atrollappears

It's a typo, it should read hyperthyroidism, my bad..

Age should work against that theory due to a decline in natural testosterone levels, unless BF% was higher, therefore aromatase enzyme numbers would be greater, leading to an increase of aromatisation of the available testosterone...

The half life of propionate ester is about 0.8 days, so should ideally be pinned ED @ lower dose.. Enanthate or cypionate might be better, as their longer esters can be pinned once/twice a week.. Unsure why you would wish to add clenbuterol if on a first cycle wishing to maximise gains? You either cut or bulk, you can't do both at the same time.. Over the longer term stimulants like clenbuterol can negatively impact cardiovascular health..

There is a greater likelihood of aromatisation, due to increased BF% and subsequent increase in the aromatase enzyme, but only in those individuals showing increased BF%.. In normal individuals (lean) aromatisation would be lower as the precursor (testosterone) would be reduced due to age factors.. Unsure how aromatising would be easier.?

Older males are more likely to carry a higher proportion of BF, as we know the aromatase enzyme that converts testosterone to estrogen is largely found in adipose (fat) tissue... Although testosterone may be reduced in older males, there is a possibility greater aromatisation will take place due to increased enzymes, thefore Test:Estrogen ratio may favour increased Estrogen %.. Estrogen increases the binding of Thyroxine to TBG, which in turn can lower metabolism.. = Greater likelihood of fat retention..

Hi... I've previously discussed the above T-3 protocol starting at 25mcg's, it was at that time considered by others to be on the low side, hence the recommendation of 50mcgs.. I know of patients in their 80's on T-4 25mcgs/day.. Like anything it can be person / size/ BF% dependent.. Levothyroxine (T-4) is prescribed in NZ to patients with reduced thyroid function..

I have a few notes on T-3 that may be helpful: Important to keep protein intake high, 250- 350g a day. T3 is catabolic but with ASS and high protein muscle losses can be kept to a minimum. Can also add in clen, ECA stack etc if you so wish. See if you can find out if there is any history of hypothyroidism hyperthyroidism in your family, if so then T3 is a no no. Chances are you will be fine but as you well know everytime we put something into our bodies it carries a risk which I don't have a problem with but I also like to minimise the risk as much as possible. You will need T3 an 'in ear thermometer' One week before starting the T3 take your morning temperature as soon as you wake up (while still in bed) for 7 consecutive mornings (record in notebook). These will be your base readings. Start T3 at 50mcg per day for 2 days then stop for 2 days then on for 2 days then off for 2 days and so on and so on. You needs to keep measuring your temperature daily and if after 7 days your temperature is not 0.3-0.6 higher than your base readings then increase T3 by 25mcg. If after another 7 days your temperature is still not higher than 0.3-0.6 then increase the dose by another 25mcg. Very unlikly that you would have to go above 125mcg. So you are measuring your temperature each day, when your temperature drops 0.6 celsius below your base readings for 3 mornings in a row it is time to stop using the T3 as your body has begun to down regulate it's own thyroid production. You needs to keep measuring your temperature on a daily basis every morning (still in bed!) and once your temperature has reached it's average base readings again the thyroid has recovered fully. Normally this will take 2-4 weeks depending on the individual. With this method a rebound (putting weight back on) is unlikely as your own thyroid has only been marginally suppressed. Once your temperature has reached your average base readings you can start the whole procedure again. T3 is best taken on an empty stomach (better absorption rate) in the morning and then wait 30mins before eating.

You are within that 10% range, I don't see there's a problem..

Boldenone takes a while to show effects due to the long carbon-chain ester producing a long half-life, and its also molecular weight lowering the amount of active hormone available.. Its sometimes best to front load with double the normal dose, to spike plasma levels beginning of cycle...

Please explain his diabetes, is it type1, type2, does he inject insulin, if so what type, how often, what time in relation to meal times etc.. Maybe post an accurate account of everything he eats, times, amounts etc...

As previously stated you appear to be within normal range, self prescribing exogenous test could negatively impact your future endocrine function unnecessarily... You seem to be suffering motivational issues, maybe you should be looking at dopaminergic system dysfunction.. Get out exercise, eat healthy, and think positive..

