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I researched a bit but its making me sick to look at the computer so here it goes... I've basically had a migraine-like headache since Monday... its fu*king wicked, fellas. I stopped taking the clen on Thursday (so my last dose was Wednesday) and the headaches are still bad. Any advice? More taurine? Use a pain killer? How long does it usually take to subside? Thanks, guys... I'm gonna go back to bed now...
the headaches go away for me after the 1rst week. taurine is at approx 4 grams a day for me. after 7 to 8 days they seem to go away.
never had headaches with clen...weird
I get clen headaches horribly. I just drink tons of water and it seems to do the trick.
which you should do anyway...problem solved....Quote:
Originally Posted by ******
no headache and your hydrated....thats doubly good!
I get terrible clen headaches, I was starting back on it but I just couldn't take the migraines it basically left me non functional for 3 days and I only took 20mcgs, I didn't have the problem as bad the first time I used it, I'm not really sure what the difference was.
I'd rather run on a treadmill until I pass out than have those migraines again.
it will cause headaches..very common.. but i have never experienced a headache from it that a simple tylenol couldnt handle..
clen can cause other more severe problems..
http://jap.physiology.org/cgi/conte...tract/93/5/1824
Myotoxic effects of clenbuterol in the rat heart and soleus muscle
Jatin G. Burniston1, Yeelan Ng1, William A. Clark2, John Colyer3, Lip-Bun Tan4, and David F. Goldspink1
1 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET; Departments of 3 Biochemistry and Molecular Biology and 4 Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom; and 2 Michael Reese Hospital and Medical Center, Chicago, Illinois 60616-3990
Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta 2-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 ± 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 ± 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.
anabolic adrenergic agonist; cardiomyocytes; sympathomimetic; necrosis; immunohistochemistry; beta -adrenergic antagonists
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Characterization of adrenoceptor involvement in skeletal and cardiac myotoxicity Induced by sympathomimetic agents: toward a new bioassay for beta-blockers.
Tan LB, Burniston JG, Clark WA, Ng Y, Goldspink DF.
Academic Unit of Molecular Vascular Medicine, University of Leeds, England.
Excessive levels of catecholamines have long been known to be cardiotoxic, but less well known are their toxic effects on skeletal muscle. By using an antimyosin monoclonal antibody and quantitative methods to measure the extent of myocyte necrosis, and by employing modulators of adrenoceptors (ARs), including clenbuterol, bupranolol, propranolol, bisoprolol, atenolol, ICI-118551, phenoxybenzamine, prazosin, and yohimbine, the involvement of ARs in isoproterenol-induced myotoxicity was characterized. In the myocardium, the toxic effects were predominantly mediated via the beta(1)-ARs. In the soleus muscle, it was almost solely via the beta(2)-ARs. Myotoxicity was also observed in the myocardium when challenged with the beta(2)-AR agonist clenbuterol. This was found to be mediated via sympathetic presynaptic beta(2)-ARs, leading to enhanced release of norepinephrine. This effect was abolished by prior treatment with reserpine. The skeletal muscle was found to be more sensitive to the myotoxic effects than cardiac muscle at lower doses of beta-AR agonists. These experiments introduce a new way of assaying beta-AR antagonists by classifying them according to their ability to prevent catecholamine-induced myotoxicity. Further research along these lines may deepen understanding of which beta-blockers work best in heart failure therapy.
PMID: 12658052 [PubMed - indexed for MEDLINE]
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Dose-dependent separation of the hypertrophic and myotoxic effects of the beta(2)-adrenergic receptor agonist clenbuterol in rat striated muscles.
Burniston JG, Clark WA, Tan LB, Goldspink DF.
Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK.
Muscle growth in response to large doses (milligrams per kilogram) of beta(2)-adrenergic receptor agonists has been reported consistently. However, such doses may also induce myocyte death in the heart and skeletal muscles and hence may not be safe doses for humans. We report the hypertrophic and myotoxic effects of different doses of clenbuterol. Rats were infused with clenbuterol (range, 1 mug to 1 mg.kg(-1)) for 14 days. Muscle protein content, myofiber cross-sectional area, and myocyte death were then investigated. Infusions of >/=10 mug.kg(-1).d(-1) of clenbuterol significantly (P < 0.05) increased the protein content of the heart (12%-15%), soleus (12%), plantaris (18%-29%), and tibialis anterior (11%-22%) muscles, with concomitant myofiber hypertrophy. Larger doses (100 mug or 1 mg) induced significant (P < 0.05) myocyte death in the soleus (peak 0.2 +/- 0.1% apoptosis), diaphragm (peak 0.15 +/- 0.1% apoptosis), and plantaris (peak 0.3 +/- 0.05% necrosis), and significantly increased the area fraction of collagen in the myocardium. These data show that the low dose of 10 mug.kg(-1).d(-1) can be used in rats to investigate the anabolic effects of clenbuterol in the absence of myocyte death. Muscle Nerve, 2006.
PMID: 16411205 [PubMed - in process]
It's been known for some time that clenbuterol at high doses causes cardiac necrosis. This study in animals shows that doses of 1 mcg/kg BW induce apoptosis (programmed cell death) in heart tissue. Humans not uncommonly ingest this much clen. For instance, in a 220 lb (100 kg) bodybuilder this translates to 100 mcg.
J Appl Physiol. 2004 Dec 10; [Epub ahead of print] Related Articles, Links
{beta}2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle.
Burniston JG, Tan LB, Goldspink DF.
Research Institute for Sports and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.
High doses of the beta2-adrenergic receptor (AR) agonist, clenbuterol, can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known if this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte specific apoptosis (detected on cryosections using a caspase 3 antibody and confirmed using annexin V, single-strand DNA labelling and TUNEL). Myocyte apoptosis was first detected at 2 h, and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 microg kg(-1), with peak apoptosis (0.35 +/- 0.005 %; P<0.05) occurring in response to 5 mg kg(-1) . In the soleus, peak apoptosis (5.8 +/- 2 %; P<0.05) was induced by the lower dose of 10 microg kg(-1). Cardiomyocyte apoptosis occurred throughout the ventricles, atria and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way from the apex towards the base. beta-AR antagonism (involving propranolol, bisoprolol or ICI 118,551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta1-AR, whereas in the soleus direct stimulation of the myocyte beta2-AR was involved. These data show that when administered in vivo, beta2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through beta1- and beta2-AR, respectively.
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just thought id push this up.. something to think about
lower the dose and run turein.
are you certain they were caused by the CLEN?Quote:
Originally Posted by fanatic
Quote:
Originally Posted by G-1000
WTF is that??
lol.. im guessing hes talking about taurine
Not 100%... I started Test P on the same day; with this in mind, I initially thought that it could be test flu (which I have NEVER gotten). After a few days, however, I knew it was the clen. I am happy to say that the headaches have gotten much better... but I am not 100% yet and I am still very sensitive to light.Quote:
Originally Posted by ****
LMFAO! I was just wondering the same thing when I read this post.Quote:
Originally Posted by HORSE
Thanks for all the info, guys (and gal). I truly appreciate it.
taurineQuote:
Originally Posted by HORSE
haha sorry
I tried everything... I ended up trying Cannabis-sativa last night and, low and behold, the nausia went away and the dizziness is gone. Thanks for all the info, guys!