Perhaps I should rephrase to clear up the point I’m trying to make.
I’m not talking about high level BBers and Strongmen, teens, freaks of nature and idiots who take enough Test to increase their test levels 1000%.
And I’m not saying the negative health effects of steroid use, such as heart disease and left ventricular hypertrophy won’t kill you and doesn’t happen. I’m saying it is very, very unlikely for the average user. Otherwise we would be hearing about it constantly and we’re not.
Steroids kill people/steroids are bad for you is often a knee jerk reaction by people to a subject area they know nothing about and pharmaceutical companies are more than happy to encourage and agree because it is in their best interest to do so. That’s all I’m trying to point out.
It seems most of AAS users don’t have a phlebotomy done as often as they should. Or if ever at all. And end up having blood like gravey that leads to clots, strokes, and heart attacks.
All users should be having a phlebotomy done every 2 to 4 months. But it’s often difficult to find a place to do this.
I want to take classes and get a phlebotomy license so I can start a mobile business. my target would be AAS users. I would show up and drain you for an affordable price. And at the same time check hemoglobin and iron/ferreritin levels. And wouldn’t be some rediculous $795 Fee.
I know someone who has done it and was fine (squatted 925 at 235 that day). In fact, there is a golden era bodybuilder named Pete Grymkowski that claims to have taken 3 bottles of orals a day along with 7 vials of injectables for a year straight (he claims that added up to 70,000 mg/wk). He is still alive too.
Maybe in extreme uses, sure. I don’t think anyone is really doing this though. I think it’s easier to od on Tylenol or vitamin c, than anavar. I don’t think there is a case of an od directly from anabolics.
Every substance taken in a high enough dose is deadly. LSD is also said to be not possible to OD on because the therapeutic window is way too large that doesn’t mean it isn’t possible.
“The treatment for marijuana intoxication is symptomatic management. The extent of management has numerous factors, including an age of individual and amount of cannabis ingested. There have been several cases of accidental cannabis poisoning in a geriatric patient resulting in intensive care admissions due to central nervous system depression.”
For cannabis from Marijuana Toxicity - StatPearls - NCBI Bookshelf
So there are substances where it’s difficult to OD on but take a pure enough sample, take a way too large dose and the right way to apply it and you’re gone. I‘m still with @mnben87, to OD is so difficult that only when you’re a complete moron you’ll get it done.
I don’t believe this statement is correct. Anabolic-androgenic steroid use can induce cardiac enlargement through a myriad of differing mechanisms, both direct and indirect. RAAS dysregulation leading to systemic vasoconstriction, hypertension and subsequently cardiac enlargment, direct AR binding within cardiac myocytes mediating a hypertrophic response, oxidative stress and more come into play.
I don’t believe cardiovascular pathology is an uncommon entity amongst AAS users, it’s more probable that most who use don’t get screened for cardiac abnormalities. I can link numerous bodies of medical literature showcasing cardiac abnormalities ranging from subclinical dysfunction to full blown CHF being present within AAS users employing dosages one would quantify to be “moderate”.
The extent of damage induced is largely mediated through genetic predisposition and lifestyle; some will get off scott free, others might drop in the midst of their first cycle. It’s playing Russian roulette with your health, the same can be said about all drugs.
A dose dependant relationship between AAS and cardiac pathology may exist, but the same linear relationship won’t exist with everyone. Put two people in a room, one guy has a strong familial history relating to CHF, hypertension. The other guy has no familial history, is generally healthy. Guy A might develop an enlarged heart secondary to hypertension at 250mg/wk over the course of a few years, guy B might be able run the same protocol for decades provided polycythemia doesn’t develop/is taken care of.
Most guys take enough test and/or androgen equivalent to increase their androgen index to 1000% + above baseline. A gram of test would typically equate to this, or 500mg test + 25-50mg anadrol/day… That’s pretty common in the grand scheme of things.
It may be unlikely/almost impossible to overdose following a single ingestion of AAS, these drugs are more subject to inducing systemic, chronic toxicity. Initially prior to marketing a drug, trials are conducted to define parameters in relation to toxicity. The “tolerable” dosage in terms of acute exposure for AAS is generally very high. Certain contraindications (autonomic dysfunction, hereditary hemachromatosis etc) come to mind as conditions that would dramatically lower the threshold for tolerability. Those at extremely high risk may be prone to fatal outcomes shortly after initiating use, but as a singular, unesterified dose it’d be very, very, very difficult to overdose on AAS.
