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Wednesday, 7 December 2011

Hep C Treatments in 5 Words

People are always asking me to put my Hep C findings into simple language and keep it short. It's hard to do this without cutting corners. But increasingly I find things falling into simple categories, each of which can be explored seperately.

  Hepatitis C in 5 words or less A Hep C protocol should protect against the following aspects of HCV infection:

  Oxidative stress (liver damage, diabetes, inflammation) – Hep C depletes antioxidants, low antioxidant levels are associated with poor outcomes. The combination of oxidative stress and hypomethylation is the preventable cause of hepatitis, fibrosis, and cirrhosis. Some genotypes also promote the accumulation of iron, which increases oxidative stress exponentially. Genetics, iron fortified foods, and poor liver function can also add to iron loads.

 Treatment – mixed antioxidants (selenium ACE type), Co-enzyme Q10, silymarin, polyphenols, OPCs.

  Hypomethylation (steatosis, fatigue, depression) – Hep C depresses methylation, which allows fats to accumulate and decreases energy output. Methylation is the process needed to supply creatine, phosphatidylcholine, carnitine, co-enzyme Q10, glycine, melatonin, adrenaline, cholesterol and steroids; methylation also inactivates histamine and niacinamide, and helps with detoxification. Methylation also plays a role in DNA synthesis and in regulating the expression of genes and the activity of proteins. All methylation in the body is carried out by the SAMe form of methionine, except for the methylation of methionine itself, which requires B12, folic acid, and/or betaine. Hypomethylation (deficient methylation) in Hep C is largely due to inhibition of vitamin B12 by oxidative stress, the poor absorption of B12 and folate when stomach acid is inadequate, and anorexia and nausea limiting intake of foods rich in methionine. So-called low fat foods that are low in high-quality protein and essential fats and high in carbohydrates are especially problematic - the liver synthesises fats from carbohydrates in any case. Overcooked fats and refined oils and spreads should be avoided, vegetable oils minimized, some PUFA from fatty fish (omega 3 EFAs) and extra virgin olive oil is acceptable but most fats should come from red meat, cream and butter, dripping, and coconut.

 Treatment – l-methionine or SAMe, B12, folic acid, phosphatidylcholine (lecithin), carnitine, betaine.

 Immunosuppression (HCV replication, co-infections, allergies) – Hep C interferes, both directly, and via oxidative stress, with immune function, allowing co-infections and autoimmune syndromes to develop. Increased levels of interferons during illness can bring about gluten and other allergies in previously tolerant individuals.

 Treatment – selenium, probiotics, zinc, vitamin A, vitamin D, vitamin C, cordyceps, astragalus, garlic, echinacea.

Note on antiviral herbs: Ginger, silymarin, grape seed OPCs, green tea extract, blueberry leaf extract, Rosa Rugosa flowers, various iridiods, stevia all directly inhibit HCV cell entry or replication; resveratrol enhances HCV replication.

  Inflammation (other inflammatory conditions, liver damage, mood disorders) – Hep C increases production of pro-inflammatory cytokines, which can promote fibrosis, and prostaglandins, which strip essential fatty acids from cell membranes, causing pain and mood changes. Inflammation and oxidative stress are closely related. Similar processes are involved in PMS, bipolar disorders, psychosis etc. so it is not surprising that moods, emotions and perceptions can be affected by Hep C. Inflammatory cytokines can also trigger sensitivity to complex proteins such as gluten (wheat, rye, barley) and casien (cow's milk), which then become an additional cause of inflammatory disease.

 Treatment – magnesium, vitamin D, ginkgo, EPA and DHA (krill oil is the best source), niacinamide, N-acetyl-glucosamine (glucosamine can be an effective substitute for NSAIDs). Gluten free, low carbohydrate diet high in saturated fat.

  Detoxification (liver damage) - Exotoxins and endotoxins requiring phase 1 and phase 2 detox – drugs, toxins, pollutants, cholesterol and steroids - must be processed by liver and kidneys. Many of the phase 2 reactions use glutathione, glycine and taurine, levels of which are reduced in Hep C, and pantothenic acid (B5). Glycine production is inhibited by hypomethylation. Improperly metabolized toxins can add to oxidative stress, damaging the liver, or inhibit enzymes, impairing liver function.

 Treatment – sulfur amino acids, B vitamins, broccoli sprouts, whey protein


Serdna said...

