Another nandrolone question, re potential cardiac issues

Bubbs

Member
I've been reading a lot of seemingly conflicting information on nandrolone and would like to know what is considered the current thinking on its cardio toxicity


Studies like this concern me but the abstract doesn't mention the dose the monkeys were given

Is ND considered benign in lower doses for heart health? As in 50 to 100mg a week
 

JimGainz

Active Member
I didn’t see any dosages in the study. I’ve asked a lot of doctors about this and the conclusion was that no one can tell. There aren’t any long term studies on this in humans, and this is a relatively new treatment for TRT patients, so no real data. I feel so good on it and was just approved for long term duration so I don’t even have to go off if blood work is good. I take a low dose statin as well as vitamin D and K2 as well as do extensive lipid monitoring. I’ll probably cycle off every now and then. There was a cardiologist on YouTube, Dr Carlson, who advocated the safety and benefits of nandrolone. Plus patients with muscle wasting disease are on long term. These helped weigh into my decision to stay on it. The joint and pain relief has been life changing for me.
 

Gman86

Member
I didn’t see any dosages in the study. I’ve asked a lot of doctors about this and the conclusion was that no one can tell. There aren’t any long term studies on this in humans, and this is a relatively new treatment for TRT patients, so no real data. I feel so good on it and was just approved for long term duration so I don’t even have to go off if blood work is good. I take a low dose statin as well as vitamin D and K2 as well as do extensive lipid monitoring. I’ll probably cycle off every now and then. There was a cardiologist on YouTube, Dr Carlson, who advocated the safety and benefits of nandrolone. Plus patients with muscle wasting disease are on long term. These helped weigh into my decision to stay on it. The joint and pain relief has been life changing for me.
Dr Lichten has also been using nandrolone with his patients for years. Isn’t there a chance that the supposed cardio and neuro toxicity of nandrolone, in studies, is due to its extremely low conversion into E2? Even without studies, all it takes is a little common sense to realize that therapeutic doses of nandrolone, by itself, would result in having chronic low E2 symptoms, which as far as I know, would increase ur risk of cardiovascular damage/ disease, as well as damage neurons overtime. Not saying that low E2 is the reason these things have shown up in nandrolone only studies, but I just think it would be a pretty crazy coincidence if these things were occurring due to some other effect(s) nandrolone was having in the body, when they line up pretty perfectly with chronic low E2 symptoms, which someone would have using therapeutic doses of nandrolone overtime. Ive seen 3 sets of labs from 3 different men, all on 300mg of nandrolone by itself. All 3 men’s E2 came back between 5-6. And in a steroid fb group a guy posted his labs while using 900mg of deca only per week, and his E2 came back at 18. A therapeutic dosage of nandrolone would be around 200mg, or less, per week I would imagine. So you can imagine where 200mg or less of nandrolone by itself would have a man’s E2 levels at. I’m assuming at the very top end 10 or less, and on the low end 5 or less

I would love to see studies done while using therapeutic doses of nandrolone, along with enough estradiol to get E2 into a healthy range, and see if the same cardio and neuro toxicity occurs
 
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madman

Super Moderator
I've been reading a lot of seemingly conflicting information on nandrolone and would like to know what is considered the current thinking on its cardio toxicity


Studies like this concern me but the abstract doesn't mention the dose the monkeys were given

Is ND considered benign in lower doses for heart health? As in 50 to 100mg a week

I would not be too concerned with using therapeutic doses (50-100 mg/week) along with therapeutic doses of T as nandrolone is considered one of the mildest AAS when it comes to side effects.

Keep in mind that the metabolites estradiol and DHT are needed in healthy amounts to experience the full spectrum of testosterones beneficial effects on mood, energy, libido, erectile function, cardiovascular/brain/bone/immune system health, body composition.


*Testosterone drugs provide a hormone identical to that already produced in the body, presenting the same spectrum of physical and physiological effects. In addition to being one of the most efficient muscle-builders available, testosterone generally has a positive (not negative) effect on libido, supports a positive mood, and supplements necessary estrogen so that cholesterol levels are less negatively shifted.




Many have added therapeutic doses of ND to their trt protocol for the relief/improvement of bone/joint pain.

Most are cycling ND using therapeutic doses and are not staying on indefinitely.

Long-term use/abuse using steroid doses of testosterone/AAS could potentially lead to negative effects on cardiovascular health but many factors come into play.

Even when looking into the use/abuse of testosterone/AAS when cycling (8-12 weeks) using doses well beyond therapeutic when it comes to health T and ND would be considered the safer AAS.
 

