You can say this because you checked LFTs and albumin levels before and after D - bol and then compared it to Tylenol and looked for statistical significance 
You so called "gurus", are exactly why bodybuilding has become a joke and a freak show. D-bol occupies cytochrome p450 and many other cytochromes MUCH more than tylenol, not that tylenol is not toxic to the liver. LFTs are always checked when giving oral anabolics, this is starded of care in most American hospitals. In fact, when you deal with cancer patients, status post chemo, and give them ORAL anabolics, such as D-bol, LFTs along with albumin are always checked. However, LFTs do not have to be checked with tylenol, assuming the patient is not overdosing on tylenol, which sadly is not always checked. No offence Disgusted, do not make blank statements without really understanding what you are talking about. Then again this is very typical of "drug gurus." Human beings should not be used as lab rats for you "gurus" to test your absurd theories on. Let the real doctors deal with real science.
cheers,
bodybuildermdpitt
Insulting me does not make you look any more credible.
BTW, as I stated above, BB at times eat very little and they also fast to some degree. Your cytochrome p450 reference is bullshit, but here's a little info for you concerning cytochrome p450 and tylenol anyway Dr.
Many commentators believe the frequent, regular use of alcohol (ethanol), when combined with APAP, "revs-up" the cytochrome P450 system producing higher quantities of the harmful metabolite/NAPQI. While this may be true, and warnings are now contained on the labels of APAP-containing products relative to dangers associated with liver damage from the use of alcohol and APAP, a growing body of evidence seems to indicate the more significant causal factor is nutrition, i.e., "fasting". Chronic alcoholics are notorious for poor nutrition and diet - often replacing food with liquid. However, retrospective studies going back over the last ten (10) years indicate a relationship between fasting, APAP, little to infrequent use of alcohol by patients, and liver damage. This includes patients who are most typically unable to eat due to nausea from the flu or flu-like symptoms, stomach virus, dental pain, and the like. Moreover, basic science studies performed and repeated over the last two plus decades add additional support to the fasting connection.
What appears to happen under these circumstances is that the "traffic" of APAP along the "expressways" of glucuronidation and sulfation slow down, and exit onto the "access road", the cytochrome P-450, CYP 2E1 pathway. Concurrent with this phenomenon is that levels of glutathione begin to become depleted, at least the glutathione available to conjugate, bind with and detoxify NAPQI. The net effect is that a patient winds up with more NAPQI, less glutathione for detoxification, and the liver's defenses are ultimately overrun and defeated. Liver death soon follows, as well as the patient's very life, unless a successful transplant is accomplished. Even if the fortuitous, successful transplant occurs, you may likely be left with a brain-damaged client who will need expensive anti-rejection drugs (that carry with them a host of potential complications, including subsequent kidney dysfunction), among other things, for the rest of their life.