As to cannabis overdose. There have been a few cases reports wherein cannabis has purportedly been the causative agent for inducing acute coronary syndrome/AMI within those already at high risk. Furthermore, cannabis hyperemesis syndrome (from extensive overuse of the drug) can induce acute renal failure, thus theoretically cannabis can kill you… It’s just extremely unlikely to do so. One must also factor in that we don’t have enough research on cannabis. Does smoking grass cause lung cancer? Cannabis smoke contains many of the carcinogens present within tobacco smoke, furthermore particular carcinogens present within cannabis smoke seem to be present at even higher concentrations comparative to tobacco. As of current it doesn’t appear to directly cause lung cancer, but quite frankly… There isn’t enough research to know for sure. Cannabis is unequivocally far less toxic than ethyl alcohol, but don’t let that fool you into thinking it’s harmless. One recent study published appears to indicate regular, chronic use of cannabis may induce subclinical cardiac dysfunction in comparison to controls/those who only use occasionally.
We don’t constantly hear about AAS related deaths because those who do drop typically aren’t well known, and the deceased may not have been public about their use. These deaths are typically chalked up to “natural causes”. If you do a little bit of digging you’ll find there’s been quite the string of deaths in the athletic/bodybuilding community over the past couple of decades, many of which have been chalked up to be sudden cardiac deaths. Cardiac hypertrophy (when the heart enlarges with an associated deterioration in cardiac contractility/output) predisposes one to arrhythmia, otherwise anabolic steroids when dosed high generally have pro-arrhymiac properties
There is definitively a “knee jerk” reaction of sorts in relation to AAS use by the generalised populace, and they aren’t entirely in the wrong. I believe it’s somewhat of a middle ground. Whilst AAS generally aren’t as terrifying as the media would have you think as they’ve been heavily politicized, they’re not nearly as harmless as many bodybuilders appear to believe. It isn’t within big pharmas best interest to demonise AAS either. Drugs like dianabol were taken off the market in part due to political pressure… But it was a profitable drug to market. As of today newer, more selective and side effect friendly drugs have been synthesised to treat the majority of conditions synthetic AAS were designed to treat.
For idiopathic short stature GH has replaced halotestin/oxandrolone, for aplastic anaemia erythropoietin/hematopoietic stem cell transplantation has replaced Nandrolone decanoate, methenolone acetate and oxymetholon etc.
For TRT, the pharmaceutical industry has formulated brand name products such as xylosted and androgel in effort to make a decent profit. Generics may not be particuarly profitable, but there’s certainly revenue to be made from selling testosterone.
It should be noted, in terms of symptomatology regarding AAS induced cardiac toxicity… The first symptom for many is sudden cardiac death. If you’re going to use these substances you’d better be damn sure you know what you’re potentially getting yourself into, whether it’s worth it.
I guess the real question at the end of the day relating to AAS/longevity is…
Well that’s a lot to process. But let’s have a go.
A lot of what you have said here is speculative, based on the studies you have read and your own conclusions that you’ve drawn from them. Which is all I’m doing. Nothing wrong with that. And you make some good points.
We can say “there’s been quite the string of deaths in the athletic/bodybuilding community over the past couple of decades, many of which have been chalked up to be sudden cardiac deaths” but, without knowing the total amount of users you are comparing this to, there is no way to determine any sort of statistical likelihood that any given person will meet this fate. Personally, I suspect it’s low but I understand why you may not agree.
On this: "Most guys take enough test and/or androgen equivalent to increase their androgen index to 1000% + above baseline. A gram of test would typically equate to this, or 500mg test + 25-50mg anadrol/day… " Well I just don’t agree. My first cycle was 400mg test, 40mg anavar. After 12 weeks my test levels were 322 on a range of 44-148 pg/ml. That’s a little over double the high end. How are you getting 1000% increase in androgen index from that?
I also don’t agree that pharma doesn’t benefit from demonizing AAS. AAS and GH, for better or worse, improve the lives of the users. Whether that improvement is actual, perceived or a road to sudden cardiac arrest is beside the point. That point being, pharma isn’t getting a piece of that pie and these black market AAS suppliers are, essentially, their competition.