Then what would happen when it comes in contact with stomach acids.. I think its a myth..lol

The biggest issue with orals is that you're overworking the liver by putting a chemical through it that it is unable to break down easily. This leads the liver to produce additional enzymes to aid in breaking down the substance (AST and ALT, which are often elevated in labs of those using oral hormones.) Because the liver is working so hard to try to break these compounds down it can lead to inhibition in its ability to break down not only the hormone but everything else it is trying to deal with. Another complicating factor is that the breakdown of 17aa hormones leads to the creation of 17-glucuronides which are toxic metabolites and which also (arguably) can lead to the majority of the negative liver effects seen with 17aas. This also causes the liver to produce additional biles (called bile salts) which work to clear toxins out of the liver and into the excretory system. When these bile sites become saturated they can stop working as effectively as they normal do and decrease or stop the production and elimination of bile from the liver. Current research is inconclusive as to the mechanism of action that 17aa hormones exhibit which specifically causes this decrease in bile production and excretion. This decrease in the liver's ability to process and expel bile results in a condition known as choleostasis. When a liver becomes choleostatic it greatly reduces or loses it's ability to process toxins out of itself. This can lead to liver damage as toxins remain in the liver, causing continued damage to hepatic (liver cells) tissues. This buildup can lead to lesions within the liver. The liver responds by increasing enyzmatic activity (leading to higher AST/ALT levels) and the circle repeats unless treated. Multiple studies indicate that after an extended period of oral steroid use clinical liver damage will occur, including lesions, drug induced hepatitis and jaundice*. However studies indicate that the extent of this damage is time and dose mediated, that is, if one is taking reasonable dosages for a period no greater than 2 months (although periods of up to 6 months have been observed with similar results) lasting damage should be non-existent. Current research indicates that if 17aa oral hormones are not used for extended periods and at sane dosages any changes in liver functioning (i.e. increased AST/ALT/Bilirubin values in labwork) should self correct with time. TUDCA is effective at decreasing liver damage because when you take it it causes your body to more effectively create and clear bile in liver tissue, which moves toxins out of the liver. TUDCA also increases the expression of certain proteins in the liver which are associated with pumping bile out of the liver, so it also helps in clearing other biles from the liver, allowing it to more effectively process all toxins coming through it. Dosing protocol is 250mg-500mg per day for maintenance with doses for up to 1000mg per day if lab works indicates significantly elevated liver values.

Liv-52 works..... The efficacy of Liv-52 on liver cirrhotic patients: a randomized, double-blind, placebo-controlled first approach. Huseini HF1, Alavian SM, Heshmat R, Heydari MR, Abolmaali K. Cirrhosis is the irreversible sequel of various disorders that damage liver cells permanently over time. Presently, the use of herbal medicines for prevention and control of chronic liver diseases is in the focus of attention for both the physicians and the patients; the reasons for such shift toward the use of herbals include the expensive cost of conventional drugs, adverse drug reactions, and their inefficacy. In the present study, the efficacy of herbal medicine Liv-52 (consisting of Mandur basma, Tamarix gallica and herbal extracts of Capparis spinosa, Cichorium intybus, Solanum nigrum, Terminalia arjuna and Achillea millefolium) on liver cirrhosis outcomes was compared with the placebo for 6 months in 36 cirrhotic patients referred to Tehran Hepatic Center. The outcome measures included child-pugh score, ascites, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total billirubin, albumin, prothrombin time, platelet and white blood cells counts. The indices were recorded in all patients before and after 6 months of drug or placebo treatment. The results demonstrated that the patients treated with Liv-52 for 6 months had significantly better child-pugh score, decreased ascites, decreased serum ALT and AST. In placebo administered patients all the clinical parameters recorded at beginning of the study were not significantly different than after 6 months. We conclude that Liv-52 possess hepatoprotective effect in cirrhotic patients. This protective effect of Liv-52 can be attributed to the diuretic, anti-inflammatory, anti-oxidative, and immunomodulating properties of the component herbs. http://www.ncbi.nlm.nih.gov/pubmed/16194047

Clinical efficacy of milk thistle is not clearly established. Interpretation of the evidence is hampered by poor study methods and/or poor quality of reporting in publications. Problems in study design include heterogeneity in etiology and extent of liver disease, small sample sizes, and variation in formulation, dosing, and duration of milk thistle therapy. http://www.ncbi.nlm.nih.gov/books/NBK11896/