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Hi fellas,
I have been trying to read some of the old posts but did not find anything related to the use of both LR3 IGF and slin together.
Most of you say to take slin for 4 weeks and then jump on the IGF for another 4 weeks....
My question is ( and this is only for the sake of learning) why are you not supposed to take both together for 4 weeks straight? What would happen if you did?
Thanks
Who made the rule you aren't supposed to take slin and LR3 IGF-1 together?
There are posts around where guys ran both concurrently.In fact I'll be doing just that next week.So whoever started that rule better come an arrest me,because I'm violating it.
~Pinnacle~
Quote:
Originally Posted by Pinnacle
lol
Yes, a remember a while back seeing posts of peaople running them together. I could not find them when I searched earlier. In any case most people here say to use 4 weeks of slin, then 4 weeks of IGF, then 4 weeks slin.....
Pinnacle, if you run them together how would you do that? If you use them both PWO, do you mix them together in the same syringe or do you take two different shots?
Thanks
Quote:
Originally Posted by warlock
eyyyyyyy both are
hypotrend (R) :owned:
take at separate moments.(same day, of course)
Thanks. I need to read and learn more about how to take them together.Quote:
Originally Posted by oswaldosalcedo
So, you would take one in the morning and one PWO?
Thanks
I train twice daily...so here's what I'm going to do...Quote:
Originally Posted by warlock
AM PWO shot(40 mcgs IGF/7 iu's slin)(same pin)<<<<4 iu's HGH(seperate pin)
Afternoon(2 pm) IGF shot 20 mcgs,4 iu's HGH also.(Different pins)
PM PWO shot(40 mcgs IGF/7 iu's slin)(same pin)
Off days..No slin....but same protocol for IGF and HGH(timing wise).
~Pinnacle~
Thanks Pinnacle.Quote:
Originally Posted by Pinnacle
So, you can take both IGF and slin together in the same pin. It's good to know.
I appreciate your replies
congrats, you are risky.Quote:
Originally Posted by Pinnacle
i see, you lower the insulin and the igf.
i use 10 ius slin, anyway i think can be dangerous.
see:
jay thread
http://forums.steroid.com/igf-1-lr3-hgh-insulin-questions/177345-slin-sides-any-advice.html
and
G-Force thread
http://forums.steroid.com/igf-1-lr3-hgh-insulin-questions/201722-think-i-went-hypo-other-night.html
Why do shoot the Afternoon shot in different pins?Quote:
Originally Posted by Pinnacle
goose4....
I read those threads already.Jays thread is 500 years old and I posted that thread in G' thread.Quote:
Originally Posted by oswaldosalcedo
How much more dangerous can it be from doing a Keto diet like you do on slin?I'll be taking in proper amounts of carbs.And meals will be timed perfect as well.
7 iu's with 40 mcgs IGF is nothing bro...shezzzz....
I'll do them together when I feel more confident in not making an error dose wise.It's an old habit of being precise with measurements.Quote:
Originally Posted by goose4
i always advocate to run them after each other for the following reasons:Quote:
Originally Posted by Pinnacle
-igf-1 increases insulin sensetivity and thus a greater risk of going hypo.this can be taken care of if you take in proper amount of dex and are educated enough to know what your doing(wich you should)
-by running them after each other you have an powerfull anabolic substance in your body for a prolonged period of time.
-when run together you will make faster gains then either one alone but if you take a look in the long haul then you prob gonna make more gains by running them after each other due to aboved mentioned reason.
i've tried both ways and i really believe in running them separetly.
-rodge
You know me Rodge...nothing exceeds like access!
Seriously though,I'll cycle them independently,that's the most logical way.But I just need to try this.Can't help myself brother.
~Pinnacle~
Quote:
Originally Posted by Pinnacle
yes i see,you lowered slin.
you have crushed, another contetion from brotelligence at worst.
(never use in same cycle, igf and slin..........congrats) .........lol..............
Here's something to add to the mix, I wish we had some on humans, but for now this is all we have
Insulin-like growth factor-I and more potent variants restore growth of diabetic rats without inducing all characteristic insulin effects.
Tomas FM, Knowles SE, Owens PC, Chandler CS, Francis GL, Ballard FJ
Cooperative Research Centre for Tissue Growth and Repair, Adelaide, Australia.
