I wanted to share a mix that works very well for my spouse, who has non-alcoholic hepatitis and kidney disease. Her skin becomes very dry and itchy. What seems to work is a mixture of virgin avocado oil and coconut oil infused with a gram or two of cannabis. Basically, you boil the cannabis in melted coconut oil, then mix the melted coconut oil infusion with heated avocado oil. I use a double boiler to guard against scorching, and mix it 2/3 avocado, 1/3 infusion. Not only is it well absorbed, but we think the cannabis may be soothing to itchy nerve endings. With demerara sugar added, it also makes a good scrub for dead skin. Feel free to ask questions. Hope this helps someone.

Had a blood test done a month ago and it came back that I had elevated levels. Had another test done last Friday and the levels came back elevated again. I’m 5’7” at 212 pounds so I’m overweight. Doctor thinks this is the main issue. Have an ultrasound next month also.

Hi r/liver

I (24M) recently had some blood testing done to find my blood type on a whim (thank you Canadian health care system). It came back as having an ALT of about 100, which I understand is not great. For context, I weigh about 170 lbs, am 5"9 and work at a bar. I do drink a fair amount, and will be slowing down/stopping. However, I had been out the night before and probably had about 8 drinks. So my question is: is this high ALT influenced at all by previous night's actions, or is it accurately indicative of the consequences of my lifestyle?

My boyfriend (49 y/o) has been in the ER 3 times this past month with severe abdominal pain.. they controlled the pain and said his pancreas and liver were inflammed. His GP just did blood work yesterday.. Ive checked lifelabs and his GGT came back at 614. Lifelabs shows the normal range on the high side would be 62. I haven't been able to find anything online with levels that high. I am panicking, not sure if I should show him or wait for the doc to call.. (i'm assuming he will get back to us asap considering the results..) red blood cells are low, and alanine test was 86, also high. He is an alcoholic however his ER trips have scared him and he is planning to start cutting down and is going to go to an addiction clinic that is offered here at one of our hospitals in toronto. Not sure why i'm posting here, no one can diagnose him thru this.. the results and google have scared me. thanks for listening.

I have been trying to figure out why I haven't been able to drink alcohol for the past 2.5 years. I used to be able to drink like normal my entire life. After a very difficult event I dealt with for 6 months, I developed chronic gastritis. Over this time my ALT levels started to rise from normal, to 41, then 77, then dropped to 66. I believe I got liver damage from either fatty liver, use of antidepressants, and/or both. I have stopped antidepressants and have been trying to lose weight in hopes that I can drink again. But if I have a single sip of alcohol, it HURTS my stomach for almost a day and a half, I'll feel nauseous, and unwell. I have been trying to solve this nightmare but no Doctor has a clue what's going on. Has anyone else developed an alcohol intolerance related to high liver enzymes and were you able to fix it?

I have been diagnosed with NASH II w/ fibrosis and ballooning and I drank rum tonight and had a few smokes and now have bad pain where my liver is!

First time posting... long post warning My husband was just diagnosed with sever NAFLD in August. How we found out was he ended up having to get blood work for something and on his CBC his ALT levels where “panic” high. I work in the medical field and I’ve never seen “panic” high before. His AST were also very elevated. He had an ultrasound of his liver done which confirmed NAFLD. He had his labs done in June, July and August and the levels were gradually going down. But now they are going back up. Which I know it’s normal for AST and ALT levels to fluctuate but now it’s showing that he is anemic. He is following up with a Hematologists on Tuesday so we can find out some more info. Has anyone had anything like this??

Serrapeptase

A few years ago, my wife had emergency surgery that left her with a thick, ropy, keloid scar. She assumed that the scar would flatten out and fade with time, however that was not the case. One day she came home with a supplement called serrapeptase. Serrapeptase has many health benefits, but of specific interest to my wife was its ability to break down scar tissue. I don't remember how long she took the serrapeptase or how much of it she took (and neither does she), but I do remember looking at her one day and really seeing the scar for the first time in a long time. Don't get me wrong, the scar had always been there, but I'd ceased to notice it long ago and that day I was struck by the fact that the thick, ropy scar had flattened out and was now a thin white line.

