Hepatitis Supplements and Diet

These are the supplements, diet and exercise regimen that I am on, along with taking 3 mg of Low Dose Naltrexone for controlling my Hepatitis C virus. It is based on Dr. Berkson's original protocol of using ALA (Alpha-Lipoic-Acid), Selenium, and Silymarin (Milk Thistle) to treat his patients with liver disease.

The 3 basic antioxidants there were used in this report are Alpha-Lipoic Acid (thioctic acid), Silymarin (milk thistle) and Selenium (selenomethionine). The Alpha-Lipoic Acid product was manufactured by Asta Medica at Frankfurt Am Main, Germany. The Silymarin was a product distributed by NOW Foods of Bloomingdale, Illinois, and the Selenium was encapsulated by Metabolic Maintenance Products Inc., of Sisters, Oregon.  Note, this is an old study prior to the newer interferons and protease inhibitors.

Berkson Clinical Study

Dr. Berkson put me on 3 mg. of Low Dose Naltrexone back in February of 2009. I am also taking the "triple antioxidants" along with other supplements that he and my own CAM doctor believe is right for me. I use primarily Metabolic Maintenance, BlueBonnet Nutrition and Now Brands, especially for the ALA, as the best source is European.

UPDATE - 2013-2014 -   Now taking the Jarrow Alpha-Lipoic-Sustain as my integrative doctor insisted - I have had much better results in all liver and other tests using this formula though the above are all great.

 

DOSAGES

ALA -  I take 300 mg. two times daily with food - some folks take it without food but if you have problems with your blood sugar levels, ALA can lower them, so it is probably better to take with food.  At Dr. Berkson's clinic, they would make sure that you had eaten something prior to the IV ALA treatments - which are, of course, different than oral supplementation.  However, with the Jarrow ALA Sustain, you can get by with one dose once your enyzmes have normalized.

B-Complex - It is also very important to take a B Complex along with ALA as the ALA will use up the B vitamins in the body. I use Bluebonnet B Complex - I also take additional Biotin, B-12, and Pantothenic Acid (B5) as a vitamin diagnostic test showed that I have low levels of those 3 B vitamins.

From Dr. Berkson's book "


"User's Guide to the B Complex Vitamins"
 
 

"Both ALA and the B vitamins are essential in helping the cells mitochondria make energy. When mitochondria function correctly, they require a number of enzymes.


ALA is the major key that turns on these enzymes. thiamine, niacin, riboflavin, biotin, and other B-complex vitamins are also involved in this system of enzymatic processes and becove depleted as the mitochondria produce energy. Therefore, if a person supplements with ALA, he or she must also take at least on B-complex capsule with it. In other words, since ALA revs up mitochondrial activity and uses up B vitamins in the process, there's a chance a person can become deficient in many key B vitamins without proper supplementation."

Selenium - 200 Mcg. in two doses - and try not to exceed 400 Mcg. daily - take into consideration if any of your other supplements contain Selenium as well.  Also, foods such as brazil nuts contain high amounts of selenium, so use caution if you eat a lot of foods that contain selenium.

Silymarin (milk thistle) - 600-900 mg daily     I have been using the Pharma Thistle Gold brand lately - very cost efficient and works well.

Vitamin D-3 is very important as well. My doctor regularly tests me and says that levels should be at least above 50 and optimally around 75. I am taking from 2,000 to 8,000 IU daily as my levels are not ideal. Most people with liver disorders, particularly with Hepatitis C, are deficient in Vitamin D.

Ideally, I like to take other supplements that help support the methylation cycle, which in turn helps boost glutathione levels that are crucial for the liver and overall cellular growth. NAC, SAMe, Taurine, Whey protein (mixed in a daily fruit smoothie), help the cycle. I can't always afford all of these supplements, but always try and have the "triple antioxidant's and B Complex on board, as well as an iron-free daily vitamin. Digestive enzymes are also very beneficial and help the entire digestive cycle.

I also use a great deal of L-Lysine, an amino acid, which helps control the various Herpes viruses that I have. Grapefruit seed extract is very beneficial for viral infections and yeast - I take the GSE for a couple of months and then switch over to Olive Leaf extract.

