Adding mast to cruise?

[Mr.BB]

Yes, about 30 plus years of literature.

Ok. Thought you were older

[cousinmuscles]

Only if the lipids are causing systemic inflammation.

True, while you're correct with the argument and we do know other factors esp sugar cause inflammation, it's documented ex AAS users have hardened arteries... Despite not having perfect control over exactly what they did we do have a little data
https://www.ncbi.nlm.nih.gov/pubmed/17085981

But enter this situation: would you live the rest of your years with tanked HDL (lessened ability to clean arteries, AFAIK only a rat study showed there is a possibility of doing so with low HDL but everything else showing correlation low HDL = higher risk) and high LDL, knowing how it will amplify risks?

[Couchlockd]

You can do whatever you want, but the purpose of cruising is to let your body and organs stabilize in normal levels to avoid health problems.

Drostanolone is one of harshest compounds on blood lipids and RBC production. Even on small doses it will significantly drop your hdl, and increase your hematocrit.

is mast really as bad as say oxandrolone?

I picked up mast based on our front pages profile saying it was one of the mildest interns of side effects after primo.

[Bigbadwolf250]

Curious to see what happens. Hear some guys say 100mg a week on cruise made then feel so much better while others say it needs to be run at higher doses

[Mr.BB]

is mast really as bad as say oxandrolone?

I picked up mast based on our front pages profile saying it was one of the mildest interns of side effects after primo.

In my opinion? Yes. Anavar has other problems like liver toxicity.

But only my opinion. HDL and hematocrit have problems when I take mast.

[Mr.BB]

very unlikely that cruising on a small dosage of Masteron for a couple months is going to have any negative impact

This is just wrong to say. Its like saying smoking for a couple of months is not going to have any negative impact.

[GearHeaded]

This is just wrong to say. Its like saying smoking for a couple of months is not going to have any negative impact.

"negative impact" in the context that i stated, ie., hardening your blood vessels. very unlikely that Mast itself is going to directly cause this from cruising on a small dosage for a short time.

if you think it is , fine be a fear monger and don't run AAS yourself, but don't tell someone else its going to cause all these negative health issues without proof. and there is no proof that a low dose of Mast for a short time is going to directly cause heart disease

[Charlie67]

I'm at 600 mast e (up,from 400) and 300 test e (down from 500) and I feel better at 600 Mast & 300 test than I did at 400 mast & 500 test.

Was there something specific that made you change the dosage of each? Were you trying to fix something? Or did you just decide to make a change and it worked out? I'm on a similar cycle, so i was just curious.

Best,
C-

[Couchlockd]

Was there something specific that made you change the dosage of each? Were you trying to fix something? Or did you just decide to make a change and it worked out? I'm on a similar cycle, so i was just curious.

Best,
C-

I was playing with TEST base daily for 6 weeks on top of 500 test e. completely fucked up my estrogen levels, went through the roof.

got gyno symptoms, and such.

so,I backed it down a bit.

[Mr.BB]

"negative impact" in the context that i stated, ie., hardening your blood vessels. very unlikely that Mast itself is going to directly cause this from cruising on a small dosage for a short time.

if you think it is , fine be a fear monger and don't run AAS yourself, but don't tell someone else its going to cause all these negative health issues without proof. and there is no proof that a low dose of Mast for a short time is going to directly cause heart disease

Nobody is saying that low dose of anything is going to directly cause heart disease, why are you distorting the conversation? And please stop the name calling, I dont know what is a fear monger, but calling a user this kind of names will inflame the thread, and the discussion will gain nothing. And I dont accept you commenting on what AAS I take or dont take it is nothing of your business, and again of this discussion.

As to masteron causing hyperlipidemia, of course it does:

"After 1 to 3 months, six patients developed marked but reversible hypertriglyceridemia."
(from: https://academic.oup.com/ajcn/articl...dFrom=fulltext)

It is also clearly mentioned on the PubChem database: "Insulin resistance with a fall in glucose tolerance, and hypercholesterolemia with a fall in high density lipoprotein cholesterol, have been reported."
(from: https://pubchem.ncbi.nlm.nih.gov/com...xicity-Summary)

[Bigbadwolf250]

Prob all in my head but pinned 35 mgs of mast last night along with my test and holy shit am I a horny bastard today

[cousinmuscles]

Ex football players, Ex construction workers, Ex lawyers, Ex etc etc.. people have hardened arteries as well. and its not documented that any one of these people, including the ex AAS users, ever even used Masteron .

things like hardened arteries happen to people mainly from genetics, and adding in diet and lifestyle choices over a long period of years. very unlikely that cruising on a small dosage of Masteron for a couple months is going to have any negative impact

Show some respect when you reply to people, read both the reference and do not cut out bits you only want seen.