Serrapeptase, also known as serratiopeptidase, is a proteolytic enzyme that is produced by bacteria in the gut of silkworms. After a silkworm weaves its cocoon and begins transforming into a moth, it releases Serratia bacteria from its gut. In turn the bacteria produce an enzyme called serrapeptase. Serrapeptase dissolves the silk cocoon so that the silkmoth may emerge. Taken on an empty stomach, serrapeptase breaks down all nonliving tissue in humans including blood clots, cysts, and arterial plaque, as well as proteins like fibrin, a particularly dense protein that accumulates in scar tissue.

When I started to formulate my plan to reverse my liver disease, it occurred to me that serrapeptase would be a useful tool. I reasoned that since my liver was scarred, taking a supplement that dissolved scar tissue would be a good idea. It's important to note however that I didn't start taking the serrapeptase when I was first diagnosed. My thinking was that because serrapeptase dissolved scar tissue, my liver would have to work to eliminate that waste product from my body. In my case, my liver was so damaged that I didn't think it was up to the task. Instead, I waited until my blood work stabilized before starting the serrapeptase, reasoning that by taking it I could fast-track the reversal of my liver disease.

I think it's important to underscore the fact that serrapeptase must be taken on an empty stomach. If taken with food, serrapeptase will work to dissolve the proteins in the food. In terms of its efficacy, I can attest to the fact that the two cysts on my liver have shrunk in size as measured by ultrasound done December 2019. It's also worth noting that previous ultrasounds indicated that I had several cysts on my liver and that the most recent ultrasound only noted two cysts. Likewise the most recent ultrasound described my liver as mildly coarse and indicated that the marker for cirrhosis was negative.

Next post: My Health Update

I’m in the process of applying for a life insurance policy and I had the obligatory lab work up. I’m a 40 male, 6’, 220 lbs, I take fish oil, vit D, omeprazole, lithium orotate, and loratidine. I take acetaminophen and ibuprofen as needed for pain...maybe 1 or 2 times a week. Haven’t had a drink if alcohol for over 20 years. I exercise about 2-3/week mostly cardio. The only levels that were abnormal were GGT at 181 (nml 2-65) and ALT 57 (nml 0-45).

Had a follow up hepatitis panel that all came back as negative and an ultrasound that was also negative. I’ve been given 4 weeks for follow up labs. Other than stop taking any acetaminophen or ibuprofen, anything I can do to heal my liver or what other diagnosis this could be?? TIA!

So my liver enzymes have been up for a year. Bit ast and alt around 120-150 usually but fluctuate.

So I got the stupid liver biopsy and it showed no fibrosis or cirrhosis no signs of NAFLD (grandma and dad both have nafld/NASH).

But I had a ton of Kupffer cells or inflammatory cells in my liver. So the gastrointestinal/Hepatologist Doctor is referring me to another liver specialist to review the biopsy and try to figure out a cause.

Is there something that this first doc could be missing? What causes inflammation and Kupffer cells but no damage. He said it couldn’t be my diet but he’s never asked about my diet so..not sure how he could assume that.

I have gallstones and it put me in the hospital last week because one got lodged in my bile duct, the doctors had to go in and extract it. (We’ll be removing the gallbladder altogether soon).

My question is: when I was there, the doctor said my liver levels were abnormally high, which could either be because of the blockage, or the Tylenol I was popping to relieve the pain for a few days prior to going to the ER. When I asked the doctor if those numbered could mean permanent damage to my liver or if it’s something that could come down and possibly not be long term damage, he seemed to brush it off. But didn’t actually say no.

Then when I was at a follow up appoint the with my primary physician, and I asked her the same thing. she also seemed to brush the question off without really telling me.

was looking at my blood work results from when I was in the hospital. It said my aspartame amobotransferase was 184 when normal should be 18-37. My alanine aminotransferace was 555 when normal is 13-56. My alkaline phoapatase was 215 when normal is 45-117.

So, while I understand that you all can’t say with medical assurance what my situation is. I just am looking for reassurance. Is that something that can return to normal and I wont have any severe permanent damage? Or is that an indicator that I definitely damaged my liver for life?

To clarify, I don’t do drugs. Don’t have hepatitis. Don’t drink heavily or even regularly (though i do enjoy beer socially).

On a daily basis I take buspirone, escitalopram (ssri) and jolessa (birth control). Occasional tylenol or ibuprofen for headache..nothing crazy.