The effects of graded doses of insulin-like growth factor-I (IGF-I) and two variants which bind poorly to IGF-binding proteins were investigated in 160 g streptozotocin-induced diabetic rats. The two variants were the truncated form, des(1-3)IGF-I, and another with arginine at residue 3 and an N-terminal extension, termed LR3-IGF-I. The peptides were infused via mini-osmotic pumps. Reference groups received either vehicle or insulin (30 i.u. per day). Treatment led to a marked dose-dependent increase in growth rate and nitrogen balance. The highest dose (695 micrograms/day) of IGF-I increased body weight by 48.1 +/- 1.7 g/7 days, compared with 11.0 +/- 2.8 g/7 days for the vehicle-treated group. The two variants were 2.5-3 times more potent than IGF-I in restoring growth. The insulin-treated group gained more weight (64.5 +/- 1.6 g/7 days), but the added gain was fat (92.5 +/- 4.8 g of fat/kg carcass wet wt., compared with 32.2 +/- 2.1 for all other groups) rather than protein. [u]All peptides increased muscle protein-synthesis rates and RNA levels by up to 50%, with IGF-I the least potent. These high doses of IGFs did not decrease either the glucosuria or the daily excretion rate of N tau-methyl-histidine (N tau-MH). On the other hand, insulin treatment markedly decreased both glucosuria (from 82.7 +/- 5.4 to 4.5 +/- 3.3 mmol/day) and N tau-MH excretion (from 9.3 +/- 0.3 to 7.1 +/- 0.4 mumol/day per kg). This experiment shows that, although IGF-I and variants can restore growth in diabetic rats, other insulin-dependent metabolic processes in liver, muscle and adipose tissue are not restored.
The fat gains with slin treated is a bit scary, but I'd like to know how it would effect none insulin dependent subjects if at all.
JohnnyB
that study is from 1993.
(Biochem. J. (1993) 291, 781-786)
if you substract the fat from the gain for LR3 and SLIN are almost the same.
AGENT: GR PROT CARCASS ANIMALS (Rats):
INSULIN------------192
IGF1---------------206
DES IGF1-----------207
LR3----------------211
NO BIG DIFFERENCE WITH SLIN.
------------------------------------------
AND FOR LR3 STUDIES DONE IN HUMANS:
Dear Mr. Salcedo,
In reply to your question, there are no studies (LR3) in man to the best of my knowledge. Some of the IGF-I analogues have been found to be potent mitogens. What is the reason you asked? Do you have any patients?
We are at present performing a worldwide survey on the prevalence of malignancy in patients with IGF-I deficiency and their family relatives. If you see or know such patients I would appreciate your cooperation in providing us data on a simple questionnaire.
Please reply and we shall send you further details.
Best regards,
Zvi Laron, MD
_______________________
Prof. Zvi Laron
Endocrinology and Diabetes Research Unit,
Schneider Children's Medical Center
Petah-Tikva 49202
Israel
Fax: 972-3-9222996
--------------------------------------------------
he is one of the world leaders in igf 1 studies.
.
LR3 was made in 1992
I'm not understanding what the date it was performed, has to do with information in it. It's posted for informational reasons, we don't even know if this would happen in humans. It's just posted to give another possibility, but without human studies, we don't know for sure if this would happen or not in humans. It could be done on humans and turn out worst then this, but without any human studies we don't know what will happen.
So it's posted as a possibility to what could happen, one more thing to consider. I wish we has access to human studies with LR3, but I have yet to find one. There are plenty done with rhIGF-1, but they're not the same so they don't apply. LR3 has 13 amino acids more then rhIGF-1, with the structure being different, the results can be different as well.
JohnnyB
Do you have access to his studies? It says he is the leader in studies on humans with IGF-1, I'm looking for studies done with LR3 IGF-1, not IGF-1. There is a differance, that is why I like calling it LR3, instead of IGF-1. There are plenty of studies in IGF-1 in humans, but I've yet to see any done on humans with LR3 IGF-1. So if you have some I'd love to read them.Quote:
Originally Posted by oswaldosalcedo
JohnnyB
..........................................
Mech Ageing Dev. 2005 Feb;126(2):305-7.
Do deficiencies in growth hormone and insulin-like growth factor-1 (IGF-1) shorten or prolong longevity?
Laron Z.
Endocrinology and Diabetes Research Unit, Schneider Children's Medical Center, WHO Collaborating Center for the Study of Diabetes in Youth, Tel Aviv University, Tel Aviv, Israel.