Gman86

Member
What baffles me tho is that a bunch of HIV positive individuals were prescribed nandrolone, and seemed to do well. But I wonder if they were on nandrolone only or not. I just can’t imagine anyone feeling good using 200mg, or less, or nandrolone only per week, due to the extremely low E2 conversion rate. Maybe @Nelson Vergel can chime in, I believe he was on nandrolone only for years.
 

Bubbs

Member
I would not be too concerned with using therapeutic doses (50-100 mg/week) along with therapeutic doses of T as nandrolone is considered one of the mildest AAS when it comes to side effects.

Keep in mind that the metabolites estradiol and DHT are needed in healthy amounts to experience the full spectrum of testosterones beneficial effects on mood, energy, libido, erectile function, cardiovascular/brain/bone/immune system health, body composition.


*Testosterone drugs provide a hormone identical to that already produced in the body, presenting the same spectrum of physical and physiological effects. In addition to being one of the most efficient muscle-builders available, testosterone generally has a positive (not negative) effect on libido, supports a positive mood, and supplements necessary estrogen so that cholesterol levels are less negatively shifted.




Many have added therapeutic doses of ND to their trt protocol for the relief/improvement of bone/joint pain.

Most are cycling ND using therapeutic doses and are not staying on indefinitely.

Long-term use/abuse using steroid doses of testosterone/AAS could potentially lead to negative effects on cardiovascular health but many factors come into play.

Even when looking into the use/abuse of testosterone/AAS when cycling (8-12 weeks) using doses well beyond therapeutic when it comes to health T and ND would be considered the safer AAS.
There is one infamous idiot kid on getbig who gave himself a heart attack by running 2 grams of deca for months with pre existing conditions, but otherwise yes I haven't seen anyone with issues from it.

My Dr has me doing a echo and treadmill stress test to see if everything is OK next month so I will report back on the results. My last one was 2014 and was perfect then
 

Bubbs

Member
What baffles me tho is that a bunch of HIV positive individuals were prescribed nandrolone, and seemed to do well. But I wonder if they were on nandrolone only or not. I just can’t imagine anyone feeling good using 200mg, or less, or nandrolone only per week, due to the extremely low E2 conversion rate. Maybe @Nelson Vergel can chime in, I believe he was on nandrolone only for years.
I have friends from my time living in SF who were HIV+, and who were on nandrolone for long periods with no issues beyond them all looking amazing for their age
 

Gman86

Member
I have friends from my time living in SF who were HIV+, and who were on nandrolone for long periods with no issues beyond them all looking amazing for their age
Do u know how much nandrolone most of them were using per week? And do u know if most of them were on nandrolone by itself? Like was there just a very standard cookie cutter nandrolone protocol that all HIV+ men were prescribed? I’m dying to know whether it was always nandrolone by itself, or say nandrolone with test
 

Bubbs

Member
Do u know how much nandrolone most of them were using per week? And do u know if most of them were on nandrolone by itself? Like was there just a very standard cookie cutter nandrolone protocol that all HIV+ men were prescribed? I’m dying to know whether it was always nandrolone by itself, or say nandrolone with test
I honestly can't say, the guy I was closest to (as in he would show me his medicine cabinet lol) was on test as well as ND. His doctor was a lot more generous than mine at the time so I assume he was pushing the upper limits of whatever is legal to prescribe

He was also on serostim but he felt that made him bloat and feel awful at the doses prescribed (I believe the protocol is ridiculous for the prescription doses) so he swapped to semorelin
 

Fluoxymesterone

New Member
Hi guys, I’m new to the forums.
Anyways I’m a medical student and I would like to add my opinion. This heart and nandrolone conversation will never end sadly because doctors can’t experiment on their patients and see if scar tissue accumulates in the heart, liver, kidneys with nandrolone.
Yet there are many preclinical studies done on mice, rats, rabbits etc that do show that nandrolone increases the activity of the ACE enzyme in the heart and this leads to progressive fibrosis; this WILL occur I believe in humans too and quite possibly in YOU if you take this hormone (I’m not against nandrolone)

The good news is that these studies also show that this fibrosis can EASILY be prevented with the use of an ARB such as Telmisartan because it prevents the ACE enzyme from working (in my opinion the best one at this). A supplement called Astaxanthin will also wonders at preventing deleterious changes related to fibrosis, and “ain’t that bad either” at helping joint pain (like a baby nandrolone).

I don’t take nandrolone, but will in the future for a knee issue ( astaxanthin) keeps the problem OK for now).

Doctors don’t prescribe telmisartan with nandrolone and they definitely should. Maybe, maybe even with regular TRT too. Not taking it is a risk. I would at least take the astaxanthin with TRT

thanks for reading. Just trying to help guys!
 