It seems that you have found some information about vitamin C and hepatitis C. Are you aware of the anecdotal data about it curing the disease? Andrew W. Saul seems to think it works, at least using intravenous vitamin C (there are two papers about hepatitis and IV vitamin C in this book, and there is at least another one about oral vitamin C and hepatitis A). One recent study using 2g/day of oral vitamin C and 10g IV vitamin C twice weekly got some positive results. I think that higher doses should do better (I have taken more than 60g/day oral vitamin C —seeking bowel tolerance— just for a flu).

Another more DIY approach could be liposomal vitamin C (the one used by the family of Alan Smith when he was able to swallow) instead of the IV one. A quick risk-benefit analysis, given the low toxicity of ascorbic acid, should give rise to a positive result.

Another treatment even less investigated seems to be using BHT. Steven Wm. Fowkes talks about some anecdotal cures of hepatitis C in his book.

Best regards.

Puddleg said...

I know people who have done IV ascorbate and felt better, but not cleared the virus.
It's possible that high-dose vit C would increase clearance of early infection. Later on, I'm not so sure.
However, I think any vit C intervention with a chronic infection should be sustainable.
Start with something like IV or liposomal if you like, to see if it works, but if so, it's also worth doing it everyday thereafter at a rate you can afford, even if that's just a cheap 500mg tablet 2x a day.

A low carbohydrate diet will make lower intakes of ascorbate more effective (glucose and ascorbate compete for receptors). Linus Pauling himself ate a high-fat diet, bacon and eggs for breakfast, and lived to be 93.

I'm not brave enough to take BHT, but the Fowkes book is very well written and I take him seriously.

Serdna said...

Although commercial Lypo-Spheric Vitamin C is too expensive for more than 2g/day maintenance, you could check its effectiveness in a short trial (15 days with something like 5g/day? It is hypothesized that it is directly absorbed by the liver, so...), and if you get positive results you could try the do-it-yourself approach (I would use sodium ascorbate —dirty cheap—, though, that is the one used in the Lypo-Spheric product). You may find some more information about the do-it-yourself approach googling " home made lypo C".

I have no personal experience with do-it-yourself lypo C though.


Serdna said...

I have to correct myself: "It is hypothesized that it is directly absorbed by the liver". I have just recently realized that liposomal vitamin C is absorbed into the lymphatic system (thanks to Roland), so no direct access to the liver.

Puddleg said...

Fats are hydrolysed and repackaged by intestinal cells; being re-formed in the lymph vessels as it were. MCTs behave differently for some reason. You'd have to run a radioactive tracer on Lipospheric C to know exactly what happens.

Bowel tolerance I suspect is unabsorbed ascorbate (a sugar, basically soluble fibre) being fermented by E. Coli.
This also explains why overuse of ascorbate increases frequency/urgency of urination in some people; basically a UTI fed by ascorbate in the bladder, irritating urethra and/or prostate, creating a vicious cycle.

Serdna said...

Ok. I see that I have been too quick in finding liposomes so obviously efficient delivering ascorbic acid directly into cells. Nevertheless Section 3.2 of Liposomal formulations for enhanced lymphatic drug delivery gives some plausibility to the hypothesis. It would fit with Dr. Levy clinical experience too.

About UTIs and ascorbic acid. It has been known E. colia and other bacteria are capable of fermenting ascorbic acid for quite a long time. What I am unable to find is any reference about an infection promoting effect of ascorbic acid in urine, just the oppositefrom majkinetor— (another one, along some anecdotal experience). Since the diuretic effect of ascorbic acid seems sufficient to explain those symptoms I don't think that your hypothesis UTI-fed-by-ascorbate has a lot of support.

Puddleg said...

There was a bit of discussion on Hyperlipid some time ago about whether the diuretic effect of ascorbate had been seen since 1944.
If ascorbate inhibited the polyol pathway in the kidneys of some species, which is plausible, it could cause diuresis due to the role of this pathway in conserving water.
(Aldose Reductase-Deficient Mice Develop Nephrogenic Diabetes Insipidus

However, if I assume excess ascorbate will act as a diuretic, that doesn't help me use it effectively or treat any consequences of over-dosing.
If I assume instead that it is a prebiotic that can cause a UTI by feeding e. coli (which is a species common to UTIs), then I have effective treatments for any after effects (d-mannose or hibiscus) and an additional guide to how much is too much.
"Escherichia (E.) coli is responsible for most uncomplicated cystitis"