purplehaze

Originally posted by BANE

So I guess I suck now... I don't even have secure access now.o:(

Man that sucks bro....

Nice post bro./

IGF-1 for tendinitis?

We had a thread recently where GH given to horses resulted in weaker tendons that were less stiff. The authors concluded GH is probably not a good treatment for tendinitis.

 

http://www.cuttingedgemuscle.com/Fo...hp?threadid=438

 

In this study they injected IGF-1 directly into the tendon and got good results, although the tendon was stiffer than the controls (just the opposite from the GH study; I wonder if this effect is real or the result of some "flaw" in one of the studies?).

 

J Orthop Res 2002 Sep;20(5):910-9

 

Insulin-like growth factor-I improves cellular and molecular aspects of healing in a collagenase-induced model of flexor tendinitis.

 

Dahlgren LA, van der Meulen MC, Bertram JE, Starrak GS, Nixon AJ.

 

Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Veterinary Medical Center, Ithaca, NY 14853, USA.

 

Flexor tendinitis is a common and debilitating injury of elite and recreational athletes. Healing may be improved through intratendinous injection of insulin-like growth factor-I (IGF-I), which has been shown in vitro to stimulate mitogenesis and enhance tendon matrix production. This study investigated the effects of intratendinous injection of IGF-I on tendon healing in an equine model of flexor tendinitis. Collagenase-induced lesions were created in the tensile region of theflexor digitorum superficialis tendon of both forelimbs of eight horses. Treated tendons were injected with 2 microg rhlGF-I intralesionally every other day for 10 injections, while controls received 0.9% NaCl. Tendon fiber deposition and organization were evaluated serially using ultrasonography throughout the 8 week trial period. Following euthanasia, the tendons were harvested and DNA, hydroxyproline, and glycosaminoglycan content determined, mechanical strength and stiffness evaluated, gene expression and spatial arrangement of collagen types I and III assessed by northern blot and in situ hybridization, and tendon fiber architecture assessed by polarized light microscopy. Local soft tissue swelling was reduced in the IGF-I treated limbs. Similarly, lesion size in IGF-I treated tendons was smaller 3 and 4 weeks after initiation of treatment. Cell proliferation and collagen content of the IGF-I treated tendons were increased compared to controls. Mechanically, IGF-I treated tendons showed a trend toward increased stiffness compared to saline treated controls. Considered together with the decreased soft tissue swelling and improved sonographic healing, these data support the potential use of intralesional IGF-I for treatment of debilitating tendon injuries.

More bad news about lifting

There have been at least a couple of posts here about lifting leading to cardiomyopathy. It seems that lifting also stiffens the arteries (a decrease in arterial compliance), making a person more prone to develop hypertension and vascular disease.

 

Hypertension 2003 Jan;41(1):130-5

 

Greater age-related reductions in central arterial compliance in resistance-trained men.

 

Miyachi M, Donato AJ, Yamamoto K, Takahashi K, Gates PE, Moreau KL, Tanaka H.

 

Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder, Colo, USA.

 

Reductions in the compliance of central arteries exert a number of adverse effects on systemic cardiovascular function and disease risk. Using the cross-sectional study design, we determined the relation between chronic resistance training and carotid arterial compliance. A total of 62 healthy normotensive men, 20 to 39 years of age (young) and 40 to 60 years of age (middle-aged), who were either sedentary or resistance-trained, were studied. In both activity groups, carotid arterial compliance (simultaneous ultrasound and applanation tonometry) was lower (P<0.05) in the middle-aged compared with the young men. There was no significant difference between young sedentary and resistance-trained men. In the middle-aged group, carotid arterial compliance in the resistance-trained men was approximately 30% lower (P<0.01) than their sedentary peers. Femoral artery compliance and arm pulse wave velocity (measures of peripheral artery stiffness) were not different among any groups. Left ventricular hypertrophy index (echocardiography) was greater (P<0.05) in resistance-trained compared with sedentary men and was associated with carotid arterial compliance (r=-0.35; P<0.01). We concluded that (1) resistance training is associated with the smaller central arterial compliance in healthy middle-aged men; (2) age-related reductions in arterial compliance was greater in resistance-trained men than in sedentary men; and (3) the lower arterial compliance in the resistance-trained men is associated with left ventricular hypertrophy. In marked contrast to the beneficial effect of regular aerobic exercise, the present findings are not consistent with the idea that resistance training exerts beneficial influences on arterial wall buffering functions

Aromasin best Anti-E! Check it out...