“For idiopathic short stature GH has replaced halotestin/oxandrolone, for aplastic anaemia erythropoietin/hematopoietic stem cell transplantation has replaced Nandrolone decanoate, methenolone acetate and oxymetholon etc.”
Great point. However, GH supplementation is about 2000.00 per month and a single stem cell treatment is 5000.00 minimum. Are you seriously trying to argue that black market GH at 3.00 per IU or a vial of nandrolone at 100.00 or a bottle of oxymetholone at 100.00 is not a competitive threat to these pharma treatments?
Do you know that vaccine makers can’t be sued for harm caused by their vaccines in the United States? If you do get harmed by a vaccine you can win a no fault suit in Federal court and be paid monetary damages, though. And do you know who pays those damages? Tax payers. In other words, you. Do you know that GH was banned for import and sale once the Chinese learned to synthesize it and started shipping it to the United States, only to then have big pharma apply for off label prescribing, thereby maintaining their monopoly? I could go on but let’s just say I don’t trust big pharma and leave it at that.
"If you’re going to use these substances you’d better be damn sure you know what you’re potentially getting yourself into, whether it’s worth it.
I guess the real question at the end of the day relating to AAS/longevity is…"
I agree, 100%, which is why I share my experiences here. And I always advocate bloodwork and monitoring for that reason.
Excellent. As a famous pugilist is reported to have stated, “Everybody has a plan until they get punched in the mouth.”
My experience most likely will be different that yours. Thought I was doing the right thing with combination thyroid therapy (150 mcg T4 + 50 mcg T3 daily). Remember Feynman states “the easiest person to fool is yourself.” 2 years on various TRT dosages between 80 and 150 mg/week. No big issues, fantastic progress. Took body mass from 220 to 248 lb while dropping BF from 13% to 9%. Used both oxandrolone and ND with TRT, sure some mental sides but nothing unmanageable.
Decided hey what’s the harm, let’s try a small jump up to 350 mg/week of Test in the name of science? Split this up into twice weekly sub-Q shots of roughly 175 mg. The night after the third shot about 2:30 AM woke up with atrial fibrillation and a nice scary ride to the ER. I’ve told this in another thread, but I am sitting there and paramedic is admiring my chiseled frame asking where I work out while my life flashes before my eyes. A minute later I go into SVT with HR above 200 bpm.
They are getting ready to administer adenosine and I sit up and start using valsalva manuever. Get the HR down but afib continues. Long story short I converted back to sinus 90 minutes later on my own. 3 months later still struggling with panic and anxiety and intermittent PVCs/PACs and short bursts of SVT. Cardiologist see no problem. Still scared to bump TRT back to even modest dosage and have dropped the T3. Dropped 35 pounds. but still about 10% BF.
In the end what caused the afib? Test, T3, Test + T3 + lots of HIIT? Too much exercise? Preexisting arrythmia with Test+T3+HIIT? Getting too old such that supporting infrastructure just can’t handle the nitrous (as another person on here likes to compare AAS with)?
I can’t say. But think about your plan to the above scenario and how you would respond. Then throw that out the window cause you don’t know how you will respond. Risk vs reward. Odds are unless you can stick with modest TRT dosage the risk isn’t work the reward. An astute observation made on here is that TRT is most definitely a gateway drug to many. If a little is good, then more is better?
There have been a few meta analysis conducted on this exact topic. The mortality rate within AAS users upon followup is typically 3-6x that of controls. Granted, the prospect of using a meta analysis to legitimately gauge mortality rates in relation to a singular variable is rather flawed. If I recall one study was looking at AAS users who were currently incarcerated vs normal controls, obviously results will end up skewed towards higher mortality rates given the nature of… prison… Furthermore GENERALLY following long term use, most AAS users within medical literature have enlarged hearts coupled with associated subclinical diastolic/systolic dysfunction (generally unlike athletes heart). Also, anabolic-androgenic steroids with rodent models/in-vitro appear to be neurotoxic (to simply put it, systemic oxidative stress/redox imbalance appears to lower circulating concentrations of neuroprotective proteins, allowing beta amyloid etc buildup to occur over long periods of time. Furthermore, there is somethign to be said about AR binding within the brain potential inducing deleterious morphological alterations). Currently these results have been replaced within studies using humans, those who use have significant structural aberrations comparative to controls when neuroimaging was conducted. Many of these studies have correlated these differences with reductions in cognition amongst the AAS using cohorts (even when adjusting for the variables of recreational drug use, education etc). AAS probably aren’t neurotoxic to the extent of say… alcohol, but I digress, it’s a potential risk virtually no one talks about.
