• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

How do we stop Liver disease (Fatty Liver, Hepatic Statosis, type 2 diabetes, mitochondrial disease)

What kind of Liver Disease do you have

  • Fatty Liver

    Votes: 11 73.3%
  • Hepatic Steatosis (Liver infammation etc)

    Votes: 4 26.7%
  • Hepatic Cirrhosis

    Votes: 0 0.0%
  • Liver Cancer

    Votes: 0 0.0%
  • Liver Failure (I expect 0 responses)

    Votes: 0 0.0%

  • Total voters
    15

prioris

Senior Member
Messages
622
my urine flow is being hindered. some comes out eventually after a long while. in the past if i drank lot of water, i'd be able to urinate within hour. could be stones but maybe not. hmmmm!
 

Gondwanaland

Senior Member
Messages
5,095
Brand new randomized controlled study
https://www.ncbi.nlm.nih.gov/pubmed/?term=28593701
Hepatol Res. 2017 Jun 7. doi: 10.1111/hepr.12918. [Epub ahead of print]
Comparison of efficacy of low-carbohydrate and low-fat diet education program in non-alcoholicfatty liver disease; Randomized controlled study.
Jang EC1, Jun DW2, Lee SM3, Cho YK4, Ahn SB5.
Author information

Abstract
AIM:
Composition of macronutrient is important in nonalcoholic fatty liver disease (NAFLD). Diet education program which mainly emphasize on reducing fat consumption has been used for NAFLD patients. We compared efficacy of conventional low-fat diet education with low-carbohydrate diet education in Korean NAFLD patients.

METHODS:
One hundred and six NAFLD patients were randomly allocated to low-fat diet education or low-carbohydrate education group for 8 weeks. Liver chemistry, liver/spleen ratio, and visceral fat using abdominal tomography were measured.

RESULTS:
Intrahepatic fat accumulation decreased significantly in low carbohydrate group compared to low fat group (Liver/spleen 0.85 vs. 0.92, p < 0.05). Normalization of alanine transaminase activity at week 8 was 38.5% for the low-carbohydrate and 16.7% for the low-fat group (p = 0.016). Not only liver enzyme, but also low density lipoprotein-cholesterol, and blood pressure levels significant decreased in low carbohydrate group. Total energy intake was also more decreased in low carbohydrate group compare to low fat group. Although body weight changes were not different between two groups, carbohydrate group more decreased total abdominal fat amount.

CONCLUSIONS:
Low-carbohydrate diet program is more realistic and effective in reducing total energy intake and hepatic fat contents in Korean NAFLD patients.
 

Gondwanaland

Senior Member
Messages
5,095
Having said that, I tried lower carbs for 2 years (up to 100mg daily), and my brain fog only went away when I upped carbs to at least 150 mg during most days of the week :rolleyes:
 

Eastman

Senior Member
Messages
526
Mark Hyman suggests that we should be eating slow carbs, not low carbs. I think the distinction between different types of carbs needs to be better highlighted in studies, as in the following:

Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index.
CONCLUSION:
This study suggests that replacing SFAs with carbohydrates with low-GI values is associated with a lower risk of MI, whereas replacing SFAs with carbohydrates with high-GI values is associated with a higher risk of MI.
 

prioris

Senior Member
Messages
622
Having said that, I tried lower carbs for 2 years (up to 100mg daily), and my brain fog only went away when I upped carbs to at least 150 mg during most days of the week :rolleyes:

my brain fog never goes away, it just varies ... :-(

about 40 years ago, when carbs made me sick, i went to a protein diet and that eventually made me sick so i got sick eating almost anything ...

i seem to have some type of male uti ... doesn't hurt when i pee, maybe slight burning, no urgency to pee, just a little pee now and then ... maybe effecting bladder and kidney some but i take uva ursi+baking soda to keep things in check ... can't figure out what microbe i'm fighting ... e-coli most common ... i need something that matches particular uti bacteria/virus with symptoms

...
 

pamojja

Senior Member
Messages
2,398
Location
Austria
Mark Hyman suggests that we should be eating slow carbs, not low carbs. I think the distinction between different types of carbs needs to be better highlighted in studies, as in the following:

I think as practical application nothing replaces a blood-glucose meter and testing each food you eat postprandially. There is just too large variations in blood-glucose reactions to the same foods in different individuals, as to subscribe to any one conceptual differentiation.
 