Present knowledge on the effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I) deficiency on aging and lifespan are controversial. Studying untreated patients with either isolated GH deficiency due to GH gene deletion, patients with multiple pituitary hormone deficiency due to PROP-1 gene mutation and patients with isolated IGF-I deficiency due to deletions or mutations of the GH receptor gene (Laron syndrome); it was found, that these patients despite signs of early aging (wrinkled skin, obesity, insulin resistance and osteopenia) have a long life span reaching ages of 80-90 years. Animal models of genetic GH deficiencies such as Snell mice (Pit-1 gene mutations) the Ames mice (PROP-1 gene mutation) and the Laron mice (GH receptor gene knock-out) have a statistically significant higher longevity compared to normal controls. On the contrary, mice transgenic for GH and acromegalic patients secreting high amounts of GH have premature death. Those data raise the question whether pharmacological GH administration to adults is deleterious, in contrast to policies advocating such therapies.
Rev Endocr Metab Disord. 2002 Dec;3(4):347-55.
Growth hormone insensitivity (Laron syndrome).
Laron Z.
Bro we're not talking about the samething, I'm talking about LR3 IGF-1, not the results of HGH use on IGF-1 levels.
IGF-1 is not LR3 IGF-1, I know people call it IGF-1. That's where the confusion comes in, you are trying to apply a study done with HGH and it's results on IGF-1 levels. That has nothing to do with LR3 IGF-1. LR3 IGF-1 is an anolog of rhIGF-1, but they are not the same, nor is IGF-1 elevated by the use of HGH.
JohnnyB
sure ? ...lol.......... oh sorry i am deadly wrong .........lol.......
i just posted to point out dr laron works.
and for LR3 studies i asked him and he answered me:
Dear Mr. Salcedo,In reply to your question, there are no studies (LR3) in man to the best of my knowledge. Some of the IGF-I analogues have been found to be potent mitogens. What is the reason you asked? Do you have any patients?
We are at present performing a worldwide survey on the prevalence of malignancy in patients with IGF-I deficiency and their family relatives. If you see or know such patients I would appreciate your cooperation in providing us data on a simple questionnaire.
Please reply and we shall send you further details.
Best regards,
Zvi Laron, MD
_______________________
Prof. Zvi Laron
Endocrinology and Diabetes Research Unit,
Schneider Children's Medical Center
Petah-Tikva 49202
Israel.
god ! the moderators dont read relevant posts !Quote:
Originally Posted by JohnnyB
see:
The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 11 5221-5226
2003, by The Endocrine Society.
"High Dose Growth Hormone Exerts an Anabolic Effect at Rest and during Exercise in Endurance-Trained Athletes
M. L. Healy, J. Gibney, D. L. Russell-Jones, C. Pentecost, P. Croos, P. H. Sönksen and A. M. Umpleby
Department of Diabetes and Endocrinology, GKT School of Medicine, St. Thomas Hospital, London, United
r-hGH-treated
------------------ Baseline --------- 1wk-----------4 wk--------- /Placebo-
