BB lifestyle and my heart problems

[BigJJ]

Ah, pretty severe then Were you developing oedema in your legs? Do you know what your ejection fraction is?

my EF was 25-30 but its upto 40 now with meds

JJ

 

[embryo923]

It would probably be extremely beneficial to adopt a plant based diet.

 

[Eryximachus]

OP has CHF. The last thing he would want to do is lower his red blood cell count. Please found your opinion in more thorough research before just dropping it out there as if it was based on some depth of knowledge.

I have had polycythemia due to steroid abuse. The symptoms are exactly the same as congestive heart failure. What led me to the emergency room was shortness of breath while skiing on a particularly high mountain. My knowledge on the topic far exceeds your own. This isn't even something that is subject to debate. While anemia is often associated with CHF, this is likely your body compensating for heart failure, and certainly is not the cause. Since he has been abusing steroids for a long time, it is entirely possible if not likely that his hematocrit levels remain elevated.

"Besides the known association of anemia with poor prognosis, more severe symptoms, decreased functional capacity and impaired kidney function, we found a significant and very consistent inverse correlation between HB and HCT and ventricular contractility. Both left ventricular ejection fraction and right ventricular fractional area change improved with a decrease in HB and vice versa. We hypothesize that this effect can result from a change in viscosity, which decreases with a decrease in HCT, and may facilitate adaptation of the heart to a volume overload state accompanied by hemodilution."

https://www.ncbi.nlm.nih.gov/pubmed/22846848

 

[Genetic Freak]

I have had polycythemia due to steroid abuse. The symptoms are exactly the same as congestive heart failure. What led me to the emergency room was shortness of breath while skiing on a particularly high mountain. My knowledge on the topic far exceeds your own. This isn't even something that is subject to debate. While anemia is often associated with CHF, this is likely your body compensating for heart failure, and certainly is not the cause. Since he has been abusing steroids for a long time, it is entirely possible if not likely that his hematocrit levels remain elevated.

"Besides the known association of anemia with poor prognosis, more severe symptoms, decreased functional capacity and impaired kidney function, we found a significant and very consistent inverse correlation between HB and HCT and ventricular contractility. Both left ventricular ejection fraction and right ventricular fractional area change improved with a decrease in HB and vice versa. We hypothesize that this effect can result from a change in viscosity, which decreases with a decrease in HCT, and may facilitate adaptation of the heart to a volume overload state accompanied by hemodilution."

https://www.ncbi.nlm.nih.gov/pubmed/22846848

Elevated haematocrit isn't really that big a deal, ensure regular venesection or donation...

shortness of breath while skiing on a particularly high mountain

Don't you think the elevation in altitude, and subsequent low O2 levels was a contributory factor to your presentation with SOB.... Also high altitude is known to increase HB, and this could explain increased HCT..

My knowledge on the topic far exceeds your own

Sits down with popcorn...

 

[Eryximachus]

Elevated hematocrit is a very big deal. Sorry guys, but you're going to find more intelligent discussion on the likes of thinksteroids.com or eroids or uk-muscle.co.uk.

I'm out from this sub-forum, but I highly suggest that if you are truly interested in harm reduction, you read and learn. I can already tell both of you mods are probably not even in your 30s. Trust me, when you've been in the game as the long as the OP, or myself, you'll definitely refrain from naive comments like "elevated hematocrit isn't really that big of a deal". Why is this? Friends have died.

 

[Serotonin101]

Elevated hematocrit is a very big deal. Sorry guys, but you're going to find more intelligent discussion on the likes of thinksteroids.com or eroids or uk-muscle.co.uk.

I'm out from this sub-forum, but I highly suggest that if you are truly interested in harm reduction, you read and learn. I can already tell both of you mods are probably not even in your 30s. Trust me, when you've been in the game as the long as the OP, or myself, you'll definitely refrain from naive comments like "elevated hematocrit isn't really that big of a deal". Why is this? Friends have died.

Both mods have used gear longer than I've been alive (im 26) and I know gf works in the health field. Elevated hematocrit isn't such a big deal if it's not for prolonged periods of time and way outside of range. Professional endurance athletes purposely elevate it for better oxygen transport (epo anyone?) and better performance. In the grand scheme of things short term elevation won't kill you, same as elevated liver enzymes, bad cholesterol, etc.