If one looks here, over ten years the mortality rates stemming from AAS users are roughly 3x that of the general populace. Keep in mind the avg age was only 26 y/old, and 1.2% died over the next twelve years. Given the toxicity induced by AAS is chronic, prolonged use increases the chances of a deleterious outcome. The mortality rate already appears to be accelerated over a period of 12 years, let alone 30+ years. Steroid users were far more likely to develop cardiomyopathy (obviously) and atrial fibrillation (@readalot).
I don’t know much about the adult demographic that uses, however I can say from anecdotal knowledge those who use within my age demographic also tend to be heavily involved within the use of other substances of which elicit cardiotoxic effects. That being said, there is a slight difference between a night of drinking and consistently having toxic concentrations of androgens coursing through you’re veins 24/7. Combine both and long term, you’re looking for trouble
To be fair, I’ve briefly dabbled once or twice out of curiosity. I’ve been around those who use more extensively. It’s not as if I’ve fallen for the hysterical antics the generalised populace tend to harbour in relation to the use of anabolics. I’m relatively pro-anabolics, in the right situations they can be tremendously therapeutic… but I also like to be fully realistic about the potential for devastating consequences down the line. Whatever goes up must come down… with every positive there is an equatable negative…
You’re relating to 200% of baseline to correlate to 2x the upper end of the ref range. The average male certainly isn’t at the top of said reference range. Lets say the average, healthy, lean male is in the top 33% in terms of FT (of which ref ranges will differ based upon assay variation… but at the same time there is still unexplained variability within ref ranges that have no clinical significance at all).
Let’s say, for reference you had a FT of 105pg/ml… Oxandrolone will also crank up you’re androgen index despite it not being registered as testosterone. When I state androgen index I’m referring to the total amount of hormone taken per week. On a milligram per milligram basis (despite the belief of many) oxandrolone is quite a bit more potent comparative to testosterone regarding it’s a ability to increase the amount of pure, lean contractile tissue one has, I can link data to prove this. Regardless, 100mg test e/c equates to 69-70mg base testosterone per week
(molar mass of testosterone = 288.42g/mol, molar mass of test E = 400.603 g/mol, Molar mass of test C = 412.6047g/mol)
288.42/400.603 = .719 (so 71.9mg pure test/100mg test E)
288.42/412.6047=.699 (69.9mg pure test/100mg test C)
so roughly 10mg anavar/day = an extra 100mg test E/C/wk, AND var is somewhat more potent. So lets state an equatable FT in response to total amount of hormones taken in PW was 644 at minimum, still probably around 600% that of baseline (not particularly of clinical significance, but you said “take enough to increase their test levels 1000%”. Furthermore this was you’re first cycle, the dosages creep up over subsequent cycles.
Also, get you’re lipids checked on anavar, or any c-17 alpha alkylated anabolic steroid for that matter. 20mg var/day is enough (according to literature) to cut HDL in half whilst skyrocketing LDL.
True, however in other countries with more universal healthcare… these drugs are typically subsidised. GH is also preferable over giving fluoxymesterone and/or oxandrolone to children due to the potential for virilization (esp for girls), furthermore excess androgenicity (less of a concern with oxandrolone) can accelerate the process of epiphyseal fusion, though oestrogen is far more culpable in relation to inducing epiphyseal fusion comparative to androgens. The “anabolic” effect of AAS actually stimulates linear bone growth.
Aplastic anaemia alone can induce CHF/arrhythmias and not all cases are responsive to androgens. Androgens stimulate the release of erythropietin within the kidney through unspecified mechanisms (likely mediated via AR binding) and increase responsiveness to erythropoietin within bone marrow. With aplastic anaemia bone marrow is failing, thus the hope is “pump them full of androgens, lets hope we can get a response”… and in many cases you do see a response, but AAS aren’t selective enough to treat this condition without potentially inducing a host of other undesirable side effects, ESPECIALLY for women (though the increase in muscular strength/function would be quite beneficial, I can def see a rationale for giving a patient in a debilitated condition modestly pharmacological dosages).
