EVERYTHING you need to know about LIQUIDEX / ARIMIDEX.....courtesay of my girlfreind

[OMEGA]

EVERYTHING you need to know about LIQUIDEX / ANASTROZOLE.......NOW GIVE ME KARMA!!!!

CLINICAL PHARMACOLOGY

Mechanism of Action

Many breast cancers have estrogen receptors and growth of these tumors can be stimulated by estrogens. In post-menopausal women, the principal source of circulating estrogen (primarily estradiol) is conversion of adrenally-generated androstenedione to estrone by aromatase in peripheral tissues, such as adipose tissue, with further conversion of estrone to estradiol. Many breast cancers also contain aromatase; the importance of tumor-generated estrogens is uncertain.

Treatment of breast cancer has included efforts to decrease estrogen levels by ovariectomy premenopausally and by use of anti-estrogens and progestational agents both pre- and post-menopausally, and these interventions lead to decreased tumor mass or delayed progression of tumor growth in some women.

Anastrozole is a potent and selective non-steroidal aromatase inhibitor. It significantly lowers serum estradiol concentrations and has no detectable effect on formation of adrenal corticosteroids or aldosterone.

Pharmacokinetics

Inhibition of aromatase activity is primarily due to anastrozole, the parent drug. Studies with radiolabeled drug have demonstrated that orally administered anastrozole is well absorbed into the systemic circulation with 83 to 85% of the radiolabel recovered in urine and feces. Food does not affect the extent of absorption. Elimination of anastrozole is primarily via hepatic metabolism (approximately 85%) and to a lesser extent, renal excretion (approximately 11%), and anastrozole has a mean terminal elimination half-life of approximately 50 hours in post-menopausal women. The major circulating metabolite of anastrozole, triazole, lacks pharmacologic activity. The pharmacokinetic parameters are similar in patients and in healthy post-menopausal volunteers. The pharmacokinetics of anastrozole are linear over the dose range of 1 to 20 mg and do not change with repeated dosing. Consistent with the approximately 2-day terminal elimination half-life, plasma concentrations approach steady-state levels at about 7 days of once daily dosing, and steady-state levels are approximately three- to four-fold higher than levels observed after a single dose of ARIMIDEX. Anastrozole is 40% bound to plasma proteins in the therapeutic range.

Metabolism and Excretion: Studies in post-menopausal women demonstrated that anastrozole is extensively metabolized with about 10% of the dose excreted in the urine as unchanged drug within 72 hours of dosing, and the remainder (about 60% of the dose) excreted in urine as metabolites. Metabolism of anastrozole occurs by N-dealkylation, hydroxylation, and glucuronidation. Three metabolites of anastrozole have been identified in human plasma and urine. The known metabolites are triazole, a glucuronide conjugate of hydroxy-anastrozole, and a glucuronide of anastrozole itself. Several minor (less than 5% of the radioactive dose) metabolites have not been identified.

Because renal elimination is not a significant pathway of elimination, total body clearance of anastrozole is unchanged even in severe (creatinine clearance less than 30 mL/min/1.73 m2) renal impairment; dosing adjustment in patients with renal dysfunction is not necessary (see Special Populations and DOSAGE AND ADMINISTRATION sections). Dosage adjustment is also unnecessary in patients with stable hepatic cirrhosis (see Special Populations and DOSAGE AND ADMINISTRATION sections).

Special Populations

Geriatric: Anastrozole pharmacokinetics have been investigated in post-menopausal female volunteers and patients with breast cancer. No age related effects were seen over the range <50 to >80 years.

Race: Anastrozole pharmacokinetic differences due to race have not been studied.

Renal Insufficiency: Anastrozole pharmacokinetics have been investigated in subjects with renal insufficiency. Anastrozole renal clearance decreased proportionally with creatinine clearance and was approximately 50% lower in volunteers with severe renal impairment (creatinine clearance less than 30 mL/min/1.73 m2) compared to controls. Since only about 10% of anastrozole is excreted unchanged in the urine, the reduction in renal clearance did not influence the total body clearance (see DOSAGE AND ADMINISTRATION).