 

[CFC]

I have had polycythemia due to steroid abuse [...] What led me to the emergency room was shortness of breath while skiing on a particularly high mountain.

As do many AAS-using bodybuilders. I'm not sure why you imagine this would make you uniquely knowledgeable on the subject.

The symptoms are exactly the same as congestive heart failure.

No, they aren't. To suggest they are clearly indicates you don't know what you're talking about. This is not an insult, but an observation. The study you posted doesn't support your assertion either. It's not an instruction for physicians to induce anaemia in CHF patients, but an attempt to understand some of the mechanisms causing that symptom.

Low HB is often linked to heart disease because the heart has to work harder to pump more blood and oxygen through the body. Even the most cursory glance at the literature would have made you realise that anaemia and low HB/HCT and haemodilution are something doctors actively try to prevent in CHF patients - indeed sometimes by giving them EPO to boost RBC concentration.

The fact that you're attempting to argue this is like arguing day is night and night is day. But for the sake of others genuinely interested in the subject, here's a small snapshot of the vast literature documenting the problems of low HB in CHF:

About half of all the patients with CHF are anemic (they have a hemoglobin of < 12 g%). The prevalence and severity of this anemia increases with increasing severity of the CHF. The anemia is caused by a combination of poor nutrition, associated renal insufficiency causing inappropriately low Erythropoietin (EPO) levels, bone marrow depression and EPO resistance caused by excessive TNF alpha and other factors, gastrointestinal blood loss caused by aspirin, ACE inhibitors, EPO loss in the urine with proteinuria, and hemodilution caused by the excessive plasma volume. Studies have shown that anemia is an independent risk factor for death in CHF, almost doubling the mortality rate. Correction of the anemia with subcutaneous EPO and IV iron improves cardiac function and functional capacity, helps prevent the progression of renal failure, markedly reduces hospitalization and diuretic doses, and improves self assessed quality of life. This so-called Cardio Renal Anemia Syndrome is very common in CHF. Its successful treatment demands close cooperation between cardiologists and nephrologists.

https://www.ncbi.nlm.nih.gov/pubmed/12453537

Anemia is a frequent comorbidity of heart failure and is associated with poor outcomes. Anemia in heart failure is considered to develop due to a complex interaction of iron deficiency, kidney disease, and cytokine production, although micronutrient insufficiency and blood loss may contribute.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569049/

Systemic review also revealed that the severity of anemia is closely related to the rate of mortality and hospitalization for heart failure. Anemia is associated with an increased risk of mortality and rate of hospitalization for heart failure. Anemia is an independent risk factor for adverse outcomes in patients with CHF.

https://www.ncbi.nlm.nih.gov/pubmed/19522961

Anemia is found in about one-third of all cases of congestive heart failure (CHF). The most likely common cause is chronic kidney insufficiency (CKI), which is present in about half of all CHF cases. The CKI is likely to be due to the renal vasoconstriction that often accompanies CHF and can cause long-standing renal ischemia. This reduces the amount of erythropoietin (EPO) produced in the kidney and leads to anemia. However, anemia can occur in CHF without CKI and is likely to be due to excessive cytokine production (for example, tumor necrosis factor-alfa (TNF-alfa) and interleukin-6 (IL-6)), which is common in CHF and can cause reduced EPO secretion, interference with EPO activity in the bone marrow and reduced iron supply to the bone marrow. The anemia itself can worsen cardiac function, both because it causes cardiac stress through tachycardia and increased stroke volume, and because it can cause a reduced renal blood flow and fluid retention, adding further stress to the heart. Long-standing anemia of any cause can cause left ventricular hypertrophy (LVH), which can lead to cardiac cell death through apoptosis and worsen the CHF. Therefore, a vicious circle is set up wherein CHF causes anemia, and the anemia causes more CHF and both damage the kidneys worsening the anemia and the CHF further. We have termed this vicious circle the cardio renal anemia (CRA) syndrome. Patients with CHF who are anemic are often resistant to all CHF medications resulting in being hospitalized repeatedly. Many studies also demonstrate that these patients die more rapidly than their non-anemic counterparts do. In addition, they have a more rapid deterioration in their renal function and can end up on dialysis. There is now evidence from both uncontrolled and controlled studies that early correction of the CHF anemia with subcutaneous EPO and intravenous (i.v.) iron improves shortness of breath and fatigue, cardiac function, renal function and exercise capability, dramatically reducing the need for hospitalization. For these reasons, it is not surprising that quality of life has also been shown to improve. As both CHF and end-stage renal disease (ESRD) are rapidly increasing, the possibility that these twin conditions can be improved by the adequate treatment of anemia offers new hope for slowing the progression of both conditions.

