Alcoholic and non-alcoholic fatty liver (ALD and NAFLD) – Part 4

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Did you already read in our first part where a fatty liver comes from and where it leads? The second part was about what you can do against the possibility of fatty liver disease.
In the third part, we informed you about the treatment of alcoholic fatty liver disease (ALD). This fourth part now deals with the treatment of non-alcoholic fatty liver disease (NAFLD).

What should you know?

This topic is of interest to at least 35% of the population, because that is how many people have already developed a fatty liver. We have therefore decided to deal with the topic extensively in several parts.

Short summary of parts 1-3: Diagnosis, severity, therapies against fatty liver disease (FLD)

There are two recommendations to treat fatty liver: Dietary changes and exercise. There is no generally accepted therapy that is evidence-based (= validated by so-called double-blind studies*), is there? We already mentioned the treatment with PPC, which is a highly enriched lecithin from the soy bean, in the third part. What applies to alcoholic fatty liver applies equally to non-alcoholic fatty liver. Here, too, PPC is the remedy of choice. We will explain why in the following sections. Before we do so, we would like to point out that fatty liver goes through several degrees of severity: Fatty accumulation of the liver, NASH, i.e. swelling of the liver (= inflammation, hepatitis), followed by fibrosis, the formation of scars until cirrhosis, the destruction of the liver called the final stage, which is often fatal if not treated. Fatty liver is not easy to detect: If obesity, diabetes mellitus or metabolic syndrome* are present, fatty liver can be assumed. Before that, there are only very diffuse signs that something is wrong with the liver, such as nausea or pressure on the upper abdomen, but sometimes the patient has no symptoms at all. There is then the possibility of taking an ultrasound picture, taking the blood values, taking a biopsy (= a piece of tissue) from the liver or taking a fibroscan, which is an alternative to the biopsy (an imaging procedure).

*Double-blind studies – what does that mean? Studies are designed to find out whether a certain active substance works and how strongly it works. A good example is the vaccines against Covid-19 that have just been approved: Here, two roughly equal groups of patients are formed and these two groups receive an injection. One group receives an injection without the active substance, a so-called placebo, while the other group receives the active substance. Neither the injecting doctors nor the patients (= double blind) know which syringe contains vaccine and which contains the placebo. Only for the evaluation is the collected data made open, so that each patient is then assigned to the corresponding group.

*Metabolic syndrome
Metabolic syndrome is the term used to describe the combination of several diseases or symptoms. Cardiovascular diseases, the most common cause of death in our country, can usually be traced back to the “fatal quartet”. Quartet because 4 aspects are combined to form the metabolic syndrome:

  • Overweight (obesity)
  • A disturbed fat balance
  • High blood pressure (hypertension)
  • Elevated blood sugar level

How exactly do the liver cells change in fatty liver?

This question is important because it helps you understand why PPC is so important in fatty liver disease. So it’s about the cell membranes in the liver cells changing. This has been studied. On the one hand, more cholesterol accumulates in the membranes, and on the other hand, the phosphatidylcholine, which ensures the permeability of the membranes, decreases considerably. Both together then cause the liver cells to no longer function properly because they become stiff or rigid instead of being nice and flexible and permeable for the substances that are introduced into the liver cells. In other words, the ratio of phosphatidylcholine and free cholesterol in the membranes shifts or changes to the disadvantage of phosphatidylcholine.

But there is more going on: our blood fats, i.e. the proportions of fat in the blood that we also call triglycerides, are increasingly accumulated in the liver, because the liver cells no longer function properly and the process of metabolising these fats is disturbed. This process is called hepatic triglyceride lipase (HTGL). If you give PPC to a fatty liver, for example by taking it as a capsule, then this lipase is strongly activated again. By the way, this only works optimally with the PPC, which you have already heard a lot about here in our blog.

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PPC as evidence-based therapy for non-alcoholic fatty liver disease (NAFDL)

You have already learned that the recommendations of the medical societies for this disease are all about changing one’s own lifestyle (diet and exercise). This is 100% correct and makes sense in every case. However, there have been studies that have compared groups that have only made lifestyle changes with groups that have also taken PPC. And there are considerable differences. Yes, there is even a meta-analysis – that is an analysis of the results of several scientifically accepted studies – and this meta-analysis also clearly shows that all study results point to the fact that PPC is useful for the treatment of the different stages of the disease. That is why we call this treatment evidence-based, i.e. backed up by high-quality studies.

We do not want to list or discuss in detail the many studies on this whole complex of topics here (you will find a bibliography at the bottom). However, we have tried to distil from these recommendations what we would like to present to you here in generally understandable English.

  1. Treatment with PPC for this disease is not a short-term therapy. It is important for anyone hoping for improvement to know that almost all study results refer to a period of at least 1 year up to 2 years. So taking a few capsules or having a few infusions or injections is nonsense. PPC must be taken on a long-term basis.
  2. The dosage and the duration of PPC intake depend strongly on the severity of the disease and also on whether additional diseases are already present, e.g. diabetes mellitus. It is simply different whether I have mild symptoms of NAFDL or am already more seriously ill due to hepatitis and scarring of the liver. It also depends on the form in which I take the PPC, as a capsule or as an injection/infusion, or even whether I combine the two.
  3. The combination is recommended by the Extended Medicine Network, for example. Carry out a course of injections 2-3 times a year with 10 injections each and take the capsules in between so that the PPC level does not drop sharply again.
  4. Exercise and a low-fat, low-sugar and low-carbohydrate diet are important building blocks for reducing health impairments.
  5. If you have been eating an unhealthy diet for several years (e.g. mainly fast food), do not exercise and frequently consume alcohol, then you do not really need to think about whether your liver is already struggling with these effects. In this case, network doctors definitely recommend taking PPC in capsule form for prevention. Of course, not without also changing your lifestyle. What is not recommended, of course, is: drinking in the evening, PPC in the morning. That is not the purpose of treatment with this active ingredient.

Conclusion

We would like to let the two authors, the Kuntz brothers, of the basic work for physicians on hepatology (on liver diseases) have their say here:
“…Based on these pharmacological and clinical data, EPL/PPC appears to be the drug of choice to significantly reduce or eliminate fatty liver of various origins, e.g. due to alcohol or obesity, even if the causative noxious agent cannot be eliminated, as is the case with diabetes-associated steatosis…”

Selected literature (article links on request)

Puri P et al: Hepatol 2007; 46: 1081-90
Ling J et al: Hepatology 2012; 55: 1094-102
Desreumaux C. et al.: Drug Res. 1979; 29: 1581-3
Kharchenko NV, Korulya IA: Such Gastroenterol 2004;19:46-9
Sas et al: Hepatol. Int. 2013; 7(Suppl.1): S71
Dajani AIM et al: Arab. J. Gastroenterol. 2015; 16: 99-104
Ohbayashi H et al: J. Rural Med. 2007; 1: 67-73
Théret CG et al: L’Ouest Méd. 1977; 30: 1595-1614
Alliet J et al: L.Ouest Méd. 1976; 29: 85-104
Dinakaran N: Ind. J. Clin. Pract. 2003; 14: 51-8
Padma L et al: Indian J. Clin. Practice 2013; 23: No.11
Arvind N et al: Ind. J. Clin. Pract. 2006; 16: 21-4
Hu G et al: Liver 2005; 10: 5-7
Ye F et al: China Modern Doctor 2015; 53: 102-107
Kuntz E, Kuntz H-D: Hepatology- Textbook and Atlas -, 3.Ausgabe Springer Verlag, Heidelberg 2008; Kapitel 40: p.896

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