non-diabetic HCV patients.

http://www.ncbi.nlm.nih.gov/pubmed/19148751?ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

[CoWriter]

I'll share the full text with you as soon as I can secure it without having to pay for it.  Call me Scrooge...LOL

Co

[jmjm530]

Call me Scrooge...LOL
--------------------------------
Do I know you from somewhere? Your name sounds familiar, but what is this thing called "Insulin Resistance", never heard of it :)

[CoWriter]

"Do I know you from somewhere? Your name sounds familiar, but what is this thing called "Insulin Resistance", never heard of it :) "
-----------------
I'm starting to think you like the sound of my voice...LOL.  No problem.  I'll explain it to you again ; )


Here's a great article......yes Sir...full text....

Co
P.S.  To Mark60...let me know if there are questions I can answer for you.


Annals of Hepatology 2009
Insulin Resistance & Steatosis in Chronic Hepatitis C.

Abstract
In chronic hepatitis C, insulin resistance (IR) and type 2 diabetes mellitus (DM) are more prevalent than in healthy controls or in chronic hepatitis B patients.  HCV infection promotes IR mainly through increased TNF-α and cytokine suppressor (SOCS-3) production.  Both events inhibit insulin receptor and IRS-1 (insulin receptor substrate) tyrosine phosphorylation. Hepatic steatosis is also 2.5 fold more frequent in hepatitis C virus (HCV) infected patients as compared to the general population. Metabolic factors play a crucial role in the etiology of hepatic steatosis genotype non-3 related, which are also the genotypes with a greater association to IR. However, genotype 3, and particularly 3a, has a greater direct steatogenic capacity, and consequently, in those patients, the association with metabolic factors is weaker. Instead, in genotype 3, steatosis associates with viral factors like viral load. Those metabolic factors influence not only the natural history of HCV infection, as well as associate to an accelerated hepatic fibrosis progression, to a worse prognosis when hepatic cirrhosis is present, namely an increased risk of hepatocellular carcinoma, and to a lower sustained viral response rate. On the other hand, in patients who achieve viral eradication, IR and hepatic steatosis may regress, and return if viral infection recurs, which once
again indicates an intrinsic steatosis and IR promoter action by HCV.


For the full text (9 pages) see...

http://www.medigraphic.com/pdfs/hepato/ah-2009/ahs091k.pdf

[jmjm530]

Thanks for the full-text.

At the bottom of this post is "Treatment implications" section excerpted from the article.. The advice (see last paragraph) still appears to be weight loss and diet as a first line strategy to improve treatment outcomes. As to IR sensitive agents, it reads " however medication with insulin sensitizer agents in this context still do not have an evidence based fundament"

To be fair this has to be put in the context of perhaps even more recent studies, but as "Willing" pointed out in an older thread, the newer data may not yet be clear cut.

Here, for example, a good case is made for the IR sensitizer agents such as Metformin, which showed improved SVR rates but especially in the subset of "heavier weight women". Again, the question might be asked should these women have at least attempted  a program of diet and exercise instead.
http://www.hivandhepatitis.com/2008icr/aasld/docs/112108_a.html

And here's another recent article where the insulin-sensittizing agent, Pioglitazone (Actos) did Not Improve Response to Re-treatment with Pegylated Interferon plus Ribavirin. http://www.hivandhepatitis.com/hep_c/news/2008/082908_a.html

Also of interest is the difference types of steatotis for genotypes 3 (viral induced) as opposed to 1, 2 and 4 (primarily metabolic reduced), a topic covered more in depth in the body of the study.

From the full-text study:

"Treatment implications

Obesity and steatosis decrease anti-viral treatment response.
40,54,118-122 However, that negative influence seems
to be limited to metabolic steatosis and not to viral one,
since genotype 3 associated steatosis does not seem to
change the response to anti-viral treatment.40 Patients
with BMI higher than 30 kg/m2 have a 4 fold lower
chance of sustained viral response.118 A pilot study
showed that weight loss, even if mild, associates to an
improvement not only in steatosis, but also in fibrosis, in
patients with chronic hepatitis C, after as little as 3
months.123,124
There are 3 mechanisms which may explain why obesity
compromises anti-viral treatment response. First,
obesity may interfere with interferon bio-availability. In
fact, subcutaneous administration of pegylated interferon
in obese patients may decrease its absorption as a consequence
of defective subcutaneous lymph drainage, leading
to lower plasma levels.125
Another proposed mechanism is obesity as a pro-inflammatory
state126 with a negative influence in immune
response to therapy. Several adipokines may have a major
role in that immune deregulation. Leptine is an adipocyte
secreted cytokine that is increased in obesity.
However, in obesity, despite there is hyperleptinemia,
there is also resistance to leptin actions.127 Leptine has a
pro-inflammatory action promoting Th1 immune response,
which is believed to be essential in achieving a
sustained response to interferon. Therefore, leptin resistance
may have a negative influence in anti-viral treatment.
128 Another important cytokine is adiponectin,
which has an anti-inflammatory activity antagonizing
TNF-α,129 being decreased in obesity and HCV infection.
130,131 On the contrary, TNF-α not only has a pro-inflammatory
activity, as directly promotes IR, and inversely
correlates to anti-viral treatment response.132
MV Machado et al. Insulin resistance and steatosis in chronic hepatitis C S71
www.medigraphic.com
Lastly, obesity promotes IR, which is known to associate
to a negative influence in anti-viral treatment response.
133-135 In fact, Romero-Gómez et al. showed 33%
sustained viral response rate in genotype 1 in patients
with IR, as opposed to 66% in patients without IR.136
Also, Poustchi et al. found a 6.5 times lower sustained viral
response in patients with IR.135 The association between
IR and no response to anti-viral treatment may be a
due to a SOCS-3 activation, which not only promotes IR,
but also inhibits STAT-1 (signal transducer and activator
of transcription).137 After α interferon binds to its receptor,
it activates tyrosine kinases that phosphorylate
STAT-1, promoting its migration to the nucleus, where it
regulates several anti-viral genes transcription. SOCS-3
protein inhibits that tyrosine phosphorylation, thus inhibiting
α interferon action.138
We still do not know whether treating IR actually
translates in a better response to α interferon. At the moment,
patients should be advised to change to healthier
life styles that promote less IR, as weight loss and physical
exercise; however medication with insulin sensitizer
agents in this context still do not have an evidence based
fundament,139 although a small retrospective study suggests
that a better glycemic control may improve survival
in these patients.140 However, a pilot study in previously
non responders to standard anti-viral therapy with IR,
showed no benefit of a triple therapy with pioglitazone"

###

[portann]

Jim makes a crucial point. The study itself shows that relying exclusively on Metformin is a second-best tactic. The real strategy requires us to deal head-on with the need for better nutrition and more exercise.