Hepatic Insufficiency: Hepatic metabolism accounts for approximately 85% of anastrozole elimination. Anastrozole pharmacokinetics have been investigated in subjects with hepatic cirrhosis related to alcohol abuse. The apparent oral clearance (CL/F) of anastrozole was approximately 30% lower in subjects with stable hepatic cirrhosis than in control subjects with normal liver function. However, plasma anastrozole concentrations in the subjects with hepatic cirrhosis were within the range of concentrations seen in normal subjects across all clinical trials (see DOSAGE AND ADMINISTRATION), so that no dosage adjustment is needed.

Drug-Drug Interactions: Anastrozole inhibited reactions catalyzed by cytochrome P450 1A2, 2C8/9, and 3A4 in vitro with Ki values, which were approximately 30 times higher than the mean steady-state Cmax values observed following a 1-mg daily dose. Anastrozole had no inhibitory effect on reactions catalyzed by cytochrome P450 2A6 or 2D6 in vitro. Administration of a single 30 mg/kg or multiple 10 mg/kg doses of anastrozole to subjects had no effect on the clearance of antipyrine or urinary recovery of antipyrine metabolites. Based on these in vitro and in vivo results, it is unlikely that co-administration of ARIMIDEX 1 mg with other drugs will result in clinically significant inhibition of cytochrome P450 mediated metabolism.

Pharmacodynamics

Effect on Estradiol: Mean serum concentrations of estradiol were evaluated in multiple daily dosing trials with 0.5, 1, 3, 5, and 10 mg of ARIMIDEX in post-menopausal women with advanced breast cancer. Clinically significant suppression of serum estradiol was seen with all doses. Doses of 1 mg and higher resulted in suppression of mean serum concentrations of estradiol to the lower limit of detection (3.7 pmol/L). The recommended daily dose, ARIMIDEX 1 mg, reduced estradiol by approximately 70% within 24 hours and by approximately 80% after 14 days of daily dosing. Suppression of serum estradiol was maintained for up to 6 days after cessation of daily dosing with ARIMIDEX 1 mg.

Effect on Corticosteroids: In multiple daily dosing trials with 3, 5, and 10 mg, the selectivity of anastrozole was assessed by examining effects on corticosteroid synthesis. For all doses, anastrozole did not affect cortisol or aldosterone secretion at baseline or in response to ACTH. No glucocorticoid or mineralocorticoid replacement therapy is necessary with anastrozole.

Other Endocrine Effects: In multiple daily dosing trials with 5 and 10 mg, thyroid stimulating hormone (TSH) was measured; there was no increase in TSH during the administration of ARIMIDEX. ARIMIDEX does not possess direct progestogenic, androgenic, or estrogenic activity in animals, but does perturb the circulating levels of progesterone, androgens, and estrogens.

Clinical Studies

Anastrozole was studied in two well-controlled clinical trials (0004, a North American study; 0005, a predominately European study) in post-menopausal women with advanced breast cancer who had disease progression following tamoxifen therapy for either advanced or early breast cancer. Some of the patients had also received previous cytotoxic treatment. Most patients were ER-positive; a smaller fraction were ER-unknown or ER-negative (the ER-negative patients were eligible only if they had had a positive response to tamoxifen). Eligible patients with measurable and non-measurable disease were randomized to receive either a single daily dose of 1 mg or 10 mg of ARIMIDEX or megestrol acetate 40 mg four times a day. The studies were double-blinded with respect to ARIMIDEX. Time to progression and objective response (only patients with measurable disease could be considered partial responders) rates were the primary efficacy variables. Objective response rates were calculated based on the Union Internationale Contre le Cancer (UICC) criteria. The rate of prolonged (more than 24 weeks) stable disease, the rate of progression, and survival were also calculated.

