THINKING OF USING LIQUID CLEN

[BOWLSCOTT]

JUST GOT DIVORCED AND HAVE TO GET BACK IN THE GYM. IM LOOKING IN TO USING CLEN. DO YOU GUYS HAVE ANY SUCSESS STORIES OR BAD STORIES ON THIS STUFF.

[Skyefire]

All caps is SHOUTING. please don't. I moved your post to the correct forum. Please go read this link http://www.superiormuscle.com/vbulle...threadid=15450

my condolences on your divorce.

[popichulo]

Ive used liquid clen with much success, what brand do you have?

[BOWLSCOTT]

thanks

[BOWLSCOTT]

have not got it yet. have done research on it but just wanted to get some real people feed back.

[RUI-Products]

you won't go wrong with fruit punch clen from the lion

[LuvMuhRoids]

In researching this product. I did find some interesting studies. Clenbuterol does have some effects such in Reproductive toxicity, Long-term toxicity/carcinogenicity, Skin irritation, Intramuscular tolerance. I think the study on pup birth rate in high dosages should be looked at.

I found this to be interesting....

Clenbuterol, like other ß-agonists, leads to tachycardia and
hypotension. This probably results in reduced myocardial perfusion at
a time when oxygen demand is high because of increased cardiac rate.
The end result is hypoxia which probably leads to the necrotic lesions
seen in the left ventricular papillary muscles (Rosenblum et al.,
1965; De Busk & Harrison, 1969; Poynter & Spurling, 1971; Roberts &
Cohen, 1972; Magnusson & Hansson, 1973; Balazs & Bloom, 1982). This
explains the cardiac effects noted in the repeated dose (and other)
studies with clenbuterol.

Observations in humans

A single blinded cross-over study was carried out to examine the
acute bronchospasmolytic effect and possible side-effects following
oral administration of placebo and three doses of clenbuterol (1, 2.5
and 5 µg/day) in patients (three male and three female) with chronic
obstructive airway disease over a 3 day period. The drug was given
orally, diluted with water. Observations were carried out over a
2-hour period following dosing. The average age of the patients was
55.7 years and they had an average body weight of 73.16 kg.

None of the 3 doses produced any clear, consistent effects on
bronchial resistance, thoracic gas volume, radial pulse frequency or
blood pressure, and no side effects were seen.

The pharmacological NOEL in this study was 5 µg/day, equivalent
to 0.08 µg/kg bw per day (Kaik, 1978).

The bronchospasmolytic effect was examined in two groups of
patients:

Group A: ten patients aged 46-75 years with chronic obstructive
respiratory disease resulting from pulmonary tuberculosis.

Group B: five patients aged 56-67 years with chronic obstructive
respiratory disease not related to tuberculosis, plus five
patients aged 34-57 with bronchial asthma.

The bronchospasmolytic effect was examined after single oral doses of
1, 2.5, 5, 10, 20, 25 or 30 µg/person, and after a placebo dose.

In Group A patients, intrathoracic gas volume was significantly
reduced and vital capacity and pneumometer values significantly
increased at all dose levels. In Group B patients, airway resistance
was significantly reduced, but no dose relationship could be
demonstrated. No significant placebo effect was seen in either group.
When compared with placebo values, a significantly greater increase
for both vital capacity and pneumometer values was observed in Group
A, even at the lowest dose used in this group (5 µg). However, at the
two lowest doses used in Group B (1 and 2.5 µg), there were no
significant differences from placebo values. The pharmacological NOEL
in this study was 2.5 µg, equivalent to 0.042 µg/kg bw (Nolte &
Laumen, 1972; Nolte, 1980).

Children who consumed between 0.05-0.075 mg of clenbuterol showed
only mild tachycardia. A 30-year-old woman who consumed 30 tablets
equivalent to 0.6 mg clenbuterol (10 µg/kg approximately) developed
tachycardia and slight hypertension approximately 1 hour after
consumption. No tablet remains were found on gastric lavage, and
medicinal charcoal and a saline laxative were given. The following
day, the patient's pulse rate and blood pressure had returned to
normal (Boehringer, 1991a).

