Well, here you go guys. BLOODWORK. A 2.5yr glimpse...

[captain caveman 1234]

It’s posts like this that bring me to this site day after day. I probably spent 30 mins reading over every detail. My chlosterol is extremely high so I’m working on getting it back to normal

 

[someday]

Yeah, IGF was 308 when on Seros 4.5iu 4 to 5 days a week.

Clearly then MK-677 wins the bang for the buck argument if just looking at igf levels. Thanks again for the factual results.

 

[Stewie]

Mr. BMJ and Rex (nice to Rex posting again, wealth of practical and clinical knowledge) summed it up very well with their point of views. To echo what they stated really isn't necessary, as they pretty much nailed it. Although, I'll throw a few thoughts out of why I suggested the couple of "exotic" lab's you pulled---myeloperoxidase and NT-proBNP. I noticed you've pulled Lp(a) in the recent past. This is a helpful biomarker that's an independent risk factor for CVD and thrombosis. Sadly enough, this is a slightly elevated genetic marker I'm faced with. I've been working diligently on lowering Lp(a)-P and increasing Lp(a)-mass. Not an easy task.

All to often, I see individuals hyperfixating on the numerical value of HDL and LDL. Not that this isn't fundamentally important as a whole, tho I look at it a little differently. To sidestep a topic on the subfractions and lipoprotein particle size(s), this in-and-of itself would be lengthy. Rather instead, I'll touch on something a little different that pertains to the assay you pulled, Myeloperoxidase (MPO).

As with subfractions of lipoproteins, this particular topic regarding the biological, cellular and molecular actions would be endless. So I'll try to be as concise as I can. Myeloperoxidsae levels generally stay constant under normal physiological conditions. As with most inflammatory markers (blood tests) these enzymes (protiens) act as acute phase reactants, meaning if there's some sort of trauma, bacterial or viral infection or even exersice, these values will transiently rise. Unless there's chronic, long-term inflammation going on.

This triggers an immunological chain of events that produces helper cells, if present, results in pathogenic destruction (phagocytosis) of the pathogen (host). Such as in the situations of infection(s). Here again I don't want to get to carried away and I'll keep it at the topic at-hand--- lipoproteins--HDL and LDL. Incidentally, myeloperoxidsae is exceptionally capable of oxidizing these lipoproteins. In which isn't necessarily a bad thing under normal physiological and biological conditions, as oxidation is necessary for many reasons. Given that, in contrast when these lipoproteins become heavily oxidized from an abundance of MPO, in this case of HDL, HDL now can become rogue or dysfunctional losing its antioxidant properties, loss of function in reverse cholesterol transport, as well possibly leading to atherosclerotic plaques, endothelial dysfunction, ect. It's of my opinion that it's pertinent to at least once a year to get a baseline of one's MPO levels. If one's running a progestin based anabolic(s), I would probably pull it before and halfway though your cycle. As progestins are notorious for increasing hepatic copper levels, thus potentially setting the stage for copper induced dysfunctional HDL. Keep in mind. Pulling your MPO levels, doesn't represent that specifically HDL is soley oxidized. It's the net fallout that MPO can inflict on lipoproteins. Hopefully that doesn't cause confusion?


I'll leave it there at that and end with, there's several different causes that can give false-positives when assessing elevated MPO levels. Yet, this doesn't mean this should be ignored.

Hopefully Rex sees this, as I'd like to scratch his mind on his thoughts of tamoxifen's impairment of reverse cholesterol transport? As well his clinical use of either levothyroxine or liothyronine with his patients that have subpar lipids?

It does have it's place with cholesterol efflux and reverse cholesterol transport.

I'll do my best to hit on NT-proBNP tomorrow.

-Kirk

 

[specter]

Mr. BMJ and Rex (nice to Rex posting again, wealth of practical and clinical knowledge) summed it up very well with their point of views. To echo what they stated really isn't necessary, as they pretty much nailed it. Although, I'll throw a few thoughts out of why I suggested the couple of "exotic" lab's you pulled---myeloperoxidase and NT-proBNP. I noticed you've pulled Lp(a) in the recent past. This is a helpful biomarker that's an independent risk factor for CVD and thrombosis. Sadly enough, this is a slightly elevated genetic marker I'm faced with. I've been working diligently on lowering Lp(a)-P and increasing Lp(a)-mass. Not an easy task.

