Blood tests. 3 problems.

eraexshoku

New Member
I did blood tests. Pretty good but ferritin and prolactin are high and HDL cholesterol is low.
The values ??are as follows:

Ferritin: 336 ng/ml, on a range of: 22-274
Prolactin: 25.51 ng/ml, on a range of: 3.5-19.5
HDL Cholesterol: 46 mg/dl, (it is written > 55 normal - 35-55 medium risk)
"General" Cholesterol is OK: 160 mg/dl on range of <200

I state that I was an idiot because the day before blood collection I trained, I ate red meat and I integrated with Vit C, Bcaa and Vit B12.


1) Concerning the Ferritin, may be due to too much red meat, too much protein powder, high-protein feed etc etc?
What can you do to lower it?
2) To lower the prolactin, can be useful 2 pills of 0.5 of caber (dostinex) per week for 3-4 weeks?? PS: I'm off by about 2 months, PCT ended in mid-September.
3) The HDL cholesterol is the good one and so I think this is a problem, I'm going to assume 1-2g a day of Omega 3? Other solutions?

PS: Cycle was Winstrol, Proviron and Test Prop. PCT done with HCG, Clomid and Nolva. The problem is that I want to start my Test E/deca/dbol cycle the next month (beginning of december), so it is possible to lower the prolactin in a month? :(

Thank you very much.
 
That's what I wonder. Maybe it will be caused by the hormonal rush between androgens and estrogens when I started doing the HCG. But I must say that I used testosterone propionate for 10-12 consecutive weeks. And I've never used an anti-estrogen during this cycle. (big mistake). It can be caused by this? I do not know.

The fact is that now I have this problem, how can I lower the prolactin level?
thanks
 
You can just lower the prolactin with caber. Did you get bloods before your cycle? Maybe your prolactin has always been this high.
 
Never. So it's possible because I did 3 cycles of AAS in less then a year, therefore may be high from a long time.

I will use 0.5 of caber twice a week for a month. Hope it works.
Regard the other things, what can I do?
 
The Prolactin can be elevated from hCG or testosterone. It is marginally elevated and might even be wnl on re-testing. It might be worthwhile to check E2. [Interestingly, there is a E2-Hepcidin connection that might explain the Ferritin results.]

Evidence for the causal relationship between testosterone replacement and a rise in PRL was suggested by the observation that PRL levels declined when testosterone was temporarily discontinued and rose again with its readministration.

It is postulated that the rise in PRL was a result of the aromatization of testosterone to estradiol, which in turn stimulated PRL synthesis and release. An accumulating body of evidence suggests that estrogen plays an integral role in the pathogenesis and progression of lactotroph tumors. Specifically, estrogen exerts a stimulatory effect upon PRL secretion by disrupting the inhibitory influence of dopamine; chronic exposure to estrogen functionally uncouples the anterior pituitary D2 receptor from its G protein-coupled receptor.

Estradiol in vitro stimulates PRL gene transcription and prevents the ability of dopamine agonists to inhibit PRL synthesis and secretion. In vivo, large doses of estrogens have induced prolactinomas in rats and may induce them in humans as well.


Sodi R, Fikri R, Diver M, Ranganath L, Vora J. Testosterone replacement-induced hyperprolactinaemia: case report and review of the literature. Ann Clin Biochem 2005;42(Pt 2):153-9. Testosterone replacement-induced hyperprolactinaemia: case report and review of the literature

Half of all men with prolactin (PRL)-producing macroadenomas present with hypogonadism, decreased libido and impotence, and therefore require testosterone replacement. However, very little is known about the effect of testosterone on prolactinomas. We report a case of an 18-year-old obese man who presented with hypogonadism and hyperprolactinaemia and underwent a transphenoidal hypophysectomy after a computer tomography scan showed the presence of a suprasellar macroadenoma. On separate occasions, we documented a rise in PRL when testosterone replacement was started and a fall in PRL when testosterone replacement was stopped (r = 0.6090, P = 0.0095). Furthermore, imaging studies suggested the possibility of tumour re-growth after testosterone therapy. We hypothesize that the exogenous testosterone was aromatized to oestradiol, which stimulated the release of PRL by the anterior pituitary. This was supported by the increase in oestradiol levels after testosterone replacement, although statistical significance was not achieved due to the availability of only a few data points. This case highlights the need to be aware of testosterone-replacement-induced hyperprolactinaemia, an under-recognized complication of androgen replacement in this setting. The use of aromatase inhibitors together with testosterone-replacement therapy or the use of non-aromatizable androgens might be indicated in such patients. Taken together, this report and previous studies show that dopamine agonists apparently do not suppress the hyperprolactinaemia induced by testosterone replacement.