The study shows the ex steroid abusers had much more damage to their CV system than average.

You are clearly avoiding the important point I made about lipids and keeping them in range.

The idea of cruising on something that will keep lipids wrecked is reckless, suggesting it in an open forum as if it won't be harmful is highly immoral.

[hammerheart]

Nobody is saying that low dose of anything is going to directly cause heart disease, why are you distorting the conversation? And please stop the name calling, I dont know what is a fear monger, but calling a user this kind of names will inflame the thread, and the discussion will gain nothing. And I dont accept you commenting on what AAS I take or dont take it is nothing of your business, and again of this discussion.

As to masteron causing hyperlipidemia, of course it does:

"After 1 to 3 months, six patients developed marked but reversible hypertriglyceridemia."
(from: https://academic.oup.com/ajcn/articl...dFrom=fulltext)

It is also clearly mentioned on the PubChem database: "Insulin resistance with a fall in glucose tolerance, and hypercholesterolemia with a fall in high density lipoprotein cholesterol, have been reported."
(from: https://pubchem.ncbi.nlm.nih.gov/com...xicity-Summary)

Hey, it might help with my trys being actually too low lol

[MuscleScience]

Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.

Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review | BMJ Open

Ok. Thought you were older

It’s all there for you to read, last time I posted studies you dismissed them all out of hand.

And besides, I was teasing cousins a bit. We’ve been going back and forth on this over pm for a long while

True, while you're correct with the argument and we do know other factors esp sugar cause inflammation, it's documented ex AAS users have hardened arteries... Despite not having perfect control over exactly what they did we do have a little data
https://www.ncbi.nlm.nih.gov/pubmed/17085981

But enter this situation: would you live the rest of your years with tanked HDL (lessened ability to clean arteries, AFAIK only a rat study showed there is a possibility of doing so with low HDL but everything else showing correlation low HDL = higher risk) and high LDL, knowing how it will amplify risks?

To me, as long as my inflammatory markers and blood Glucose and A1c are all low, i would be fine with lower HDL and LDL. One thing that is missed and forgot about. When a cell is inflamed and swelling outside of enzymes and other things it’s also leaking of what? Cholesterol!

Every single cell wall is composed of the stuff. If you have high systemic inflammation for any number of things, let’s say chronically high blood glucose. You will get an increase in circulating cholesterol. This is well know, it’s even used as a marker for over training syndromes in athletes when coupled with increase in CK and Troponin levels. High circulating cholesterol levels is a symptom not the singular cause of athlosclerosos. At least in my very humble opinion

[cousinmuscles]

Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.

Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review | BMJ Open





It’s all there for you to read, last time I posted studies you dismissed them all out of hand.

And besides, I was teasing cousins a bit. We’ve been going back and forth on this over pm for a long while



To me, as long as my inflammatory markers and blood Glucose and A1c are all low, i would be fine with lower HDL and LDL. One thing that is missed and forgot about. When a cell is inflamed and swelling outside of enzymes and other things it’s also leaking of what? Cholesterol!

Every single cell wall is composed of the stuff. If you have high systemic inflammation for any number of things, let’s say chronically high blood glucose. You will get an increase in circulating cholesterol. This is well know, it’s even used as a marker for over training syndromes in athletes when coupled with increase in CK and Troponin levels. High circulating cholesterol levels is a symptom not the singular cause of athlosclerosos. At least in my very humble opinion

I'm a believer of maintaining a healthy lifestyle first and foremost - but we do know why we need HDL to reverse buildup. Nice study and convincing but still not convinced it is at any way safe to assume bad lipid profile for extended periods is OK, unfortunately most AAS wreck the good lipoproteins too. The study mentions LDL not HDL though I get it, you can have more cholesterol and LDL, as long as there isn't inflammation there isn't much to worry about.