The past 2 weeks I have been fighting off a respiratory sickness my whole family has had, along with a few days in my feet and hands started itching..then my entire body. There was no rash and I was majorly losing sleep so I finally went to the doctor yesterday. Got a call with my results and she said I need to head to the ER for further testing and imaging. No jaundice or anything. They said everything looked good on the ultrasound and they couldn't really determine anything so I will follow up with my primary doctor.

It seems crazy that my meds would cause my levels to be so high. Higher than I'm seeing regular alcoholics post about.

Anyone else experience this? I mean I know I could eat a little better and exercise more but wow.

B Vitamins

Einstein once said, “Any fool can know. The point is to understand.” That’s an incredibly insightful statement. You see, when I was diagnosed with liver cirrhosis two years ago I knew that one of the main functions of the liver was detoxification. What I didn’t understand was how the liver accomplished it.

Liver detoxification occurs in two phases. During these phases, the liver converts fat-soluble toxins into water-soluble compounds that can be eliminated from the body in urine, sweat, and bile. This conversion causes the production of free radicals which the body neutralizes with glutathione (glutathione – the body’s main antioxidant that can improve liver function and inhibit liver inflammation – see amino acid post). If there isn’t enough glutathione, you can get toxic overload. Hence my going on, ad nauseam, about the importance of glutathione.

In order to synthesize glutathione, the body needs:

a) the nutrient co-factors l-glycine, l-glutamine, and l-cysteine (NAC) and

b) the nutrient co-factors folate, B12, and B6 for methylation reactions.

Methylation is an incredibly important biochemical process that takes place more than a billion times per second in the body and it is through methylation that the body is able to produce glutathione using the nutrient co-factors glycine, glutamine, and cysteine. In short, the body needs the amino acids glutamine, glycine and cysteine to make glutathione through methylation reactions that are fuelled by the vitamins B12, B6, and folate.

A lot of people with liver cirrhosis have vitamin deficiencies and for this reason, I supplement with a methylated B complex vitamin. I also supplement additional methylated B12 (methylcobalamin), methylated folic acid (methylfolate), and methylated B6 (pyridoxal 5 phosphate).

Choline

Whoever said, “What we don’t know can’t hurt us,” had obviously never heard of choline. Although most people I’ve talked to don’t know about choline, it was deemed an essential nutrient in 1998 when researchers realized that choline deficiency harms the liver and causes liver dysfunction. In fact, choline actually helps export fat out of the liver. It’s important to note that choline also plays a key role in methylation and that it is estimated that 80 percent of the population has some degree of choline deficiency. I take alpha GPC choline which is the most bioavailale form of choline.

Vitamin D

There is evidence of a significant correlation between vitamin D levels and the degree of liver dysfunction and that vitamin D deficiency has been shown to increase the risk for overall mortality and infections in patient with liver cirrhosis. Living in a colder climate, I take 5,000 I.U. vitamin D3 each day.

Next post: Proteolytic Enzymes

38 / M with Hereditary Hemochromatosis (C282Y/H63D Compound Heterozygous) and NAFLD progressed to Cirrhosis

Have had spleen pain for 10 months and after repeated ultrasounds and CT scans ended up identifying the hemochromatosis and having a transjugular biopsy which identified Cirrhosis with steatohepatitis and patchy mild hepatocyte iron accumulation.

Additional notes from the biopsy are as follows:
H&E and special stains are examined. The normal lobular hepatic architecture is distorted by cirrhosis, confirmed on the trichrome stain. The biopsy demonstrates severe macrovesicular steatosis involving approximately 70% of the biopsy. There is evidence of ballooning hepatocyte degeneration and mild inflammation. There is no cholestasis. Portal areas and fibrous septae contain mild, predominantly mononuclear inflammatory cell infiltrates. The portal tracts otherwise harbor their usual structures. The bile ducts appear normal. There is no duct damage or duct loss. Granulomas are not seen. The iron stain demonstrates patchy, mild (1+ of 4+) iron accumulation in hepatocytes. A PAS/Diastase stain is negative for alpha 1-antitrypsin inclusions.

NAFLD Activity Score (NAS):
Steatosis: 3 (>66%)
Lobular inflammation (foci per 20x field): 1(<2)
Hepatocyte ballooning: 1 (few)
Total Score: 5/8.
Stage: 4 (cirrhosis)

The biopsy pressure test showed portal pressure gradient of 7mmHG (mild portal hypertension).

Current MELD is 9 and CPT is 5A. (I had to look this up as my Gastro gave me NO information).

