Not acutely… Or perhaps even over an intermediate duration of time
You could probably go five straight years with HDL 20 LDL 130 or something without serious detriment.
The effect is cumulative, no one runs one blast… Or at least very few only run 1-2 and call it quits.
The cumulative exposure over one decade + of bad lipids is a concern.
The health risk knowledge today is way more than anything available in the '70’s, '80’s, and ‘90’s. When I started it was exclusively Dianabol. It was 1971 when I started with a prescription for 30 days of 10mg of Dbol per day. After a couple of 30 day cycles I bought a PDR (Physicians’ Desk Reference) and looked up all the anabolic steroids it contained. I read the details of Dianabol, Winstrol, and Anavar. There was very little in depth specifics. (I bought an updated one a few years later and found two more orals: Halotestin and Anadrol.) I don’t recall seeing either Deca or any injectable testosterone. I started my first Deca at 100mg/week in 1977; and my first testosterone at 200mg/week in 1978.
Most all the steroid information was word of mouth. In those days only one was considered risky, Anadrol. When I used Anadrol it was only 50mg per day and for between 3 and 4 weeks at the start of a cycle and changed to another oral for the remainder of the 8 or 12 weeks of the cycle (contest cycles were 12 weeks).
Word of mouth in those days held Primobol acetate as the Holy Grail of the steroids for contest prep. I never had the opportunity to try it, but it was considered about worthless for adding size and strength (do know that we took much lower dosages than is common place today).
So for all the years of taking AAS’s I, thus far, don’t seem to have any long lasting consequences for their use. I should say I got Dermatamyositis when I was 48 which totally removed my capability of ever being capable of a physique worthy of being on stage. I had what was know as a cyclic version and fought may cycles of flare ups until I was selected for a test group for the use of rituximab as a treatment for Dermatamyositis. BTW, the disease affects women twice as often as men. And at the time, via a national support group for my disease, I found not even a weight lifter that had the disease, much less a steroid user. But of course, as people will talk, some claimed that the AAS’s caused my disease.
So, age 48 was the last year I did any AAS cycles. But due to some rather low testosterone, I started TRT at about the age of 58. So at 72 I still am plugging along, trying to retain as much muscle as I can.
In conclusion, though I am a very small sample size of 1, I believe AAS’s (70mgs/wk to 600mg/wk) can be cycled over many years and not be your undoing. So far, at least…
Thanks for sharing.
Have you or anyone you know had trouble peeing from enlarged prostate or prostate cancer? I have never heard of anyone personally who had that problem, only have read about it. They say that if someone has their prostate removed, often the life gets really difficult. no erections and hard to control the bladder. I’m curious if steroids really cause this… because in any case it can happen to a non-user as well.
I agree to a degree. I think there’s even a huge difference between a cumulative five year period and a strung together five year period.
5 years blasting >>>> 5 years blasting in 3 month cycles over a 10+ year period >> a few blasts over a decade > no blasts and TRT or no AAS
The time given for the body to reverse remodeling in an ideal case (granted: no dyslipidemia off cycle, no high blood pressure,…) is in my opinion equally as important as how much you are on cycle with bad lipids. Ideally you are way less time on cycle than off. Arteriosclerosis takes time to develop and can be reversed if parameters are in line and the body has enough time.
So, I agree that it is a concern over decades of on and off cycling but I think how these decades are composed plays a big role and damage prevention can definitely be achieved.
Sadly, we don’t know the dynamics well enough to give clear guidelines. I think the time on = time off is an absolute bare minimum requirement and probably not enough for damage prevention.
That’s good to know, thanks.
I’ve been lucky with HDL, it’s always been around 75-80, so it’ll be interesting to see what happens with Primo and Anavar.
For what it’s worth I’m thinking of adding something like 10-15 mg/day of either to my 18 mg/day of Test C. I’m not looking to run huge blasts, just TRT+ here and there and maybe even permanently as I keep an eye on my cholesterol and run regular ultrasounds to monitor my heart
I have no idea. I’d think 5 cumulative years, then going off forever supercedes being on and off (time on = time off) rule for decades on end.
That’s why I added in the 10+ years so it would be clear that I don’t mean 30 years. But the same time in around double the period.
Perma blasting forever > blasting and cruising forever > everything I wrote before
Everyone has different genetics as it pertains to both positive and negative response to AAS’s. I only have an idea how my body has responded, and as I have said before, I am a sample of 1.
I have been blessed with low cholesterol. My total cholesterol has always tested below 150. But I never had HDL numbers included in my blood tests until the 2000’s, so I don’t know how low they dipped during my AAS cycles. The '70’s, '80’s, and most of the '90’s, most of my cycles were 8 weeks “on” followed by 4 weeks “off”. I quit all injectables two weeks before my cycles ended, which means the last 2 weeks was all orals. I wanted to feel like I actually had a full 4 week “off” period. So, for the most part my ratio of weeks “on” to weeks “off” was 2:1. In 1997 I quit AAS’s altogether, at the age of 48 years and 9 months. Still alive and counting my blessings, knowing fully that life is fragile.