All to often, I see individuals hyperfixating on the numerical value of HDL and LDL. Not that this isn't fundamentally important as a whole, tho I look at it a little differently. To sidestep a topic on the subfractions and lipoprotein particle size(s), this in-and-of itself would be lengthy. Rather instead, I'll touch on something a little different that pertains to the assay you pulled, Myeloperoxidase (MPO).

As with subfractions of lipoproteins, this particular topic regarding the biological, cellular and molecular actions would be endless. So I'll try to be as concise as I can. Myeloperoxidsae levels generally stay constant under normal physiological conditions. As with most inflammatory markers (blood tests) these enzymes (protiens) act as acute phase reactants, meaning if there's some sort of trauma, bacterial or viral infection or even exersice, these values will transiently rise. Unless there's chronic, long-term inflammation going on.

This triggers an immunological chain of events that produces helper cells, if present, results in pathogenic destruction (phagocytosis) of the pathogen (host). Such as in the situations of infection(s). Here again I don't want to get to carried away and I'll keep it at the topic at-hand--- lipoproteins--HDL and LDL. Incidentally, myeloperoxidsae is exceptionally capable of oxidizing these lipoproteins. In which isn't necessarily a bad thing under normal physiological and biological conditions, as oxidation is necessary for many reasons. Given that, in contrast when these lipoproteins become heavily oxidized from an abundance of MPO, in this case of HDL, HDL now can become rogue or dysfunctional losing its antioxidant properties, loss of function in reverse cholesterol transport, as well possibly leading to atherosclerotic plaques, endothelial dysfunction, ect. It's of my opinion that it's pertinent to at least once a year to get a baseline of one's MPO levels. If one's running a progestin based anabolic(s), I would probably pull it before and halfway though your cycle. As progestins are notorious for increasing hepatic copper levels, thus potentially setting the stage for copper induced dysfunctional HDL. Keep in mind. Pulling your MPO levels, doesn't represent that specifically HDL is soley oxidized. It's the net fallout that MPO can inflict on lipoproteins. Hopefully that doesn't cause confusion?


I'll leave it there at that and end with, there's several different causes that can give false-positives when assessing elevated MPO levels. Yet, this doesn't mean this should be ignored.

Hopefully Rex sees this, as I'd like to scratch his mind on his thoughts of tamoxifen's impairment of reverse cholesterol transport? As well his clinical use of either levothyroxine or liothyronine with his patients that have subpar lipids?

It does have it's place with cholesterol efflux and reverse cholesterol transport.

I'll do my best to hit on NT-proBNP tomorrow.

-Kirk

Holy Shit my brain just melted

 

[G.I.Bro]

All my numbers were recently OK but my HDL took a nose dive to the lowest levels I've ever had, I assume because I've increased some AI usage lately (no orals though). My HDL was fucking 8. I've got to work on that.

HS-CRP was only .3 though. Anything under 1 is low risk.

 

[G.I.Bro]

I also talked to regular doc (not a specialist) about getting an echo. At 35 he said it's pretty hard to substantiate. So today he gave me an EKG. He said if there was anything slightly off he'd use it to substantiate an echo. Unfortunately it was perfect. He said if I had an enlarged heart, you'd most likely see some minor voltage flags or "noises" but there weren't any. I couldn't convince him to rx an echo...

 

[AthleticApe123]

I also talked to regular doc (not a specialist) about getting an echo. At 35 he said it's pretty hard to substantiate. So today he gave me an EKG. He said if there was anything slightly off he'd use it to substantiate an echo. Unfortunately it was perfect. He said if I had an enlarged heart, you'd most likely see some minor voltage flags or "noises" but there weren't any. I couldn't convince him to rx an echo...

no..
my ecg is also perfect but i have a slightly dilated lv and also a slightly lowered ef (47-49%)

 

[G.I.Bro]

no..
my ecg is also perfect but i have a slightly dilated lv and also a slightly lowered ef (47-49%)

I know, EKG is not enough to rule anything out. It's frustrating. I don't have any symptoms, only a family history, so he's being conservative.