Gillam MP, Middler S, Freed DJ, Molitch ME. The Novel Use of Very High Doses of Cabergoline and a Combination of Testosterone and an Aromatase Inhibitor in the Treatment of a Giant Prolactinoma. J Clin Endocrinol Metab 2002;87(10):4447-51. http://jcem.endojournals.org/cgi/content/full/87/10/4447 (The Novel Use of Very High Doses of Cabergoline and a Combination of Testosterone and an Aromatase Inhibitor in the Treatment of a Giant Prolactinoma)

Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia. A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 {micro}g/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 {micro}g/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 {micro}g/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.


Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F. Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation. Acta Endocrinol (Copenh) 1984;105(2):167-72. Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation

A case of a patient with hypopituitarism due to a disturbance of hypothalamo-pituitary regulation is presented, who developed high-grade hyperprolactinaemia after the initiation of substitutive therapy with testosterone esthers. The increase in serum Prl was strictly related to testosterone aromatization to oestradiol, since anti-oestrogen compounds were effective in reducing (clomiphene) or abolishing (tamoxifen) the enhanced Prl secretion. The oestrogen effect in raising Prl release was not attributable to a reduction in the dopamine inhibition of Prl-secreting cells, as the dopamine-antagonist domperidone failed to increase Prl serum levels in the same patient. This suggests that, in man, the oestrogen effect in enhancing Prl release is mainly enacted directly on the pituitary lactotrophs rather than exerted through a reduction in the hypothalamic dopamine activity.


Prior JC, Cox TA, Fairholm D, Kostashuk E, Nugent R. Testosterone-related exacerbation of a prolactin-producing macroadenoma: possible role for estrogen. J Clin Endocrinol Metab 1987;64(2):391-4. http://jcem.endojournals.org/content/64/2/391.abstract (Testosterone-Related Exacerbation of a Prolactin-Producing Macroadenoma: Possible Role for Estrogen)

Men with PRL-producing macroadenomas often present with hypogonadism and impotence. This report documents exacerbation of a PRL-secreting tumor after two separate 200-mg testosterone enanthate (T) injections despite continued bromocriptine (BRC) therapy. A 37-yr-old man with a 60-mm invasive tumor and a serum PRL level of 13,969 +/- 332 ng/ml (mean +/- SD) responded to BRC therapy with rapid disappearance of visual field defect, headache, and facial pain as well as decrease in serum PRL to 5,103 +/- 1,446 ng/ml. T injection was followed by severe headache, facial pain, and increase in PRL to 13,471 ng/ml. Visual field deterioration and increased tumor size (height, 40-43 mm) by computed tomography were documented. A relationship between T injection and exacerbation of the prolactinoma was not recognized until after a second T injection 3 months later. After that therapy, baseline PRL increased from 6,900 to 12,995 ng/ml. The hypothesis that T was aromatized to estradiol, directly stimulating lactotrophs, was supported by an increase in serum estradiol from 24 to 51 pg/ml after the second T injection. Although T treatment is accepted as appropriate therapy for hypogonadism in men with prolactinomas, it may not only interfere with the response of the tumor to BRC therapy, but even stimulate tumor growth and secretion.
 
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Why would your AAS use raise your prolactin when u didn't use Tren or Deca?

Test *can* affect PRL - with a frequency similar to that of Deca. There is no evidence that I'm aware of showing that tren affects it at all.

That's what I wonder. Maybe it will be caused by the hormonal rush between androgens and estrogens when I started doing the HCG. But I must say that I used testosterone propionate for 10-12 consecutive weeks. And I've never used an anti-estrogen during this cycle. (big mistake). It can be caused by this? I do not know.

The fact is that now I have this problem, how can I lower the prolactin level?
thanks

You don't have a problem. Your PRL is barely outside NLs and it's certainly not significant enough to worry about, let alone be a factor in your next cycle.

