Test level increase and cancer risk
Test level increase and cancer risk
Hi folks. I'm a 56 year old athletic old dude. At one time I was in great shape... weight lifting and martial arts competitor.Doing both for approx 36 years. 2 years ago I was diagnosed with and treated for prostate cancer. For the past 2 years I have tested cancer free. I've read alot of conflicting reports on test boosting and cancer risks. Some reports say no connection and some say excess test, in addition to other factors, can cause increased cancer risk. Anyone out there know the real scoop on this? I'm just getting back into shape again and wanted to jump start my weightlifting/muscle production, as I have successfully done in the past, with a couple of cycles of light weight juice or even the new prohormone replacements, Methyl 1-D or Superdrol. I hate needles so I've made a topical, in the past, from Denkall Aqua Test (evaporated the water and marinated the crystals in DMSO). Worked really well. Extra Test makes me feel great. Any opinions on this issue from the pro's? I'm getting a Test check at the end of July. Suspect it will read low, since I'll be finished by about a week or so, with a Superdrol cycle.
"2 years ago I was diagnosed with and treated for prostate cance" = No steroids ever again son.
damn! I was afraid of that. Been feeling really nasty these last two years and really want to recover and get back into shape. The surgery was easy to recover from. The emotional toll was tougher.
At 56 you can talk to your Doctor about HRT, and the possible problems it might cause with your history of cancer.
Yeah... that's why he's testing me. I asked him for HRT a couple of days ago. Too bad if I can't do it, the extra Test feels so damned good, the workouts are great, and the muscle comes on fast. Once you get cancer there's so much to watch out for..... sugar, red meat, fat, nitrites etc.... tough way to live, but at least I'm still alive and kicking.
Living another 50 years cancer free is better than living just a few more with some extra muscle.
Let's all join together and SPEAK ENGLISH IN AMERICA.
ABSOLUTELY NOT! The two most prone cells with the biggest receptor sites for anabolics are the breast and the prostate. 99% of cutting edge steroid books agree that injectable steroids are usually harmless if used in under a gram dosages, UJNLESS one is predisposed to genetic baldness or has a family history of porstate cancer... Much less already having had it yourself. Sounds like a death wish to me.
Why genetic baldness? Grateful, as a male pattern baldness sufferer, for pointers to any supporting evidence between this and prostate cancer please.
Originally Posted by Ironhorse
Hmm.. I'll look for the article, however, I believe there is supportive evidence at www.lef.org. Perhaps do a search at thier site. As I reflect on this and several other articles, some peoples genetic traits have a predisposition to turn test into DHT.. the hormone responsible for causing hormonal hair loss. Some anabolics are very likely to turn to DHT (a bad thing) like tren especially. Different anablolics have different affinities to turn to DHT but tren is the worst, probably followed by sus and prop. Of course, there are some slow to aromatise anabolics out there such as deca, primo and anavar come to mind.
It may be a good idea to buy the book 'anabolics' that digs much deeper into this subject available at meso-rx. Good luck putting a safe cycle together and slowing the inevatable.
No more prostate.... no more cancer
Just to set the record straight. I don't have a prostate anymore. I had it removed with robotic surgery two years ago (the DiVinci robot). Very interesting experience, also a testament to being in shape as an old fart. The docs said I had the fastest recovery they had ever seen. I got in really great shape before I went in. Anyway.... I don't have a prostate anymore. Also don't have a couple of glands and seminal vessicles. Those were all removed and biopsied just to be sure the cancer hadn't spread. It hadn't. They got it all, And for the last two years I have tested with a PSA of zero. I get tested every 6 months now. It was every three months for the first year.
So..... does this change anything? I can't get prostate cancer anymore. I did a long cycle of low dose aqua test last year, with no rise in any cancer related variables. Thanks for all the feedback guys I really do appreciate it. I'm working hard to get back in shape. Those six holes in my belly and peeing all over myself slowed me down a bit. Everything is much better now. Erections are even back, with or without ciallis, though ciallis makes them rock hard. Very cool invention, that stuff.
one more thing...
Oh, one more thing.... I have no family history of prostate cancer. My dad is 87 and his PSA is 1.5. Pisses me off. I have an uncle on mothers side, with a PSA of 15 for last 10 years.... but.... no cancer. Very strange. I'll tell you what though, I eat very little red meat now... or hot dogs or sausages etc.
