PROOF? You Decide.

[ceo]

Bro, this is BEFORE I EVER USED STEROIDS.

I TESTED 1850 at 20 years old NATURAL bro, I didn't TOUCH anabolics until I was 21.

What happened between 20 and 21 to cause your very high natural test levels to drop so low that you needed to supplement with anabolics?

 

[Ross]

What happened between 20 and 21 to cause your very high natural test levels to drop so low that you needed to supplement with anabolics?

When I turned 21, I decided I wanted to take my physique to the next level.

My first 2 cycles were 30mgs Anavar ED for 4 weeks. I didn't use Testosterone until I was 23 years old.

 

[njmuscleguy]

Nelson,

I get what you're saying about free test and the merits of Unleashed (via reducing SHBG).

You're also saying that it's wise to help the body maintain *some* natural test production while administering exogenous test. So aside from running a low dosage (or the lowest dosage necessary), are you suggesting anything else to do this? The only other way I can think of is by running a very low dosage of HCG every week.

And just for reference, I've been on HRT for almost 2 years now.

100mg (injectable) test puts me in the 900 range - I feel "ok" on this dosage, not great
50mg (injectable) test puts me in the 500-600 range - I feel like crap on this dosage
A 5g dosage of androgel also puts me in the 500 range - Feel ok on this dosage (probably due to greater DHT conversion)

 

[Nelson Montana]

Nelson,

I get what you're saying about free test and the merits of Unleashed (via reducing SHBG).

You're also saying that it's wise to help the body maintain *some* natural test production while administering exogenous test. So aside from running a low dosage (or the lowest dosage necessary), are you suggesting anything else to do this? The only other way I can think of is by running a very low dosage of HCG every week.

And just for reference, I've been on HRT for almost 2 years now.

100mg (injectable) test puts me in the 900 range - I feel "ok" on this dosage, not great
50mg (injectable) test puts me in the 500-600 range - I feel like crap on this dosage
A 5g dosage of androgel also puts me in the 500 range - Feel ok on this dosage (probably due to greater DHT conversion)

HCG does nothing to maintain T production. HCG SIMULATES LH excretion, which is a great way to get your balls up and running and give them a head start in taking over for themselves, but (here we go again) if they have "nothing to do" what's the point?

I AM NOT an advocate of using HCG every week, either on cycle or on HRT. It should be an occasional "boost" and that's all.

Ross, if you've been using anabolics since you're 21 how in the world can you talk about making natural gains, or maintaining high levels or using supps to gain an advantage? Fuck, I didn't use anabolics until I was 41! I went from age 36 at a scrawny 150 pounds to a 180 pound body model at age 38 NATURALLY -- with my training and supplement techniques. You had a T level of 1850 and went on gear a year later? Dude, get your stories straight.

 

[njmuscleguy]

HCG does nothing to maintain T production. HCG SIMULATES LH excretion, which is a great way to get your balls up and running and give them a head start in taking over for themselves, but (here we go again) if they have "nothing to do" what's the point?

I AM NOT an advocate of using HCG every week, either on cycle or on HRT. It should be an occasional "boost" and that's all.

Yes, HCG doesn't directly boost test, but keeps the boys primed... or to put it another way, prevents total testicular shutdown.

So back to my original question then... what do you recommend to keep your body's natural test production going, other than maintaining a low exogenous test dosage.

 

[Ross]

HCG does nothing to maintain T production. HCG SIMULATES LH excretion, which is a great way to get your balls up and running and give them a head start in taking over for themselves, but (here we go again) if they have "nothing to do" what's the point?

I AM NOT an advocate of using HCG every week, either on cycle or on HRT. It should be an occasional "boost" and that's all.

Ross, if you've been using anabolics since you're 21 how in the world can you talk about making natural gains, or maintaining high levels or using supps to gain an advantage? Fuck, I didn't use anabolics until I was 41! I went from age 36 at a scrawny 150 pounds to a 180 pound body model at age 38 NATURALLY -- with my training and supplement techniques. You had a T level of 1850 and went on gear a year later? Dude, get your stories straight.

Bro, I am only 25.

When I decided I wanted to juice after my 21st B-day, I wanted to have my Testosterone level checked. At 20 years old, my level was 1850.

 

[alphatest]

Yes, HCG doesn't directly boost test, but keeps the boys primed... or to put it another way, prevents total testicular shutdown.

So back to my original question then... what do you recommend to keep your body's natural test production going, other than maintaining a low exogenous test dosage.

Maybe Nelson can clear this up. If 100mg is just as suppressive to LH and FSH as 300mg it would appear that there is no way to maintain any sort of "natural" test production while on. Restoring a suppressed system is probably more of a function of time on, then dosage (at least once you get above 100mg per week).

 

[muscleup]

Yes TIME...With time anyone can recover from ANY cycle...As long as those people do not have a pre-exisiting condition that will lead them to primary hypogonadism.

Maybe Nelson can clear this up. If 100mg is just as suppressive to LH and FSH as 300mg it would appear that there is no way to maintain any sort of "natural" test production while on. Restoring a suppressed system is probably more of a function of time on, then dosage (at least once you get above 100mg per week).

