Liver Tests and Info from GotFina.com – by acid_doctor and fukkenshredded
acid_doctor:
As usual IA is dead on here. Resistance training, especially vigorous training will raise the ALT and AST, the 2 main liver enzymes doctors watch. And I would venture to guess that since so few people train like we do that almost no doctors, even good ones know this. (Probably only sports med docs and hepatologists would.) High protein intake will artificially raise your BUN levels which also may make him think you have a kidney problem (just threw that in as an aside). You can have high levels of platelets or white blood cells due to a phenomenon called "demargination" from physical exertion and muscle strain.
NJ, see if your doc or lab have any of that same blood sample left in the lab (many times they will) and have them run a CPK and GGT. The CPK should be very high indicating what a stud you are in the weight room and that you tear the shit out of your muscles training them. Here's the MOST IMPORTANT POINT: the GGT should be NORMAL. If your GGT is normal, then your liver is normal and the AST, ALT values were artificially raised due to resistance training. At that point blow it off and don't waste anymore money chasing it. My guess is that unless you are taking large amounts of an oral steroid and have been for months, your liver is actually fine. Injectables have very little IF ANY effect on your liver.
Hepatitis patients can recover because of the reserve the liver has. As I pointed out, the cells do regenerate and that fact alone has led to the myth especially among nutritionists, supplement pimps, etc that the liver has this "amazing ability" to regenerate. Well it does when you compare it to the brain which cannot reproduce one single brain cell that dies. HOWEVER this "regenerative" capability of the liver is non functional. Liver cells are laid out in a very precise pattern of rows and columns. There is an intricate pattern of blood vessels, which bring the portal venous supply (from the gut), the arterial supply (bringing oxygen) and the regular venous supply (taking away de-oxygenated blood). It also has a very intricate network of tubules or ducts, which carry bile. Anyway, the key to these cells working is the pattern and very precise framework that they are laid out in. When liver cells are DAMAGED structurally or destroyed, the liver regenerates them (with amazing speed, true). However, and this is the KEY which is conveniently ignored by the supplement pimps and others who are just ignorant to the facts, the cells are regenerated in a completely haphazard and irregular array of clumps of cells that do not metabolize toxins or produce bile. This is just the simple fact of hepatic pathophysiology. For those who will vehemently disagree based on this or that source that they find or were told about, try going to your local medical library and checking out a textbook on pathology or hepatic pathology before you become convinced you are correct. Regenerated liver cells do not function. As I said, your liver has a VAST reserve, which can be called into play when needed.
There is one other factor though and that might be what a lot of people are actually referring to. That would be liver cells that aren't ACTUALLY DAMAGED but starting to show a fall off in function due to some chemical insult such as booze or drugs.
IA, probably what saved you was that you had many CELLS that were on their last leg but weren't actually damaged and once you stopped insulting them they started functioning properly again. But a DAMAGED liver cell is kaput. So we may be arguing here over semantics about what is simply a stressed out and practically non-functioning liver cell versus a liver cell that is completely trashed. Yes, when we have alcoholics stop drinking they usually appear to get normal liver function back. This is partly due to cells which weren't dead yet getting normal function back after the alcohol was withdrawn and partly due to the vast reserve of extra liver tissue we are born with. So in this light we can both be right.
I would caution again though that livers are nothing to screw with and that they can be irreparably damaged.
fukkenshredded:
Alpha-lipoic acid's primary feature--separating it from other antioxidants--is its exceptional ability to act as a reducing agent. This means it more readily donates electrons to molecules with a net positive charge than many antioxidants and is easily recycled back to its reduced state by intracellular glutathione reductase. The main task of this enzyme is to transform oxidized glutathione (GSSG) back to the active reduced form, GSH. This recycling mechanism is not nearly as efficient in recycling alpha-lipoic acid, but it significantly adds to the appeal of using it as a treatment for oxidative stress (Passwater, 1995).
Through this antioxidant action, alpha-lipoic acid helps to keep NF-kB, a cellular protein, which activates HIV expression (see below). Other features of alpha-lipoic acid important to PWAs are its ability to aid in the recycling of vitamins C and E; its ability to replace lost glutathione in intracellular free radical defense; and its ability to reduce or eliminate plaque formation (clumping) of CD4 lymphocytes (syncytia), which is a suspected mechanism in the killing of uninfected T cells (Passwater, 1995; Suzuki, 1994; Suzuki, 1992).