IP-6 is important as it helps keep ferritin levels down.  I usually take one or two 500 mg. capsules twice daily - note, it is very important to take IP-6 away from any other supplements or food for at least a half hour to an hour.  I find that if I wake up during the night to use the restroom, I will take one dose then.  The Jarrow formula works very well and is very inexpensive compared to others.

I've found that iHerb has very inexpensive prices on most supplements (but not Metabolic Maintenance) - Use this code to get $5.00 off your first order: KOV896

iHerb

Amazon.com has Metabolic Maintenance at variable prices. This site has Metabolic Maintenance products at lower prices - but they do not ship as fast:

My Health-Store


Or just go to amazon.com


Diet is very important with any type of liver disease. When you consider that everything that you eat is processed by the liver, it makes all the more sense to pay attention to your diet. Organic foods contain a lot less harmful elements than those produced in mass, or those that have been genetically engineered. Avoid processed foods, particularly those with gluten (the protein found in wheat and barley), and fried, greasy foods. Many people with immune disorders also cannot tolerate dairy products or are lactose intolerant. Avoid "fake" foods - like margarine or MSG. I like to use Stevia instead of sugar or any of the artificial sweeteners like Splenda.  And newer research indicates that going low carb, high fat might be very beneficial, particularly in those with fatty liver and insulin resistance.

One of my favorite bloggers is George Henderson and one of his best posts is:

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 casein (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




Nutrition


Fresh vegetables and fruits - lean meats - brown rice, gluten-free grains such as quinoa - avoidance of processed or "fast food".  Eat several small meals as opposed to a few heavy ones as it is easier for the liver to digest.   Here is more:

New, also from George Henderson - thank you George!  Glad I found you again!

 High-Fat Hep C Diet



DIET AND NUTRITION FOR LIVER DISEASE AND HEPATITIS

Nutrition And The Liver

Video - Foods to avoid when living with Hepatitis C



Easy Fruit SmoothieFresh fruit - strawberries, pineapple, banana - half fresh and half frozen - add juice -   - Add whey protein(gluten-free!) for more punch

GLUTEN FREE DIET

I maintain a strict gluten and dairy free diet - most folks with Hep C or liver disorders (or really just about any disease) have problems or sensitivities to the proteins in these food sources.  A great resource is called
"The Gluten File"  Check out the page on "Liver Disease"  for many studies and abstracts.  One study is:

Celiac disease in patients with severe liver disease: gluten-free diet may reverse hepatic failure.


BACKGROUND & AIMS: Mild liver abnormalities are common in patients with celiac disease and usually resolve with a gluten-free diet. We investigated the occurrence of celiac disease in patients with severe liver failure.

METHODS: Four patients with untreated celiac disease and severe liver disease are described. Further, the occurrence of celiac disease was studied in 185 adults with previous liver transplantation using serum immunoglobulin A endomysial and tissue transglutaminase antibodies in screening.

RESULTS: Of the 4 patients with severe liver disease and celiac disease, 1 had congenital liver fibrosis, 1 had massive hepatic steatosis, and 2 had progressive hepatitis without apparent origin. Three were even remitted for consideration of liver transplantation. Hepatic dysfunction reversed in all cases when a gluten-free diet was adopted. In the transplantation group, 8 patients (4.3%) had celiac disease. Six cases were detected before the operation: 3 had primary biliary cirrhosis, 1 had autoimmune hepatitis, 1 had primary sclerosing cholangitis, and 1 had congenital liver fibrosis. Only 1 patient had maintained a long-term strict gluten-free diet. Screening found 2 cases of celiac disease, 1 with autoimmune hepatitis and 1 with secondary sclerosing cholangitis.

CONCLUSIONS: The possible presence of celiac disease should be investigated in patients with severe liver disease. Dietary treatment may prevent progression to hepatic failure, even in cases in which liver transplantation is considered.