Determined aren't we?.. Joking. You may have removed some glands and body parts that were suseptable to cancer risk yes. However, JAMA said that everybody on the planet has cancer, it's the part of the immune system that keeps it in check. I do, to be clear, have had a lifting partner that juiced to the gills after a nasty bout with skin cancer. DURING his cancer his PSA was well within limits, and his family had a predisposition to prostate cancer. Hey, we all take tremendous risks when "juicing", I'd be more concerned about what exactly is in the bottle I'm getting ready to put in my body. That could lead to instant death, not just a quickening.
JAMA = Journal of the American Medical Association
DHT binds much more tightly to androgen receptor than testosterone. MPB (alopecia aerata), as result of DHT imbalance in skin, may result from hypersensitivity to DHT, from androgen receptor (AR) upregulation (meaning a physical increase in AR from gene expression) or from an increase in the cytochrome P450, 5-alpha reductase, an enzyme that converts test to DHT in dermal tissue.
Androgen receptor itself doesn't cause cancer, it does however signal for a cascade of events in cells in which its enriched, muscle, and sex steroid responsive tissues. It also signals for immune system function, as muscle requires support tissue function (tissue peripheral to muscle fiber - connective, repairs and blood and lymph supply).
Now, here's why tight binding DHT is a problem. Its not DHT binding to androgen receptor, its DHT binding to other nuclear receptors that also regulate immune system function, that the rub. Its not test, its DHT, the point IronHorse was trying to bring out, in his comments on the relative binding strength of AR receptor activators.
But here's a hint; its also a function of the presence of other nuclear receptor activators, common in a well balanced diet. They also compete for time at the docking stations (receptor binding sites) of nuclear receptors present in all tissue, but they vary in their combiantion. Its not so much AR being goosed by anabolics, its also who else is being tickled by tight binding steroid analogs, overactivating otherwise carefully maintained cell turnover control elements.
Who would have thought, just a decade ago, that the secret to ultimate homeostatic health and disease prevention, including cancer, lies in the action of bioactive lipids in your food, many of them potent antioxidants. Nearly all of these compounds originate in vegetables and fruits. And they are all present at low physiological concentrations.
Hence, the comment about AAS dose effects made earlier in this thread by IronHorse, an astute observation well worth considering.
You are what you eat.
I've just re-read Ironhorse'e original post and realised it could be read two ways: firstly, if you have the genetic predisposition you are more likely to get MPB or prostate cancer; secondly (the way I read it first time around) if you have a genetic predisposition to MPB you are more likely to get prostate cancer.
I understand how DHT is the culprit here, whether as DHT-derived AAS including the other wise mild primobolan or as the result of conversion from test. What I still don't understand is whether there is any (scientific) evidence to suggest that because I am prone to MPB (I am) I am more likely to get prostate cancer.
Hey, but I'm going to eat more fruit and veg!
Thanks in advance,
Sure, let me clarify my previous answer, which did indeed address your question, but it must not be real clear to you.
1. If you have DHT sensitivity, you're gonna scale up the response of androgen receptors on prostate cells.
2. Just bout all the darned biomedical research on androgen receptor (AR) relates to prostate cancer. That should tell you something right there.
3. DHT sensitivty has been correlated to AR upregulation and cancer forming potential (hyperplasia) in susceptible males.
1 + 2 = 2
Sensitivity generally means that you have an altered transcript of the androgen receptor gene, and that gives you a slightly different androgen receptor protein than you would normally have. Sometimes its genetic cause, and sometimes its a change in the nuclear receptor activator promoter elements.
Thats an area I'm working on, on the side.
I think you got the latter case, and if so, don't matter hill o beans if you got hairy assed apes in your gene pool. Its environmental factors or exposure to certain steroid analogs, or maybe exposure to some pesticide, thats done changed your programming.
I got threads in other forums that talk about the sophisitcated molecular handwaving explanations of nuclear receptor cross talk. Thats not needed here, just for you to know that yeah, theres a connection.
(does that) Answer your question, RF?
Weighing in as a prostate cancer survivor...
Everything I read, and everyone I talked to, including the cancer pro's at UCSF Medical Center and MD Anderson in Huston, TX. STRONGLY suggest that if you have prostate enlargement or a family history of Prostate cancer.... STAY AWAY FROM ANABOLIC STEROIDS. The research data is pretty cle ar now, that there is a strong connection to pre existing conditions or family history, and full blown prostate cancer. I can't help but think that some of my playing with orals in years prior to my condition, led me to my problem. The doctors also said that there may be a connection between a mothers breast cancer and a sons prostate cancer.
very good point
Originally Posted by ForemanRules
I'm having trouble here (no pun intended). I think I understand the links between DHT sensitivity and AR responsitiveness. I guess what I am asking is whether male patter baldness is a direct result of DHT sensitivity i.e.