Your HDL can be increased with niacin if you are so inclined.

Regards
CBS
 
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So now I have the confirm that all these problem are causated by HCG. I had also fuckin acne after the first shot HCG (1000 UI for 3times E5D) :mad:

However thanks so much guys, to be sure I'll wait another month to start my next cycle. ;)
 
Test *can* affect PRL - with a frequency similar to that of Deca. There is no evidence that I'm aware of showing that tren affects it at all.



You don't have a problem. Your PRL is barely outside NLs and it's certainly not significant enough to worry about, let alone be a factor in your next cycle.

Your HDL can be increased with niacin if you are so inclined.

Regards
CBS

The HDL decrease seen with AAS is resistant to niacin.
 
You will not find a cite or link. Instead, what I have is focused long-term efforts to prevent, minimize, &/or eliminate the HDL decrease with those using nonprescription AAS all for naught.

Your clinical experience is certainly good enough for me. Good to know, nonetheless. I guess this is another example of how understudied this class of drugs is.
 
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Then we have the whole HDL & CVD hypothesis. PCSK9 might just rewrite treatment. PCSK9 drugs - FierceBiotech

Ng DS, Wong NCW, Hegele RA. HDL - is it too big to fail? Nat Rev Endocrinol;advance online publication. http://www.nature.com/nrendo/journal/vaop/ncurrent/full/nrendo.2012.238.html

The HDL hypothesis has suffered damage in the past few years. Clinical trials have shown that raising HDL cholesterol levels does not improve cardiovascular disease (CVD) outcomes. In addition, Mendelian randomization studies have shown that DNA variants that alter HDL cholesterol levels in populations are unrelated to incident CVD events. Balancing this deluge of negative data are substantial basic science data supporting the concept that raising HDL cholesterol levels reduces CVD risk. Also, functionally relevant HDL subfractions might be more important determinants of risk than overall HDL cholesterol levels. But, while wobbly, the HDL hypothesis is still standing, seemingly too big to fail owing to past intellectual, economic and psychological investments in the idea.


Schwartz GG, Olsson AG, Abt M, et al. Effects of Dalcetrapib in Patients with a Recent Acute Coronary Syndrome. New England Journal of Medicine. MMS: Error

BACKGROUND - In observational analyses, higher levels of high-density lipoprotein (HDL) cholesterol have been associated with a lower risk of coronary heart disease events. However, whether raising HDL cholesterol levels therapeutically reduces cardiovascular risk remains uncertain. Inhibition of cholesteryl ester transfer protein (CETP) raises HDL cholesterol levels and might therefore improve cardiovascular outcomes.

METHODS - We randomly assigned 15,871 patients who had had a recent acute coronary syndrome to receive the CETP inhibitor dalcetrapib, at a dose of 600 mg daily, or placebo, in addition to the best available evidence-based care. The primary efficacy end point was a composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, unstable angina, or cardiac arrest with resuscitation.

RESULTS - At the time of randomization, the mean HDL cholesterol level was 42 mg per deciliter (1.1 mmol per liter), and the mean low-density lipoprotein (LDL) cholesterol level was 76 mg per deciliter (2.0 mmol per liter). Over the course of the trial, HDL cholesterol levels increased from baseline by 4 to 11% in the placebo group and by 31 to 40% in the dalcetrapib group. Dalcetrapib had a minimal effect on LDL cholesterol levels. Patients were followed for a median of 31 months. At a prespecified interim analysis that included 1135 primary end-point events (71% of the projected total number), the independent data and safety monitoring board recommended termination of the trial for futility. As compared with placebo, dalcetrapib did not alter the risk of the primary end point (cumulative event rate, 8.0% and 8.3%, respectively; hazard ratio with dalcetrapib, 1.04; 95% confidence interval, 0.93 to 1.16; P=0.52) and did not have a significant effect on any component of the primary end point or total mortality. The median C-reactive protein level was 0.2 mg per liter higher and the mean systolic blood pressure was 0.6 mm Hg higher with dalcetrapib as compared with placebo (P<0.001 for both comparisons).

CONCLUSIONS - In patients who had had a recent acute coronary syndrome, dalcetrapib increased HDL cholesterol levels but did not reduce the risk of recurrent cardiovascular events.
 