Gman86

Member
Hi guys, I’m new to the forums.
Anyways I’m a medical student and I would like to add my opinion. This heart and nandrolone conversation will never end sadly because doctors can’t experiment on their patients and see if scar tissue accumulates in the heart, liver, kidneys with nandrolone.
Yet there are many preclinical studies done on mice, rats, rabbits etc that do show that nandrolone increases the activity of the ACE enzyme in the heart and this leads to progressive fibrosis; this WILL occur I believe in humans too and quite possibly in YOU if you take this hormone (I’m not against nandrolone)

The good news is that these studies also show that this fibrosis can EASILY be prevented with the use of an ARB such as Telmisartan because it prevents the ACE enzyme from working (in my opinion the best one at this). A supplement called Astaxanthin will also wonders at preventing deleterious changes related to fibrosis, and “ain’t that bad either” at helping joint pain (like a baby nandrolone).

I don’t take nandrolone, but will in the future for a knee issue ( astaxanthin) keeps the problem OK for now).

Doctors don’t prescribe telmisartan with nandrolone and they definitely should. Maybe, maybe even with regular TRT too. Not taking it is a risk. I would at least take the astaxanthin with TRT

thanks for reading. Just trying to help guys!
Great info. Really appreciate ur reply and contribution. How do the doses in the studies compare to say using 50-100mg of nandrolone in a male human? Do u think they’re comparable, or the doses in the studies were much higher than say a 150lb male human using 50-100mg/ week? Obv hoping a good amount of the negative effects in these studies are dose dependent. Is that wishful thinking? Lol
 

Fluoxymesterone

New Member

So this study is done on rats (so to get the human equivalent dose you would divide the rat dose by 6.2 to get a human dose). In this case in "group 4" the human equivalent does was 90 mg/week for a 70kg human. This DID have negative effects, but with the addition of antioxidants and anti-inflammatory supplements (sylimarin and antox) there was a VERY strong protective effect. In other words be careful with steroids even at therapeutic doses (90mg/week). This work is on rats and may not be 100% applicable to humans. Each rat month is roughly equivalent to 2.5 human years, so they took nandrolone for "5 years nonstop when made equivalent to humans".

My opinion is if you take nandrolone for years and have excellent antioxidant reserves (as in no other medical condition that depletes the body), nandrolone may not have such a negative impact. In the end, the therapy must be individualized, no cookie cutter approach because its tricky.

I take Bioastin astaxanthin 12 mg bid
 

madman

Super Moderator
Hi guys, I’m new to the forums.
Anyways I’m a medical student and I would like to add my opinion. This heart and nandrolone conversation will never end sadly because doctors can’t experiment on their patients and see if scar tissue accumulates in the heart, liver, kidneys with nandrolone.
Yet there are many preclinical studies done on mice, rats, rabbits etc that do show that nandrolone increases the activity of the ACE enzyme in the heart and this leads to progressive fibrosis; this WILL occur I believe in humans too and quite possibly in YOU if you take this hormone (I’m not against nandrolone)

The good news is that these studies also show that this fibrosis can EASILY be prevented with the use of an ARB such as Telmisartan because it prevents the ACE enzyme from working (in my opinion the best one at this). A supplement called Astaxanthin will also wonders at preventing deleterious changes related to fibrosis, and “ain’t that bad either” at helping joint pain (like a baby nandrolone).

I don’t take nandrolone, but will in the future for a knee issue ( astaxanthin) keeps the problem OK for now).

Doctors don’t prescribe telmisartan with nandrolone and they definitely should. Maybe, maybe even with regular TRT too. Not taking it is a risk. I would at least take the astaxanthin with TRT

thanks for reading. Just trying to help guys!

Much more involved when it comes to the potential negative effects on the cardiovascular system let alone numerous other side-effects from testosterone/AAS use/abuse.

Keep in mind that any androgen even nandrolone has the potential to cause side effects especially when using doses well beyond what would be considered therapeutic.

Comes down to the type of AAS, doses used, duration of use, overall lifestyle factors let alone one's genetics.




Steroid Side Effects

While anabolic/androgenic steroids (AAS) are generally regarded as therapeutic drugs with high safety, their use can also be associated with a number of adverse cosmetic, physical, and psychological effects. Many of these side effects are often apparent during therapeutic-use conditions, although their incidence tends to increase profoundly as the dosages reach supratherapeutic ranges. Virtually everyone that abuses anabolic/androgenic steroids for physique- or performance-enhancing purposes notices some form of adverse effects from their use.
According to one study, the exact frequency of tangible side effects in a group of steroid abusers was 96.4%. This shows very clearly that it is far rarer to abuse these drugs and not notice side effects than it is to endure them.90 In addition to the side effects that anabolic/androgenic steroids can have on various internal systems, there are others that may not be immediately apparent to the user. The following is a summary of the biological systems and reactions affected by AAS use.