 

[nothuman]

All my numbers were recently OK but my HDL took a nose dive to the lowest levels I've ever had, I assume because I've increased some AI usage lately (no orals though). My HDL was fucking 8. I've got to work on that.

HS-CRP was only .3 though. Anything under 1 is low risk.

I also talked to regular doc (not a specialist) about getting an echo. At 35 he said it's pretty hard to substantiate. So today he gave me an EKG. He said if there was anything slightly off he'd use it to substantiate an echo. Unfortunately it was perfect. He said if I had an enlarged heart, you'd most likely see some minor voltage flags or "noises" but there weren't any. I couldn't convince him to rx an echo...

ECG is kind of useless. I mean it's useful if something comes up but it's silly your doctor wouldn't order the echo. Why do you think your HDL is so low? Have you been able to get an NMR Lipoprofile and check your HDL-P and particle size, etc.? Good news about the CRP. Mine is the same.

 

[G.I.Bro]

ECG is kind of useless. I mean it's useful if something comes up but it's silly your doctor wouldn't order the echo. Why do you think your HDL is so low? Have you been able to get an NMR Lipoprofile and check your HDL-P and particle size, etc.? Good news about the CRP. Mine is the same.

No haven't checked particle size yet. My HDL is lower because I've been using slightly more AAS and more AI than normal the past 6 months. I was using a low enough amount before I didn't use much AI. I blame the AI use for this because I haven't messed with orals.

I need to get it up though. It's usually around 30-40, so even when it's good it's still shit.

This is a genetic thing, runs in my family. Dad has the same lipids. I'm on Praluent.

 

[ThinkTank]

I also talked to regular doc (not a specialist) about getting an echo. At 35 he said it's pretty hard to substantiate. So today he gave me an EKG. He said if there was anything slightly off he'd use it to substantiate an echo. Unfortunately it was perfect. He said if I had an enlarged heart, you'd most likely see some minor voltage flags or "noises" but there weren't any. I couldn't convince him to rx an echo...

Seek out a cardiologist. They will certainly take you most seriously.

 

[Rex Feral]

Thanks a lot for the response, brother. It's funny my true baseline is 19.6 with vitamin D. I got that twice while eliminating it. Once on purpose and another time out of laziness.
I like to have my levels around 60 so I will aim for that. 10,000iu seems to get me to over 60 but I didn't have supplemental magnesium at the time so maybe 1-2g of magnesium would elevate it further.

Do you really think H and H top off at my current levels? I have never donated before. I'm torn on whether to donate or ride the wave, continue to monitor and ride the wave. I was planning on perhaps implementing superdrol and trestolone and maybe doing NMRs while on among a few other tests.

Have you seen any sure fire ways to raise free test?

Sent from my SM-N900V using Tapatalk

Hey bro, yeah I think it will top off near where it is regardless. I've never been big on phlebotomy personally as long as platelets are good. I remember several years ago there was a big push around here for therapeutic phlebotomy. One of the biggest proponents on here did it himself at home. I remember looking into this in depth as a result (I had seen few MDs utilize therapeutic phlebotomy at this point) and I found a fair % increase in risk in of thrombosis. I remember seeing no evidence in increased risk of anything for elevated H & H in absence of increased platelets. I believe I even posted a question here as to why we worry about H & H. Then this big phlebotomy proponent dropped dead, from thrombosis. Big Bapper was his name I believe. Many will remember. Coincidence? I didn't know him. There has been some debate on here lately because of what some MD posted on YouTube. You can do the research yourself but I've concluded, after talking to several MDs and looking at the available evidence, that elevated H & H is not deserving of the concern most here have placed on it in the absence of elevated platelets. The increased risk of thrombosis from phlebotomy outweighs it in my mind.

Honestly, and I may seem ignorant in admitting this, I have never really focused on free T. I'd say you take enough drugs to advance you towards your goal whatever that may be. i.e. dose determines the outcome and not some focus on minutia like free T. Not to say that increasing free T will not somehow marginally benefit those who are seeking to limit doses as much as possible. But I'd have to ask what is the point? You can't be a competitor or you will just lose to someone who could give a fuck about his free T and takes larger doses. So then it's just for you. Then you have to assess the gain vs whatever you choose to increase free T and the sides you may incur. To my mind, you could add 600 mg EQ or Primo for example and have a better outcome both results wise and healthwise than adding say oral winstrol to get whatever small decrease in SHBG you may get along with whatever small increase in performance comparatively.