IGF-I (nmol/liter) 24.6 ± 3.0 / 89.6 ± 12.21-- 106.3 ± 16.41/ 25.8 ± 2.7-- 25.4 ± 2.7-- 25.2 ± 2.6
fT3 (pmol/liter) 5.1 ± 0.3 6.0 ± 0.12 6.1 ± 0.22 4.8 ± 0.2 4.9 ± 0.2 4.8 ± 0.1
fT4 (pmol/liter) 15.5 ± 1.5 11.5 ± 1.02 10.6 ± 0.92 15.8 ± 1.6 15.6 ± 1.7 15.8 ± 1.5
Testosterone (nmol/liter) 18.3 ± 3.2 18.5 ± 3.4 18.5 ± 3.3 16.7 ± 2.6 16.3 ± 2.6 16.4 ± 2.2
Glucose (mmol/liter) 4.7 ± 0.3 5.5 ± 0.5 5.3 ± 0.2 4.5 ± 0.4 4.2 ± 0.2 4.4 ± 0.3
Insulin (mU/liter) 7.9 ± 1.6 22.6 ± 3.92 16.0 ± 9.32 6.0 ± 0.3 5.6 ± 1.9 9.3 ± 2.4
HOMA IR 1.4 ± 0.2 5.1 ± 1.02 3.3 ± 0.62 1.1 ± 0.4 1.0 ± 0.3 1.6 ± 0.5
Total cholesterol (mmol/liter) 4.3 ± 0.3 4.0 ± 0.5 4.1 ± 0.3 3.4 ± 0.3 3.3 ± 0.3 3.5 ± 0.6
Triglyceride 1.1 ± 0.2 2.0 ± 0.5 1.3 ± 0.1 0.6 ± 0.1 0.7 ± 0.1 0.5 ± 0.1
LDL cholesterol (mmol/liter) 2.6 ± 0.3 2.2 ± 0.3 2.3 ± 0.3 1.6 ± 0.4 1.6 ± 0.3 1.6 ± 0.5
HDL cholesterol (mmol/liter) 1.2 ± 0.1 1.0 ± 0.1 1.1 ± 0.1 1.5 ± 0.1 1.5 ± 0.1 1.7 ± 0.2
Body weight (kg) 74.4 ± 1.1 76.5 ± 1.72 77.9 ± 1.62 74.9 ± 3.4 74.9 ± 3.4 74.7 ± 3.3
Lean body mass (kg) 57.6 ± 1.1 61.0 ± 1.22 61.6 ± 2.5 61.8 ± 2.4
Total body fat (kg) 11.4 ± 1.4 11.6 ± 1.7 9.8 ± 1.9 10.1 ± 2.0
Trunk fat (kg) 4.7 ± 0.7 4.5 ± 0.9 2.8 ± 0.9 2.8 ± 0.9
There was no change in IGF-I levels in the placebo-treated group throughout the observation period. In contrast, in the r-hGH-treated group, IGF-I levels rose markedly, reaching levels outside the physiological range (P < 0.001; Table 2 ). These changes occurred within 7 d of commencing r-hGH administration and did not change further over the remaining 21-d period of r-hGH administration."
------------------------------------
igf is elevated 4 fold ! from hgh.
and now like always, johnny b dissapears..................
Bro I could say the same about you, but say things about each other is useless and leads no where and the post needs to be relevent to the discussion, which is LR3 IGF-1. I'm talking about LR3 IGF-1 and you are talking about IGF-1 and rhIGF-1. So since we are not talking about the same thing it's useless to continue. Bro there is a difference and a big one at that, when we are looking at studies.Quote:
Originally Posted by oswaldosalcedo
The studies we do have on LR3 IGF-1 are on rats and pigs, which aren't humans, so they can only be used as references, not solid proof of what would happen in humans.
It seems you think LR3 IGF-1 is a waste, which is fine, but by posting studies on IGF-1 and rhIGF-1, you're not proving your point, cause they don't apply. Studies done with LR3 IGF-1 in them, will say IGF-1 and it's analog(s) in them or say LR3 IGF-1. Those studies were done with IGF-1, rhIGF-1 and/or LR3 IGF-1, some may include IGF-II.
Have you every tried LR3 IGF-1?
You are getting frustrated, because we are not talking about the samething, but you think we are. It's not that hard, if it doesn't say IGF-1 anolog(s) or LR3 IGF-1 in the study, it doesn't apply to LR3 IGF-1
JohnnyB
men, get to the point.
you are anchored.
you said textually (literatim,verbatim):
"nor is IGF-1 elevated by the use of HGH"
-----------------------------------------
and i posted:
The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 11 5221-5226
2003, by The Endocrine Society.