[CoWriter]

You know what I'm concerned about Jim?  Some people are trying to reduce their HOMA with exercise and diet and have done great.  Their weight, total cholesterol, LDH, triglycerides and blood pressure are down...but not the HOMA.  Blood sugar and insulin have remainedc exactly the same as 3 months ago.

And get this....either with or without Metformin (some needed the Metformin because their blood sugar was high).

Co

[portann]

In terms of the posted study, this is the conclusion:

"We still do not know whether treating IR actually
translates in a better response to α interferon. At the moment,
patients should be advised to change to healthier
life styles that promote less IR, as weight loss and physical
exercise; however medication with insulin sensitizer
agents in this context still do not have an evidence based
fundament,139 although a small retrospective study suggests
that a better glycemic control may improve survival
in these patients."

Based on the study provided, the conclusion speaks for itself. Perhaps we need further studies to conclude otherwise. Until then, "we still do not know whether treating IR actually translates in a better response to α interferon".

[jmjm530]

  Some people are trying to reduce their HOMA with exercise and diet and have done great.  Their weight, total cholesterol, LDH, triglycerides and blood pressure are down...but not the HOMA.  Blood sugar and insulin have remained exactly the same as 3 months ago.
------------------
That's a good point, and I'm certainly not disputing that IR sensitizer agents such as Metformin do not have a role, a role that really needs more study and attention by the medical community.

As to the people not being able to raise their HOMA with exercise and diet, first we don't know whether diet or exercise will work until it's tried, that's why it's called a first line attack.

And where it was tried and failed, perhaps their compliance was less than reported, and perhaps compliance may be an unrealistic expectation in some cases. Or perhaps, some as you suggest may simply not react to diet and exercise in terms of reducing HOMA. Wondering if inthose studies per these HOMA/exercise issues how things broke down by genotype, gender, and starting/ending BMI, for example.

I think we're both onboard how important this issue is, and anyone who has been around here awhile knows how much I harped on lowering BMI through diet and exercise prior to treatment because it is one of those things in our control that can significantly affect treatment outcome. And it's such a shame that so many here have started treatment over the years without their treating doctors even mentioning the BMI factor as those studies have been out there. And now the Metformin and similar studies are giving even more hope where diet and exercise for whatever reason will not work. I was mean and lean when I started tx but it wasn't because anyone told me to in terms of HCV treatment, I just lucked out because I was somewhat of a health freak.

Sometimes I think gastro's shouldn't be allowed to treat HCV patients because they are so behind. I mean let's face it, many of us here learn many of the important lessons *after* we start treatment the first time instead of before. It should be the other way around.

-- Jim

[bajawoman]

let me see if this makes any sense to anyone here feed back appreciated these are my labs from november



INSULINA         12 uUl/ml

GLUCOSA      103   mg/dl
UREA              31  mg/dl
BUN                14 mg/dl
CREATININA        0.94 mg/dl
URICO             4.0  mg/dl
COLESTEROL      171
TRIGLICERIDOS  198
VLDL               40


These labs below were taken last week  also my CAT scan showed NO fatty liver and the Ultra sound I had in November showed stage two fatty liver  ???
HOMA IN NOVEMBER 08    3


HEMOGLOBINA GLICADA 4.5
INSULINA 11.9  uUl/ml
GLUCOSA 102  mg/dl
UREA         49   mg/dl
CREATININA   1.1   mg/dl
ACIDO URICO  4.2  mg/dl
COLESTEROL  183   mg/dl
TRIGLICERIDOS 140  mg/dl  this was the major change in my labs as I see it but I am not a professional

I would have expected a drop in Glucose and Insulin with the diet I am on but nothing ???  HOMA IN MARCH 09  2.99  NO CHANGE   NOW WHAT TRY HARDER HOW?

baja

[bajawoman]

Forgot to add the weight I have lost is minimal and YES I know it is about excercise it is difficult for me to excercise if I excercise it totally wipes me out  I need to start small 5 minutes of walking  I am not terribly obese but am obese at 30 pounds overweight I was able to take 10 pounds off but am stuck   I eat well oatmeal with bran  lots of large salads and chicken or fish and some red meat but not often I cut way back on carbohydrates my downfall is peanuts in the shell but will stop those and see if that makes a difference  I do not let me body go into starvation mode and try very hard to eat balanced snacks during the day  I do eat beef jerky and yougart no fat or sugar  eat berries and fresh picked lettuce  and other greens and flowers in all my salads
I am taking all my sups regularly  I have done research and except for the curcumin not one seem to mess with  insulin levels?

baja

[jmjm530]

The discussion above was about the general population, but in the real world things have to be addressed case by case.

So for that reason it's  impossible to answer your question because so much depends on exactly what type of diet and exercise program you're on, how well you are complying, your pre-program BMI, your BMI right now, and how much of a strain boosting the diet and exercise program would be. Maybe it's a good idea to have your program re-evaluated by a doctor and/or nutritionist or perhaps it's not and you should explore other options such as the IR sensitizes discussed.

My suggest to you has always been the same. Get a liver biopsy to pin point exactly how much damage you have and then find yourself a good hepatologist who can help put the whole thing together. And given the new research on the IR sensitizers, if it were me, I'd print out a whole lot of those studies and bring them with me to the doctor. If the aforementioned is unrealistic, then I guess you have to do the best you can do but I'm not sure how anyone can tell you too much more unless theyre a medical professional without your complete charts, etc.

I do wish you the very best, however, as you do seem determined to fight this thing which is a long way from when you first joined here and were only relying on input from your local doctor.

-- Jim

[Trinity4]

Well said Jim.

[jmjm530]

Last sentence, third paragraph should read in part...

"...then I guess you have to do the best you can do but I'm not sure how anyone can tell you too much more unless theyre a medical professional WITH your complete charts, etc."

[jmjm530]

Just read your second post.

Look, diet and exercise can be difficult and not everyone responds the same and maybe you are doing all you can do, it's really hard to say as all I know is from the other end of a computer screen.

Did you check out the South Beach Diet Links I sent you some time back?

If interested, check out "PHASE 1" and give it a try for 2-3 weeks. I think you will find it more carb restricted than what you are doing and I wouldn't be surprised if it will bring down some of those numbers you posted.