https://www.ncbi.nlm.nih.gov/pubmed/15593047

Anemia exacerbates CHF, causing a vicious circle, where renal dysfunction and neurohormonal and proinflammatory cytokine activation participate in the development of anemia. On the other hand, anemia increases myocardial workload and worsens cardiac dysfunction. So, it is important to recognize any possible causes of anemia. It would also be beneficial to treat them, if possible. Administration of iron and ESAs seems to be promising, since they can both also improve factors other than anemia, but still there are many questions to be answered. These mainly concern their safety, the goals in Hb elevation, and probably their cost.

https://www.hindawi.com/journals/isrn/2012/246915/

In two recent studies from Israel, Silverberg and colleagues noted that anaemia was common in chronic heart failure (CHF). Moreover, treatment with combined erythropoietin and intravenous ferrous sulfate not only increased haemoglobin concentrations but, more importantly, was associated with improvements in cardiac function

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1767058/

26 patients with heart failure and anaemia treated for an average of 7.2 months with EPO and intravenous iron were reported to show an increase in haemoglobin from 10 to 12 g/dl, an increase in left ventricular ejection fraction from 27% to 35%, a decrease in hospitalisations for heart failure by 91%, an improvement in mean NYHA class from 3.6 to 2.6, and a reduction in the use of diuretics.

In a second report with a control group 16 patients with moderate to severe CHF and haemoglobin values persistently between 10.0–11.5 g/dl received subcutaneous EPO and intravenous iron to increase the concentration of haemoglobin to at least 12.5 g/dl. Over a mean (SD) period of 8.2 (2.6) months, the mean NYHA class improved by 42.1%, the left ventricular ejection fraction increased by 5.5%, and the need for oral and intravenous furosemide (frusemide) decreased by 51.3% and 91.3%, respectively. In addition the number of days spent in hospital compared with the same period of time before entering the study decreased by 79.0%

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768415/

My knowledge on the topic far exceeds your own. This isn't even something that is subject to debate.

I almost fell for the pompous act, but actually I think this is just trolling, since you would have very quickly figured out you were completely wrong when you went looking for a study to support your view. You successfully made me waste time correcting your nonsense, and I'm going to have to do the same on the other thread you're trolling as well. It's not funny and you're advocating something which would be dangerous for OP. If you keep it up you're going to get infracted.

 

[CFC]

Elevated hematocrit is a very big deal.

Yes, it is. We never said it wasn't, and we advocate controlling HB levels in AAS using bodybuilders. But this has absolutely nothing to do with the discussion at hand about OP's CHF. To attempt to conflate the two is asinine and disingenuous.

 

[Genetic Freak]

Elevated hematocrit is a very big deal. Sorry guys, but you're going to find more intelligent discussion on the likes of thinksteroids.com or eroids or uk-muscle.co.uk.

I'm out from this sub-forum, but I highly suggest that if you are truly interested in harm reduction, you read and learn. I can already tell both of you mods are probably not even in your 30s. Trust me, when you've been in the game as the long as the OP, or myself, you'll definitely refrain from naive comments like "elevated hematocrit isn't really that big of a deal". Why is this? Friends have died.

I live with elevated hematocrit and have done for a number of years which I manage via regular venesection every 3 months, so to me it's no big deal.. To others with similar condition we have always advised seek medical help, with the view to obtaining blood tests and possible venesection or donation, combined with consideration to lower dose/switch compounds, time off, regular cardio, and healthy nutrition..