Cardiovascular System


The use of anabolic/androgenic steroids in supratherapeutic (and often therapeutic) doses can have a number of adverse effects on the cardiovascular system. This may be noticed in several areas including unfavorable alterations in serum cholesterol, thickening of ventricular walls, increased blood pressure, and changes in vascular reactivity. In an acute sense, these drugs are admittedly very safe. The risk of an otherwise healthy person suffering a heart attack from an isolated steroid cycle is extremely remote. The risk of stroke is also extremely low. When these drugs are abused for long periods, however, their adverse effects on the cardiovascular system are given time to accumulate. An increased chance of early death due to heart attack or stroke is, likewise, a valid risk with long-term steroid abuse. In order to better understand this risk, we must look specifically at how anabolic/androgenic steroids affect the cardiovascular system in several key ways.


*Cholesterol/Lipids

Anabolic/androgenic steroid use can adversely affect both HDL (good) and LDL (bad) cholesterol values. The ratio of HDL to LDL cholesterol fractions provides a rough snapshot of the ongoing disposition of plaque in the arteries, either favoring atherogenic or anti-atherogenic actions.
The general pattern seen during steroid use is a lowering of HDL concentrations, which is often combined with stable or increased LDL levels. Triglyceride levels may also increase. The shift can be unfavorable in all directions. Note that in some cases, the total cholesterol count will not change significantly. The total cholesterol level can, therefore, give a false representation of uncompromised lipid health. Almost invariably the underlying HDL/LDL ratio will decrease. While this ratio should return to normal following the cessation of steroid intake, plaque deposits in the arteries are more permanent. If unfavorable shifts in lipids are exacerbated by the long-term use of steroidal compounds, significant damage to the cardiovascular system can result.


*Over time, plaque deposits may begin to narrow and clog arteries

Anabolic/androgenic steroids are most consistent in their lowering of HDL levels. This adverse effect is mediated through the androgenic stimulation of hepatic lipase, a liver enzyme responsible for the breakdown of HDL (good) cholesterol.91 With more hepatic lipase activity in the body, the favorable (anti-atherogenic) HDL cholesterol particles are cleared from circulation more quickly, and their levels drop. This is an effect that seems to be very pronounced at even modest supratherapeutic dosage levels.
For example, studies with testosterone cypionate noted a 21% drop in HDL cholesterol with a dosage of 300 mg per week.92 Increasing this dosage to 600 mg did not have any significant additional effect, suggesting that the dosage threshold for strong HDL suppression is fairly low.

Oral steroids, especially c-17 alpha-alkylated compounds, are particularly potent at stimulating hepatic lipase and suppressing HDL levels. This is due to first-pass concentration and metabolism in the liver. A drug like stanozolol may, therefore, be milder than testosterone with regard to androgenic side effects, but not when it comes to cardiovascular strain. A study comparing the effects of a weekly injection of 200 mg testosterone enanthate to only a 6 mg daily oral dose of stanozolol demonstrates the strong difference between these two types of drugs very well.93 After only six weeks, 6 mg of stanozolol was shown to reduce HDL and HDL-2 cholesterol levels by an average of 33 and 71% respectively. HDL levels (mainly the HDL-3 subfraction) were reduced by only 9% in the testosterone group. LDL cholesterol levels also rose 29% with stanozolol, while they dropped 16% with testosterone. Esterified injectable steroids are generally less stressful to the cardiovascular system than oral agents.

It is also important to note that estrogens can have a favorable impact on cholesterol profiles. The aromatization of testosterone to estradiol may, therefore, prevent a more dramatic change in serum cholesterol.
A study examined this effect by comparing the lipid changes caused by 280 mg of testosterone enanthate per week, with and without the aromatase inhibitor testolactone.94 Methyltestosterone was also tested in a third group, at a dose of 20 mg daily, to judge the comparative effect of an oral alkylated steroid. The group using only testosterone enanthate in this study showed a small but not significant decrease in HDL cholesterol values over the course of the 12-week investigation. After only four weeks, however, the group using testosterone plus the aromatase inhibitor displayed an HDL reduction of an average of 25%. The group taking methyltestosterone experienced the strongest HDL reduction in the study, which dropped 35% after four weeks. This group also noticed an unfavorable rise in LDL cholesterol levels.