I did blood tests. Pretty good but ferritin and prolactin are high and HDL cholesterol is low.
The values ??are as follows:

Ferritin: 336 ng/ml, on a range of: 22-274
Prolactin: 25.51 ng/ml, on a range of: 3.5-19.5
HDL Cholesterol: 46 mg/dl, (it is written > 55 normal - 35-55 medium risk)
"General" Cholesterol is OK: 160 mg/dl on range of <200


I state that I was an idiot because the day before blood collection I trained, I ate red meat and I integrated with Vit C, Bcaa and Vit B12.


1) Concerning the Ferritin, may be due to too much red meat, too much protein powder, high-protein feed etc etc?
What can you do to lower it?
2) To lower the prolactin, can be useful 2 pills of 0.5 of caber (dostinex) per week for 3-4 weeks?? PS: I'm off by about 2 months, PCT ended in mid-September.
3) The HDL cholesterol is the good one and so I think this is a problem, I'm going to assume 1-2g a day of Omega 3? Other solutions?

PS: Cycle was Winstrol, Proviron and Test Prop. PCT done with HCG, Clomid and Nolva. The problem is that I want to start my Test E/deca/dbol cycle the next month (beginning of december), so it is possible to lower the prolactin in a month? :(

Thank you very much.

Do you have blood work that shows your HDL when not on AAS?
Did the lipid panel include triglycerides? If yes what was the reading?

Using Niacin to Improve Cardiovascular Health - Life Extension
 
How to Make “Good Cholesterol” Work to Reverse Heart Disease
How to Make “Good Cholesterol” Work to Reverse Heart Disease | Guest Blog, Scientific American Blog Network

Large population studies have shown an inverse relationship between HDL and CVD risk such that people with low HDL levels have a higher risk of CVD events (3, 4). These findings underlie what has been termed the “HDL hypothesis” which states that raising HDL should lower CVD risk (1). Studies of a similar nature suggested that lowering LDL was beneficial and helped in forging a simple but direct relationship between LDL and CVD risk such that: ‘The lower the LDL, the higher the reduction in CVD risk’. When we turn to HDL, it is tempting to think that the converse would apply. If so, then higher HDL levels should lead to decreased CVD risk. While the large population studies support this idea, there are inconsistencies.
 

http://www.nytimes.com/2012/05/17/h...-cholesterol-found-not-to-cut-heart-risk.html
a new study that makes use of powerful databases of genetic information has found that raising HDL levels may not make any difference to heart disease risk. People who inherit genes that give them naturally higher HDL levels throughout life have no less heart disease than those who inherit genes that give them slightly lower levels. If HDL were protective, those with genes causing higher levels should have had less heart disease.

Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study
 
Then we have the whole HDL & CVD hypothesis. PCSK9 might just rewrite treatment.

The whole HDL thing is confusing. Heart disease risk seems to be correlated with total cholesterol and LDL. The relationship between serum cholesterol and heart disease is perfectly log-linear (at least down to cholesterols of 150 or so), with correlation coefficients exceeding 0.95 in multiple studies (r2 around 0.9). Epidemiologically, heart disease mortality rises starting at about cholesterol 160 (total) or LDL about 100 in men. Is the focus on keeping the ratio of total to HDL cholesterol less than 5, and preferably less than 3 misplaced? Is the idea wishful thinking in a society that continues to eat a high fat diet?

Maintaining that ratio doesn't seem to be a necessity for the prevention of heart disease - at least in populations that eat a very low fat diets. For example, Tarahumara Indians have total cholesterols averaging 135 and TC/HDL ratios averaging about 5.5 - not impressive at all. Yet they have virtually no heart disease. You'll find similar in rural China. Eating low fat drops LDL but HDL usually goes with it.

And the ratio doesn't seem to matter to the Finns who eat a much higher fat diet than the average American. In that population, only LDL correlates to heart disease.

Regardless, it seems humans - at least those at high risk - are doomed to drug therapy to prevent heart disease. The diet needed to get LDL below *safe* levels is too strict for MOST people to adhere to. We're genetically programmed to like calories - lots of calories. Nature places more importance on the avoidance of starvation than dying of an MI at 60.