Of course, run the diet by whatever doctor you're seeing for HCV to make sure it's OK in your case. Maybe that will help or maybe the IR sensitizers are the way to go. As prev stated, I'm not the right person to make that call.

Again, you should be commended on your determination. Good luck!

-- Jim

[GreatBird]

When I was about twenty, I was diagnosed with hypoglycemia (something they don't seem to talk about anymore) and put on a *very* strict high-protein, low carbohydrate diet.

I'm wondering if you are low carb/low sugar enough? You said you eat oatmeal? I was allowed 1/2 cup. I got 1/2 a piece of fruit in an entire day and my carb portion per meal would be the equivalent of 1/2 a piece of bread.

I was supposed to have six meals a day (breakfast, snack, lunch, snack, dinner, snack) and they all had 2 or more ounces of protein in them, some fat, and a small amount of carb.

Are peanuts fat or carb? Technically they are legumes. Maybe you would do better snacking on cashews or almonds?

That diet they gave me eased up slightly after four weeks, (so that I got a whole slice of bread at lunch, for instance), but it was still very strict and there were certain foods I was supposed to stay away from completely: corn, potatoes, and the easy burning starches. They even differentiated between low sugar and high sugar veggies (like onions, carrots, artichokes were high sugar and to be eaten in very limited quantity). Absolutely NO refined sugar.

If CoWriter reads this, can you tell me why I am not IR but my blood sugar still does a  crash at hour four? I had a four hour GT test done over a year ago and my numbers were:

Fasting 84
1 hour 119 (that was after drinking that gawdawful stuff)
2 hour 83
3 hour 76
4 hour 53

Which indicates I'm still hypoglycemic.

The fasting insulin was 7.8 so my HOMA is okay at 1.6.

Anyway, sorry if I've rambled on and slightly hi-jacked the thread, but I'm very curious about this.

BTW--I just cranked up the protein back up in my diet and I'm noticing that I'm feeling much better overall. (I had slacked off during the weeks I felt nauseous because carbs were gentler on my tummy.)

[GreatBird]

Check the ingredients in your beef jerky. It's almost always cured with sugar.

[bajawoman]

I felt very comfortable in HR's hands with my Fibroscan and he had all my charts I am meeting with a nutritionist here next week to see what we can do to get the weight off but as we all know our own bodies  I would have thought I would have lost more weight

yes I agree without a complete record of all my tests so far it is hard to tell  I prefer not to get a bx at this point  CAT scan show no abnormalities at all and was different than the ultra sound in the respect showed no gall stones nor fatty liver
Higado sin alteraciones actuales
sin esteatosis ni abscesos
ni actividad neoplasica primaria ni mts
vesicula biliar, bazo, pancreas normales
sin evidencia de adenomegalias retropertoneales
sin ascitis ni colecciones adbominales
grandes vasos normales
rinones normales

bases pleuropulmonares si engrosamientos ni derrames pleurales, sin  datos de reflujo gastroesofagico, a nivel abdominal, espacios retrocrurales sin adenomegalias, ni plastrones ni evidencia de tumoraciones, estomago y duodeno sin alteraciones, bazo sin  megalias, higado, de forma, tamano, situacion, contorrios normales, sin evidencia de tumoraciounes soidas ni quisticas, ni abscesos, ni lesiones de caracteristicas metastasicas, sin datos de infiltracion grasa hepatica, con densidad de 64 UH, sin dilationcion de las vias biliares intra ni extrahepaticas, sistema venoso suprahepatico sin alteraciounes.  VESICULA bilar piriforme sin septos,ne vegetaciones,ni calcificaciones intralumianles, sin edema de pared, ni colecciones peridcolecisticas, mide 65x24 mm. retroperitoneo sin ademomegalias ni plastrones actuales. pancreas de forma, tamano, situacion, contornos y densidad normal, sin tumoraciones solidas ni quistacas, ni calificaciones ni pseudoquistes mide a nivel de acbeza 24 mm. cuerpoo y cola de 25 ateromas parciales de pared, sin evidencia de compresion de la via billar extrahepatica, espacios de Morrison, gastrohepatico, esplenomenal y correderas paretocolicas sin colecciones ni aspecto normal, rinones de forma, tamano, situacion, contornos y densidad normal, sin tumoraciones solidas ni quisticas, sistemos pielocalicial sin litos ni ectasias ni hidronetrosis, RD mide 105 x 50 x 56 mm. RI mide 105 x 48 x 51 mm. grasa mesenterica y asas intestinales sin alteraciones.

Tras la adminmistracion del medio de contraste se obeserva perfusion hpatica, esplenica y renal normales, sin neformaciones vasculares.

I know Co can read this and HR which I plan to send it to I have a cd of the CAT scan
From what I read you would think I am a health person
except for the HCV  IR  RA  and Depression   lol

[portann]

Five months is not a very long time to expect big changes based on your lifestyle improvements. I hope you recognize your excellent achievements and exercise patience for at least another year or two. Like being on HCV tx, you have to take it a day at a time and eventually, miraculously, you arrive at your goal. It takes time to reap the rewards, the road can be rough but the prize is worth it. Like tx.

Most of the people I know on the forum are slim, including me, so weight loss is not a priority. In fact, many of us are trying to put on weight. You have a difficult challenge but you can do it, a day at a time. Never give up hope.

That said, I also see a liver biopsy as a priority. How else can you make an informed treatment plan whether to wait, without such a critical piece of information?

[GreatBird]

I just checked out the South Beach Diet Phase 1 and that's as close to the high-protein, low carb diet that worked for me as I've ever seen.

The thing is that both diabetics and hypoglycemics have to eat about the same even though the way their bodies handle the insulin is different.

In fact, it's a really healthy diet for anyone. (I just wouldn't touch the artificial sweeteners myself.)

[Trinity4]

I know Co can read this and HR.  What the heck is that supposed to mean?  That was a rather cynical.

[jmjm530]

Yes, SB Phase 1 is on the money and falls into a family of other metabolic specific diets. It's also doable, the trick is to print it all out, including foods allowed and "not allowed" list.  Basically what I did was first take the "foods not allowed list" and throw out anything in the fridge or cabinets that was on the list.

Then I'd take the "foods allowed" when I went shopping and ONLY buy from the list. That way I knew I was on the diet.

Eating out was more of a challenge but can be accomplished if you really study up on the diet and really analyze what you're being served which includes asking enough questions to annoy even the most patient waiter or waitress. LOL. Frankly, I'd say no eating out for the first month on the diet as that would keep things simpler.