PMID: 11910339 [PubMed - indexed for MEDLINE]



If you have undergone interferon treatment, chances are that it triggered gluten intolerance or full blown celiac disease:

Silent celiac disease in chronic hepatitis C: impact of interferon treatment on the disease onset and clinical outcome.

http://www.ncbi.nlm.nih.gov/pubmed/15492610


Unmasking of coeliac disease on interferon treatment for hepatitis c

A 45-year-old woman with chronic hepatitis C, contracted 25 years previously from intravenous drug use, was referred to our hepatitis C clinic by her general practitioner. She was noted to have persistently elevated serum transaminases, with alanine transaminase of 158 U/L (normal < 34) and aspartate aminotransferase of 92 U/L (normal < 31), but was clinically well. She had an albumin of 34 g/L (normal 36–48), bilirubin of 17 µmol/L (normal < 18) and International Normalized Ratio of 1.3. A normal sized liver but coarse echotexture with no mass lesions was noted on abdominal ultrasound. There were no signs of portal hypertension on examination or on ultrasound.

She had an upper gastrointestinal endoscopy done 4 years prior to investigate transient mild diarrhoea in which small bowel biopsies were taken. On histological examination, the villi appeared slightly short and broad, and there was some branching of crypts, but no characteristic degenerative or inflammatory changes of coeliac disease was seen.

As there were no contraindications to anti-viral therapy, she was commenced on pegylated interferon alpha (180 µg subcutaneously, weekly) and ribavirin (400 mg twice a day). She initially tolerated treatment well, but after 12 weeks developed abdominal pain and bloating, nausea, vomiting and watery diarrhoea. She was provided a course of oral metronidazole, which did not improve her symptoms. As it was felt that these symptoms were due to the interferon treatment, her interferon dose was gradually reduced to 90 µg/week, and she was provided with loperamide.



Despite this, her symptoms progressively worsened and by week 20 of treatment, she was noted to be anaemic with a haemoglobin level of 97 g/L (normal 115–165) and ferritin of 7 µg/L (normal 18–464). She was also folate deficient with a serum folate of 4.5 nmol/L (normal > 6.8) and had a bilirubin of 17 µmol/L and albumin of 30 g/L. As she had genotype 1 with evidence of cirrhosis and was managing treatment relatively well, we decided to continue antiviral treatment despite her symptoms to complete a 48-week course. She continued to have four to six episodes of watery diarrhoea a day and by completion of therapy, her weight had dropped from 67.2 to 57.8 kg. Of note there was no fever, no haematemesis, no melaena and no per rectum bleeding.

She was reviewed 12 weeks post treatment, when she was noted to have a negative hepatitis C RNA PCR, but her liver function tests remained abnormal with alanine transaminase of 51 U/L and aspartate aminotransferase of 81 U/L. As abdominal bloating, nausea, lethargy and diarrhoea were persistent, she had a repeat upper gastrointestinal endoscopy. Small bowel biopsies this time revealed striking total villous atrophy and marked crypt elongation with prominent epithelial lymphocytosis consistent with untreated coeliac disease. Her anti-gliadin and anti-endomysial IgA were also positive.

She was commenced on a gluten-free diet with resolution of both symptoms and liver function tests over 3 months. Further small bowel biopsies were taken 9 months after commencement of gluten-free diet showed preserved villous architecture with no significant acute inflammatory process. Repeat anti-gliadin and anti-endomysial antibodies at this time were also negative. Twelve months after completion of interferon and ribavirin treatment, she remains hepatitis C PCR negative.

Hepatitis C is associated with a myriad of autoimmune conditions including autoimmune thyroiditis1 and Sjogren's syndrome.2 More recently, coeliac disease as well as dermatitis herpetiformis have also been associated with hepatitis C.3 In addition, hepatitis C is associated with autoantibody production. Antinuclear antibodies, rheumatoid factor, anti-cardiolipin antibodies, smooth muscle antibodies, or anti-thyroid antibodies are detected in 40–65% of patients, but usually in low titre.4 Additionally, both coeliac disease and hepatitis C are common and so any coexistence may simply be a conjunction of two common conditions.