The potential positive effect of estrogen on cholesterol values also makes the issue of estrogen maintenance something to consider when it comes to health risks. To begin with, one may want to consider whether or not estrogen maintenance drugs are actually necessary for any given circumstance. Are side effects apparent, or is their use a preventative step and perhaps unnecessary? The maintenance drug of choice can also have a measurable impact on cholesterol outcomes. For example, the estrogen receptor antagonist tamoxifen citrate does not seem to exhibit antiestrogenic effects on cholesterol values, and in fact, tends to increase HDL levels in some patients. Many individuals decide to use tamoxifen to combat estrogenic side effects instead of an aromatase inhibitor for this reason, particularly when they are using steroids for longer periods of time, and are concerned about their cumulative cardiovascular side effects.


*Enlarged Heart

The human heart is a muscle. It possesses functional androgen receptors and is growth-responsive to the male steroid hormones.
This fact partly accounts for men having a larger heart mass on average than women.95 Physical activity can also have a strong effect on the growth of the heart. Resistance exercise (anaerobic) tends to increase heart size by a thickening of the ventricular wall, usually without an equal expansion of the internal cavity. This is known as concentric remodeling. Endurance (aerobic) athletes, on the other hand, tend to increase heart size via expansion of the internal cavity, without significant thickening of the ventricles (eccentric remodeling). Even with concentric or eccentric remodeling, diastolic function usually remains normal in the athletic heart. The heart muscle is also dynamic. When regular training is removed from a conditioned athlete, the wall thickening and cavity expansion tend to reduce.

Anabolic steroid abusers are at risk for thickening of the left and right ventricular walls,96 known as ventricular hypertrophy. Hypertrophy of the left ventricle (the main pumping chamber) in particular is extensively documented in anabolic/androgenic steroid abusers.97 While left ventricular hypertrophy is, again, also found in natural power athletes, substance-abusing athletes tend to have a much more profound wall thickening. They also tend to develop pathological issues related to this thickening, including impaired diastolic function, and ultimately reduced heart efficiency.98 The level of impairment is closely associated with the dose and duration of steroid abuse. A left ventricle wall exceeding 13mm in thickness is rare naturally and may be indicative of steroid abuse or other causes.99 It may further, suggest that pathological left ventricular hypertrophy has developed. Additional testing of such patients is recommended.

Left ventricular hypertrophy (LVH) is an independent predictor of mortality in overweight individuals with high blood pressure.100 It has also been linked to atrial fibrillation, ventricular arrhythmia, and sudden collapse and death.101 While LVH in non-steroid-using athletes tends to be without clinical significance, pathological increases in QT dispersion are noticed in steroid abusers with LVH. 102 These changes tend to be similar to the increases in QT dispersion noted in hypertensive patients with LVH. 103 Among other things, this could leave a steroid abusing individual more susceptible to a serious adverse event, including arrhythmia or heart attack. Isolated medical case studies of longtime steroid abusers support an association between LVH and related pathologies including ventricular tachycardia (arrhythmia originating in the left ventricle), left ventricular hypokinesis (weakened contraction of the left ventricle), and decreased ejection fraction (reduced pumping volume and efficiency).104

Heart mass can increase or decrease in relation to the current state of anabolic/steroid use, the average dosage, and duration of intake. Likewise, the heart usually begins to reduce in size once anabolic/androgenic steroids are no longer being used. This effect is similar to the way the heart will reduce in size once an athlete no longer follows a rigorous training schedule.105 Even with this effect, however some changes in heart muscle size and function caused by the drugs may persist. Studies examining the effects of steroid use and withdrawal on left ventricular hypertrophy noted that athletic subjects who abstained from steroid abuse for at least several years still had a slightly greater degree of concentric left ventricular hypertrophy compared to nonsteroid-using athletic controls.106 The disposition of pathological left ventricular hypertrophy following long-term steroid abuse and then abstinence remains the subject of investigation and debate.


*Heart Muscle Damage

Anabolic/androgenic steroid abuse is suspected of producing direct damage to the heart muscle in some cases.
Studies exposing heart cell cultures to AAS have reported reduced contractile activity, increased cell fragility, and reduced cellular (mitochondrial) activity, providing some support for a possible direct toxic effect to the heart muscle.107 108 Furthermore, a number of case reports have found such pathologies as myocardial fibrosis (scar tissue buildup in the heart), myocardial inflammation (inflammation of heart tissue), cardiac steatosis (accumulation of triglycerides inside heart cells), and myocardial necrosis (death of heart tissue) in long- term steroid abusers.109 110 111 112 A direct link between drug abuse and cardiac pathologies is assumed in these cases, but cannot be proven given the slow nature in which these cardiac pathologies develop, and the influence many other factors (such as diet, exercise, lifestyle, and genetics) can have on them. Individuals remain cautioned about the possibility of cardiac muscle damage with long-term steroid abuse.


