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, which should be kept in the 30-80 ferritin range.
Treatment – mixed antioxidants, silymarin, polyphenols.
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 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. Cooked fats and hydrolysed fats should be avoided, omega-6 EFAs and PUFAs - most vegetable oils - and saturated fats minimised, while fatty fish (omega 3 EFAs) and extra virgin olive oil (monunsaturated omega 9 fatty acid) should be eaten whenever possible.
Treatment – l-methionine, B12, folic acid, phosphatidylcholine (lecithin), carnitine.
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, zinc, vitamin A, vitamin C, cordyceps, astragalus, garlic.
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, evening primrose oil.
Coagulation (liver damage, inflammation) – rapid coagulation (clotting time) is associated with fibrosis, thinner blood with better outcomes. Blood clots often become a focus of inflammation, leading to fibrosis. Most anti-fibrotics and anti-inflammatories are anticoagulants; for example:
Treatment – ginkgo, vitamin E, fish oil, garlic
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) as acetylCoASH, which instead becomes tied up with unprocessed fats in steatosis. 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