Whilst it might be prudent for some to increase their knowledge, I am regularly audited on treatment options/diagnosis of my patients... This is a legislated requirement of Emergency Medicine here in NZ, needed to retain my Authority to Practice.. Whilst I thank you for your concern, I am well versed on cardiovascular health.

 

[Serotonin101]

What's weird is having been on for three and a half years and only donating twice, all my blood work I've got done and my hematocrit is only slightly elevated (nothing alarming by any means). Think there's a genetic component to it? Or maybe environmental? I've heard living in warmer climates, the body is supposed to thin the blood to make for more efficient cooling and vice versa for cooler climates. Where I live it's typically above 85F for 75% of the year and I spend a lot of time in the heat.

 

[CFC]

Both mods have used gear longer than I've been alive (im 26)

I just noticed this lol. Nah, I've been using for about 17-18 years. I'd have had to start when I was 11 to be on that long GF, however, started about the time I was born I think

What's weird is having been on for three and a half years and only donating twice, all my blood work I've got done and my hematocrit is only slightly elevated (nothing alarming by any means). Think there's a genetic component to it? Or maybe environmental? I've heard living in warmer climates, the body is supposed to thin the blood to make for more efficient cooling and vice versa for cooler climates. Where I live it's typically above 85F for 75% of the year and I spend a lot of time in the heat.

Do you know what you're hb/hct is when not on? Is there much change on cycle? Altitude plays the bigger role naturally, but in terms of changes on cycle in the same circumstances, it's almost certainly genetic variation.

 

[Serotonin101]

I just noticed this lol. Nah, I've been using for about 17-18 years. I'd have had to start when I was 11 to be on that long GF, however, started about the time I was born I think



Do you know what you're hb/hct is when not on? Is there much change on cycle? Altitude plays the bigger role naturally, but in terms of changes on cycle in the same circumstances, it's almost certainly genetic variation.

Hb is usually mid 14s and hct is usually mid 40s off gear or at actual trt doses (150/week). While on Hb maybe hits 15 and hct hits 48-49. So I'll hit the high end of normal and it just stays there.

 

[Genetic Freak]

I just noticed this lol. Nah, I've been using for about 17-18 years. I'd have had to start when I was 11 to be on that long GF, however, started about the time I was born I think

.

You're both making me feel old... about to start my 37th year..

 

[chompy]

This is why I powerlift all natural. 1 year of training and im at 3 plates. How long did it take u with roids to do that?

 

[Serotonin101]

This is why I powerlift all natural. 1 year of training and im at 3 plates. How long did it take u with roids to do that?

3 plates for what? That's my buffet rule is 3 plate minimum. Always get the expensive stuff to get your money's worth.

 

[Genetic Freak]

3 plates for what? That's my buffet rule is 3 plate minimum. Always get the expensive stuff to get your money's worth.

Used to rep dips with 4 plates, when I was your age...

 

[CFC]

You're both making me feel old... about to start my 37th year..

You're only as old as your arteries say you are!

 

[CFC]

3 plates for what? That's my buffet rule is 3 plate minimum. Always get the expensive stuff to get your money's worth.

A buffet isn't a buffet unless you hit 10 plates in the first half hour

 

[Eryximachus]

Yes, it is. We never said it wasn't, and we advocate controlling HB levels in AAS using bodybuilders. But this has absolutely nothing to do with the discussion at hand about OP's CHF. To attempt to conflate the two is asinine and disingenuous.

It is a rare thing to have such a forceful condemnation presented so eloquently. This certainly is very different from every other bodybuilding forum where cogent writing is a rarity. I'm not going to argue this point, mostly because I respect the research you have done and I have too many work deadlines this week to read anything else that is technical.

But, I do wish to clarify that I was not in any way trolling. I like this site a lot specifically because the quality of discourse is high.

 

[CFC]

^ It's water under the bridge, I don't hold a grudge Some of us have backgrounds in internal medicine and cardiological issues, so tend to be pretty strict on that, but we're always open to a well-reasoned argument from anyone, with or without papers to back it up.