[Trinity4]

OK Trin, you're getting side tracked her.  IR seems to have become a religion which I do not follow so I must look at other topics which have equal if not greater importance.

[bajawoman]

I ordered a book from Amazon Insulin Resistant diet and it is balancing like the south beach diet and  the zone diet  being one very familiar with diets over the many years
I do think the Insulin Resistance diet is a very good one  I use stevia as a sweetner and HR also recommended for morning coffee which I drink decaf  lactosa or something like that but I have not found it here

I thank you all for your always sincere comments  it means a lot to me as here we do not have support groups and I do not discuss my HCV with anyone except the forums and my doctor here

Diabetes runs in my family on my Dad's side  Co spotted the IR factor or thought I may be IR after a few posts I made back in September and send me a PM  I started to communicate with her through PM's and she helped translate my blood work and also find studies for my Doctor in Spanish   You have to realize we did not have interferon or treatment here until a year ago my GI is the Hep Doctor for Baja Sur and has only been a monitoring doctor as all patients had to go to see a  Hep doctor in Guadalajara to recieve their meds fly back and he would monitor the treatment and report to the doctor there in Guadalajara  Well he has read the studies and the continuing emails from me with further studies and is now testing his patients HOMA  this is Great  He is also sending them to an Endo for treatment of the Diabetes  as it is a big problem here all ages groups  
now we have interferon here and he is now as far as my insurance co. goes my doctor for me to be covered has to order all test etc.  He will work with me and he is anxious for me to start treatment  HR said I can but need to be sure to take alinia and metaformina for a better chance of success
I am grateful that I found out about my IR before just jumping in to tx possibly keeping me from going through relapse
sorry for the long drawn out datribe   baja

[bajawoman]

not cyinical sorry you took it that way
it is in Spanish they both read Spanish that is all I was referring to  baja

[jmjm530]

OK, maybe you can clarify things.

I believe you've now had a Fibrotest (or something similar), a Fibroscan, and now a Spanish CatScan LOL. Can you tell us what stage of fibrosis each suggested, and what your medical team thinks what stage of fibrosis you have based on all input so far?  The reason I mentioned "liver biopsy" -- other than it being the gold standard -- is because sometimes individual markers -- like mentioned above -- give conflicting results and therefore you have to dig deeper, so to speak. Since you brought up "HR", I do remember him posting on a similar topic that (this is a paraphrase) the more "points" you have, the more accurate you can draw the line.  The "points" he was referring to included blood marker tests, fibroscan and liver biopsy. It seemed clear to me that he advocated ALL THREE especially in difficult to diagnose cases. Since you're about to contact him, you might ask him about that and see what his opinion is.

-- Jim

[jmjm530]

Just want to add that I agree with HRs "points" theory and personally expand it to include doctors, even hepatolgists, i.e. the more pointed expert opinions you get, the more apt you are to go in the right direction. During the course of my treatment I had at least four such points (hepatolgists) giving input at critical junctures. This may be excessive, but I don't think second opinions are.

-- Jim

[portann]

I'm also really glad you didn't jump into treatment. You and I  joined the forum at about the same time and I wish I'd been lucky enough to pause and consider my options. Instead, I plunged in.

I'm almost finished now, so I did it.

Would I have done it, if I knew then what I know now? No, definitely not, in my situation. Based on a liver biopsy that showed mild progression, I would have waited for the PI's for one reason only. Do you think for better odds? Actually, no. Only for shorter treatment time. It's like your diet. Would you take the one that could show results in 24 weeks or 48 weeks? Dieting is so hard but tx can bring you to your knees.

Go for your biopsy if you can, and maybe that will give you the option of waiting for the PI's. The more time on tx, possibly the more opportunity for underlying autoimmune disorders to rise to the surface and give you a run for your money the rest of your days.

You've learned so much in a few months. Good luck.

[jmjm530]

PA: . Do you think for better odds? Actually, no. Only for shorter treatment time. It's like your diet.
----------
Interesting and on-the-mark comment.

When I was at my doc's office while treating one day, I was asked if a Vertex rep could interview me for a few minutes, as they were in the office that day doing some sort of survey.

The one thing that stuck in my mind -- and this was very early on -- before it was called Telaprevir and maybe even before they started human trials -- the one thing that stuck out was they were focusing in even then on the number 24 (as in weeks) because apparently their research/interviews had shown that after 24 weeks is when a lot of people start to go downhill in terms of side effects. It's not that you necessarily have more sides in the last 24 but it seems you just keep getting more and more and more worn down and never get to recover. I'm sure that if I had stopped at 24, my post tx recovery would have been a lot easier and I might have been spared some of the lingering issues.

-- Jim

[Willy50]

I agree with Portann, but of course, the benefits don't stop with shorter TX time and all the other alluded issues that can come from extended chemotherapy.

I think the most recent TVR SVR results in EU were over 80%- nearly double that one could expect in the USA for SOC.

Reigning in the discussion back to the topic...... folks in Europe often do better than their North American counterparts.  Why??????  It could be they they get more exercise, have better diet and (no question about this I think) have less IR issues than the United States.  (but then who has more?)

best,
Willy

[jmjm530]

It could be they they get more exercise, have better diet and (no question about this I think) have less IR issues than the United States.  (but then who has more?)
----------
That has been the theory for some years now and in fact one reason why some of the early european trial results may have over-estimated SVR results in terms of the U.S. population. Hopefully this does not get me into too much trouble - getting ready to duck -- but when in Europe I could always spot a European woman (from an American) at 100 yards, they just didn't have that "healthy" farm-fed look :) And European men also appear much leaner. It's a different aesthetic. Whenever I drop down to my ideal BMI through diet I always get comments like "you look thin" or "did you lose weight" but the sub-text isn't necessarily complimentary because I think what Americans think looks "healthy" is about 10-15 pounds overweight.

-- Jim

[apache1]

Baja, I see exercise is the 1 element missing in your routine.

By the end of tx, I gained 18lbs.
I did stop most all exercise on tx. First time I consistently did not work out in 25 years.

I could not lose weight on tx, even for weeks after tx, even going on a strict diet.
THEN,
started brisk walking for an hour a day, then progressed to running and lifting again ...slowly.
The first week I started my exercise routine, I droped 4 lbs (mostly brisk walking)
After 8 weeks lost 12 lbs. No dieting. Just good healthy meals with realistic portions size

My point being, diets did nothing for me, maybe I was eating good enough already. I am not on a diet now, but eat good. Even have a piece of cake or ice cream once in a while, and my weight/bmi stays the same...as long as I don't miss my EXERCISE. I recently got a cold/flu (first time in 20 years) and stopped exercise for a week, gained 4lbs, quick.