Gondwanaland

Senior Member
Messages
5,095
i seem to have some type of male uti
http://www.acu-cell.com/dis2.html
Urinary Bladder Infection: High potassium, low chromium, low magnesium, low manganese, low sulfur,
(opt. cranberry juice, probiotics, 2-3 mg chelated chromium for a few days, then 500 mcg for maintenance).
A lot of info also here http://www.acu-cell.com/pna.html

I don't know if it is all true though.

Edited to add - I am reading a Mast Cell questionnaire:
The patient complains about occasional or continuing pain in the urinary bladder and/or pelvis accompanied by painful desire to void and/or blood in the urine. There is no bacteriuria.
 
Last edited:

Eastman

Senior Member
Messages
526
There is just too large variations in blood-glucose reactions to the same foods in different individuals, as to subscribe to any one conceptual differentiation.

But that's my point. We shouldn't be subscribing to anything until we understand the variations better.
 

ryan31337

Senior Member
Messages
664
Location
South East, England
I think as practical application nothing replaces a blood-glucose meter and testing each food you eat postprandially. There is just too large variations in blood-glucose reactions to the same foods in different individuals, as to subscribe to any one conceptual differentiation.
I agree and from my own experience I also have enormous variations in how I handle the same foods from one day to the next, likely a result of variable rapid gastric emptying. This seems to be very unpredictable and usually in tune with my other symptoms of autonomic dysfunction (POTS etc.).

Just to add my anecdotal evidence to the study posted by @Gondwanaland: My endo suspected NAFLD, I had increasingly deranged ALT, bilirubin and mildy enlarged liver shown on CT. Liver enzymes went almost back to within normal range at the next test, after just a couple of months on a keto diet.
 

Gondwanaland

Senior Member
Messages
5,095
my urine flow is being hindered.
Insulin-resistance and benign prostatic hyperplasia: the connection.

Abstract
Benign prostatic hyperplasia (BPH) is a highly prevalent disease in the aged men population characterized by augmented cell proliferation and contractility of the prostate gland. Prior studies have demonstrated the relationship between BPH and insulin-resistance syndrome. During insulin-resistance, hyperinsulinemia develops to combat the decreased responsiveness of the body towards insulin. Although, the compensatory hyperinsulinemia prevents development of fasting hyperglycemia in insulin-resistant individuals, the increased level of circulating insulin directly and/or indirectly affects different molecular signaling and can promote prostatic growth. Insulin-resistance syndrome includes group of disorders, such as obesity, dyslipidemia, sympathetic overactivity, hyperinsulinemia and each individually reported as risk factor for the development of BPH. The present review describes the inter-relationships between different insulin-resistance associated factors and their possible involvement in the pathogenesis of BPH.
 

prioris

Senior Member
Messages
622
P.S The most common cause of kidney infection is from a UTI. I don't have enlarged prostate (yet but maybe down the road ... LOL). So BPH unlikely. Finding root causes and addressing them heads off many other problems. I just started taking Prostrate supplement to help with any UTI infection and as a prevention.
 

stetson28

If it aint broke don't fix it...but.
Messages
49
Location
Richmond Virginia
Some weeks back I came to realize that my liver had inflammation. This has been going on for some years but it wasn't as severe. I remember years back whenever I had too much gas in my colon, it would cause pain in the middle bottom of my rib cage sternum. Once I pushed the air out, the pain subsided. Looking back, my liver likely had some more milder inflammation. I also thought maybe the pain was from gallstones pain I had.

I started doing some liver/gallstone cleanses about 6 weeks back which I am not done and will write about later. About a couple weeks ago I felt really deathly. I got hit with kidney stone attack first. I took rememdy and that calmed down. Neuropathy started to flare all over especially feet. I didn't know what was going on. After I found that L-carnitine calm down the neuropathy, I started researching further.


First thing I came across was mitochondrial disease. I noticed a lot of people suffering with disease have neuropathy.

Second thing I noticed was that the supplements that people with type 2 diabetes were the same ones that people with mitochondrial disease take.