 

[njmuscleguy]

But there is no "recovering" for (most) people on HRT... so time isn't the answer according to what Nelson was saying about maintaining natural test production along with exogenous test supplementation. So initially he said that keeping HRT dosage low will help in this endeavor... just curious if he suggests anything else.

I'm not saying I'm convinced either way, I'm no expert and I haven't seen any studies proving or disproving... what I know is that when I'm on test, even minimal HRT dosages, my LH and FSH are practically zero if not zero... so I'm guessing that my body isn't doing much in the way of test production while on HRT.

 

[Tatyana]

Granted, 1850 is insanely high, I have great genetics indeed. Many 19-21 year olds will test that high though, which is why it is TRUE that teenagers don't need steroids!

I think this is something a lot of people overlook.

Personally, I don't think that taking advice from the 'genetic freaks' is always the best idea.

Genetic freaks can usually eat or train or eat any sort of diet and still put on muscle.

Those comments, 'well Jay/Ronnie/Flex did it this way', completely irrelevant to the majority of the population.

I have come to realise that the best advice and knowledge are from those who:

1. Are hardgainers/ectomorphs, have had to work hard to put on muscle (I think women are also in this category as well )

2. Have pushed their physique to the max nattie, and then used or kept it nattie



This is an example of how you would post scientific papers on the internet so that people can actually find them and check out the original source themselves.

If you notice, aspirin doesn't work on everyone, so claims that some herbs can replace steroids is a bit over the top.

I also included the introduction as I thought it was interesting.

http://www.bmj.com/cgi/content/full...in&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

BMJ 2008;336:195-198 (26 January), doi:10.1136/bmj.39430.529549.BE (published 17 January 2008)

Research

Aspirin "resistance" and risk of cardiovascular morbidity: systematic review and meta-analysis

George Krasopoulos, cardiovascular surgery fellow1, Stephanie J Brister, associate professor1, W Scott Beattie, R Fraser Elliot chair in cardiac anaesthesia2, Michael R Buchanan, professor3

1 University Health Network, Division of Cardiovascular Surgery, Toronto General Hospital, 2 University Health Network, Department of Anaesthesiology, Toronto General Hospital, 3 McMaster University, Department of Pathology and Molecular Medicine, Hamilton, ON, Canada L8S 4L8

Correspondence to: M R Buchanan [email protected]


Objective To determine if there is a relation between aspirin "resistance" and clinical outcomes in patients with cardiovascular disease.
Design Systematic review and meta-analysis.

Data source Electronic literature search without language restrictions of four databases and hand search of bibliographies for other relevant articles.

Review methods Inclusion criteria included a test for platelet responsiveness and clinical outcomes. Aspirin resistance was assessed, using a variety of platelet function assays.

Results 20 studies totalling 2930 patients with cardiovascular disease were identified. Most studies used aspirin regimens, ranging from 75-325 mg daily, and six studies included adjunct antiplatelet therapy. Compliance was confirmed directly in 14 studies and by telephone or interviews in three. Information was insufficient to assess compliance in three studies. Overall, 810 patients (28%) were classified as aspirin resistant. A cardiovascular related event occurred in 41% of patients (odds ratio 3.85, 95% confidence interval 3.08 to 4.80), death in 5.7% (5.99, 2.28 to 15.72), and an acute coronary syndrome in 39.4% (4.06, 2.96 to 5.56). Aspirin resistant patients did not benefit from other antiplatelet treatment.

Conclusion Patients who are resistant to aspirin are at a greater risk of clinically important cardiovascular morbidity long term than patients who are sensitive to aspirin.





There is no debate that long term aspirin use attenuates the risks of myocardial infarction, stroke, and vascular related deaths in patients with cardiovascular disease,1 but a significant number of patients prescribed aspirin as antithrombotic therapy have major adverse vascular related events each year.2 Consequently other antiplatelet agents in addition to aspirin have been prescribed for certain patients.w16-w20

The major controversy about aspirin therapy is why particular patients do not benefit from such therapy and how they might be identified. It has been suggested that some patients require a higher dose of aspirin than is normally recommended to achieve the expected antiplatelet effect—for example, inhibition of platelet function or inhibition of platelet thromboxane A2 synthesis.3456 w10 It is unclear whether these patients simply receive too low an aspirin dose, are not compliant, have differing abilities to absorb aspirin, or have an underlying genetic disposition that renders aspirin ineffective.2 7891011 Such patients have been labelled aspirin "resistant"—that is, their platelets are not affected in the same way or are affected differently from the platelets of those who seem to benefit from aspirin therapy (aspirin "sensitive" patients with no subsequent adverse cardiovascular event).121314151617 w1 w4-w9 w11-w13 Little consistency exists about which measure should be used to identify patients who seem resistant to aspirin.121314151617 w1 w4-w9 w11-w13 Also, few studies have assessed the effect of aspirin resistance on clinically important outcomes.

We systematically reviewed studies of aspirin resistance and its effect on adverse cardiovascular outcomes. We hypothesised that aspirin resistance is real and is clinically relevant—that is, it significantly affects the risk of cardiovascular, cerebrovascular, and vascular related events.11 w6