Rex.

 

[Rex Feral]

Rex, what have you seen with patient's (or users) on Toremifene?

I know that alpha6164 was in favor of it too over long-term nolva, IIRC, due to the blood clotting factors. It's seems to also have some positive benefits on cholesterol as well...i'd have to look at the designs on the research again, as it's been years since I've looked over them. I've tried it Torem myself, but never got blood work on it.

Not real sure of the quality of the research places that I used though. I know that online pharmacies have it. I guess the only way to see is by getting blood work on it.

I just wanted to see what experiences you've had with it, or those you kjnow who have. Thanks, and good seeing ya post

I have very limited personal experience data, only 4. But those 4 would echo what I've seen in the data, a completely unaltered lipid profile with HRT doses and a significantly improved lipid panel vs what would normally be observed at higher doses.

The Journal of Urology
Volume 199, Issue 4, Supplement, April 2018, Page e1171



Sexual Function/Dysfunction: Medical, Hormonal & Non-surgical Therapy II

MP85-06 TOREMIFENE CITRATE IMPROVES HIGH-DENSITY LIPOPROTEIN LEVELS IN MEN ON TESTOSTERONE REPLACEMENT THERAPY


INTRODUCTION AND OBJECTIVES
Decreases in high-density lipoprotein (HDL) levels have been observed in men on testosterone therapy (TTh). Niacin is commonly used as a therapy for low HDL, although its side effect (SE) profile often leads to frequent discontinuation. Toremifine citrate is an oral selective estrogen modulator (SERM) that is well tolerated and can improve lipid profiles by raising HDL levels in both breast and prostate cancer patients. Here we assess the role of toremifene in the management of HDL abnormalities in men on TTh.

METHODS
Men on TTh with low HDL levels (<39 mg/dL) at a single andrology clinic treated between October 2015 and August 2017 with either toremifine (60 mg daily), niacin (titrated to 1,000 mg daily over 2 months) plus krill oil (1,000 mg daily) (NKO), or no treatment (patient refusal) were reviewed in a retrospective intent-to-treat analysis. Patient age, type of TTh, length of follow-up, and baseline and subsequent non-fasting lipid panels, total testosterone (TT) levels, and estrogen (E) levels were determined. Analysis of variance (ANOVA) was used to determine differences between groups.

RESULTS
A total of 75 men with low HDL levels on injectable TTh were included (34 treated with toremifine, 17 treated with NKO, and 24 untreated). No differences in the mean (SD) age between the cohorts (39.2 (10.2) years for whole cohort), baseline laboratory values, or the mean duration of follow-up (6.4 (4.1) months, for whole cohort). Changes in laboratory values are listed in Table 1. Only the change in HDL was significant between the groups during follow-up, with both toremifine and NKO resulting in significant improvements in HDL when compared with untreated men (p = 0.02 and 0.01, respectively). No significant difference in the change in HDL between toremifine vs NKO was observed. 3 men (17.6%) stopped niacin prior to follow up secondary to intolerable SEs (flushing), whereas no men stopped toremifine due to SEs.

CONCLUSIONS
Toremifine results in improvement in HDL in men with low HDL on TTh similar to that observed with niacin + krill oil. However, toremifine is better tolerated than niacin and could serve as an reasonable alternative treatment for low HDL in men on TTh. Prospective studies are needed to validate these results.

And also in the opposite, though this may not seem applicable to us for many, it is actually.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049948/

Toremifene significantly decreased total cholesterol, LDL cholesterol, and triglycerides, and increased HDL cholesterol in men receiving ADT for prostate cancer.