Both trials included over 375 patients; demographics and other baseline characteristics were similar for the three treatment groups in each trial. Patients in the 0005 trial had responded better to prior tamoxifen treatment. Of the patients entered who had prior tamoxifen therapy for advanced disease (58% in Trial 0004; 57% in Trial 0005), 18% of these patients in Trial 0004 and 42% in Trial 0005 were reported by the primary investigator to have responded. In Trial 0004, 81% of patients were ER-positive, 13% were ER-unknown, and 6% were ER-negative. In Trial 0005, 58% of patients were ER-positive, 37% were ER-unknown, and 5% were ER-negative. In Trial 0004, 62% of patients had measurable disease compared to 79% in Trial 0005. The sites of metastatic disease were similar among treatment groups for each trial. On average, 40% of the patients had soft tissue metastases, 60% had bone metastases, and 40% had visceral (15% liver) metastases.

As shown in the table below, similar results were observed among treatment groups and between the two trials. None of the within-trial differences were statistically significant.


. ARIMIDEX
1 mg ARIMIDEX
10 mg Megestrol
Acetate
160 mg
Trial 0004
(N. America) (n=128) (n=130) (n=128)
Median Follow-up (months)* 31.3 30.9 32.9
Median Time to Death (months) 29.6 25.7 26.7
2 Year Survival Probability (%) 62.0 58.0 53.1
Median Time to Progression (months) 5.7 5.3 5.1
Objective Response
(all patients) (%) 12.5 10.0 10.2
Stable Disease for >24 weeks (%) 35.2 29.2 32.8
Progression (%) 86.7 85.4 90.6
* Surviving Patients
Trial 0005
(Europe, Australia, S. Africa) (n=135) (n=118) (n=125)
Median Follow-up (months)* 31.0 30.9 31.5
Median Time to Death (months) 24.3 24.8 19.8
2 Year Survival Probability (%) 50.5 50.9 39.1
Median Time to Progression (months) 4.4 5.3 3.9
Objective Response
(all patients) (%) 12.6 15.3 14.4
Stable Disease for >24 weeks (%) 24.4 25.4 23.2
Progression (%) 91.9 89.8 92.0
* Surviving Patients



More than 1/3 of the patients in each treatment group in both studies had either an objective response or stabilization of their disease for greater than 24 weeks. Among the 263 patients who received ARIMIDEX 1 mg, there were 11 complete responders and 22 partial responders. In patients who had an objective response, more than 80% of the patients were still responding at 6 months, from randomization and more than 45% were still responding at 12 months from randomization.

When data from the two control trials are pooled, the objective response rates and median times to progression and death were similar for patients randomized to ARIMIDEX 1 mg and megestrol acetate. There is, in this data, no indication that ARIMIDEX 10 mg is superior to ARIMIDEX 1 mg.

Trials
0004& 0005
(Pooled Data) ARIMIDEX
1 mg

(N=263)
ARIMIDEX
10 mg

(N=248)
Megestrol Acetate 160 mg

(N=253)

Median Time to Death (months) 26.7 25.5 22.5
2 Year Survival Probability (%) 56.1 54.6 46.3
Median Time to Progression (months) 4.8 5.3 4.6
Objective Response
(all patients) (%) 12.5 12.5 12.3



Objective response rates and median times to progression and death for ARIMIDEX 1 mg were similar to megestrol acetate for women over or under 65. There were too few non-white patients studied to draw conclusions about racial differences in response.

 

[OMEGA]

ADVERSE REACTIONS

ARIMIDEX was generally well tolerated in two well-controlled clinical trials (ie, Trials 0004 and 0005), with less than 3.3% of the ARIMIDEX-treated patients and 4.0% of the megestrol acetate-treated patients withdrawing due to an adverse event.