MPB means you have DHT sensitivity which means you have greater AR respons iveness which means you have a greater chance of developing prostate cancer - a direct causal iink, even if each link in that logical chain is not 100%.
So if I have MPB I have x% more chance than someone who doesn't of developing prostate cancer if we both ran the same cycle - what is x roughly - 10%? 100%? 200%?
Apologies if I'm being unusually slow here but Im not a scientist..
All he best,
oh ... now I understand what you're wondering about. I think one of the other members had the science down better than me. I have friends who do anabloics and are bald and have no prostate cancer yet. I have no family history of prostate cancer and played with very strong anabolics and topicals for a few years.... and I ended up with prostate cancer. I personally haven't read anything about the DHT/Prostate cancer connection. Most reasearchers say steroid use will increase any man's risk by a significant percentage. Some research says there is no strong link. If you want to be sure you don't end up like me, under the knife of a surgeon or robot, and don't want to suffer the long term aftermath of such surgery, then be safe and don't do the roids. Stick to Nitric oxide, creatine, whey protein etc. If you like taking risks, then talk to your doctor first and let him weigh in, then do short, low dose cycles. I'm doing that, right now, to get jump on getting back in shape. I'll do two 3 week cycles with a couple of weeks rest in between, then I'll stay with the non-roid supps. I'm doing HIT workouts right now, and my bod's responding after only 1 and 1/2 weeks. Could be the mild roids or could be the hard work and other supps, or a combo. Either way, when my current supply is gone, that's it. I'll be tested right after my second cycle is completed. Good luck
OK, lets try again.
Prostate cancer ---> high level of very sensitive androgen receptor (AR)
DHT---> relatively tight binder to AR --> increases AR concentration in cell membranes on the surface of cells.
Increased AR receptor on protstate cells ---> increased chance of excess arachidonic acid activating cell turnover (cell division and replacment).
Increased cell turnover = hyperplasia = increased opportunity for DNA fuckups during cell replication
Increased DNA fuckups + DNA repair / immune suppression by AAS = higher cancer risk
Now thats as simple an explanation as I can make here, RF. And it underlines the last posters helpful comments, perfectly. Understand that I have simplified at rather complex cascade that leads to cancer promotion by AAS in susceptible induhviduals.
Anybody with the balls to read the eyeglazing details on arachidonic acid intitiation of cancer events, can scan this abstract for proof of what I say here.
Where do you get the excess arachidonic acid?
Simple, you make it from the the excess of dietary intake of omega-6 fatty acids and the shortage of omega-3 fatty acids (fish oil) that controls arachidonic acid formation in specific tissues.
Ahhh, you see? You are what you eat! And your health is also a product of your lifestyle choices.
Excess stress ---> increased arachidonic acid formation, suppresses immune controls, and increases the chance of cellular hypeplasia in key tissues.
Hope this helps you understand my earlier post comments.
Yup, I understand all of the terminology and most of the sentences.... but you don't answer my question. There is no mention of MPB in your response.
I'm looking for a cause-and-effect chain here, even if event or condition A does not lead in 100% of cases to event or condition B, I need to know whether event or condition A increases the chances of event or condition B. For example, DHT sensitivity/receptivity leads to increased chance of both MPB and prostate cancer; AAS use leads to increased DHT levels; DHT sensitivity plus AAS usage leads to significantly greater probability of prostate cancer. I'm not looking for certainty, just probabilities.
Very specifically, would the following be true: MPB is caused by enhanced sensitivity to DHT; enhanced sensitivity to DHT also increases the chances of developing prostate cancer; it is therefore reasonable to assume OR there is scientific/clinical evidence [delete as applicable] that having MPB means that you are more likely to suffer prostate cancer problems as a result of AAS use than someone who does not have MPB.
Does that make sense?
Oh boy, you really make a mod work...
...for her cookies!
DHT is produced from testosterone through the action of 5-alpha reductase.
AAS also bind to the nuclear receptor that activates it, as do other dietary lipids.
In susceptible induhviduals, when DHT is 'up-regulated' (overproduced), it causes blockage of the retinoid RXR receptor in skin and scalp, and that leads to an inflammation control problem. Its the inflammation that causes both excess sebum (skin oils) and increases the rate of hair follicle maturation, so that they turn over very quickly and fail to mature (gain thickness, so they become fine) and eventually "burn out", causing MPB.