I repeat, exercise made a drastic and immediate difference for me. I have exercised regularly for decades without ever stopping, until TX. Never realized how much it effected my metabolism and spirit, till I stopped for months, than started back up.
EXERCISE, also helped elevate my mood.

See a Dr and get the ok to slowly start an exercise program.
I hope you can get the Dr's ok.
Its not easy to start exercise, but it grows on you till it becomes part of your life. It is work, and you do sweat.
Sweat is good. You need to sweat, and get the fluids/blood pumping thru you.

Even a continuous semi brisk walk for 1hour per day, every day, will probably see immediate results. Thats what I did for my first couple weeks before I started running again. For me, exercise and weight control go hand in hand.

Please don't take this as criticism or me judging you. I am not.
I am only trying to motivate you into the world of exercise. IMO it is the key to good health.
For you, exercise is at least worth a try, especially since diets don't seem to work for us.


jmo
apache

[bajawoman]

fibrotest showed   DONE IN  NOV 08
score: .0.82  
(f1-f2)

ActiTest

Score: 0.23
(A0-A1)

Fibro Scan showed   JAN 09

8.7  k Pa
1QR  6.9

the only test I have had done in the USA are the original PCR
blood test  Genotype 1b viral load 47,300,000 HCV RNA, PCR. QUAT 7.67 in JULY 08
LAB SPECIALTY LAB VALENCIA CALIFORNIA
besides the Fibro Scan WITH HR

Ultra sound  stage two fatty liver and gall stones  JAN 09 BEFORE MY TRIP TO HR

Cat Scan  which was MARCH 09 2 months later showed no fatty liver or gall stones?

HOMA tests done here November 08 and March 09  showed practically the same results
3 and 2.99

Alt levels in June 08  TGO  12  TGP 16
In November 08   41

Oct 08 test done here  
anticueros anti-virus de la hepatitis C ANTI-HCV  11.90
indice S?CO  Menor a 1 NO REACTIVO  Mayor o igual a 1 REACTIVO
METHOD  QUIMIOLUMINISCENCIA CMIA ABBOTT

NOTA  La Investigacion de anti-HCV es una prueba de escrutinio En caso de reactividad se debera realizar prebas complementarias. Se recomienda las siguientes pruebas si el indice S/CO es de 1 a 13.99 realizar RIBA mayor o iqual a 14.00 realizar RNA HCV (PCR)
MY MEDICAL TEAM LOL WHAT MEDICAL TEAM  HR AND THE FORUMS AND THE INFO I CAN FEED MY GI  I GUESS I AM WITH ALL OF THE HELP I HAVE GOTTEN MY MEDICAL TEAM LOL

[bajawoman]

Hey I like your comments don't be sorry you are dead on   I was going to the gym love weights and excercise I really do it is the only times with excercise that my weight was good except for fad diets that definatley don't work  but all that said  What happened to me is I had an accident I was in great health (didn't know about the HCV ) but in 2001 I fell off my second story and a piece of rebar when though my forearm trying to stop the fall I flipped and landed on my back  breaking ribs etc and almost lost my arm I still am missing a part of my forearm  super lucky there  but needless to say the excercise stopped and then when I was almost ready to go again I took a vacation and tripped on a step and broke my leg just above my ankle  Geez ruined the vacation
and I wasn't even drunk
so now it is 2009 and I have been carrying around this weight for about 8 years  post menopausal didn't help either or the stress of work  
So I am going to try  It is just now the HCV really makes me tired  the supps help  since the fall I suffer from Vertigo so have to really watch my step  fast walking for me is not possible yet but could be in my future with starting with baby steps
I do need a trainer and I do some stretching but get incredibly wiped out with any attempts at excercise  and I do not overdue just feel wiped out like the flu the next day

but I have discussed this with my GI he wants me to begin with 5 min a day on my treadmill I invested in a few months back  something in my brain just won't click on I guess I have to be dragged to the thing  boy am I pitiful   baja

[jmjm530]

Fibro Scan showed   JAN 09

8.7  k Pa
1QR  6.9
-----------
So what does that kpa translate to -- stage 1-2 leaning toward 2? If so, and if your other scores are also around stage 1-2, then what's the rush to treat? What is the justification to treat now as opposed to waiting for the newer drugs?

If you're really f1-2, and are 60 something, and have had this disease for many years -- then you're obviously showing very slow progression. In this scenario, personally I'd go into watch and wait mode (liver healthy lifestyle, etc) with periodic (every 6-12 months) fibroscans as well as periodic visits to a hepatologist. I'd still do the biopsy, but that's been already discussed.

As long as you're running things by HR, you might want to ask him why he suggests treating at F1-F2 as opposed to waiting two years until the PIs come out of trial.

-- Jim

[Bill1954]

Bill1954 previously) "I am a type 2 diabetic that SVRrd. Although I had a slow response during the first treatment, the second time I cleared relatively early, and went on to achieve sustained viral response."
--------------------
CO previouly) I am going to take a wild guess and say that perhaps your blood sugar control was better the second time?
================================================================
Bill1954) I believe my BG control was adequate both times; although it wasn’t as tight as I recall during the latter part of the second treatment.

Bill1954 previously) "Type 1 diabetes typically involves underproduction of insulin from the beta cells in the pancreas."
--------------

CO previously) Actually Bill, Type 1 means that you don't produce ANY insulin at all.  
===============================================================
Bill1954) You got me there. I was responding to another poster that had used the term “underproduction”. I should have been more precise.

Bill1954 previously) " A type 1diabetic typically requires very little exogenous insulin; they can get by with injecting small amounts."
----------------

CO previously) Think about it.  They don't produce any insulin at all.

Bill1954) I hold my position on this; a type 1 diabetic typically requires far less insulin than a type 2 DM patient due to IR. I required up to 100+ units of insulin during treatment to maintain BG control, presumably due to existing insulin resistance. A type 1 diabetic would have become ill with that much insulin, I’d imagine.

Bill1954 previously) "but it doesn’t *preclude* SVR"
------------------
CO) I disagree with that, however, I do agree that IR is only one of many hurdles.
So you assert that insulin resistance precludes SVR? That’s a pretty strong statement, in light of the fact that diabetics with IR continue to achieve sustained viral response. I assume that type 2 DM patients continue to  have some level of insulin resistance.