 

Quoted from "Zyglamail" from EF:

"Anastrozole is the same as liquidex. femara is slightly better as an anti-e but both seem to have more of a negative impact on lipid profiles than aromasin which is much more powerfull than both of them."

 

Quoted from "CandianBro" From EF:

"There can be NO DEBATE!

 

Aromasin is the king of all anti-e's!

 

After using 2mg/day of Arimidex during a 1000mg/week

Test cycle and STILL getting quite a bit of water weight as well as slight gyno, I decided to try Aromasin.

 

Well, needless to say, after shooting 1gram + of test per week and taking ONE 25mg Aromasin per day, I literally had ZERO water bloat and gyno........ZERO!!!

 

Aromasin is simply INCREDILE

 

I think the reason Arimidex is much more popular is because it is much readily available as there are SEVERAL generic and undergorund versions.

 

However, it one has access to real Aromasin (Pharmacia), then there should be no choice between the two.

 

I'm sure those that have used BOTH will concur."

 

Quoted from "DrJMW" from EF:

Interesting Facts about Aromasin (post #1)

 

1. It is an irreversible, steroidal aromatase inactivator

 

2. Structurally related to androstenedione

 

3. Significantly lowers estrogen and has no detectable effect on adrenal biosynthesis of corticosteroids or aldosterone

 

4. Aromasin 25mg daily reduced whole body aromitization by 98%

 

5. Has a slight affinity for the androgen receptor (.28% relative to dihydrotestosterone)

 

6. The binding affinity of its 17-dihydrometabolite for the androgen receptor is 100-times that of the parent compound.

 

7. Daily doses had no effect on levels of testosterone, androstenedione, dehydroepiandrosterone, or 17-hydroxyprogesterone.

 

8. A dose-dependent decrease in sex hormone binding globulin (SHBG) has been observed.

 

9. Slight, non-dose dependent increases in serum LH and FSH have been observed.

 

These are the links i quoted people from. I don't take any credit for this post. I didn't write any of it, all i did is research it and post it to make it easier for everyone to read in a condensed post. And you can go back and read the threads I copied them from.

 

http://boards.elitefitness.com/foru...hlight=aromasin

 

http://boards.elitefitness.com/foru...hlight=aromasin

 

http://boards.elitefitness.com/foru...hlight=aromasin

Drug Side Effects - Gynecomastia Male Breast Enlargement

 

There are many possible reasons for male breast growth. If caused by a medical problem, this should be corrected first. Such issues can be investigated by your internist or an endocrinologist. In most cases there is no known cause. A complete discussion of the many possible causes for gynecomastia is beyond the scope of this introduction.

 

These drugs (according to the Physician Desk Reference) can cause gynecomastia as a side effect. The risks are generally very low for male breast enlargement from these medications, but breasts in men can be a cause for embarrassment. Some medications may be important for your other medical problems.

 

Adalat

 

Aldactazide

 

Aldactone

 

Aldoclor

 

Aldome

 

Aldoril

 

Anadrol

 

Androderm

 

* Android

 

Atromid-S

 

Avonex

 

Axid

 

Baycol

 

Betaseron

 

Calan

 

Captopril

 

* Casodex

 

Catapres

 

Celexa

 

Cipro

 

Clinoril

 

Clorpres

 

Combipres

 

Compazine (No incidence data in labeling)

 

Covera-HS

 

Duraclon

 

Effexor

 

Elavil (No incidence data in labeling)

 

Etrafon

 

* Eulexin

 

Flexeril

 

Haldol

 

Humatrope

 

Humegon

 

Indocin

 

Intron A

 