Patients (100+) administered doses of 20-60 µg/day (0.3-1.0 µg/kg
bw per day) for up to 1 year or 20 µg/day (0.3 µg/kg bw per day) for
up to 6 months showed no adverse effects except for slight tremor and
occasional, mild tachycardia (Laumen, 1978; Tullgren & Lins, 1987).

3. COMMENTS

The Committee considered toxicological data on clenbuterol,
including the results of acute, short-term and reproductive toxicity
studies, as well as studies on teratogenicity, genotoxicity and
carcinogenicity. Results of pharmacokinetic and pharmacodynamic
studies in animals and humans were also considered.

Clenbuterol is well absorbed after oral administration in a
number of animal species and in humans. An oral dose is largely and
rapidly excreted in the urine, and the majority of the remainder is
excreted in the faeces. The biotransformation of clenbuterol is
complex and a number of metabolites are formed. The major compound
found in a number of species was unchanged clenbuterol. After oral
administration of therapeutic doses to lactating cattle, clenbuterol
was found in the milk.

When radiolabelled clenbuterol was given orally to pregnant rats,
dogs, baboons and cattle, radioactivity was detected in the fetuses.

Clenbuterol was moderately toxic in mice and rats after oral
administration, LD50 values being in the range of 80-175 mg/kg bw.
It was less toxic in the dog (LD50 = 400-800 mg/kg bw). It was more
toxic after parenteral administration, with LD50 values in the range
of 30-85 mg/kg bw after intravenous administration. The main signs of
toxicity included lethargy, tachycardia and tonic-clonic convulsions
after oral administration.

The main effects noted in the repeat-dose studies were
tachycardia and, at higher doses, myocardial necrosis. These effects
are common with ß-agonist drugs. The myocardial necrosis was
considered to be secondary to hypoxia, due to reduced myocardial
perfusion at a time of high oxygen demand resulting from increased
cardiac rate.

In 30-day repeat-dose studies in mice and rats, NOELs of 2.5 and
1 mg/kg bw per day, respectively, were identified, largely based on
cardiac lesions. However, in a range of repeat-dose studies in rats
using doses of 0.01 to 100 mg/kg bw per day for durations of up to
18 months, administered through the oral, intravenous and inhalation
routes, no NOELs were identified. Effects were usually related to
cardiac function and were seen even at the lowest doses used.
Similarly, no NOELS could be identified in a range of repeat-dose oral
studies in dogs. These studies used doses ranging from 0.1 to 40 mg/kg
bw per day. In a 26-week inhalation study in cynomolgus monkeys, the
NOEL was 25 µg/kg bw per day, based on a number of observations
including cardiac effects.

No evidence of carcinogenicity was noted in a two-year oral study
in mice with doses of up to 25 mg/kg bw per day. In a two-year study
with doses of up to 25 mg/kg bw per day in the Chbb:THOM rat, no
evidence of carcinogenicity was seen. However, in Sprague-Dawley rats
given 25 mg clenbuterol/kg bw per day orally for 2 years, an increased
incidence of mesovarian leiomyomas occurred. With the related
compounds salbutamol in rats and medroxalol in mice, the effects could
be abolished by administration of the ß-blocking agent propranolol.
Mesovarian leiomyomas in rats and uterine leiomyomas in mice are known
to occur following long-term treatment with ß-adrenoceptor agonists
and the Committee concluded that these were due to adrenergic
stimulation and not to any genotoxic mechanism. Clenbuterol was not
genotoxic in a range of in vitro and in vivo genotoxicity studies.

Epidemiological studies indicate that there have been no
increased incidences of uterine leiomyomas in women following the use
of ß-adrenoceptor agonists.