Bill1954) "some members on this board have become obsessed by insulin resistance"
-------------------

CO previously) You can't be talking about me.  I didn't just become.  I've been obssessed with it for years...LOL

Bill1954) LOLOL! Your words, not mine!!
===============================================================
CO previously) I find your case incredibly interesting and wish I could see what the difference was between the two times you treated (same with FlGuy) since high levels of insulin make interferon ineffective and that includes injected insulin...and you were on quite a bit of Lantus insulin.

It's fascinating.  I would love it if you share more details.

Co

Bill1954) I’d be delighted to share any info you find relevant. Co. You can ask questions here, or feel free to ask me in private message (PM might be better; we won't take up bandwith on this thread). .

I’m not sure how much help I can be; while I kept good BG diaries throughout HCV treatment, they were forwarded to my doctor for the most part; I don’t generally keep copies for myself. I do have copies of A1c test results, but as we’ve discussed previously, they probably don’t accurately reflect control *or* insulin resistance.

Thanks again for your participation in the forum; you continue to provide thought-provoking, valuable  information here.

Best to you—

Bill

[bajawoman]

HR thought I was stage 2 approaching stage 3  but he also thought I could wait for the newer drugs believe he mentioned Vertex but if I decided I did not want to wait and wanted to treat now not to do it without alinia and metaformin  so I am waiting but in the meantime trying to get a handle on my IR but like others have mentioned too this is not an overnight or fast process   thanks for all your input and suggestions
baja

Bill I would personally like to see what you post to Co I find it very interesting and in my opinion this type of information will be beneficial to some here on the forum with diabetes problems   thanks  baja

[Marc1955]

I think there is something that is (perhaps) being overlooked in this discussion on IR. According to the article originally cited in the Journal of Hepatology, there is evidence that HCV can create IR. So the IR among HCV patients may not simply be related to lifestyle issue, but perhaps to the HCV itself.

I don't disagree with what has been said above – lifestyle changes need to be the first line of defense. But if the HCV is somehow implicated in the presence of the IR, then there are going to need to be different approaches.

(Sorry for extending this overly long thread -;))

[mikesimon]

I am a type 2 diabetic and I too achieved SVR after 2 failed tries. My glucose control was the same during all three treatments. What changed was dose and duration. The 3rd time I increased my ribavirin and treated with Pegasys whereas the first 2 was  regular interferon/ribavirin and the second was Peg-Intron/ribavirin. I don't think the choice of Peg made a difference. I think the increased ribavirin was the determinative factor and the extended treatment probably didn't hurt either.
My genotype was 1b and VL from 2.5 million to 6.5 million - highest at the start of my third and successful treatment.
Mike

[Gee704]

I was dx'd with Geno 1 July 08'. I have not yet begun tx but am about to begin a diet study this week concerning HCV and IR. One of the aims of this study is to find out if by changing the diet, can they change the ability of the HCV virus to grow.

In the purpose of the study paragraph for consent to participate it states that Hepatitis C can lead to insulin resistance. It also states that insulin is a hormone that helps your body use the sugar in the food you eat as fuel. In some people, the liver, muscle and fat stops responding to insulin as well as it should  and results in a condition called insulin resistance.

Hope this helps in the conversation here. I can post updates if I receive the information after completion of the study.

Gee704

[jmjm530]

Could you tell us more about the diet study? Is it part of a trial where you will be taking drugs to kill the virus, or is the diet study separate and after that you will treat privately. Thanks for joining the conversation, it all sounds interesting and I'm sure a lot of us would like to hear more if you are able to share.

-- Jim

[willing]

until recently I wasn't aware that three of the SVRs whose posts I find very helpful were/are diabetic. Among the  documented and overlapping associations in this area (hcv associated with  higher incidence of ir; hcv+ir associated with higher steatosis/fibrosis and lower  tx odds; pre-treatment with IS may/may-not improve svr odds) is data suggesting improvement in glucose abnormalities *after* svr, eg

http://www.ncbi.nlm.nih.gov/pubmed/17065685

Since all 3 of you, with repeated effort and in spite of the unfavorable odds described above, *did* svr, did you see any improvement in your glucose profiles after tx?

[Bill1954]

Thanks for the link, Willing; I’ll take a look in a bit. Regarding blood glucose control; I was able to delete all insulin from my regimen about 4 months post HCV treatment due to multiple low BG results. However, recently, I’ve been having difficulty again, and have had to increase two of the three oral ant diabetes meds. One of the problems with diabetes management is other factors… weight, exercise etc. are all critical to tight control. It’s hard to determine whether or how much IFN directly influences this. Still no insulin, but…

Take care—

Bill

[Gee704]

As more information becomes available, I would be happy to share.

This study is independent from tx. Although I am hoping IF I decide to treat, I will have a chance with a study with a PI within the same research environment. What interest me about this study (and possibly of one with a PI) is a shorter duration of treatment. If in fact diet plays a role in replication, not only should the duration for treatment shorten but maybe the success rate for SVR may go up? I am doing the study not only to help in the cure but also to broaden my knowledge.

There are three groups in the study. Healthy without Hep C or fatty liver, those with fatty liver, and Geno 1's not yet treating. They believe fatty liver develops in those with Hep C because the virus negatively affects a particular gene in the liver that is responsible for exporting fat. The gene, stearoyl CoA desaturase-1 creates a fat called oleate from another fat called stearate. Oleate is more easily exported than stearate from the liver. They will compare the amounts of oleate to stearate in the blood of the control groups while on two different diets. The first three weeks is a diet high in poly unsaturated fats and the 2nd three weeks will be a high carb diet.

Blood will be saved to run genetic studies from the Hep C control if they do find that a certain diet changes the ability of the virus to grow. This just may be helpful in future treatments - hopefully mine! Stay tuned.

[CoWriter]

Second person just got the results of his 2 Week viral load....89.  And we made sure he wasn't IR before startin g Tx.  AND he is also a previous non-responder.  (he used the same approach as CS).

Co

[CoWriter]

Remember what we were discussing the other day?  Take a look at this....
"The number of P-STAT1 observed correlated significantly with the body mass index  and homeostatic model assessment"

: )
Co


Intervirology. 2009 Mar 4;51(6):394-399.

Predictive Value of the Phosphorylation of Signal Transducers and Activators of Transcription in the Outcome of Interferon Therapy for Chronic Hepatitis C.

Miyaaki H, Ichikawa T, Nakao K, Takeshita S, Shibata H, Ozawa E, Akiyama M, Miuma S, Eguchi K.
First Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.