But, at least drug therapy works. There are more recent examples but the Scandinavian Simvastatin Survival Study is a favorite (Lancet 345:1274-1275, 1995). 4444 people with coronary disease and with cholesterols between 220 and 300, were all given dietary treatment, and then further divided more or less equally into drug treatment vs non drug treatment groups. Addition of Simvastatin to diet lowered cholesterols by 25%, MI mortality by 42%, total cardiac mortality by 35%, and total mortality by 30%. NOTHING like this has ever been done with dietary therapy.

CBS
 
The whole HDL thing is confusing. Heart disease risk seems to be correlated with total cholesterol and LDL. The relationship between serum cholesterol and heart disease is perfectly log-linear (at least down to cholesterols of 150 or so), with correlation coefficients exceeding 0.95 in multiple studies (r2 around 0.9). Epidemiologically, heart disease mortality rises starting at about cholesterol 160 (total) or LDL about 100 in men. Is the focus on keeping the ratio of total to HDL cholesterol less than 5, and preferably less than 3 misplaced? Is the idea wishful thinking in a society that continues to eat a high fat diet?

Maintaining that ratio doesn't seem to be a necessity for the prevention of heart disease - at least in populations that eat a very low fat diets. For example, Tarahumara Indians have total cholesterols averaging 135 and TC/HDL ratios averaging about 5.5 - not impressive at all. Yet they have virtually no heart disease. You'll find similar in rural China. Eating low fat drops LDL but HDL usually goes with it.

And the ratio doesn't seem to matter to the Finns who eat a much higher fat diet than the average American. In that population, only LDL correlates to heart disease.

Regardless, it seems humans - at least those at high risk - are doomed to drug therapy to prevent heart disease. The diet needed to get LDL below *safe* levels is too strict for MOST people to adhere to. We're genetically programmed to like calories - lots of calories. Nature places more importance on the avoidance of starvation than dying of an MI at 60.


But, at least drug therapy works. There are more recent examples but the Scandinavian Simvastatin Survival Study is a favorite (Lancet 345:1274-1275, 1995). 4444 people with coronary disease and with cholesterols between 220 and 300, were all given dietary treatment, and then further divided more or less equally into drug treatment vs non drug treatment groups. Addition of Simvastatin to diet lowered cholesterols by 25%, MI mortality by 42%, total cardiac mortality by 35%, and total mortality by 30%. NOTHING like this has ever been done with dietary therapy.

CBS

http://www.abc.net.au/catalyst/heartofthematter/download/The4SStudy.pdf
Abstract

Drug therapy for hypercholesterolaemia has remained controversial mainly because of insufficient clinical trial evidence for improved survival. The present trial was designed to evaluate the effect of cholesterol lowering with simvastatin on mortality and morbidity in patients with coronary heart disease (CHD). 4444 patients with angina pectoris or previous myocardial infarction and serum cholesterol 5.5-8.0 mmol/L on a lipid-lowering diet were randomised to double-blind treatment with simvastatin or placebo. Over the 5.4 years median follow-up period, simvastatin produced mean changes in total cholesterol, low-density-lipoprotein cholesterol, and high-density-lipoprotein cholesterol of -25%, -35%, and +8%, respectively, with few adverse effects. 256 patients (12%) in the placebo group died, compared with 182 (8%) in the simvastatin group. The relative risk of death in the simvastatin group was 0.70 (95% CI 0.58-0.85, p = 0.0003). The 6-year probabilities of survival in the placebo and simvastatin groups were 87.6% and 91.3%, respectively. There were 189 coronary deaths in the placebo group and 111 in the simvastatin group (relative risk 0.58, 95% CI 0.46-0.73), while noncardiovascular causes accounted for 49 and 46 deaths, respectively. 622 patients (28%) in the placebo group and 431 (19%) in the simvastatin group had one or more major coronary events. The relative risk was 0.66 (95% CI 0.59-0.75, p < 0.00001), and the respective probabilities of escaping such events were 70.5% and 79.6%. This risk was also significantly reduced in subgroups consisting of women and patients of both sexes aged 60 or more. Other benefits of treatment included a 37% reduction (p < 0.00001) in the risk of undergoing myocardial revascularisation procedures. This study shows that long-term treatment with simvastatin is safe and improves survival in CHD patients.
 
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