Clenbuterol had no effects on fertility in a reproductive
toxicity study in rats using oral doses of 1-50 mg/kg bw per day from
10 weeks prior to mating in males and two weeks prior to mating in
females. However, doses of 50 mg/kg bw per day resulted in the deaths
of pups soon after birth. To investigate the cause of the high pup
mortality at this dose level, the litters of control dams were
exchanged with those from dams given 50 mg/kg bw per day. Pups from
rats given 50 mg/kg bw per day died on the first day of lactation
regardless of whether they suckled on treated or control dams. The
mechanism involved in this lethal effect is unknown. A NOEL was not
identified in this study, because pup weights at birth were reduced in
all treated animals.

In a reproductive toxicity study in which male rats were treated
with 1.5-15 µg clenbuterol/kg bw per day orally for 70 days prior to
mating and females with the same dose range for 14 days prior to
mating, no adverse effects on reproduction were noted. The NOEL was
15 µg/kg bw per day.

In teratogenicity studies in rats, oral doses of 10 and 100 mg/kg
bw per day produced teratogenic effects that included hydrocephalus,
anasarca, umbilical hernia, anophthalmia, rib variations and
splintering of vertebrae. These were accompanied by signs of maternal
toxicity. The NOEL was 1 mg/kg bw per day. In three studies in rabbits
using doses of 30 µg to 50 mg per kg bw per day, signs of feto-
toxicity, including delayed ossification and cleft palate, occurred.
The NOEL was 30 µg/kg bw per day.

Clenbuterol produced a range of pharmacodynamic effects in a
number of animal species including tachycardia, hypertension and
muscle relaxing effects. These were seen at single doses as low as
0.8 µg/kg bw.

Four metabolites of clenbuterol that had been shown to be present
in the kidneys of treated target animals were tested for pharmaco-
logical activity. Of these, only one (N-A 1141) was shown to have
activity. Its broncholytic effect in the guinea-pig was less than
20% that of clenbuterol. In addition, it accounted for only 1-2% of
residues in the liver and kidney of target animals 6 hours after
treatment.

In humans, clenbuterol produced a bronchiolytic effect when a
single dose of 10 µg (0.167 µg/kg bw) was given by the inhalation
route, but no evidence of tachycardia was seen at this dose. With oral
doses of clenbuterol of up to 5 µg/day (0.08 µg/kg bw per day) over a
3-day period, there were no effects on bronchial resistance, thoracic
gas volume, cardiac rate or blood pressure. The NOEL in this study was
5 µg/day (0.08 µg/kg bw per day). In a study to investigate the
bronchospasmolytic effect in humans, patients with obstructive lung
disease were given oral doses of up to 30 µg per person. Patients
administered doses of 5 µg or more exhibited bronchospasmolytic
effects, and the pharmacological NOEL in this study was 2.5 µg per
person, equivalent to 0.04 µg/kg bw.


Clen almost reminds me of the selectivness of nolvadex and clomid. Being clen's selective binding to ß2-adrenoceptors on uterine smooth muscle cell membranes.

Clenbuterol is a ß-adrenoceptor agonist that exerts a potent
bronchiolytic effect by preferential action on ß2-adrenoceptors in
smooth muscle, resulting in the relaxation of bronchial smooth muscle
and a decrease in airway resistance. Similarly, through selective
binding to ß2-adrenoceptors on uterine smooth muscle cell membranes,
relaxation of the uterus (tocolysis) occurs.


Here are two excellent reading matierials on animal and human studies. I read through most of it and have yet to completely understand the differences.

http://www.inchem.org/documents/jecf...no/v38je02.htm

http://www.emea.eu.int/pdfs/vet/mrls/003095en.pdf

Clen is usually ran 2 weeks on 2 weeks off. In your off time run what is called an ECA stack (Ephedrine, Caffeine, Aspirin). This has a thermogenic and anabolic effect as well. Clen can be run for post cycle treatment to help retain gains because it is anti-catabolic. Clen properties are known to have thermogenic effects (raise body temp) and nerve stimulant. Clen effects the main nervous system.