DHT also induces the same hyperplasia and inflammation response in prostate, and we know that its coupled to action of arachidonate on AR in both skin and prostate tissue.
And that sir, is about as cutting edge as you will find for an explanation of the chain of events that cause these DHT-induced cellular control dysfunctions.
Originally Posted by Trouble
Disclaimer: All health, fitness, diet, nutrition, anabolic steroid & supplement information posted here is intended for educational and informational purposes only, and is not intended as a substitute for proper medical advice from a medical doctor. We do not condone the use of anabolic steroids (AAS), all information about AAS is for educational and entertainment purposes only. If you choose to use AAS it's your responsibility to know the laws of the country that you live in. Consult your physician or health care professional before performing any of the exercises, or following any diet, nutrition or supplement advice described on this website.
arachidonic acid formation...I've never heard of this. Is there an alkaloid that can reduce the amount in your system? Sorry for less than an educated post, but, would vinagar or celery have a positive effect? I know these two natural ingredients have a neutralizing effect on many alkaloids and acidic compounds in the body and can help get your ph balance in line. Thanks Trouble. I hope you're not entirly what you eat... celery would be a bit woosey, should I add a little piss to my vinagar? lol
Thanks Trouble... now I get it!
I was not bald in my twenties but I do have seriously thinning hair in my forties. Guess I'm more likely than most then to develop prostate problems.
Final request - has there ever been any published research which demonstrates a higher prevalence of prostate issues in those with MPB than without? I understand the theory but it would seal it for me if someone had identified a linkage; I'm not doubting the theory, but practice carries more weight if it exists.
Many thanks for your patience in restating what I'm sure to you is the bleedin' obvious.
One more fact.....
Gee.... Look what I started here!
I'm not as science savvy as Trouble is, but I want to bring into focus a fact I neglected to mention. I have a full (and I mean full) head of hair. No MPB with me, my dad or my grandfathers or any of my uncles. As a matter of fact, I have very little grey as well hair (at 56). I was extremely healthy and in great shape. Most people thought I was 10 to 15 years younger than I was, and yet....... I had prostate cancer. I don't think using MPB as a barometer works. I have known plenty of AAS users with very little hair left, and no prostate cancer. Has anyone asked what degree of significance the statistical analysis indicated in the research? I think becoming knowledgable with prevention is a better use of mental energy at this point. Also... get your PSA tested often. Early detection can save your life. I'm sure I had cancer for at least a year before I was tested, at my wife's urging. I could have lost my life or at least shortened it, if I hadn't gone in when I did. I had a moderately fast growing form of the cancer (a Gleason score of 7 and PSA of 8.3).
Blood doesn't lie
I get my blood checked every three months, it's about 30 bucks including prescription, flebotomist, and results and a phone call to a doc if you have any questions. Go to lef.org. for more info.
Okey dokey, good point raised by almcg2:
5-alpha-reductase P450 is present in two flavors in humans: isozyme types I and II.
Characterization, expression, and immunohistochemical localization of 5 alpha-reductase in human skin. Luu-The V, Sugimoto Y, Puy L, Labrie Y, Lopez Solache I, Singh M, Labrie F. J Invest Dermatol.(1994) 102(2):221-6.
Human skin has been shown to contain a high level of 5 alpha-reductase activity, the enzyme that catalyses the conversion of the weak androgen testosterone into dihydrotestosterone, the most potent androgen. Because two types of 5 alpha-reductase genes have been characterized in humans, we have cloned 5 alpha-reductase cDNAs from adult human keratinocyte and skin fibroblast cDNA libraries to identify and gain better knowledge of the 5 alpha-reductase expressed in normal human skin. Nucleotide sequence analysis shows that the clones obtained correspond to the type I 5 alpha-reductase. RNase protection analysis using (poly A)+ RNA obtained from human skin and prostate also confirms that type I 5 alpha-reductase is the predominant type expressed in normal skin, whereas type II 5 alpha-reductase is the major form found in the prostate. Following polymerase chain reaction amplification of human keratinocyte and skin fibroblast cDNA, a low level of type II 5 alpha-reductase cDNA has been detected. Using antipeptide antibodies raised in rabbits against the peptide sequence covering amino acids 227 -240 to perform immunohistochemical localization of 5 alpha-reductase, we have found that 5 alpha-reductase is distributed in sweat and sebaceous glands, as well as in the epidermal cell layers, thus providing the basis for the important role of androgens in human skin and its appendages.