Objective: Signal transducers and activators of transcription (STATs) play a critical role in antiviral defense. To better understand pegylated interferon (IFN)-alpha and ribavirin combination therapy resistance, we examined the STAT expression in the liver. Methods: We immunostained Phospho-STAT1 (P-STAT1) and Phospho-STAT3 (P-STAT3) in 59 hepatitis C virus (HCV)-infected liver tissues and compared the expression of these STATs proteins and the clinicopathological factors. Results: The number of P-STAT1 observed correlated significantly with the body mass index (BMI; p = 0.03) and homeostatic model assessment (p = 0.007). The number of P-STAT3 observed correlated significantly with the ALT level (p = 0.002) and platelet count (p = 0.002). The number of P-STAT1 nuclei in the sustained virological response (SVR) group was significantly larger than in the non-SVR group (p = 0.003). On multivariance analysis, the number of P-STAT1 nuclei (p = 0.004) and age (p = 0.016) were significant predictors of SVR. Conclusions: P-STAT1 in the liver tissue prior to IFN therapy correlated with an increased BMI and increased insulin resistance, and might be a useful predictor of HCV clearance by IFN therapy. On the other hand, P-STAT3 might play a critical role in the hepatocellular response against inflammatory damage.

[CoWriter]

"I don't disagree with what has been said above – lifestyle changes need to be the first line of defense. But if the HCV is somehow implicated in the presence of the IR, then there are going to need to be different approaches."
-------------------

That's right Mark.  There are two different types of IR.  Hepatic IR caused by the Hep C virus and peripheral IR caused by obesity.


"(Sorry for extending this overly long thread -;)) "
------------------

I, for one, like to hear what people have to say on this subject.  Thank you for jumping in!

Co

[CoWriter]

Fasting 84
1 hour 119 (that was after drinking that gawdawful stuff)
2 hour 83
3 hour 76
4 hour 53

----------------

My guess is that at that time you're producing too much insulin.  Next time you have a 3 or 4 hr GTT, ask your doctor to see if he would check the insulin.

Co

[bajawoman]

Can a person have both types of IR?

[CoWriter]

Bill....Lantus controls fasting blood sugar.  What was your fasting blood sugar like the first time you treated?  The second?  

Mike....how much Riba?  Same question as Bill....what was your fasting like?

Co

[CoWriter]

I certainly do speak Spanish.  Wasn't it funny how much time I spent translating your results and HR ended up speaking Spanish....LOL

Love ya!

Co

[mikesimon]

Willing,
I don't recall any difference in my glucose post treatment. Recently I put on some weight and that seems to have increased my BG. And, often the weight comes with increased carbohydrate intake so that played a role as well. I have lost some of the weight by abstaining from carbs and as a result my insulin requirement has decreased.
CO,
After 2 years of treatment I lost a lot of weight. I weighed between 140 & 145 lbs and I had treated with 800 mg ribavirin per day my first 2 treatments. For the third treatment my ribavirin dose was 1000 mg per day.
During my second treatment I did become undetectable but quite late in my treatment - guessing I would say between week 20 to week 28. I stopped at week 52/53 and relapsed immediately.
My third treatment I was undetectable per Heptimax at week 12 but I assume I was clear at week 11 because week 10 VL was 15 IU/ml or thereabouts.
Mike

[merryBe]

sevral things:

yes one could have both HCV caused and peripheral.

Your BS's are not bad but have you had your thyroid checked. The easiest way to correct for triglycerides is to be sure you stay in the .1-1.5 range, if your TSH number is 2,3,4 or higher this will rei triglycerides, so a low dose of synthroid can really help there.
It used to be a 2 or 3 was consider fine, but not anymore.

not only can you have 2 types IR, but MANY types of diebetes (diabetes):

A number of other types of diabetes exist. A person may exhibit characteristics of more than one type.

For example, in latent autoimmune diabetes in adults (LADA), also called type 1.5 diabetes or double diabetes, people show signs of both type 1 and type 2 diabetes.

Other types of diabetes include those caused by

genetic defects of the beta cell—the part of the pancreas that makes insulin—such as maturity-onset diabetes of the young (MODY) or neonatal diabetes mellitus (NDM)

genetic defects in insulin action, resulting in the body’s inability to control blood glucose levels, as seen in leprechaunism and the Rabson-Mendenhall syndrome

diseases of the pancreas or conditions that damage the pancreas, such as pancreatitis and cystic fibrosis

excess amounts of certain hormones resulting from some medical conditions—such as cortisol in Cushing’s syndrome—that work against the action of insulin

medications that reduce insulin action, such as glucocorticoids, or chemicals that destroy beta cells

infections, such as congenital rubella and cytomegalovirus

rare immune-mediated disorders, such as stiff-man syndrome, an autoimmune disease of the central nervous system

genetic syndromes associated with diabetes, such as Down syndrome and Prader-Willi syndrome

[Deb_c430]

http://www.sciencedaily.com/releases/2009/03/090327072801.htm

[merryBe]

I think getting the BMI is important, much more than my doc thinks.

However, one has to be careful how one achieves that with HCV.and especially with any iron overload or IR on board.

reason being is fasting causes big issues as does too much excercsie with oxidative stress which in turn causes more liver harm.

So dieting should be renamed portion contol and excersise should be light to moderate to avoid oxidative stressand muscle acid build ups.

Because once on tx red blood cells can be cut by 30-50% of normal, activity is not always an option.

However, one can help ones blood sugar out a lot by 7 small  half meals a day.
the 7th meal should be a glass of milk and grahm cracher, or a small piece of chesse with a couple slices of apple, taken at mifnight or upon wakinf during the night,
CTUALLY EATING THAT LATE WILL HELP YOUR MORNING BLOOD SUGARS TO BE LOWER believe it or not, by having some available fuel through the night it slows the production of hormones that tend to raise BS overnight,

I'd really recommend you take a look at Barry's Sears "The Zone" diet...in paperback everywhere.
This is the only diet book I know of that explains IR and diebetes (diabetes) and food matabolism so that any person of average intelligence can fully understand it. His chapter on Insulin Production alone is worth the price of admission.
Even if you don't like "the point" system he used for keeping track of foods, you can still follow the principal of combining protein/carbs/fats in the right proportion is each meal or snack, and this combing alone will greatly effect IR.

