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LondonGirl wrote:
Somehow I think there are some links between how our bodies are responding to the medicines, especially if a slower response,
If I talk about this GT2 is probably going to start a petition to get me kicked out of the forum
Okay, but keep in mind that this is my favorite subject and I can talk about it for days.
With interferon treatment, being insulin resistant lowered treatment sucess (But it doesn’t seem to be important with DAAs). Multiple mechanisms cause the development of INSULIN RESISTANCE in patients with Hepatitis C.
1. Steatosis which is metabolic in genotype 1 and caused by the virus in genotype 3. So they are two different types of steatosis.
2. The chronic inflammation of the liver caused by the Hep C virus causes an overproduction of pro-inflammatory cytokines. Activation of inflammatory pathways, together with increased levels of free fatty acids disrupt intracellular pathways in liver cells and inhibit insulin signalling…. leading to insulin resistance.
3. The core protein of the Hepatitis C virus can directly inhibit the insulin signalling pathway and increase reactive oxygen species production, both of which can further exacerbate insulin resistance.
4. Obesity….because fat cells are not sensitive to insulin.
5. Endotoxemia from leaky gut.
The liver is the first organ that encounters venous blood from the small and large intestines via the portal vein. So that makes the liver vulnerable to exposure of bacterial products coming from the intestines. Translocation of large amounts of gut-derived products is usually prevented by an intact barrier system made strong by intestinal epithelial cells. In general, the liver tolerates small amounts of bacterial products in order to avoid harmful responses, but damage of the intestinal epithelial barrier results in a leaky gut that lets large amounts of bacterial products reach the liver. When they reach the liver, they act as ENDOTOXIN and elicit a strong reaction from our immune system.So as you can see, it isn’t just about diet. People have a hard time accepting the possibility of being insulin resistant but if you’ve had the virus for many years, chances are some of those things are happening. Being insensitive to insulin makes your pancreas produce high levels of insulin to compensate, and having high levels of insulin made Interferon ineffective.
BUT thankfully, it doesn’t seem to matter with DAAs. People are clearing even if they have high blood sugar or diabetes. So don’t let that worry you. This study says.
“with the advent of potent direct acting antiviral therapies, viral eradication may be possible despite poor glycemic control and may actually be an effective means of improving diabetic control.”I tend to be hyper vigilant, especially with signs of insulin resistance because I’ve been doing it for so long they sort of jump out at me from the posts. It’s my “job” to watch after you. But remember, I’m not always right and I’ll probably get lynched for saying this…
When you say things like “I had a huge craving for carbs”, “gaining too much fat, losing too much weight”. It makes me suspect high blood sugar. Insulin is like the key that opens muscle cells so glucose can go in to feed them, and when you don’t have enough insulin to open doors, food can’t go in to feed them and they start loosing weight. Fat tends to accumulate on your belly.A fasting blood sugar will let you know for sure and then you can come and tell me that I was wrong and you’re signing GTs petition.
P
Hi Price,
There didn’t appear to be a lot of correlation between this post and genotype 3 relapse and retreatment options with DAAs so I’ve split it off into its own thread.
G3a since ’78 – Dx ’12 – F4 (2xHCC)
24wk Tx – PEG/Riba/Dac 2013 relapsed
24wk Tx – Generic Sof/Dac/Riba 2015/16 relapsed
16wk Tx – 12/01/17 -> 03/05/17 NS3/NS5a + Generic Sof
SVR7 – 22/06/17 UND
SRV12 – 27/07/17 UND
SVR24 – 26/10/17 UND
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