"High Dose Growth Hormone Exerts an Anabolic Effect at Rest and during Exercise in Endurance-Trained Athletes
M. L. Healy, J. Gibney, D. L. Russell-Jones, C. Pentecost, P. Croos, P. H. Sönksen and A. M. Umpleby
Department of Diabetes and Endocrinology, GKT School of Medicine, St. Thomas Hospital, London, United
r-hGH-treated
------------------ Baseline --------- 1wk-----------4 wk--------- /Placebo-
IGF-I (nmol/liter) 24.6 ± 3.0 / 89.6 ± 12.21-- 106.3 ± 16.41/ 25.8 ± 2.7-- 25.4 ± 2.7-- 25.2 ± 2.6
fT3 (pmol/liter) 5.1 ± 0.3 6.0 ± 0.12 6.1 ± 0.22 4.8 ± 0.2 4.9 ± 0.2 4.8 ± 0.1
fT4 (pmol/liter) 15.5 ± 1.5 11.5 ± 1.02 10.6 ± 0.92 15.8 ± 1.6 15.6 ± 1.7 15.8 ± 1.5
Testosterone (nmol/liter) 18.3 ± 3.2 18.5 ± 3.4 18.5 ± 3.3 16.7 ± 2.6 16.3 ± 2.6 16.4 ± 2.2
Glucose (mmol/liter) 4.7 ± 0.3 5.5 ± 0.5 5.3 ± 0.2 4.5 ± 0.4 4.2 ± 0.2 4.4 ± 0.3
Insulin (mU/liter) 7.9 ± 1.6 22.6 ± 3.92 16.0 ± 9.32 6.0 ± 0.3 5.6 ± 1.9 9.3 ± 2.4
HOMA IR 1.4 ± 0.2 5.1 ± 1.02 3.3 ± 0.62 1.1 ± 0.4 1.0 ± 0.3 1.6 ± 0.5
Total cholesterol (mmol/liter) 4.3 ± 0.3 4.0 ± 0.5 4.1 ± 0.3 3.4 ± 0.3 3.3 ± 0.3 3.5 ± 0.6
Triglyceride 1.1 ± 0.2 2.0 ± 0.5 1.3 ± 0.1 0.6 ± 0.1 0.7 ± 0.1 0.5 ± 0.1
LDL cholesterol (mmol/liter) 2.6 ± 0.3 2.2 ± 0.3 2.3 ± 0.3 1.6 ± 0.4 1.6 ± 0.3 1.6 ± 0.5
HDL cholesterol (mmol/liter) 1.2 ± 0.1 1.0 ± 0.1 1.1 ± 0.1 1.5 ± 0.1 1.5 ± 0.1 1.7 ± 0.2
Body weight (kg) 74.4 ± 1.1 76.5 ± 1.72 77.9 ± 1.62 74.9 ± 3.4 74.9 ± 3.4 74.7 ± 3.3
Lean body mass (kg) 57.6 ± 1.1 61.0 ± 1.22 61.6 ± 2.5 61.8 ± 2.4
Total body fat (kg) 11.4 ± 1.4 11.6 ± 1.7 9.8 ± 1.9 10.1 ± 2.0
Trunk fat (kg) 4.7 ± 0.7 4.5 ± 0.9 2.8 ± 0.9 2.8 ± 0.9
There was no change in IGF-I levels in the placebo-treated group throughout the observation period. In contrast, in the r-hGH-treated group, IGF-I levels rose markedly, reaching levels outside the physiological range (P < 0.001; Table 2 ). These changes occurred within 7 d of commencing r-hGH administration and did not change further over the remaining 21-d period of r-hGH administration."
------------------------------------
igf is elevated 4 fold ! from hgh.
--------------------------------------------
who is wrong?
The point is, you still are posting studies that don't apply to LR3, I can't say it any planner then that. So you're not getting the point, that's the point, do you get my point :wg:
JohnnyB
"nor is IGF-1 elevated by the use of HGH"
you said that,not me.
It looks like you are, didn't you post that HGH was a waste, but this prove it raises IGF-1, which is a good thing when looking for muscle growth, so this would make your point of HGH being a waste, de-bunked.Quote:
Originally Posted by oswaldosalcedo
But explain to me how this applies to LR3 IGF-1, the original point of this thread?
JohnnyB
i said that igf is good thing ?
No the study you posted said that and thank you for proving that point. You failed to read further, you stopped at IGF-1 was not raised, if you would of read further, it says in the "placebo-treated group" but the thing that really throws me off, is you put in bold letters "IGF-1 was elevated 4 fold! from HGH"Quote:
Originally Posted by oswaldosalcedo
Which make me wonder what the you are talking about. You disprove stuff you try to promote, you make thread trying to say HGH is a waste, then you post this and put into bold letters, the HGH does work at raising IGF-1. Raised IGF-1 levels will help with muscle growth, so that means HGH is a good thing.
We clearly aren't talking about the samething, but you post good stuff on the use of HGH raising IGF-1 levels, which are good for muscle growth. I don't understand your line of reasoning, it's not logical, this is not a put down. If your reasoning is HGH is a waste, you should be posting studies showing it to raise IGF-1 levels, you just disproved your own line of reasoning.
Are you trying to say you don't need LR3 to raise IGF-1? Cause I really don't know where you are coming from, here.
JohnnyB
Okay, but you are also trying to say LR3 is bad or what?Quote:
Originally Posted by oswaldosalcedo
JohnnyB