mb

[bajawoman]

thank you for the information here is my thyroid panel
INDICE DE TIROXINA LIBRE ITL                 2.20  %
T3 CAPTIACION                                       25.3   %
T3 TRIYODOTIRONINA LIBRE T3F       3.39  pg/ml
T3 TRIYODOTIRONINA TOTAL              108               ng/dl
T4 TIROXINA LIBRE T4F                 1.09     ng/dl
T4 TIROXINA TOTAL                           8.72   ug/dl
RTH TSH TIROTROPINA                 1.50     uUl/mL

My doctor said it was fine?
I have the Zone very good diet plan and very similar to the Insulin Resistance diet
which I think I follow pretty good but the PORTION CONTROL  is a factor for me  I am so hungry  I am eating breakfast for the first time in years
but am really starving at 11am and again throughout the day

fasting before a blood test is really hard on me to do I dread it as I feel so woosy and dizzy and feel very bad when my body is in starvation mode

there is another factor I think for some that eating time can bring anxiety from past experiences or lifestyle and I think most people in a rush do not enjoy what they eat
or how they eat  this is something I personally want to work on but always being in a hurry is a definate factor for me and with people on tx it is an anxious time as stated here as they cannot keep it down or most foods just are not appealing

Excercise I get so much bad excercise at work I am very active moving things and it is tiring and causes pain but that is part of my job decoration in my one business I love it but it tires me out to no end  
I am very strong and overdo  also being on my feet which has always been easy for me is now painful but so is laying down after sleeping there is a lot of pain upon waking
too much info???

but thanks for your post I have to admit I do not understand much of the IR Diabetes Info
just wondering if I could have both as having HCV for the length of time I have had I figure it is throughout my body rather than damaging my liver which you would think would be the case it seems to have affected my body in many ways and not my liver??
Can a person who is always in survival mode have less damage to the liver? does having HCV in your brain stem or brain cause other issues in your body?  or is it the virus in those organs?  
baja

[CoWriter]

Thyoid looks fine.

Co

[CoWriter]

I sent you the full text of the initial study MYS posted.

Anybody else who would like a copy please contact me via PM.

Co

[CoWriter]

Thanks for posting the link.  Very interesting.  According to the Gomez-Romero study, Blacks are considered "difficult to treat" because they are IR.  So it seems that the topic of IR just got alot more complicated and alot more interesting.

Thanks again!

Co

[FlGuy]

I am wondering if you are familiar with the 'life' of metformin.  Using riba as an example, it works up to a saturation level over time and eventually reaches a steady state.  Is it the same for metformin, or is the life of metformin much shorter. And further, is dosing of metformin strategic in terms of meals? Thanks.

[CoWriter]

Half life of Metformin is very short 6.2 hours and it's excreted in the urine.

Metformin should be taken with meals.  For example, if you take it twice a day, then it should be taken with breakfast and dinner.

Co

[FlGuy]

Thank you. Now for a follow-on.  The doc asks me to take readings, he suggests taking a fasting reading (upon waking) and on alternating days two hours after lunch.  (I usually have three meals a day, can't manage  5-6 small feedings per day).  If I take the met. with breaksfast (after the fasting reading) and take the pm metformin with dinner (7 PM) am I getting a reliable reading if I take the reading after lunch which would be 7.5 hour after AM dose and 4.5 hours before PM dose?

[bandman54]

"Second person just got the results of his 2 Week viral load....89.  And we made sure he wasn't IR before startin g Tx.  AND he is also a previous non-responder.  (he used the same approach as CS). "

question - did this person have insulin resistance??  And if so, did he take metformin before and during tx??

Just wondering....

bandman

[CoWriter]

Yes, it is.  Because you will be doing the same thing every day.  What your doctor wants to see is PATTERNS.

So you can't eat 5 small meals a day?  

I once saw a patient on a referral.  He worked at a car wash on commission.  So obviously, he couldn't stop to eat whenever he wanted.  After I explained to him that having meals on a regular schedule was one of  the most important things in obtaining glucose control, he said he would try.  

Next time I saw him he was very happy.  His blood sugar was great and with a big smile on his face he told me that he was taking a sandwich or a burrito to work....and when it was lunch time, he would hide between the cars and quickly eat the food he'd taken with him.

For some reason, I think about him every time somebody says, "I can't".  Eating a snack simply means eating a few nuts or a cheese stick.  

Co

[CoWriter]

His HOMA was below 2.  His diet is good and he exercises.  He followed a plan like CS's.  AND his side effects are not bad at all.  Some of the supplements seem to work very well in preventing side effects.

Co

[FlGuy]

Thanks again, and I promise to give the meals a better effort.  Nuts and cheese are doable.
But it brings me to another question. Based on the transitory life of meformin, I'm beginning to think that even a religious adherence to the daily dosing of metformin will have no affect on an a1c test over time.  And, short of a steady diet of riba the only thing that can impact the a1c results for me is diet, exercise, several meals a day including nuts and cheese. Am I correct about metformin and a1c, or am I asking the wrong questions?

[willing]

Bill, Mike : thanks for the information; seems the DB-control dividend from svr is real but by no means conclusive..

Co: so is there a supplement that promotes phosphorylation of stat1 to take along with the SAMe? I'm starting to repeat myself here, but I still think the Magdalena S-F paper show fixing  ifn signaling is only going after a part, and possibly not the most significant part, of the problem. Even after those 200 or so ISG get translated and go about their business they're still not getting the job done in NRs.

As a card-carrying member of the Alinia fan club, I found the following
http://www.ncbi.nlm.nih.gov/pubmed/18710916
(referenced in a CME review Jim posted recently) to be very good news. Though cells saturated with the stuff can lose their response to NTZ, the virus cannot mutate away from it and the cells actually become significantly *more* responsive to ifn. There's no real reason to *not* take the SAMe, but I think adding the Alinia is likely the more significant factor. (also:
http://www.ncbi.nlm.nih.gov/pubmed/19135998

[CoWriter]

Diabetes questions are never the wrong questions.

I think what you're thinking is that Metformin lowers your blood sugar....and that is not so.  Metformin makes the cells in your body more sensitive to insulin but it doesn't lower your blood sugar 40 or 50 points.  It doesn't do that.

On my journal, which you can access through my profile, there's an explanation of diabetes and there's a section on how Metformin works.  I think it will help you understand what Metformin does.

Your HgA1C is the average fasting blood sugar over the last 3 months.  How can you lower the fastin g blood sugar?  By having a protein snack half hour before you go to bed so the liver won't give you any sugar during the night.

Co

[FlGuy]

One more time, thank you.  I'll see the journal and go to the protein.