Third thing I found was a you tube video on curing type 2 diabetes. This guy was curing diabetes by limiting fats. He would have most people stop taking their insulin first day and they were allowed to eat carbohydrates. I later realized it was the saturated fats he was curtailing.

Fourth thing I found led me to fatty liver disease. When fatty liver disease leads to inflammation of the liver, it is called hepatic steatosis. If it progresses further, it is called cirrhosis, cancer/liver failure.

So I came to realize that my liver was clogged with saturated fats. That makes sense since I ate a lot of butter and use only coconut oil. It also solved the mystery why some people have difficulties with coconut oil too so should suspect they have fatty liver disease build up.

I did have the standard liver tests before I did gallstone cleanse about two months ago. The test results for liver came back normal. I had it done about 6 months ago also. My A1C came back 5.0. It wasn't detecting any abnormality so I crossed the liver as a possible problem back then and must be something else.

My normal way of diagnosing is taking the remedy so I researched hepatic stetosis.


It can be treated with PolyenthylPhosphatidylCholine (PPC I use Life extension Hematopro because it is lowest cost), SiliPhos (10X better absorption), L-carnitine and lowering saturated fats/raising Omega 3 can heal and cleanse the liver.

Here is the treatment I put together

------------------------------------------------------------------
Polyenylphosphatidylcholine
1 at end of each meal so 2 per day (I tried 3 but too much)

Siliphos Two 360 mg (120mg silybin) after each meal (Twice a day)

Omega 3 Kril Oil + Udol oil with each meal

ON EMPTY STOMACH at least hour before meals
L-Carnitine Tartrate 500mg 2Xday
NA-R-ALA 100mg
Benfotiamine 300mg/therapeutic (or 150mg/maintenance) 2xday

5-Lox (morning and night for inflammation for first week)

DIET

REMOVE Coconut oil and Butter from diet and high saturated foods
I still get some saturated fats.
USE GMOFree Canola Oil, Safflower Oil
Take ConjugatedLinoleicAcid 3 capsules/day ( with any saturated fat meal )

Setria sublingual glutathione 50 mg (dissolve under tongue 3Xday for week because I just had it available)

MISCELLANEOUS

With FOOD
Ubiquinol 100mg 2xday with fatty meal


On EMPTY STOMACH
PQQ 10mg
Coenzyme B complex 1 capsule (has B5 Pantethine, B6 P5P)
1.25 mg Sublingual methylcobalamin(B12)
-----------------------------------------------------------------
RESULTS
The sternum area was painful when I started. At day 8 I noticed major progress. After second week, I feel better. I will continue this for maybe 6 months but not sure. I slightly lower dosage as symptoms resolve. My neuropathy calmed down more. The Benfotiamine is most impoortant for neuropathy.

I do feel much healthier but usually another problem strikes that I need to figure out how to solve... a continuing saga LOL


Perusing around the internet I notice many doctors dealing with fatty liver solutions don't mention PPC or the above. They have people resolve fatty liver thru their diets instead and more indirect method. That is a weak approach I think and would take much longer. Some people ask for stronger approaches but they claim their way is the only way. They don't even mention the connection of saturated fats to diabetes. There are doctors who know what they are doing but too many just follow the official treatment line.

If something can treat hepatis steatosis, wouldn't it make sense to use it for the less severe fatty liver too.

As I clean out my liver, I will try to introduce more saturated fats but I will take these supplements to help me metabolize fats better. I will try to balance the Omega fats with it also.

I will make adjustments as I find out new things

Chinese medicine says that the Liver is the General of your army of other organs so I will go all out to take care of that organ. The thing I hate about Chinese medicine is that it is very cryptic about the liver and other organs talking about chi, dampness, heat etc when there is no need.

If the liver starts becoming dynfunctional so many ailments can develop in the body.

NOTE: Normally I would have difficulty taking Phosphatidylcholine (13% choline) or any choline since I had severe MTHFR reaction taking folate and b12. Lithium orotate solved that. I posted about it.

They say about 1/3 of the population has fatty liver disease or worse so I have to assume most people with ME/CFIDS have it. You can give your experience.