[hammerheart]

I just ate six eggs for breakfast. Am I going to die?

[cousinmuscles]

I just ate six eggs for breakfast. Am I going to die?

Almost out of sand in the sand timer glass...

MS from what I have in my bookmarks it is not about any single lipid marker but ratios and the combination of TC and ratios...

[Mr.BB]

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review | BMJ Open

It’s all there for you to read, last time I posted studies you dismissed them all out of hand.

Come on, I told no Dr. Lard lol, this makes it too easy.

You say I dismissed the studies you posted, in fact, its not me who dismissed it, its their own medical peers.
If you read medical studies for 30 years, as you have said before, you know that there is always peer reviews and only when a document is reviewed by peers, and it shows to be truthful, unbiased and well designed, it is considered viable to its conlcusion to become guidelines or, change current situations.

There are several problems with the study you posted, I will just post the conclusion of the CEBM review, if you want you can go read the whole document and check all the flaws found on it:

Conclusions
There are a number of studies that seek to explore associations between LDL-C and mortality in samples of elderly people from the general population, despite a known positive association with cardiovascular disease. Given its significance, there is some justification for a rigorous and systematic review of the available literature related to cholesterol and mortality in the elderly.

Ravnskov and colleagues attempt to provide such a review. However there are serious methodological flaws with their study, not least the lack of a published protocol, searching of only one database, nonuniform application of inclusion/exclusion criteria, a lack of critical appraisal of the methods used in the included studies, no indication of the quality or uncertainty of the included data and issues with the accuracy of data extraction. A lack of controlling for confounding due to the effect of lipid-lowering treatment and HDL-C levels presents major bias and more likely underpins the majority of the observed inverse associations.

Given that the authors failed to account for this significant confounding as well as the methodological weaknesses of both the review and its included studies, the results of this review have limited validity and should be interpreted with utmost caution. At this time it would not be responsible, or evidence-based, for policy decisions to be made based on the results of this study.

(full text: CEBM response: “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review” – a post publication peer review)

[Mr.BB]

I just ate six eggs for breakfast. Am I going to die?

Probably, you and anyone else around you, if you fart.

[MuscleScience]

Come on, I told no Dr. Lard lol, this makes it too easy.

You say I dismissed the studies you posted, in fact, its not me who dismissed it, its their own medical peers.
If you read medical studies for 30 years, as you have said before, you know that there is always peer reviews and only when a document is reviewed by peers, and it shows to be truthful, unbiased and well designed, it is considered viable to its conlcusion to become guidelines or, change current situations.

There are several problems with the study you posted, I will just post the conclusion of the CEBM review, if you want you can go read the whole document and check all the flaws found on it:

Conclusions
There are a number of studies that seek to explore associations between LDL-C and mortality in samples of elderly people from the general population, despite a known positive association with cardiovascular disease. Given its significance, there is some justification for a rigorous and systematic review of the available literature related to cholesterol and mortality in the elderly.

Ravnskov and colleagues attempt to provide such a review. However there are serious methodological flaws with their study, not least the lack of a published protocol, searching of only one database, nonuniform application of inclusion/exclusion criteria, a lack of critical appraisal of the methods used in the included studies, no indication of the quality or uncertainty of the included data and issues with the accuracy of data extraction. A lack of controlling for confounding due to the effect of lipid-lowering treatment and HDL-C levels presents major bias and more likely underpins the majority of the observed inverse associations.

Given that the authors failed to account for this significant confounding as well as the methodological weaknesses of both the review and its included studies, the results of this review have limited validity and should be interpreted with utmost caution. At this time it would not be responsible, or evidence-based, for policy decisions to be made based on the results of this study.

(full text: CEBM response: “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review” – a post publication peer review)

I guess I keep forgetting to go back and look at the epidemiological data that shows CVD and obesity has decreased drastically since the recommendation of the low fat/low cholesterol diet. Coupled with the use of statin drugs. Who could POSSIBLE argue with all the improvements that have been made. All that other evidence is pseudoscience and the cholesterol link is fact and not hypothesis at this point. :

[DarthFlex]

Statins have been revealed as bunk meds. Right?

[DarthFlex]

https://www.google.com/search?q=doct...TV7rXgBQ_0:878