In this patient, the chronic hypertransaminaesemia was attributed to hepatitis C. However, the alanine aminotransferase remained high despite the clearance of hepatitis C, and did not normalize until a gluten-free diet was instituted. Thus occult coeliac disease may have been the cause. She probably had pre-existing subclinical coeliac disease, which only became symptomatic upon treatment with interferon. It has been noted that coeliac disease may be associated with nonspecific mild chronic elevation in serum aminotransferase levels in 40% of patients,13 and adherence to a gluten-free diet results in normalization of these abnormalities. Coeliac disease can cause progressive hepatitis and hepatic steatosis without apparent reason. Even if a patient has severe liver disease as a result of untreated coeliac disease, a gluten-free diet may reverse liver failure.14


We recommend that all patients be screened for coeliac disease prior to anti-viral treatment. The coeliac autoantibodies should be checked and if any suggestive symptoms are present or if antibodies are positive, upper gastrointestinal endoscopy with small bowel biopsies should be considered.

Weight loss and diarrhoea are common side effects of interferon therapy, but marked weight loss or excessive diarrhoea should prompt a search for coeliac disease, as the activation of silent coeliac disease during interferon treatment is common. Symptoms often subside after interferon withdrawal.


The investigation of chronic transaminitis should include coeliac serology as coeliac disease can cause liver disease.

http://onlinelibrary.wiley.com/doi/10.1111/j.1445-5994.2009.02087.x/full





The prevalence of celiac autoantibodies in hepatitis patients


Celiac disease has been associated with other autoimmune disorders such as autoimmune hepatitis, moreover it is known that T cell mediated immune response to dietary gluten and released cytokines are important for the entheropathy seen in celiac disease. We investigated celiac autoantibodies in patients with autoimmune hepatitis (AIH), and chronic hepatitis B (CHB).Sera from 84 patients with Autoimmune Hepatitis (AIH) type 1 and 88 patients with Chronic Hepatitis B (CHB) were tested for Immunoglobulin A and G antibodies to Gliadin, Immunoglobulin A antibodies to tissue transglutaminase using enzyme immunoassay, and Immunoglobulin A anti-endomysial antibodies by both indirect immunofluorescence, and enzyme immunoassay. The patients positive for anti-endomysial antibodies and/or anti tissue transglutaminase antibodies were considered for deuodenal biopsy. The study was approved by Research Center for Gastroenterology and Liver Disease Ethics Committee and all patients gave their written informed consent to participate.Immunoglobulin A anti-endomysial and Immunoglobulin A anti-gliadin antibodies were positive in two out of 84 patients with AIH. Moreover, Immunoglobulin A anti-gliadin antibodies were positive in another patient who was also positive for anti tissue transglutaminase antibodies. Tissue transglutaminase antibodies were positive in eight (9.1%) of 88 patients with CHB, two of which were also positive for anti-endomysial antibodies. One of the patients with CHB was only positive for anti-endomysial antibodies.

Compared with the general population, the prevalence of celiac autoantibodies in CHB and AIH patients is relatively high, and it is noteworthy that most positive patients were asymptomatic for celiac disease. We suggest screening for celiac disease before and during treatment in patients with viral and autoimmune hepatitis.

PMID: 20952805 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/20952805







I'll also reference George Henderson again here - he says it so well - thank you George!

Gluten and Casein as Factors responsible for the Characteristic Diseases of Chronic Hepatitis C

Not everyone exposed to HCV develops a chronic infection. The rate of natural clearance is unknown, because most people are not aware they are infected until the condition becomes chronic. One known factor in chronic infection with viral hepatitis (A&B) is selenium deficiency in malnourished populations. Celiac disease, the most easily diagnosed form of gluten toxicity, is known to cause selenium deficiency in well-fed populations. Celiac also causes a general deficiency of many antioxidants, protein, and minerals and vitamins. There is a strong association between HCV and celiac disease in many populations tested. There is an even stronger association between interferon-alpha treatment and celiac disease. Interferon-alpha is the cytokine that triggers celiac disease naturally.

Celiac disease is only the easiest to diagnose of the gluten sensitivity syndromes. It results in destruction of the intestinal cell vilii, damage which can be detected on biopsy.