Tamox has a similar benefit, maybe better. But as mentioned clotting issues for those susceptible. There is also the carcinogen issue for tamox, but this seems to be related to uterine CA specifically which is not applicable to us. Then there is the evidence of cognitive decline but this is questionably related to males. 90 mg of torem citrate is = 60 mg torem. So if you're using torem citrate vs a pharmaceutical 60 mg torem tab like almost everyone here be aware of the dose difference. Nolva receives a lot of bad publicity here but it actually has a very long safety history and most don't seem to understand that the carcinogen classifications have to do with uterine cancer. As long as you're not one of the 10% or so susceptible to clotting from it, which is why I'd agree torem is the better is option. Ralox will not have not have the same positive effect on lipids so it also not SERMS in general.

Rex.

 

[MyNameIsJeff]

Hey bro, yeah I think it will top off near where it is regardless. I've never been big on phlebotomy personally as long as platelets are good. I remember several years ago there was a big push around here for therapeutic phlebotomy. One of the biggest proponents on here did it himself at home. I remember looking into this in depth as a result (I had seen few MDs utilize therapeutic phlebotomy at this point) and I found a fair % increase in risk in of thrombosis. I remember seeing no evidence in increased risk of anything for elevated H & H in absence of increased platelets. I believe I even posted a question here as to why we worry about H & H. Then this big phlebotomy proponent dropped dead, from thrombosis. Big Bapper was his name I believe. Many will remember. Coincidence? I didn't know him. There has been some debate on here lately because of what some MD posted on YouTube. You can do the research yourself but I've concluded, after talking to several MDs and looking at the available evidence, that elevated H & H is not deserving of the concern most here have placed on it in the absence of elevated platelets. The increased risk of thrombosis from phlebotomy outweighs it in my mind.

Honestly, and I may seem ignorant in admitting this, I have never really focused on free T. I'd say you take enough drugs to advance you towards your goal whatever that may be. i.e. dose determines the outcome and not some focus on minutia like free T. Not to say that increasing free T will not somehow marginally benefit those who are seeking to limit doses as much as possible. But I'd have to ask what is the point? You can't be a competitor or you will just lose to someone who could give a fuck about his free T and takes larger doses. So then it's just for you. Then you have to assess the gain vs whatever you choose to increase free T and the sides you may incur. To my mind, you could add 600 mg EQ or Primo for example and have a better outcome both results wise and healthwise than adding say oral winstrol to get whatever small decrease in SHBG you may get along with whatever small increase in performance comparatively.

Rex.

I agree with you that if platelets aren't elevated and Hematocrit isn't too high (<53), then phlebotomies may not be necessary.
But to my knowledge phlebotomies do not increase the risk of thrombosis. That conclusion was based on an observational study leading to issues with selection bias. A more recent paper looked for evidence from randomized clinical trials and found no correlation between the number of phlebotomies per year and the risk of thrombosis.

These results, based on a more powerful analysis of PV patients treated with HU in the settings of controlled prospective trials, do not confirm those recently reported by Alvarez-Larran et al.,10 who showed a correlation between the number of TP and a higher incidence of thrombosis in HU treated patients in an observational cohort. It should be underlined that the median value of HCT in the group treated with 3 or more phlebotomies (46.03%) of the ECLAP study was lower than the median value of hematocrit in the high-HCT arm of the Cyto-PV trial (always above 47.5%), and that this latter value was comparable to the group treated with 3 or more phlebotomies of the Spanish cohort in which higher risk of thrombosis was reported. Clearly, the increased number of phlebotomies is obviously related to the need to reach the target hematocrit level. Thus, it could be argued that the higher risk of thrombosis might be related to an uncontrolled hematocrit value, rather than to the use of phlebotomies per se.

In conclusion, our results indicate that the frequency of phlebotomies in PV patients on HU does not represent a risk factor for future thrombosis in PV patients and do not support the need to shift from HU plus TP to second-line drugs, indirectly reinforcing the fact that a low HCT is the key variable to reduce thrombotic risk in PV patients.

No correlation of intensity of phlebotomy regimen with risk of thrombosis in polycythemia vera: evidence from European Collaboration on Low-Dose Aspirin in Polycythemia Vera and Cytoreductive Therapy in Polycythemia Vera clinical trials | Haematologi

 

[Stewie]

I agree with you that if platelets aren't elevated and Hematocrit isn't too high (<53), then phlebotomies may not be necessary.
But to my knowledge phlebotomies do not increase the risk of thrombosis. That conclusion was based on an observational study leading to issues with selection bias. A more recent paper looked for evidence from randomized clinical trials and found no correlation between the number of phlebotomies per year and the risk of thrombosis.