You’re not an anti-vaxxer are you? The benefits regarding the creation of herd immunity by vaccinating the populace for something like measles far outweighs the minute chance of an adverse reaction induced by vaccination.
I believe the majority of healthy adult men could PROBABLY run a few cycles, perhaps even a few more on top of that… and get away with it. Get in, quickly get out ASAP and perhaps you’ll get away with it. As we all know, the results stemming from AAS use are profound, these are very powerful drugs… the feeling of unrivalled confidence, power and energy can be intoxicating and therefore many feel the need to continually hop back on and/or add new, harsher compounds at escalating dosages. Anabolic-androgenic steroids aren’t physically addictive per-se, but they certainly have psychologically reinforcing properties. It takes quite a lot of willpower/insight to look in the mirror at peak condition, pecs bulging, delts veiny and flaring with skin the consistency of an erect penis and to say “this is temporary, if I wish to live a long/healthy life, then this can’t be permanent”. After which when one comes off/drops to TRT it’s rather difficult to re-acclimate to not being superhuman, and this is why we now get non-competitive bodybuilders cruising on like 350mg test/wk, cruising on low dose tren etc.
All in all, it doesn’t really matter to me what others do so long as they’re aware of what they’re doing. Risk/reward is subjective, if you’re aware of the risks yet you’re okay with blasting/cruising til the day you die; then all the more power to you. The problem with most who decide to hop on at times is insight. If you’re a 17y/o kid, 98% of the time you have no idea what you really want out of life, neurological hardwiring generally impedes one to have this capabilitiy. Bodybuilding may be the prime objective today, but six months, two years from now? This can even cross over with ideology harboured adults. I’ve noticed there is a distinct breed of adult in his/her mid 20’s or early thirties that will still act is if they’re stuck in high school, it’s very individualistic in nature. if you’re taking the plunge, the prospect of maturity/insight harboured over choices made is pivotal. I get the feeling many wouldn’t get into gear to begin with if they knew the full spectrum of risk. There was one dude on here running like 700mg tren, a ton of winny, test and clen… and he smokes to curb his appetite. His last cycle a mere couple/few months ago was also 700mg tren (looking up it’s @ukben) … This kind of use is a surefire way to end up dropping dead ten or twenty years from now. Perhaps he’s oblivious to the risks, perhaps he doesn’t care? If he doesn’t care, that’s fine… but the problem arises within the fact that many legitimately aren’t aware of the damage they’re inducing. Fucking one cigarette per day increases long term risk of myocardial infarction 3-fold… If you’re going to smoke, PLEASE don’t smoke while you’re on gear…
Sorry you had to experience this, must’ve been awful. Testosterone/AAS in general upregulate beta-adrenergic receptors, rodent models indicate ND increases the number of/expression of beta 2 adrenergic receptors within the myocardium. Inducing a hyperthyroid state will also predispose one to arrhythmia. HIIT + predisposition + test + T3/T4 + high body mass, probably the perfect storm…
If you still feel you have PAC’s/PVC’s (most of the populace statistically will have a few every 24 hrs) could you ask you’re cardiologist/GP about medication (cardioselective beta blockers etc). There are certainly risks/rewards in regards to just about every medication/supplement available, so it’s a discussion you’d have to have with your doctor. However I can relate to just how much having persistent anxiety sucks… It’s very possible the reward (ameliorating anxiety) could outweigh the risk.
We’re not talking about the same thing here anymore. When I say “average user” I’m talking about a healthy adult doing a cycle or two per year of 400ish test and something like 40 Anavar, having bloodwork, being monitored. That’s my qualification of an “average user”.
You’re talking about 17 year olds and peoples cycles creeping up in dosage over time and some guy on 700mg of tren, people who think they’re still in high school, involved with other cardiotoxic substances, have high blood pressure, etc. I’m not talking about these people. Also, that Endocrinology Advisor morbidity study you linked has no information on compounds, dosages, frequency, etc. There’s no way you can say these are “average users” using the definition I use for that group. These are still good points, and worth stating, but not a good a basis for comparison in terms of what I consider “average use”.
On the lipids, I’m with you. Anavar certainly wrecks mine and I’ve mentioned that in other posts.