Disclaimer: I don’t advise anyone that what I did is safe for everyone. We all are different on how our bodies respond. I will say that I consider myself on what I call the “Goldman Dilemma spectrum”. That is, I was willing to accept the risk for the reward I was hoping to achieve, but not to the total extent of the Goldman Dilemma. But I was on that “spectrum”.
@bfg1
I didn’t read every post so forgive me if i missed it but what is your cycle history? Most of the posts on here suggest you really didn’t do much research on the compounds you propose to use.
Please note, I incorporated the use of the word “spectrum” to denote that I was willing to assume some risk (on a sliding scale of risk, where one end is no risk and the other Goldman’s death result in five years)) for a desired benefit.
I like the Goldman Dilemma, because I believe everyone who is thinking about AAS usage needs to understand the that there are many who are willing to risk all for a great moment in time, only to die shortly thereafter.
Did you generate the data for this histogram to make a point?
I base all my decisions on real data, if available. Murphy’s Law is a defeatist attitude that I refuse to accept.
Thanks for the tag @anon18050987 ! I’ve actually been diving deeply into how to minimize (or even completely prevent) the negative effects of blasting. I’m not going to post sources, as I’ve been through too many and that would be cumbersome, but they are easily found. Some of this is not definitive; it’s new research.
Dyslipidemia: It’s my understanding that the rise in LDL is mostly an issue with the presence of systemic inflammation, since it’s used by the body to “fix” lesions in the circulatory system.
This inflammation, as far as AAS use, can be heightened dramatically by the type of carrier oils and co-solvents that are used in the drug product. Propylene glycol is frequently used as a co-solvent for drugs (like tren) that are poorly soluble in pharma-grade carrier oils like cottonseed oil and castor oil, and causes an increase in C-reactive protein, which is a marker of systemic inflammation. Peanut oil does the same thing, due to the presence of peanut agglutinin.
The way to fix this is by the use of ezetimibe, using only pharma-grade gear (like test and Bayer primo), taking supplements like citrus bergamot, and by caring for the liver.
Liver: We all know the use of orals causes liver issues. The alkylation at C-17 allows the drug to survive the first pass in hepatic metabolism. This is because the C-17 hydroxyl would typically be oxidized to a ketone by oxidative enzymes in the hepatocyte, but this is blocked my the alkyl group. These oxidants cause cell death and the drug is released into the bloodstream.
The way to fix this is to allow the tablet to dissolve sublingually, which skips (mostly) the first pass in the liver. Also, treating orals as preworkout supplements instead of anabolic agents will reduce hepatic damage - leave the anabolism to the injectables. Switching between 2 or more different orals (e.g., tbol one day, anadrol the next) will prevent tachyphylaxis and eliminate the need for an increase in dose. Hepatic damage is increased significantly more by daily use; give the liver a break.
Daily use of TUDCA, vitamin E, and NAC will help with liver issues as well.
Or… don’t use orals!
Cardiac: Heart remodeling is a major concern with AAS use. This can be reduced significantly by the use of something like nebivolol and using HGH as far from lifting sessions/cardio as possible. Also, keep BP down.
Renal/CVS: Blood pressure can increase dramatically with AAS use, especially with drugs that aromatize. HGH can also cause fluid retention and spike BP. The use of telmisartan can really help with this issue. Start low and increase as needed.
19-nor derivatives can also cause renal issues. Avoid these, especially tren.
My main concern was generating random data and adding a single data point clearly much greater than 3 sigma from the mean to create a authentic looking graph is misleading to the less statistically astute person.
I can be as aware as is reasonably possible of all the potential failure modes and effects of all possible interventions or discoveries of a process and reject the common understanding of Murphy’s Law. And I do. The universe is not plotting against anyone, except in their mind.
Amen brother
Ought to be noted, I’ll link data later BUT… the deterioration in cardiac function appears to partially revert back to some semblance of normality once use is ceased
Also important to note, cutoff for LVEF varies from 50-55%
Also needs to be noted the dosages and duration of use with many of these studies tends to be quite high. Talking 500-700mg/wk over around a decade of cumulative exposure.
Ah, that’s on me man, my autism is showing again. Sometimes sarcasm is completely lost on me, especially when it’s not in-person.
Sorry being late on this reply, but are you putting Deca and NPP under Nandrolone? Or did you just mean Deca?
I’ve been told by others I’m on the spectrum. Never was diagnosed with it, but my brother is low functioning autistic, and I was diagnosed with ADHD growing up. Not claiming I’m on the spectrum, but it’s a possibility. I’ve always made friends really easily, so that would indicate that perhaps I’m not.
Yes, deca and NPP are both under the nandrolone umbrella (as is the more rare nand cyp).
Why isn’t there a nand ace or prop? Are the certain esters that just don’t bind to certain compounds?