==============================================================
Here are some excerpted stuff I collected

-------------------------------
HERE IS FREE BOOK I FOUND
https://www.liverdoctor.com/5-ways-to-reverse-fatty-liver/
------------------------------

Fatty liver disease comprises a spectrum ranging from simple steatosis to steatohepatitis which can progress to liver cirrhosis and hepatocellular cancer. Hepatic lipotoxicity may ensue when the hepatic capacity to utilize, store and export fatty acids (FA) as triglycerides is overwhelmed. Additional mechanisms of hepatic lipotoxicity include abnormal FA oxidation with formation of reactive oxygen species, disturbances in cellular membrane FA and phospholipid composition, alterations of cholesterol content and ceramide signalling. Lipotoxicity is a key factor for the progression of fatty liver disease by inducing hepatocellular death, activating Kupffer cells and an inflammatory response, impairing hepatic insulin signalling resulting in insulin resistance, and activation of a fibrogenic response in hepatic stellate cells that can ultimately lead to cirrhosis. Therefore, the concept of hepatic lipotoxicity should be considered in future therapeutic concepts for fatty liver disease.
-------------------------------
Human trials have shown that a preparation providing 376 mg silybin, 776 mg phosphatidylcholine, and 360 mg vitamin E produces therapeutic effects in patients with a variety of different forms of liver damage, improving insulin resistance, reducing liver fat accumulation, and reducing blood levels of markers of liver scarring (Trappoliere et al 2005, Federico et al 2006, Trappoliere et al 2005).

-------------------------------

Alpha R-Lipoic Acid for a Fatty Liver

While a growing body of research provides reason to consider ALA for reducing steatosis, three relatively new studies bring this consideration to the next level:

As published in a February 2012 edition of the journal Obesity, researchers found that supplementing with alpha lipoic acid prevented the accumulation of triglycerides in the liver – a major contributor to fatty liver disease. More specifically, they identified certain genes (SIRT1 and SIRT3) that ALA stimulates to achieve this goal.
As published in a March 2012 edition of The Journal of Nutritional Biochemistry, researchers found that alpha lipoic acid has an ability to prevent nonalcoholic steatosis brought on by a high-fat intake. Besides its benefit to the liver, ALA’s benefits also included preventing excessive body weight gain.

-------------------------------
Carnitine
This nutrient is critical for fat metabolism and energy production in the cellular mitochondria and is naturally produced in the liver and kidneys. It ismost concentrated in the heart and skeletal muscles where it plays an important role in energy production and detoxification. It is also found in the brain and male sperm cells.
-------------------------------
Choline & Inositol:
Choline and inositol are co-enzymes that are required for the proper metabolism of fats and have the ability to remove fat from the liver. Choline's function in fat metabolism is tied to its role in bile production because bile acts as emulsifier (allowing water and lipids to combine) to more readily transport fats.

Choline prevents fats from becoming trapped in the liver, where they can block normal metabolic functions. Choline, as well as inositol, acts as a fat emulsifier that prevents cholesterol from settling on arterial walls. Choline also works well with inositol to utilize fats and cholesterol.

Inositol is referred to as vitamin B8 and it helps to metabolize fats and cholesterol and aids in transporting fat in the blood system. Thus, inositol is an aid in the redistribution of body fat and can help to lower cholesterol levels.

-------------------------------
Benefits of PolyenylPhosphatidylCholine

Fats and lipids – these include vitamins – are insoluble in water. They need to be emulsified into small particles that are invisible to the eye before they can be digested and taken up by the body. This takes place in the intestines with the aid of PPC and of the bile acids. The excretion of water insoluble substances from the body, the purification of the body by bile, is only possible when the fats form a micellar solution with PPC, bile acids and cholesterol, so that they are taken up in the water and rendered ransportable. It has been demonstrated that there can be disruption of the organism if sufficient PPC is not available for both processes


Experiments with, for instance, red blood cells have shown that the amount of rigidity present is regulated by the incorporation of PPC with essential fatty acids into the membranes.
The importance of the membrane-regulating effect of PPC has been especially intensely investigated for the liver. It has been founded that PPC-c
ontaining primarily unsaturated fatty acids has the following effects on the membranes of damaged liver cells, The fluidity, flexibility, elasticity and enzyme activity of the membranes is increased while their rigidity is reduced.
Since the functioning of enzymes and ion channels throughout the body
is a prerequisite for the maintenance of life, it can be taken that the effect of PPC as a dietetic foodstuff taken in adequate quantities daily is not likely restricted to the liver.