*Blood Pressure

Anabolic/androgenic steroids may elevate blood pressure. Studies of bodybuilders taking these drugs in supratherapeutic doses have demonstrated increases in both systolic and diastolic blood pressure readings.113 Another study measured the average blood pressure reading in a group of steroid users to be 140/85, which was compared to 125/80 in weight lifting controls not taking steroids.114 Hypertension, or consistently high blood pressure at or above 140/90 for either systolic or diastolic measures, has been reported in steroid users,115 although in most cases the elevations are more modest. Increased blood pressure may be caused by a number of factors, including increased water retention, increased vascular stiffness, and increased hematocrit. Aromatizing or highly estrogenic steroids tend to cause the greatest influences on blood pressure, although elevations cannot be excluded with non-estrogenic anabolic/androgenic steroids. Blood pressure tends to normalize once anabolic/androgenic steroids have been discontinued


*Hematological (Blood Clotting)

Anabolic/androgenic steroids can cause a number of changes in the hematological system that affects blood clotting. This effect can be very variable, however. The therapeutic use of these drugs is known to increase plasmin, antithrombin III, and protein S levels, stimulate fibrinolysis (clot breakdown) and suppress clotting factors II, V, VII, and X. 116 117 These changes all work to reduce clotting ability. Prescribing guidelines for anabolic/androgenic steroids warn of potential increases in prothrombin time, a measure of how long it takes for a blood clot to form.118 If prothrombin time increases too greatly, healing may be impaired. The effects of anabolic/androgenic steroids on prothrombin time are generally of no clinical significance to healthy individuals using these drugs in therapeutic dosages. Patients taking anticoagulants (blood thinners), however, could be adversely affected by their use.

Conversely, anabolic/androgenic steroid abuse has been linked to increases in blood clotting ability. These drugs can elevate levels of thrombin 119 and C-reactive protein,120 as well as thromboxane A2 receptor density, 121 which can support platelet aggregation and the formation of blood clots. Studies of steroid users have demonstrated statistically significant increases in platelet aggregation values in some subjects.122 There are also a growing number of case reports where (sometimes fatal) blood clots, embolisms, and stokes have occurred in steroid abusers.123 124 125 126 127 Although it has been difficult to conclusively link these events directly to steroid abuse, the adverse effects of anabolic steroids on components of the blood coagulation system are well understood. These serious adverse effects are now regarded as recognized risks of steroid abuse among many that study these drugs.

In therapeutic levels, the anti-thrombic effects of anabolic/androgenic steroids seem to dominate physiology, and decreases in blood clotting ability may be noted. At a certain supratherapeutic dosage point, however, the prothrombic changes appear to overtake the anti-thrombic changes and physiology begin to favor fast and abnormally thick clot formation (hypercoagulability). The exact dosage threshold or conditions required to increase blood clotting has not been determined, and some studies with steroid users taking supraphysiological doses fail to demonstrate increased coagulability.128 Individuals remain warned of the potential increases in thrombic risk with anabolic/androgenic steroid abuse. Blood clotting tendency should return to the pretreated state after the discontinuance of anabolic/androgenic steroids. point until the hematocrit issues have been corrected. Minor elevations in hematocrit may be addressed with phlebotomy. For this, 1 pint of blood may be removed periodically during steroid intake, often every two months. Proper hydration is also important, as dehydration can temporarily cause the hematocrit level to elevate, giving a false positive for polycythemia. The daily intake of aspirin is also commonly advised if the hematocrit is above normal, as this will reduce platelet aggregation, or the tendency for platelets to stick together and form clots. Individuals remain cautioned of the potential cardiovascular danger of high hematocrit levels associated with anabolic/androgenic steroid use.


*Hematological (Polycythemia)

Anabolic/androgenic steroids stimulate erythropoiesis (red blood cell production). One potential adverse effect of this is polycythemia, or the overproduction of red blood cells.
Polycythemia can be reflected in the hematocrit level or the percentage of blood volume that is made up of red cells. As the hematocrit rises, so too does the viscosity of the blood. If the blood becomes too thick, its ability to circulate becomes impaired. This can greatly increase the risk of serious thrombic events including embolism and stroke. A high hematocrit level is also an independent risk factor for heart disease.129 The normal hematocrit level in men is 40.7 to 50.3%, and in women it is 36.1 to 44.3% (numbers may vary very slightly depending on the source). For the sake of scale, while a hematocrit of 50% may be normal, a hematocrit of 60% or above is considered critical (life-threatening).