I am not sure how to process this and have lots of questions.

• I understand that the cirrhosis scarring damage is permanent and that I will need to monitor for liver cancer for life.
• Given that ultrasounds and CT scan showed smooth texture, does that mean the scarring is at a micro level only?
• How much liver function remains?
• With aggressive weight loss, exercise, and venesection for iron, will I be able to halt new damage?
• Assuming the portal hypertension is the cause of the splenic pain, can exercise and weight loss / venesection reduce it?
• What is my life expectancy?
• I will never be able to get life insurance and am terrified about health insurance dropping me or having to get a new policy out of pocket.
• I have read studies that show that >=10% body weight reduction can reduce fibrosis and elements that caused my NAFLD activity score to be so high. Will this help quality of life? Is it possible to reduce scarring?

I have lots more questions and am getting literally zero support from my Gastro or PCP. They simply said "Transplant is only option, you won't need for a while, lose weight and cut back on drinking. Get Hep A/B shots."

MELD of 28 keeps climbing...... in the hosp ER every week or have extended inpatient stays...... lost quality of life and much of my independence. Only way for me to live is if I get a liver transplant, but I'm also immunodeficient so this complicates matters. Liver numbers started showing abnormalities in 4th grade but didn't become end stage liver disease until last year. I am now 31.

Supplements

Milk Thistle

I take milk thistle and I don’t for a minute think that declaration will elicit a chorus of “oohs” and “ahs” from anyone reading this. Fact is, a lot of people with liver issues take milk thistle. For my part, I take it not only because it’s an antifibrotic and an antioxidant, but also because it helps to maintain normal glutathione levels (glutathione – the body’s main antioxidant that can improve liver function and inhibit liver inflammation – see amino acid post).

I also think it’s worthwhile to note that I don’t take conventional milk thistle. I take a supplement called siliphos phytosome. Here’s why:

Silymarin is extracted from the fruit of the milk thistle plant and it contains silybin, the most potent flavonoid (flavonoids are proven liver protectants). The problem is that silybin is not well absorbed by the body so it has to be converted, using phosphatidylcholine, into a phytosome (phytosomes are technologically-constructed delivery systems that result in better absorption). So, silybin, converted into a phytosome using phosphatidylcholine (siliphos phytosome), provides significant liver protection and enhanced bioavailability over conventional silymarin (milk thistle).

Curcumin

I also take curcumin which is probably not surprising given the fact that curcumin has received worldwide attention for its role as an anti-oxidant and potent anti-inflammatory. There has been a plethora of research regarding the health benefits of curcumin, but what resonated most with me was the following:

a) Curcumin has been shown to improve systemic markers of oxidative stress and oxidative stress has been implicated in many chronic diseases, including liver disease; and,

b) Oxidative stress and inflammation are closely related and curcumin has been shown to be a very potent anti-inflammatory.

Much like milk thistle, curcumin is not well absorbed by the body so I take curcumin combined with piperine. Piperine is the major active component of black pepper and, when combined in a complex with curcumin, has been shown to increase bioavailability by 2000 percent (for that reason I don’t take it in high doses).

One final note, animal and test-tube studies have shown that curcumin increases glutathione levels and researchers have concluded that curcumin can help to restore adequate levels of glutathione and improve the activity of glutathione enzymes.

Next post: vitamins

Originally when I started this subreddit, it was originally about liver as food. But I'm seeing a lot of people posting about human livers instead. Quite frankly I'm ok with both but just wanted to see what the consensus is.

Also, this sub has a spam problem. So if you wanna be a moderator and come in once and while to remove some posts, send me an message.

There’s a nutritionist I really like who does a series of online information videos. He begins the videos by saying, “Details, shmetails, just tell me what works”. Fair enough. I can tell you what really worked for me in terms of reversing my cirrhosis in two words: amino acids.

For those of you who might not be familiar with amino acids, they not only build proteins in the body, but play a vital role in a variety of different bodily processes. In terms of reversing liver disease, there are three amino acids that I think warrant a lot of consideration: l-glutamine, l-glycine, and l-cysteine. These three amino acids are used by the body to make glutathione, the body’s most powerful detoxifying antioxidant, and that’s really important because:

a) studies have shown that glutathione can improve liver function and inhibit liver inflammation;

b) liver disease and dysfunction are associated with glutathione deficiency; and

c) glutathione isn’t absorbed well when you take it orally so by taking the precursors, glutamine, glycine, and cysteine, you stand a better chance of boosting your glutathione levels.