But this was my original point “And I’m not saying the negative health effects of steroid use, such as heart disease and left ventricular hypertrophy won’t kill you and doesn’t happen. I’m saying it is very, very unlikely for the average user.” You can post studies till the cows come home citing this group had enlarged hearts, that group had high cholesterol, this group had this, this group had that but how many of these people DIED as a result and were they “average users” in the context I have set out? That’s what I’m interested in here. Mortality. Not issues, not problems, abnormal this and that. And not so I can say, it won’t kill you, so yay steroids go take some Tren. Or to encourage people to recklessly use AAS or even use AAS at all. No. This is just how I see it based on my own AAS experiences over the last five years and the research I’ve done. Perhaps if I had had said it’s “probably” unlikely to kill you, the conservation may have went a different way. Perhaps my heart will explode later in life and I’ll then be another statistic for your argument. Maybe not. And I fully realize and accept that this is a possibility. I just don’t think it’s likely based on my experiences, thus far.
And, to be clear, the comment I made about knee jerk reactions was not directed at you, personally. You are obviously more informed than the average person on this subject.
And, no, I’m not an Anti-Vaxxer. I threw that in as another reason for why I don’t trust big pharma and don’t believe peoples health are what motivates them to be in business, nor do they care. The VICP is paid for by tax payers. It came into being in the early 80’s when vaccine makers we threatening to stop making vaccines because they were not profitable due to the payouts to harmed patients via lawsuits. So Ronald Reagan passed a law whereby people are not allowed to sue vaccine makers for vaccine damages but could win damages in federal court, paid for by tax payers, and the vaccine maker admits no fault. Off topic, but an interesting point: if vaccines weren’t causing harm, some way or other, why were these companies getting sued to the point where it was not profitable to make them?
How bad we’re you’re lipids on anavar? And at what dosages. I get curious because var/winny seriously wreck lipids, it’s rare we ever actually get to see bloods from people on var/winny though.
Also to OP. Increasing fibre intake can somewhat suppress appetite. Increasing fibre intake can also have a marginal, yet statistically significant beneficial impact on lipids.
The cycle I had them tested on was 40mg per day over 3 months with 400ish test. I don’t remember the numbers for LDL/HDL but I remember the endo telling me it was over 2x out of desired range and almost certainly due to the Anavar. I was also on a baby dose of Accutane but I doubt it was enough to contribute. He said it would go back to normal after a month or so and it did but who can say if there was any permanent damage.
I worry more about lipids than anything else, actually.
Whether troche or capsule, I can report extreme nonlinear dose response for oxandrolone on HDL. Whether I took average dose of 7.5 mg per day or 50 mg per day, HDL was still crushed by 50-70%. Curious that Lp(a) was extremely low while taking oxandrolone. On the whole, I am not comfortable with the net/net to confidently take oxandrolone given whatever long-term implications the above data indicate. And my takeaway from all the guys on here who blast away, is that my genetics clearly indicate I should leave 300 mg/week of testosterone alone.
Metoprolol makes me feel extremely lethargic and does nothing to my anxiety. Good point on the ND, I wondered if I rendered myself susceptible to afib after taking ND off and on over the course of a year. Like we’ve discussed, you are rolling the dice.
Clinical studies use surrogate endpoints when mortality isn’t available. It’s common practice for every drug before the drug gets released for sale since the clinical trials with mortality as the primary endpoint take too long. Surrogate endpoints should be equatable to lower or higher mortality. For example decrease in blood pressure is a bad one since some drugs lower it but don’t decrease mortality. There are better indicators for mortality though and if the study uses a good one, it’s nearly clear that mortality increases or decreases. Mortality studies take a long time and with AAS users it’s relatively difficult to keep enough people in the study as they are mostly younger adults.
I suppose an easy way around this would to be to look at the studies done on the surrogate endpoints to get a better overall picture? Ie. If a drug causes high blood pressure, look at studies with data on death due to blood pressure increase. Is that where you’re going?
Yes that would be the solution, but you must look at the evidence of the relationship between a surrogate and mortality. Blood pressure increase is a good one, blood pressure decrease through medication is a bad one. Cause one correlates well with death the other not so much.
My point was that only because unreal shows surrogate endpoints his points are not invalid. It’s more difficult to see the direct relationship but that doesn’t mean the relationship isn’t there. Granted your point is also valid that not every surrogate is a good indicator. That’s why you have to take a deeper look instead of just outright discarding the argument.
This would be the real endpoint but limitations were already discussed. That’s why taking a larger sample and getting some years with surrogate endpoints is justified.