When alpha-lipoic acid (which is considered its oxidized state) enters a typical cell, most of it is reduced to dihydrolipoic acid, which has greater potential than alpha-lipoic acid to neutralize reactive oxygen species. Dihydrolipoic acid has the same backbone structure as alpha-lipoic acid, except its disulfide connection is broken (Bast, 1990). Another metabolic product that comes from alpha-lipoic acid is tetranorlipoic acid, which has been shown to be very potent for inhibition of NF-kB (Suzuki, 1994). Through Suzuki and Packer's work, it is evident that two portions of this molecule are active in inhibiting NF-kB, including the hydrocarbon backbone and the cyclic disulfide side chain. The cyclic disulfide/dual SH- moieties (parts) are much more potent than the hydrocarbon chain. (The sulfhydryl group [SH] donates two hydrogen ions [protons denoted H-] to reduce oxidant molecules. Again, because repetition is good for the soul, the dihydrolipoate is oxidized, and a disulfide bridge forms between the two sulfur atoms to form the cyclic compound alpha-lipoic acid.)
Alpha-lipoic acid has also been shown to aid in the recycling of reduced vitamin C and, thereby, vitamin E. Alpha-lipoic acid reduces dehydroascorbate (oxidized ascorbate) back to vitamin C, which in turn reduces vitamin E. This maintains a steady state of both vitamins C and E (Kagan, 1992; Passwater, 1995). When Kagan's group added dihydrolipoate acid to a mixture of plasma lipoproteins (a fat-protein mixture that mimics a cell's membrane) undergoing peroxidation (oxidative stress), the ability of ascorbate to recycle vitamin E increased greatly. Thus there was more vitamin E available in a form that was effective in limiting the damage to cellular membranes induced by the oxidative stress. This effect was shown in other test situations with liposomes (balls of fat), microsomes (balls composed of a cellular organ, the endoplasmic reticulum), membranes and tissue homogenates (blended tissues) (Kagan, 1991).
The role of glutathione as the primary cellular antioxidant, and its often extreme deficiency in people with HIV, cannot be overemphasized when discussing the use of antioxidant therapy for HIV/AIDS. (Please see the Glutathione Information Sheet). Alpha-lipoic acid has the ability to recycle oxidized glutathione (GSSG) back to reduced glutathione (GSH), possibly by simply donating electrons to GSSG (although the mechanism is not clear). Alpha-lipoic acid in turn, is then reduced by glutathione reductase and other enzymes. Because intracellular alpha-lipoic acid concentrations are in the range of nanomoles (nM, extremely low concentration) and glutathione is in the range of millimoles (mM, which is relatively high), the recycling of alpha-lipoic acid takes place without interfering with the recycling of GSSG to GSH (Kis, 1996).
Fukkenshredded,
Sorry, Bro. Not trying to be flippant. Just trying to understand the full picture. You are very informed and must know that while oxidative damage CAN/DOES cause hepatocellular carcinoma, that particularly nasty cancer is about the rarest disease that steroid users will actually get as a result of taking 17aa anabolics. Clearly it is the worst, being uniformly incurable and very quickly leading to death. My point was just that hepatitis peliosis and cholestasis are other real worries and these are caused by direct damage to the cell membrane and cell function, not by oxidative damage. Various anti-oxidants are touted by most people in the BB world as "liver protectants" and I think it is just a good idea that everyone understand what we are talking about since undoubtedly most, like BP655, are totally clueless and just repeating what they have read on numerous boards. The simple fact is that these supplements are not in fact "liver protectants" but anti-oxidants. They protect against oxidative damage. I am not saying that THAT is not significant. Far from it. Most certainly it is VERY significant. All I am saying is that the term "liver protectant" is misleading. It suggests some magical power over evil, and I believe that that is about the extent of understanding that most supplement whores have about the supplements they take and recommend. I propose that we all strive for deeper understanding and not take labels like "liver protectant" at face value. The simple truth as you have eloquently stated is that there is a very real mechanism by which ALA works to protect against oxidative damage in the liver. It is not magical. It is real, scientific, and definable, and I thank you for the education you gave me on it. It protects against a certain type of damage but certainly is not a talisman against all liver disease caused by 17aa anabolics. Can we agree on that?
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