The principal adverse event more common with ARIMIDEX than megestrol acetate was diarrhea. Adverse events reported in greater than 5% of the patients in any of the treatment groups in these two well-controlled clinical trials, regardless of causality, are presented below:

Number and Percentage of Patients with Adverse Event†

. ARIMIDEX
1 mg
(n = 262) ARIMIDEX
10 mg
(n = 246) Megestrol
Acetate
160 mg
(n = 253)
Adverse Event n
%
n
%
n
%

Asthenia 42
(16.0)
33
(13.4)
47
(18.6)

Nausea 41
(15.6)
48
(19.5)
28
(11.1)

Headache 34
(13.0)
44
(17.9)
24
(9.5)

Hot Flushes 32
(12.2)
29
(10.6)
21
(8.3)

Pain 28
(10.7)
38
(15.4)
29
(11.5)

Back Pain 28
(10.7)
26
(10.6)
19
(7.5)

Dyspnea 24
(9.2)
27
(11.0)
53
(20.9)

Vomiting 24
(9.2)
26
(10.6)
16
(6.3)

Cough Increased 22
(8.4)
18
(7.3)
19
(7.5)

Diarrhea 22
(8.4)
18
(7.3)
7
(2.8)

Constipation 18
(6.9)
18
(7.3)
21
(8.3)

Abdominal Pain 18
(6.9)
14
(5.7)
18
(7.1)

Anorexia 18
(6.9)
19
(7.7)
11
(4.3)

Bone Pain 17
(6.5)
26
(11.8)
19
(7.5)

Pharyngitis 16
(6.1)
23
(9.3)
15
(5.9)

Dizziness 16
(6.1)
12
(4.9)
15
(5.9)

Rash 15
(5.7)
15
(6.1)
19
(7.5)

Dry Mouth 15
(5.7)
11
(4.5)
13
(5.1)

Peripheral Edema 14
(5.3)
21
(8.5)
28
(11.1)

Pelvic Pain 14
(5.3)
17
(6.9)
13
(5.1)

Depression 14
(5.3)
6
(2.4)
5
(2.0)

Chest Pain 13
(5.0)
18
(7.3)
13
(5.1)

Paresthesia 12
(4.6)
15
(6.1)
9
(3.6)

Vaginal Hemorrhage 6
(2.3)
4
(1.6)
13
(5.1)

Weight Gain 4
(1.5)
9
(3.7)
30
(11.9)

Sweating 4
(1.5)
3
(1.2)
16
(6.3)

Increased Appetite 0
(0)
1
(0.4)
13
(5.1)

†A patient may have more than one adverse event.



Other less frequent (2% to 5%) adverse experiences reported in patients receiving ARIMIDEX 1 mg in either Trial 0004 or Trial 0005 are listed below. These adverse experiences are listed by body system and are in order of decreasing frequency within each body system regardless of assessed causality.

Body as a Whole: Flu syndrome; fever; neck pain; malaise; accidental injury; infection

Cardiovascular: Hypertension; thrombophlebitis

Hepatic: Gamma GT increased; SGOT increased; SGPT increased

Hematologic: Anemia; leukopenia

Metabolic and Nutritional: Alkaline phosphatase increased; weight loss

Mean serum total cholesterol levels increased by 0.5 mmol/L among patients receiving ARIMIDEX. Increases in LDL cholesterol have been shown to contribute to these changes.

Musculoskeletal: Myalgia; arthralgia; pathological fracture

Nervous: Somnolence; confusion; insomnia; anxiety; nervousness

Respiratory: Sinusitis; bronchitis; rhinitis

Skin and Appendages: Hair thinning; pruritus

Urogenital: Urinary tract infection; breast pain

Vaginal bleeding has been reported infrequently, mainly in patients during the first few weeks after changing from existing hormonal therapy to treatment with ARIMIDEX. If bleeding persists, further evaluation should be considered.

The incidences of the following adverse event groups, potentially causally related to one or both of the therapies because of their pharmacology, were statistically analyzed: weight gain, edema, thromboembolic disease, gastrointestinal disturbance, hot flushes, and vaginal dryness. These six groups, and the adverse events captured in the groups, were prospectively defined. The results are shown in the table below.