Anabolic/steroid administration tends to raise the hematocrit level by several percentage points, sometimes more. As a result, many steroid-using bodybuilders will have hematocrit levels that are above the normal range. For example, one study measured the average hematocrit in a group of steroid abusing competitive bodybuilders to be 55.7%.130 This level is considered clinically high and would increase blood viscosity enough to raise the risk of a serious cardiovascular event. Although not likely to be an isolated cause, high hematocrit is believed to have been a contributing factor in the deaths of a number of steroid abusers, usually paired with high blood pressure, homocysteine, and/or atherosclerosis. The average hematocrit level in bodybuilders not taking anabolic/androgenic steroids was 45.6%, well within the normal range for healthy adult men.

Many physicians that specialize in hormone replacement therapy consider a hematocrit level of 55% to be an absolute cutoff point. At or above this point, and anabolic/androgenic steroid therapy cannot be continued safely. Drug intake would be ceased at this point until the hematocrit issues have been corrected. Minor elevations in hematocrit may be addressed with phlebotomy. For this, 1 pint of blood may be removed periodically during steroid intake, often every two months. Proper hydration is also important, as dehydration can temporarily cause the hematocrit level to elevate, giving a false positive for polycythemia. The daily intake of aspirin is also commonly advised if the hematocrit is above normal, as this will reduce platelet aggregation, or the tendency for platelets to stick together and form clots. Individuals remain cautioned of the potential cardiovascular danger of high hematocrit levels associated with anabolic/androgenic steroid use.


*Homocysteine


Anabolic/androgenic steroids may elevate homocysteine levels. Homocysteine is an intermediary amino acid produced as a byproduct of methionine metabolism. High levels of homocysteine have been linked to elevations in the risk for cardiovascular disease.131 It is believed to play a direct role in the disease, increasing oxidative stress, including the oxidation of LDL cholesterol, and accelerating atherosclerosis.132 Elevated levels of homocysteine may also induce vascular cell damage, support platelet aggregation, and increase the likelihood of thrombic events.133 134 135 The normal range for homocysteine levels in men aged 30 to 59 years is 6.3-11.2umol/L. For women of the same age, the average is 4.5-7.9umol/L. Increased risk of heart attack, stroke, or other thrombic events is noted with even modest elevations in homocysteine. According to one study, a homocysteine level exceeding 15umol/L in patients with heart disease is associated with a 24.7% increased likelihood of death within five years.136

Androgens stimulate elevations in homocysteine,137 and men have an approximately 25% higher level on average than women.138 Anabolic/androgenic steroid abuse has been associated with hyperhomocysteinemia or consistent clinically high homocysteine levels.139 One study found that the average homocysteine concentration in a group of 10 men that had been self-administering anabolic/androgenic steroids (in a cyclic pattern) for 20 years was 13.2 umol/L.140 Three of these men died of a heart attack during the investigation and had homocysteine levels between 15umol/L and 18umol/L. The average homocysteine level in bodybuilders who had never taken steroids was 8.7umol/L, while it was 10.4umol/L in previous steroid users (3 months abstinence). One study did show that administering 200 mg of testosterone enanthate (with and without an aromatase inhibitor) for three weeks failed to produce a significant elevation in homocysteine.141 It is unknown if the moderate dosage, drug type (esterified injectable vs. c17-aa), or short duration of intake were factors in the differing outcome from other studies. Individuals remain warned of the potential for elevations in the homocysteine level with steroid abuse.


*Vascular Reactivity


The endothelium is a layer of cells that line the entire circulatory system. These cells are found on the inside of all blood vessels and help increase or decrease blood flow and pressure by relaxing or constricting the vessels (referred to as vasodilation and vasoconstriction, respectively). These cells also help regulate the passage of materials in and out of blood vessels and are involved in a number of important vascular processes including blood clotting and new blood vessel formation. Having a more flexible (reactive) endothelium is generally considered desirable for health, and, likewise, the endothelium is often compromised in individuals with cardiovascular disease. Patients with endothelial dysfunction tend to notice greater vasoconstriction, restricted blood flow, higher blood pressure, local inflammation, and reduced circulatory capacity.142 This may place them at greater risk for heart attack, stroke, or thrombosis (blood clot).

Endothelial cells are androgen-responsive, which may partly account for men exhibiting less vascular reactivity than women.143 Similarly, anabolic/androgenic steroid use has been shown to impair endothelial activity and vascular reactivity.
Studies at the University of Innsbruck in Austria compared the level of endothelial dilation in 20 steroid users to a group of control athletes.144 Those individuals using anabolic steroids noticed slight but measurably impaired vascular dilation and endothelial function. Additional studies at the University of Wales in Cardiff comparing vascular dilation in active, previous, and non-steroid users, also demonstrated anabolic steroids to cause a decline in endothelial-independent vasodilation.145 These effects leave the steroid user with more relative “stiffness” in the vascular system, which could increase the chance of an adverse cardiovascular event. In both studies, vascular reactivity improved after the discontinuance of anabolic/androgenic steroids.