A large surface area is necessary for the exchange of gases between the human body and the environment, this is made possible by the presence of 30 million tiny lung cavities, the alveoli. A membrane consisting of PPC and protein coats the surface of the lung cavities and, thus, prevents them from sticki
ng together and collapsing. The integrity of the membrane on the lung surface is a requirement for efficient gas exchange. A small proportion of newborn babies do not have enough PPC in their lungs. These babies can be kept alive by introducing PPC into the amniotic fluid of the mother.

Phospholipids and especially PPC are essential components of the mucosal. Disorders leading to a reduction in the PPC content, or a disruption of the PPC membrane cause pain -or in more severe forms, gastric ulcers or cancer.


Research on nerve cells has shown that PPC can act as a substitute for the messenger substances acetylcholine. This result is supported by the finding that orally consumed PPC or Choline increases the acetylcholine content of the blood. Experience of the course taken by AZ and other degenerative diseases of the nervous system emphasized the importance of taking PPC prophylactically or at least when the first symptoms are observed. The significance of PPC as an age-dependent substitute for the nervous system is emphasized by the fact that the phospholipid and the PPC content of the brain falls from the age of 30 years on.

Polyenylphosphatidylcholine as a source of choline for the liver

The liver is the most metabolically active organ and requires an unknown quantity of the choline per day. Investigations in humans would require li
ver biopsies and production of deficiency states, and are not acceptable on ethical grounds. Hence, it is necessary to fall back on the results of animal experiments to probe the importance of choline and PPC as a choline source.
Experiments in 12 species of animals have revealed that choline-deficient diets lead to an accumulation of fat in the liver and in a chronic state to cirrhosis of the liver. It is known that these states are also brought about by excessive alcohol consumption, infections, bacterial toxins, certain chemicals, e.g. solvent carbon tetrachloride and some drugs such as tetracycline’s. Several studies have revealed that these disorders can be treated successfully with PPC containing a high proportion of essential fatty acids. The results obtained in animal experiments with choline must be translated into PPC for human application because choline is moderately toxic and taking it leads to unacceptable mouth and body odors. Therefore, it is re
asonable then to *assume that regular consumption of PPC must be regarded as the only promising prophylaxis against liver damage.

IMPORTANCE OF PPC
http://nutrasal.com/pdf_articles/sig.pdf

http://nutrasal.com/phoschol.html
-------------------------------
Useful dosages of Siliphos®:
Shows definite advantages of Siliphos® at dosages ranging from 160mg to 360mg (measured as silybin). Dose/effect relationship is also demonstrated with the highest dosage tested getting the most dramatic results.

Study shows how Siliphos® is dramatically more effective than pure silybin alone. Concludes Siliphos® may be useful in counteracting damage caused by alcohol intake.

Shows Siliphos® is more effective than its constituents, silybin and phosphatidylcholine, alone. The effectiveness of Siliphos® is considerably greater than the sum of its parts.
-------------------------------

how well a person digests fats depends on the health of their liver and gallbladder

Body Ecology's position is that people with digestive disorders usually have a problem digesting saturated fats, especially when they are cooked. Indeed, how well a person digests fats depends on the health of their liver and gallbladder. Is their liver congested? Is their gallbladder releasing adequate amounts of bile to digest the fats? Are there enough pancreatic enzymes being produced to digest the fats in the small intestine? Bottom line, saturated animal fats are too heavy for people with over-worked or congested livers, especially in the amounts recommended by GAPS.
-------------------------------
Omega 6 oil will decrease diabetes

“The overall scientific picture suggests that we should eat less saturated fat than most of us do, but it is difficult to say what we should eat instead and which types of foods with saturated fat we should avoid,” she says.

“Fat storage in the liver and around the intestines, and the lower insulin response in the saturated fat group, is associated with an increased risk of developing a number of lifestyle diseases such as type 2 diabetes,” says Dyerberg.