Pilosebacous glands are colocated in the same pores as hair follicles. This article
yaks in technical jargon about the androgen binding site differences between the two types of isozymes present in a prostate hyperplasia cell line used for research on prostate disease.
What it shows is that both forms of isozyme are expressed in abnormally dividing prostate cells, and we know from our molecular biology primers, that this also means that there is unusual 5-alpha-reductase activity present, and that means tissue specific variable expression of the enzyme, and therefore, the localized tissue concentration of DHT.
Note that the type II isozyme is expressed at very low rates in skin, and high rates in prostate.
This fact, correlated with the differences in binding stength, and therefore, enzyme sensitivity to androgen type, answers your question.
Yes, if you have high circulating levels of DHT, you may exhibit MPB. But, if you have a tumor type that has the opposite isoform as the predominant type of alpha reductase enzyme present, it, and the androgen receptor cell surface concentration (and abberations of AR are possible as well) will determine if you have both MPB and prostate hyperplasia co-symptoms.
So, MPB is a general indicator, not a specific one, for potential response to androgen receptor upregulation. Furthermore, there is no direct genetic evidence for MPB as a directly inherited trait within families. Later reports link MPB to androgen receptor polymorphism (expression variation for the androgen receptor protein).
Polymorphism of the androgen receptor gene is associated with male pattern baldness. Ellis JA, Stebbing M, and Harrap SB. J Invest Dermatol. 2001 116(3):452-5.
Certain androgen receptor polymorphisms are apparently related to prostate disease susceptibility, when coupled to insulin insensitivity - a known regulator of lipids in humans. And it has been linked to faulty nuclear receptor control of vitamin D biosynthesis in the liver.
These are all cytochrome P450 catalyzed reactions.
To bring us our eye glazing discussion full circle, when you use anabolic steroids in supraphysiological concentrations, you saturate many nuclear receptors in liver, skin, prostate and breast tissue, plus brain. These nonspecific targets are then changed from natural regulatory contols...
and molecular mayhem results. Liver lipid and immune system dysregulation, upregulation and enhanced sensitivity to xenobiotic contaminants, etc.
Do you understand my arguments and explanations?
You are now at the cutting edge of knowledge on prostate hyperplasia, the precursor condition to tumor formation. Plus, you have an inkling of the connection between LXR and RXR, as well as PXR and SXR nuclear receptor swamping by anabolic steroids and their linkage to alterations in lipids (including those that affect oil production and skin cell inflammation and overgrowth) in both hair and skin negative sides associated with AAS use.
Now that wasn't so painful...was it? *laughing*
Ironically, there is a patent for using Arachidonic Acid to "increase muscle mass in humans".
Not inronic, insightful. I know and like Bill L and his staff, whom I correspond with over at Mind and Muscle and Avant Labs forums.
In proper dose, with the right chaparones (other nuclear receptor regulators) exogenous arachidonic acid can be a very useful anabolic supplement.
The combination of AA with other lipid regulators is already under investigation and early results are promising. What most don't know, is the arachidonate works via the vitamin A pathway nuclear receptors and receptor modulators. They in turn down regulate mystatin and increase muscle protein biosynthesis many fold, a substantial action, say, when compared to the much touted use of IGF-1 long form.
It's that magic combination of NR factors and dosage thats key to keeping AA from exerting other less desirable effects.
Those negative effects are a direct result of the standard Western dietary imbalance of omega-6 to omega-3 fats, the former being the agent from which arachidonate is synthesized in cells, and the latter being its controller that helps upregulate its synthesis in many tissues.
So you see, Pirate, careful diet is also required when using this supplement. Too much AA in diet from n-6 fat sources, and you push the prostanoid biosynthetic cascade the wrong way, with inflammation and programmed cell death (apoptosis of cells), including skeletal muscle cells, as the cost borne when one doesn't know the chemical recipe very well.
Moderation and balance have their just rewards when one is attempting to season the molecular soup within cells, just so...
By Prince in forum Bodybuilding Gossip
Last Post: 07-14-2011, 09:20 PM
Last Post: 07-14-2011, 09:20 PM
By Prince in forum Bodybuilding Gossip
Last Post: 11-09-2010, 07:23 AM
By cpush in forum Diet & Nutrition
Last Post: 03-30-2009, 11:22 AM
By JJJ in forum Anabolic Zone
Last Post: 11-29-2003, 10:48 PM