Isoptin SR

 

Kadian

 

Lanoxicaps

 

Lanoxin

 

Lescol

 

Lexxel

 

Limbitrol (No incidence data in labeling)

 

Lotrel

 

Loxitane

 

Loxitane

 

Lupron

 

Matulane

 

Megace

 

Methotrexate

 

Mevacor

 

Midamor

 

Moban

 

Moduretic

 

Motrin

 

Myleran

 

Navane (No incidence data in labeling)

 

Neoral

 

* Nilandron

 

Nizoral

 

Norpace

 

Norpramin (No incidence data in labeling)

 

Norvasc

 

Novarel

 

Nutropin

 

Orudis

 

Oruvail

 

Oxandrin

 

Pepcid

 

Pergonal

 

Plendil

 

Pravachol

 

Pregnyl

 

Prevacid

 

PREVPAC

 

Prilosec

 

Procardia

 

Profasi (No incidence data in labeling)

 

Propulsid

 

Protropin

 

Prozac

 

Reglan

 

Repronex

 

Requip

 

Rifamate (No incidence data in labeling)

 

Rifater

 

Risperdal

 

Sandimmune

 

Sandostatin

 

SangCya

 

Serentil

 

Seroquel

 

* Serostim

 

Sinequan (No incidence data in labeling)

 

Sporanox

 

Stelazine (No incidence data in labeling)

Sular

 

Surmontil

 

Sustiva

 

* Tagamet

 

Tarka

 

* Testoderm

 

Testred (No incidence data in labeling)

 

Thalomid

 

Thioridazine Hydrochlorid

 

Thiothixene

 

Thorazine

 

Tiazac

 

Trecator-SC (No incidence data in labeling)

 

Triavil (No incidence data in labeling)

 

Tricor

 

Trilafon

 

Vascor

 

Vaseretic

 

Vasotec

 

Verelan

 

Vivactil (No incidence data in labeling)

 

Wellbutrin

 

Winstrol (No incidence data in labeling)

 

Xanax

 

Zantac

 

Zocor

 

* Zoladex

 

Zoloft

 

Zyban

 

Herbals

 

Digitalis Purpurea (FOXGLOVE

Before you decide that blocking progesterone is the solution to gyno, consider a few things. There is not one case of progesterone induced gyno in the medical literature EXCEPT in those cases where strong synthetic progestins, like medroxyprogesterone, were administered. In these cases the gyno is due to suppression of LH and testosterone by the progestin, NOT by a direct effect on breast tissue. On a cycle your LH is already suppressed by the AAS anyway.

 

Breasts have two components: alveoli and ducts. The alveoli are what secrete milk; they drain into ducts. Gynecomastia is the result of ductal hyperplasia, not alveolar hyperplasia. Estrogen stimulates the ductal tissue, while progesterone stimulates the alveoli. Alveolar hyperplasia does not contribute to gyno. If you want to read more on breast development, I suggest visiting this site:

 

http://www.endotext.org/male/male14/male14.htm

 

In various tissues throughout the body, including cultured neoplastic breast tissue, progestins downregulate the estrogen receptor (1). Progesterone receptor blockers like RU-486 upregulate the estrogen receptor (1). This is consistent with the fact that RU-486 CAUSES gyno in patients in whom it is used to treat Cushing's disease and meningiomas (2).

 

Progestins are also anti-estrogenic in that they induce the enzyme 17-hydroxysteroid dehydrogenase, which catalyzes the oxidation of estradiol to the less potent estrone. Progestins also induce estrogen sulfotransferase, the enzyme which catalyzes the sulfation and inactivation of estrogens.

 

So do progestins contribute to gyno, and if yes, how so? If you visit the link above you will see that progestins increase IGF-1 levels. As that article indicated, IGF-1 is essential to the the development of mammary tissue. This is also how it is believed that progestins in HRT or oral contraceptives contribute to breast cancer: by increasing IGF-1 levels. But as bodybuilders we are always trying to maximize IGF-1. Hence the futility of trying to lower IGF-1 by blocking progestins. The other anabolics we use will elevate (hopefully) IGF-1, while blocking the progesterone receptor will only increase the levels and activity of estrogen by the mechanisms outlined above.