The principal adverse event more common with ARIMIDEX than megestrol acetate was diarrhea. Adverse events reported in greater than 5% of the patients in any of the treatment groups in these two well-controlled clinical trials, regardless of causality, are presented below:

The incidences of the following adverse event groups, potentially causally related to one or both of the therapies because of their pharmacology, were statistically analyzed: weight gain, edema, thromboembolic disease, gastrointestinal disturbance, hot flushes, and vaginal dryness. These six groups, and the adverse events captured in the groups, were prospectively defined. The results are shown in the table below.

Number and Percentage of Patients

. ARIMIDEX

1 mg

(n=262)
ARIMIDEX

10 mg

(n=246)
Megestrol Acetate

160 mg

(n=253)

Adverse Event Group N
%
N
%
N
%

Gastrointestinal Disturbance 77
(29.4)
81
(32.9)
54
(21.3)

Hot Flushes 33
(12.6)
29
(11.8)
35
(13.8)

Edema 19
(7.3)
28
(11.4)
35
(13.8)

Thromboembolic Disease 9
(3.4)
4
(1.6)
12
(4.7)

Vaginal Dryness 5
(1.9)
3
(1.2)
2
(0.8)

Weight Gain 4
(1.5)
10
(4.1)
30
(11.9)




More patients treated with megestrol acetate reported weight gain as an adverse event compared to patients treated with ARIMIDEX 1 mg (p<0.0001). Other differences were not statistically significant.

An examination of the magnitude of change in weight in all patients was also conducted. Thirty-four percent (87/253) of the patients treated with megestrol acetate experienced weight gain of 5% or more, and 11% (27/253) of the patients treated with megestrol acetate experienced weight gain of 10% or more. Among patients treated with ARIMIDEX 1 mg, 13% [33/262] experienced weight gain of 5% or more, and 3% [6/262] experienced weight gain of 10% or more. On average, this 5% to 10% weight gain represented between 6 and 12 pounds.

No patients receiving ARIMIDEX or megestrol acetate discontinued treatment due to drug-related weight gain.

DRUG INTERACTIONS

(See CLINICAL PHARMACOLOGY) Anastrozole inhibited in vitro metabolic reactions catalyzed by cytochromes P450 1A2, 2C8/9, and 3A4 but only at relatively high concentrations. Anastrozole did not inhibit P450 2A6 or the polymorphic P450 2D6 in human liver microsomes. Anastrozole did not alter the pharmacokinetics of antipyrine. Although there have been no formal interaction studies other than with antipyrine, based on these in vivo and in vitro studies, it is unlikely that co-administration of a 1-mg dose of ARIMIDEX with other drugs will result in clinically significant drug inhibition of cytochrome P450-mediated metabolism of the other drugs.

Drug/Laboratory Test Interactions: No clinically significant changes in the results of clinical laboratory tests have been observed.

 

[OMEGA]

WARNINGS

ARIMIDEX can cause fetal harm when administered to a pregnant woman. Anastrozole has been found to cross the placenta following oral administration of 0.1 mg/kg in rats and rabbits (about 3/4 and 1.5 times the recommended human dose, respectively, on a mg/m2 basis). Studies in both rats and rabbits at doses equal to or greater than 0.1 and 0.02 mg/kg/day, respectively (about 3/4 and 1/3, respectively, the recommended human dose on a mg/m2 basis), administered during the period of organogenesis showed that anastrozole increased pregnancy loss (increased pre- and/or post-implantation loss, increased resorption, and decreased numbers of live fetuses); effects were dose-related in rats. Placental weights were significantly increased in rats at doses of 0.1 mg/kg/day or more.

Evidence of fetotoxicity, including delayed fetal development (i.e., incomplete ossification and depressed fetal body weights), was observed in rats administered doses of 1 mg/kg/day (which produced plasma anastrozole Cssmax and AUC0-24 hr that were 19 times and 9 times higher than the respective values found in healthy post-menopausal humans at the recommended dose). There was no evidence of teratogenicity in rats administered doses up to 1.0 mg/kg/day. In rabbits, anastrozole caused pregnancy failure at doses equal to or greater than 1.0 mg/kg/day (about 16 times the recommended human dose on a mg/m2 basis); there was no evidence of teratogenicity in rabbits administered 0.2 mg/kg/day (about 3 times the recommended human dose on a mg/m2 basis).