“Increased muscle mass, on the other hand, which the study found in the omega-6 group, prevents type 2 diabetes. This study therefore indicates that it may be a good idea to swap saturated fat with omega-6 fat from sunflower oil. This may be true in relation to type 2 diabetes, but if we look at the risk of cardiovascular disease, we might see a different picture.”

http://sciencenordic.com/saturated-fat-increases-diabetes-risk
-------------------------------
CAUSE OF TYPE 2 DIABETES
https://nutritionfacts.org/2016/11/17/fat-is-the-cause-of-type-2-diabetes/

This mechanism by which fat induces insulin resistance wasn’t known until fancy MRI techniques were developed to see what was happening inside people’s muscles as fat was infused into their bloodstream. That’s how we found that elevation of fat levels in the blood causes insulin resistance by inhibition of glucose transport into the muscles.

We can also do the opposite experiment. Lower the level of fat in people’s blood and the insulin resistance comes right down. If we clear the fat out of the blood, we also clear the sugar out. That explains the finding that on the high fat, ketogenic diet, insulin doesn’t work very well.Our bodies become insulin resistant. But as the amount of fat in our diet gets lower and lower, insulin works better and better—a clear demonstration that the sugar tolerance of even healthy individuals can be impaired by administering a low-carb, high-fat diet. We can decrease insulin resistance, however, by decreasing fat intake.

how that fat can come either from our diet or excess fat stores, and then in Lipotoxicity: How Saturated Fat Raises Blood Sugar, I show how not all fats are equally to blame.
-------------------------------
Chart down page hald way shows oil compositions and unsaturated:saturated ratio
https://oilpalmblog.wordpress.com/2014/01/25/1-composition-of-palm-oil/

Canola oil 15.7 ... very low saturated fat ratio
coconut oil 0.9 ... very very high saturated fat ratio
palm kernel oil ratio 0.2
cocoa butter 0.6 also really bad
lard 1.2

Good Oils
canola oil 15.7
safflower oil 10.1
corn oil 6.7 (maize oil)
olive oil 4.6 good
sunflower 7.3
walnut oil 5.3

Safflower Oil is naturally non-GMO. So you don't have to worry about finding a non-GMO alternative safflower oil

Of the major cooking oils, olive, sunflower, and peanut oil come from crops where no GMO technology is used. In addition, any organic versions of soy or canola oil would not make use of any GM technology.

-------------------------------------
Recommended Dosage and Administration
The recommended daily dose is 2-3 grams (2-3 capsules or 1 tsp. liquid concentrate) once daily. To be administered during meals, with a little liquid if required.

http://www.phoschol.com/prescribing-information.html

A therapeutic dose of PPC ranges from 1.8 to 2.7 grams per day. PPC has no known contraindications, side effects, or interactions with medications. It also has an excellent safety profile and is generally well tolerated. The most common reported side effect is gas, which is most strongly associated with very high doses, typically 15 grams or more per day.

I took an amino acids test that also included lithium. My lithium result was 0 as in none but what I cant figure out since it is supposedly not a required element am I suppose to be zero unless supplementing for possible benefit or should it be much higher just from the foods I eat? Thanks
 

prioris

Senior Member
Messages
622
I took an amino acids test that also included lithium. My lithium result was 0 as in none but what I cant figure out since it is supposedly not a required element am I suppose to be zero unless supplementing for possible benefit or should it be much higher just from the foods I eat? Thanks

The problem with standard measurement tests is that they can't measure levels in the tissue except thru biopsy. So we're talking about a brain biopsy. Tissue biopsies are generally a no go. It's why many tests are limited. Until they find a noninvasive way to test tissue concentrations of things then we experiment. I have found most tests are a waste. If I think I have a particular condition or deficiency, I just try the cure and see what improves. I save a lot of time and money too.

Buy the 120mg tablets (much cheap than 5mg plus you can break them up to smaller doses if you want) and just experiment taking it. See if it helps. It's a trial and error approach. You should feel some effect within a week I would think.

It will build up in tissues in about a month so after that you can ratchet down to maintenance dose. I take one 120mg tablet maybe every 10 days for maintenance but I have no idea at this point what exactly would be good maintenance dose unless my symptoms come back which they haven't.

p.s. i would edit your previous post and remove most of the text within the quote since it is a lot of clutter to wade thru .... basically shorten it