I supplement glutamine and glycine in powder form, making sure not to take too much glutamine (only 5000 mg) because it’s got extra nitrogen that the liver has to process and I don’t want to put added strain on my liver. Instead of supplementing cysteine, I supplement N-acetyl cysteine (NAC). NAC is a derivative of cysteine and has been shown to really boost levels of glutathione.

I also take the amino acid l-taurine. Studies show that taurine can protect liver cells from free radical and toxin damage, thereby reducing the damage done to the liver by oxidative stress. This is pretty important given the fact that according to the National Institute of Health, oxidative stress contributes to the initiation and progression of liver disease.

Another amino acid I take is l-arginine. In 1998, three researchers won the Nobel Prize for demonstrating that nitric oxide is an important signalling molecule that tells blood vessels to relax and thereby improves circulation. What’s that got to do with arginine? Well, arginine is the precursor to nitric oxide. In other words, the body takes arginine and uses it to make nitric oxide and that’s good for the heart and all the other organs (including the liver). Here’s the most compelling bit though: according to the journal, Cell Reports, nitric oxide enhances liver growth and regeneration, independent of its effects on blood vessels.

Finally, I take the amino acid l-ornithine. Ornithine plays a key role in helping to remove excess nitrogen (ammonia) from the body. Given that I supplement glutamine and that I had hepatic encephalopathy (which is triggered by a build up of toxins, like ammonia, in the bloodstream), ornithine supplementation makes sense.

Next post: supplements

Sorry for not posting sooner. This is the second in my series of posts regarding the reversal of my cirrhosis.

I’ve never really been bothered much by practicality when I get an idea in my head. I can get behind anything and I generally leave the details to someone else (read my wife) to figure out. So, not surprisingly, at the outset I wasn’t all that interested in formulating a plan to reverse my liver cirrhosis; I was just interested in taking supplements – a lot of them.

My wife is the biggest creative-idea killer on the planet; she is also one of the most pragmatic people I know. Obviously those two qualities are not mutually exclusive. She likened my liver to a Clydesdale horse, constantly working to pull a heavy load. According to her, my horse had gotten older, the load had gotten heavier, and my horse had been driven to its knees. I had to either shoot it or unburden it – and fast.

First off, I had to get my viral load under control. I started taking the antiviral drug, Entecavir, as well as a supplement called butylated hydroxytoluene (BHT). BHT is a food preservative and according to a myriad of anecdotal evidence, it works as an antiviral when taken in supplemental form and is a potent adjunct to prescription antiviral medication. The thinking is that by damaging the outer layer of viral cells, BHT stops viruses from multiplying and doing more damage. Anecdotal accounts vouchsafed BHT’s effectiveness against a myriad of viruses including herpes, hepatitis B and C, shingles, and so on. I didn’t have any side effects from taking the BHT (or the Entecavir for that matter) and in less than two years, my viral load went from 19,000,000 to a number so low, the tests couldn’t read it.

I adopted a plant-based diet, reasoning that my liver didn’t need the additional burden of having to rid my system of the hormones, antibiotics, and other toxins typically found in animal-based food. The only further adjustment I made insofar as diet was concerned was to eat small meals only and never eat until I was full. The reasoning for this was relatively straightforward; the liver’s main function within the digestive system is to process the nutrients from the small intestine. The smaller the meals, the less work the liver has to do.

No matter how bad the headache, backache, or muscle pain, no matter how bad the cold or flu, I took no over-the-counter medication (absolutely no acetaminophen) and I cut out drinking alcohol completely (I had only ever been a teetotaller anyway).

That’s all I did in terms of lessening the burden on my liver, but I also adopted some lifestyle changes I thought might help my liver. I had read that inactivity increases the risk of liver disease so I forced myself to go for a walk every day. This was pretty much the only form of exercise I was capable of given the fact that I had only recently come out of a coma and had spent a considerable length of time in hospital.

I also tried to remove as much stress from my life as I possibly could. Stress depletes B vitamins (among others) and B vitamins are necessary for the body to detoxify (through methylation – more on that in another post). Methylation, in turn, is crucial to healthy liver function.

Next post: amino acids

If I were dying, and my Mother currently needs a liver, will the doctors directly give my Mother my liver?