EXPLANATION OF MEDICAL REPORT BY DR. D. J. Ableman, M.D.
(Full Report Below)

"When one takes medications, drugs or alcohol, one produces free radicals (by means of the metabolism and attempts to destroy these toxins by the liver) which cause destruction to the liver cells. In doing so these free radicals result in inflammation of the liver which can be detected by liver enzyme tests, which are blood tests that demonstrate a leakage of these enzymes into the blood beyond their normal value levels.

As there is an escalation of free radicals, the liver cells become compromised and the liver is unable to perform it's functions, one being to detoxify the body. As more toxins build up in the blood system, the situation gets worse so that even toxins that would normally not cause problems add to compound the problem. The result is lack of energy, fatigue and toxic buildup.

Liverite reduces the free radicals and enables a compromised liver to increase it's function in detoxifying the body. As a result the energy level is increased. In addition, Liverite also prevents further damage to the liver as it helps in cell repair and helps damaged liver cells to function normally again. So, it both protects cells from damage and helps damaged cells to heal"

(FULL REPORT)

Liverite with it's particular combination (hereinafter referred to as "the combination") of liver hydrolysate with amino acids, niacin, B12, choline, inositol, cysteine and phospholipids, has phenomenal potential to prevent and alleviate hepatotoxicity.

There are many patients who develop different degrees of hepatotxicity as a result of medications, alcohol consumption or toxic agents (eg. acetaminophen, chemical toxins). Patients with varying degrees of existing hepatotoxicity from a variety of medical drugs are often forced to discontinue their therapeutic regimen. This might be seen with multiple drugs like the cholesterol-lowering agents, immuno-suppressant drugs, and chemotherapeutic agents which are used for treating mutiple diseases in medical practice. There are many patients who develop different degrees of hepatotoxicity as a result of medications or alcohol consumption. Liverite may be used in preventing some of the adverse effects of these drugs.

The main drug metabolizing system resides in the microsomal fraction of the liver hydrolase called the smooth endoplasmic reticulum. The enzymes responsible for this are mixed function mono-oxygenase, cytochrome c-reductase, and cytochrome P450. Reduced NADPH in the cytosol is a co-factor. The drugs are rendered more polar by hydroxylation or oxydation. The P450 system is a system that is involved particularly in drug metabolism, and production of toxic metabolytes is performed by this sytem of hemoproteins in the endoplasmic reticulum of the hepatocyte. There are fifty types or more of the P450 enzyme which have subtypes and can metabolize many drugs.

Enzyme induction, by increasing the P450 enzymes, leads to increased production of toxic metabolytes. Alcohol induces a sub-group of the P450 enzyme group.

The most important mechanism of liver injury in alcohol is the production of acetaldehyde which is a toxic substance which binds to phospholipids, amino acid residues and sulfphydral groups. It does effect the plasma membranes by depolymerizing proteins and producing altered surface antigens. Lipid peroxidation is favoured. It also binds to tubulin impairing membrane microtubules. Furthermore, there is an increase in intracellular redox potential and this is the other major mechanism of destruction. This means that there is an increase in the NADH:NAD ratio in liver cells which are actively oxidizing alcohol. This produces profound metabolic consequences. Thus, the redox ratio of lactic acid to pyruvic acid is largely increased, resulting in lactic acidosis. This, in conjuction with ketosis reduces the uric acid excretion, resulting in gout. This change in redox potential results in a fatty liver and change in steroid metabolism as well as impaired glyconeogenesis.

Hepatocellular injury is the primary event. This is rarely due to the drug itself. It is the toxic metabolytes of the drug, for example, not alcohol particularly, but the breakdown toxic metabolyte of alcohol called acetaldehyde which is usually responsible for the cellular injury. The drug metabolizing enzymes activate chemically stable drugs to produce electrophilic metabolytes. These potent alkylating, arylating or acylating agents bind to liver molecules which are essential to the life of the hepatocyte and thus, necrosis ensues. This follows exhaustion of intracellular substances such as glutathione which are capable of preferentially conjugating with the toxic metabolyte. In addition, metabolytes with an unpaired electron are produced by oxidative reactions of cytochrome P450. These free radicals also bind covalently to proteins and to unsaturated fatty acids of cell membranes. This results in lipid peroxidation and membrane damage. The end result is hepatocyte death related to failure to pump calcium from the cytosol and to depress mitochondrial function. Necrosis is greatest in zone 3 where drug-metabolizing enzymes are found in their highest concentration and where oxygen tension is lowest in the sinusoidal blood.

The hepatocellular damage in its acute form is illustrated by serum increases in enzymes which are thus released from the cells into the blood. These enzymes are in the form of AST and ALT and, to a smaller degree, LD.

The unique combination of the liver hydrolysate with it's amino acid, B12, and niacin combination results in an increase in the production of NADPH and NADH, which both help as co-factors in the reduction of metabolytes, which are increased as a result of the consumption of alcohol and which are also increased as a result of the multiple drugs referred to hereinabove. It is the reduction of these toxins and acetaldehydes that, as aforementioned, helps eliminate the toxins without hepatotoxicity. Cysteine has two actions. The first is that it actually forms glutathione in the liver cells and this forms, as mentioned, a unique ability of the liver to conjugate the drug metabolytes which in turn are responsible for the toxicity described hereinabove. In addition, cysteine can be of benefit in combining with lactic acid and thus producing pyruvic acid. It therefore prevents the build-up of lactic acid which again is a toxic metabolyte that results in hepatotoxicity.

Inositol and choline are subfractions of phosphoglyceride. They, in turn, combine with other compounds such as sphingosine and fatty acid to make sphingomyelin. It is these two molecules which comprise the essential building blocks to form the bilayers seen in cell membranes. Thus, their increased supply can improve cellular membrane integrity and therefore, they can be directly responsible in preventing further cell destruction on a cellular level.

Liverite can therefore help to prevent the build-up of acetaldehyde and thus the adverse hepatotoxicity that results.

Liverite can be used in drug regimens that will cause hepatotoxicity and that are seen in medical practice to be causing hepatotoxicity as demonstrated by increased liver enzymes in the blood. Liverite can thus be used for potentially many therapeutic regimens including the side-effects of drugs, therapeutic and toxic agents.

Dr. D.J. Ableman, Mbbch., M.D.