Proving an Association

Direct links between steroid abuse and individual cases of stroke and heart attack have been difficult to prove. There are a number of things that have made this difficult. For one, cardiovascular disease is very common in men. It also usually takes decades to develop. This makes individual contributing factors (which include many things such as diet, lifestyle, health status, and genetic variables) extremely difficult to isolate. Data concerning the long-term use of steroids in physique- or performance-enhancing doses is also very limited. It would be unethical to conduct a controlled study where participants were given abusive doses of steroids for many years, so the data that is referenced tends to be from case studies. Individual case studies are important but are usually considered too weak to meet the requirements of statistical proof.

*Still, it would be a mistake to confuse this lack of proven association with proof of nonassociation. The cardiovascular risks of steroid abuse remain well supported by both documented acute changes in cardiovascular markers and a growing body of case reports of injury or death. There are few medical experts close to the study of these drugs today that would actually deny their risks.






Anabolic/androgenic steroid abuse can produce changes in a number of areas of cardiovascular health that can work together to increase the risk of heart attack, stroke, or embolism.
Screenshot (5041).png




Numerous other potential side-effects of AAS use/abuse:

*Immune System

*Kidneys (Renal System)

*Liver (Hepatic System)


Physical

*Acne
*Hair Loss (Androgenetic Alopecia)
*Stunted Growth
*Tendon Injury

*Water and Salt Retention


*Virilization

Physical (Male)
*Dysphonia (Vocal Changes)
*Gynecomastia


Physical (Female)

*Birth Defects
*Dysphonia (Vocal Changes)
*Enlarged Clitoris (Clitoromegaly)
*Hair Growth (Hirsutism)
*Menstrual Irregularities
*Reduced Breast Size



Psychological

*Aggression
*Dependency/Addiction

*Depression/Suicide
*Insomnia



Reproductive (Male)
*Infertility

*Libido/Sexual Dysfunction
*Priapism
*Prostate Enlargement
*Testicular Atrophy
 

Bubbs

Member
Great posts guys, very informative and interesting

If ACE is an issue would that imply that an ACE inhibitor like lisinopril would be doubly cardio protective in this case?
 

Fluoxymesterone

New Member
Great posts guys, very informative and interesting

If ACE is an issue would that imply that an ACE inhibitor like lisinopril would be doubly cardio protective in this
Great posts guys, very informative and interesting

If ACE is an issue would that imply that an ACE inhibitor like lisinopril would be doubly cardio protective in this case?
Telmisartan is superior it has dual ARB and ppar-y agonist properties. It is anti-inflammatory, anti-diabetic and more
 

Bubbs

Member
Telmisartan is superior it has dual ARB and ppar-y agonist properties. It is anti-inflammatory, anti-diabetic and more
I have been taking lisinopril for a decade, hence my interest in that drug.

I can definitely ask my TRT doc for Telmisartan but I'm hoping that the lisinopril I've been using has helped mitigate some of the potential risk
 

Nelson Vergel

Founder, ExcelMale.com
Steroid Side Effects

While anabolic/androgenic steroids (AAS) are generally regarded as therapeutic drugs with high safety, their use can also be associated with a number of adverse cosmetic, physical, and psychological effects. Many of these side effects are often apparent during therapeutic-use conditions, although their incidence tends to increase profoundly as the dosages reach supratherapeutic ranges. Virtually everyone that abuses anabolic/androgenic steroids for physique- or performance-enhancing purposes notices some form of adverse effects from their use.
According to one study, the exact frequency of tangible side effects in a group of steroid abusers was 96.4%. This shows very clearly that it is far rarer to abuse these drugs and not notice side effects than it is to endure them.90 In addition to the side effects that anabolic/androgenic steroids can have on various internal systems, there are others that may not be immediately apparent to the user. The following is a summary of the biological systems and reactions affected by AAS use.
Hey @madman : what is the reference? Thanks a lot! Great article
 

Fluoxymesterone

New Member
I have been taking lisinopril for a decade, hence my interest in that drug.

I can definitely ask my TRT doc for Telmisartan but I'm hoping that the lisinopril I've been using has helped mitigate some of the potential risk
Yea the lisinopril should have helped; it’s a cardiology drug. My mentor is an interventional cardiologist and tells me good things about it. It’s a drug used to reduce cardiac fibrosis and to prevent heart remodeling in heart disease.
 

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