No correlation of intensity of phlebotomy regimen with risk of thrombosis in polycythemia vera: evidence from European Collaboration on Low-Dose Aspirin in Polycythemia Vera and Cytoreductive Therapy in Polycythemia Vera clinical trials | Haematologi

Hey, Jeff.

Sadly enough we can't extrapolate this design of those with a neoplastic disease vs those without. Moreso, the patients were also given the drug Hydroxycarbamide in which suppresses bone marrow production of blood cells.

It's an interesting observation nonetheless, yet this isn't applicable of a comparison value.

 

[Massive G]

Hey, Jeff.

Sadly enough we can't extrapolate this design of those with a neoplastic disease vs those without. Moreso, the patients were also given the drug Hydroxycarbamide in which suppresses bone marrow production of blood cells.

It's an interesting observation nonetheless, yet this isn't applicable of a comparison value.

I have seen 3 hematologists in the past 15 years currently get drained if hemo goes over 55. Said I am a big guy and that's a safe level for me.
He also mentioned the risk of problems from pulling off too much blood too quickly -he see's a few bodybuilders -ironically a few are women, but his maiin area of focus in hematology is PCV and hemochromatosis.

 

[MyNameIsJeff]

Hey, Jeff.

Sadly enough we can't extrapolate this design of those with a neoplastic disease vs those without. Moreso, the patients were also given the drug Hydroxycarbamide in which suppresses bone marrow production of blood cells.

It's an interesting observation nonetheless, yet this isn't applicable of a comparison value.

Thanks, I feared it would not be applicable to secondary polycythemia.
Upon further reading, it seems that the Hydroxyurea may prevent a possible post-phlebotomy enhancement in platelet production, thereby preventing thrombotic events. So in anyone not taking that drug, there may well be a negative effect due to increased platelet production.
Though this seems more of a theoretical consideration, I have not found any empirical evidence showing abnormal platelet levels post-phlebotomy. Still, enough evidence to 1) limit phlebotomies to serious cases, 2) monitor platelets, and 3) take low dose aspirin if you blood let.

 

[G.I.Bro]

Guys, this blood letting discussion is cool and all, but my HDL is fucking 8. I'm going to die, k.... I need to select someone here who I can reveal my real life identity to so they can alert the board of my untimely passing (and inherit by juice stash).

[emoji6]

 

[Elvia1023]

Guys, this blood letting discussion is cool and all, but my HDL is fucking 8. I'm going to die, k.... I need to select someone here who I can reveal my real life identity to so they can alert the board of my untimely passing (and inherit by juice stash).

[emoji6]

Hey I may have you beaten. I usually get blood tests done very frequently but haven't for a few months. I am sure my HDL was feeling much better about himself (not sure why it is a him but just go with it) then I started tbol last week so I imagine now he will be at about 8 and steadily declining. I should note everything else is always good and my HS-CRP was I think 0.1 and 0.3 the last 2 times. My HCT has been high in the past but the last 10 or so blood tests it's been in range and I have never given blood. The moment I touch orals but HDL goes to practically zero. I have just checked my platelet count for my last 5 blood tests and everytime it was low. It ranged from 193 to 240 with the last 2 tests being the lowest. So it looks like (fingers crossed) I won't drop dead either but if I do you guys can have a raffle for my aas stash as I have some good stuff. You can have a separate raffle for my pre workout supply

Great thread Knight. I don't really have anything to add but it was a good read and thanks for taking the time to post it. The IFG-1 and MK result was very good. I am actually a fan of tamox during cycles and have looked into torem for the reason mentioned above but never botthered just because I can get nolva and arom so easily. Rex's last post has actually motivated me to give it a go as it seems to have all of tamox's benefits without that 1 possible negative.

 

[MR. BMJ]

Yea, this is turning into a classic thread, Knight...Good job man, et al:headbang:

See GotGame looking at it too below

...and thanks for the reply, Rex!