Even so celiac is seriously underdiagnosed. It is likely that anyone in New Zealand with the symptoms of celiac disease, who is HCV positive, will be told that their symptoms are due to hepatitis C. Testing for Celiac will happen slowly and most likely not at all, unless the patient insists, and testing for other forms of gluten sensitivity is unlikely. Milder forms of gluten sensitivity might only disrupt those gut receptors responsible for functions such as immune regulation (especially endorphin receptors), mineral transport, or absorption of specific vitamins. Antibodies may form to the proline-rich gluten, gliadin and casein sequences released by peptide digestion which enter the bloodstream, which then attack the proline-rich collagenous tissues, promoting diseases such as liver fibrosis and rheumatoid arthritis.


It so happens that the auto-immune symptoms associated with celiac and gluten sensitivity diseases, including liver and gall-bladder disease, and which usually resolve slowly on a strict gluten and dairy-free diet, are essentially identical to the various syndromes seen in chronic Hep C, especially during or after interferon-alpha treatment.

Syndromes caused by gluten in celiac disease include:

- fibrosis and cirrhosis of the liver
- gall bladder obstruction
- insulin resistance
- thyroiditis
- sicca syndrome (dry eyes and mouth)
- vasculitis
- brain fog (poor memory, confusion)
- depression
- fibromyalgia
- fatigue
- optic neuritis
- deficiencies of selenium, magnesium, zinc, chromium
- deficiencies of fat-soluble vitamins (A, D, E, K)
- deficiency of those vitamins converted in the intestines (including folate, B6)
- anaemia
- thrombocytopenic purpurea (low platelets due to autoimmunity)
- GI disturbance; diarrhea, steatorrhea

These symptoms are aggravated by the nutrient deficiencies, especially antioxidant, magnesium, and chromium deficiencies, associated with gluten sensitivity. In fact, the symptoms of both Hep C and celiac disease are often partially, but significantly, relived by supplementation of these nutrients, especially when anti-inflammatory botanicals (curcumin, grape seed, ginkgo, milk thistle etc) are added. Other treatments effective against Hep C have obvious links to gluten sensitivity; for example, low dose naltrexone may exert its beneficial effects on cancer, autoimmune disease, and viral immunity by repairing damage done to endorphin receptors by gluten and casein digests. Similarly, enzyme therapy for cancers may work by promoting the complete digestion of gluten and casein exorphins, and the ketogenic diet for cancer may work by eliminating grains and lowering insulin levels (and hence inflammation), rather than merely by depriving cancer cells of glucose.

Exorphins are chemicals found in protein digests (the peptides produced by pepsin digestion of food proteins) which have an affinity for endorphin receptors. Endorphins are the messengers of emotion, and gluten sensitivity is very often found in schizophrenia, autism, ADHD, Aspergers, and the various mood disorders. However, the endorphin system also regulates the immune system, and defects of endorphins and endorphin receptors are associated with cancers and autoimmune disease, as well as AIDS. Endorphins also regulate gut motility; the well-known constipating effect of cheese is an opioid effect. Even people who have no gluten antibodies and no leaky gut (which allows gluten digests to enter the bloodstream in especially large doses) are influenced by the opioid effect of exorphins at the local, gut level.

Diagnosing non-celiac gluten and casein sensitivity without exclusion diets is difficult, if not impossible. Commonly in New Zealand a scratch test for gluten is the doctor’s first choice. This is worse than useless, because we are not talking about an allergy to gluten at all (though these do exist). When gluten, milk and maize are digested in the stomach (by pepsin and hydrochloric acid) a variety of peptides are released. The exact combination of peptides that might appear in the gut varies with the individual, the state of his digestion, and the strain of wheat, milk or maize consumed. Gliadomorphin is a characteristic wheat exorphin; beta-casomorphin-7 is thought to be the most toxic milk exorphin; and the maize exorphins have not yet been identified.

Autoimmune reaction to antigenic peptides is not the only way in which exorphins can harm us, so the current insistence on immunological testing seems limited. Also, current tests do not include antibodies to every possible peptide digest of gluten; this would probably be impossible.