 

Two drugs have shown the greatest efficacy in treating gyno: Nolvadex, and Raloxifene, another SERM. Nolvadex has the longest track record, but a recent trial with Raloxifene showed it to be superior to Nolvadex. With these drugs you attack the problem at its source: the estrogen receptor. You get the added benefit of lowering IGF-1. Not a good thing for making gains, but important for treating gyno.

In addition to elevated IGF-1, lowered DHT levels resulting from endogenous testosterone suppression may contribute to gyno from non aromatizing steroids. Gyno is a reported side effect from finasteride use. Some have attributed this to elevated estrogen levels due to the fact that there is more testosterone to be aromatized, since less test is being converted to DHT. Other researches think that DHT has a direct antiestrogenic effect on breast tissue.

 

Studies have shown that DHT can actually block estrogen from binding to the estrogen receptor in mammary tissue (1). DHT also is an aromatase inhibitor (2). Even more interesting is the fact that transdermal DHT cream has been used successfully to treat gyno (3).

 

It may be that the estrogen/DHT ratio is more important to the development of gyno than the estrogen/testosterone ratio.

here is the real deal out in the open!

 

click here for CNN report

For Those who wonder How Steroids Work....Technically Speaking

This is a breakdown of the technical effects of anabolics within the human body. Should my MU bros have anything to add, please feel free. The anabolic effects of the steroids are elicited by the action of the steroids on androgen receptors in muscle tissue. The steroid binds to the receptor and is carried to the nucleus of the cell where it tells the DNA in the cell to transcribe the steroid’s message onto messenger RNA (mRNA). The mRNA then delivers its message to the muscle cells and this causes a response in the cells that results in increased protein synthesis, which causes hypertrophy (growth) of the cells and the muscle tissue that the cells make up.

The different molecular configurations of the various anabolic steroids cause significantly different cellular responses, and even a subtle change of one atom can elicit a unique response for a specific steroid. That is why each steroid has distinct characteristics that make it more appropriate for specific therapeutic uses.

 

It should also be noted that anabolic steroids, in general, are hematopoietic (blood building) agents; they increase hemoglobin production and hematocrit.

 

 

What are your thoughts or additions.

 

 

 

 

__________________

Played real golf today and shot a 79... Not a bad day, but the putting was pissing me off...

Curious as well...I would have went with at least 4iu ED for at least 3-4 months...Bump for Merlin...

What up big T./..

Originally posted by j0yride34

Hmm..wonder if he likes that injection in the ass better than his test...:D

HA HA HA HA HA........

Originally posted by BigRed54

Becarful over there at AU.....

Be careful at any board...Au has changed things bro..There are no source checks no classifieds..We are trying to stop the bleeding believe me...BTW what sanger

Originally posted by Stripper

people are sorry, if u have to front to them or lend $ to them, they are probblly not good with their money, and will fucking lose it somewhere along the line. if u are going to front say it from the beginning u have 2 or 3 fronts that is it ,u should have saved enough $ for u to start buying out right and cut them off.

Well said..

If someone could find me a good Jimi avatar..I would appreciate it...

Really, it appears that a few are left out...Where is BR and Swoll are they still mods on here...and do we have new ones..

YOu would like it back eh....

Seems that we dont have the same mods anymore...Roll Call...WHo are mods now..?????

Originally posted by hitmeoff

For those of you who didnt catch it the first time, let me repeat my self you are ALL MY BITCHES, now be good little whores and shut your traps before I bitch slap y'all o8)

I will hold my breath for that/////:D

Originally posted by admin

You stood in the corner? Did your mommy tell you to or something? :confused:

Bro, I dont see why you get so pissed, the man has an opinion, he spoke his mind, I mean shit cut back on the test or something...Why is it that you feel it is necessary to always flame good bros...This maybe your board, but with that attitude towards a long time member and a respected vet is a little much...

Do you guys want the library back believe me I am a librarian...