Luckily, no-one needs to eat grains. Our ancestors got along in better health without them for millions of years. Grain consumption is a comparatively recent phenomenon in human history; very recent indeed in some cases; in Northern Europe and in colonized Oceania it is a habit of mere centuries, if that. In parts of the world where grain-eating goes back longest, for example the eastern Mediterranean, there is a higher rate of adaptation. This does not mean that individuals adapted to grains; individuals died young or became sterile if they lacked the more grain-adapted genes, in order that the race might adapt. But this still does not rule out the diseases of later life. Study of remains of grain-dependent societies, such as Rome and ancient Egypt, show that so-called “modern” diseases such as arthritis and cancer were prolific there. It is trendy to think that such disease results from technology; radiation, pesticides, food processing; and that it can be prevented with an organic vegetarian diet. The sad truth is that in most cases wheat and milk - even organic wheat and milk – products of the older agricultural revolution – are doing more harm than those traces of the modern industrial revolution that we cannot avoid. If our immune systems and our detox enzymes cannot cope with some new agricultural chemical, the most likely reason is the disruption they have received from the old agricultural chemicals – gluten and casein. It was also agriculture, not food processing, that first placed man in a guilty relationship with his food. Pre-agricultural man killed to eat and took from the forest, and had rituals that made peace with the animals and the plants. He took from these bounteous gods, not from captive creatures. Agricultural man kills for money, pays others to kill for him, and burns down the forest to plant his cash crops. If this was original sin, then the wages of sin have indeed been death.

It is customary to blame lead piping for the decline of Rome. The Roman people were highly wheat-addicted; they would riot for bread; “Bread and Circuses” was the formula for keeping them happy; they were so addicted that the state found it more convenient to supply bread for free (like a methadone clinic for the opiate of the people). Today the state oversees the addition of gluten, milk and maize to an ever-widening range of foods, so that a mere bread shortage is not likely to cause withdrawals. This is probably not intentional; addicts tend to assume that everyone wants to share their habit. In the case of Rome, wheat and lead may have had a synergistic toxicity. Both lead poisoning and wheat consumption tend to reduce iron and zinc absorption. This is why celiac children are often of short stature. The Romans would have become increasingly incapable of sensible planning and come to lack the stern old Roman self-control. We know that a decreasing birthrate of “true born” Romans eventually led to the conscription of barbarian armies and the opening up of Roman citizenship. Today gluten, and the antioxidant deficiency it causes, is a major cause of infertility.

Research has been done into the links between gluten sensitivity and Hep C, showing a strong association (especially after interferon therapy). There is also a strong association between Hep C and lymphoma (a cancer of the lymph glands). Lymphoma is the characteristic cancer caused by gluten; celiacs have a 30x elevated risk of lymphoma. To date no-one seems to have tested a strict gluten- and dairy-free diet for chronic Hep C or post-interferon toxicity, but a great many people with Hep C who take their health seriously have gone gluten free, often without knowing of the links between the two conditions, but motivated by their own well-being when avoiding gluten. There is no nutritional need that can only be met by grains; nuts and seeds, for example, supply the same amino acids, fats and vitamins in greater concentration (for example, sunflower and sesame seeds are superior sources of methionine and vitamin E), while legumes are rich in complex carbohydrates.

Gluten is also a cause of insulin resistance, and everyone who develops liver fibrosis has some degree of insulin resistance. Gluten itself causes a four-fold rise in insulin levels (unusual for a protein). The cure for insulin resistance is two-fold; a high-protein, low-carb diet (the Paleolithic diet is the most natural version of this diet) and replacement of the nutrients depleted by gluten which are essential for the function of insulin receptors; chromium, magnesium and the antioxidant minerals and vitamins.

Gluten also seems to cause amino acid deficiencies, including some of the very amino acids which wheat is supposed to supply, methionine and cysteine. Gluten is very much an anti-nutrient once one is sensitive to it.


Dangerous Grains by James Braly M.D. and Ron Hoggan M.A.

On milk, exorphins, and beta-casomorphin-7 (BCM7):

The Devil in the Milk by Keith Woodford

On endorphin receptors and AIDS:

Molecules of Emotion by Candace B. Pert

Read more: http://blogs.myspace.com/georgedhenderson#ixzz13Qu2vFF4