There are no adequate and well-controlled studies in pregnant women using ARIMIDEX. If ARIMIDEX is used during pregnancy or if the patient becomes pregnant while receiving this drug, the patient should be apprised of the potential hazard to the fetus or potential risk for loss of the pregnancy.

PRECAUTIONS

General

Before starting treatment with ARIMIDEX, pregnancy must be excluded (see WARNINGS).

ARIMIDEX should be administered under the supervision of a qualified physician experienced in the use of anticancer agents.

Laboratory Tests

Three-fold elevations of mean serum gamma glutamyl transferase (GT) levels have been observed among patients with liver metastases receiving ARIMIDEX or megestrol acetate. These changes were likely related to the progression of liver metastases in these patients, although other contributing factors could not be ruled out.

Drug Interactions

(See CLINICAL PHARMACOLOGY) Anastrozole inhibited in vitro metabolic reactions catalyzed by cytochromes P450 1A2, 2C8/9, and 3A4 but only at relatively high concentrations. Anastrozole did not inhibit P450 2A6 or the polymorphic P450 2D6 in human liver microsomes. Anastrozole did not alter the pharmacokinetics of antipyrine. Although there have been no formal interaction studies other than with antipyrine, based on these in vivo and in vitro studies, it is unlikely that co-administration of a 1-mg dose of ARIMIDEX with other drugs will result in clinically significant drug inhibition of cytochrome P450-mediated metabolism of the other drugs.

Drug/Laboratory Test Interactions

No clinically significant changes in the results of clinical laboratory tests have been observed.

Carcinogenesis, Mutagenesis, and Impairment of Fertility

Carcinogenesis: No long-term animal studies have been conducted to assess the carcinogenic potential of ARIMIDEX.

Mutagenesis: ARIMIDEX has not been shown to be mutagenic in in vitro tests (Ames and E. coli bacterial tests, CHO-K1 gene mutation assay) or clastogenic either in vitro (chromosome aberrations in human lymphocytes) or in vivo (micronucleus test in rats).

Impairment of Fertility: Studies to investigate the effect of ARIMIDEX on fertility have not been conducted; however, chronic studies indicated hypertrophy of the ovaries and the presence of follicular cysts in rats administered doses equal to or greater than 1 mg/kg/day (which produced plasma anastrozole Cssmax and AUC0-24 hr that were 19 times and 9 times higher than the respective values found in healthy post-menopausal humans at the recommended dose). In addition, hyperplastic uteri were observed in chronic studies of female dogs administered doses equal to or greater than 1 mg/kg/day (which produced plasma anastrozole Cssmax and AUC0-24 hr that were 22 times and 16 times higher than the respective values found in post-menopausal humans at the recommended dose). It is not known whether these effects on the reproductive organs of animals are associated with impaired fertility in humans.

Pregnancy

Pregnancy Category D: (See WARNINGS).

Nursing Mothers

It is not known if anastrozole is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when ARIMIDEX is administered to a nursing woman (see WARNINGS).

Pediatric Use

The safety and efficacy of ARIMIDEX in pediatric patients have not been established.

Geriatric Use

Fifty percent of patients in studies 0004 and 0005 were 65 or older. Response rates and time to progression were similar for the over 65 and younger patients.

 

[OMEGA]

OVERDOSAGE

Clinical trials have been conducted with ARIMIDEX, up to 60 mg in a single dose given to healthy male volunteers and up to 10 mg daily given to post-menopausal women with advanced breast cancer; these dosages were well tolerated. A single dose of ARIMIDEX that results in life-threatening symptoms has not been established. In rats, lethality was observed after single oral doses that were greater than 100 mg/kg (about 800 times the recommended human dose on a mg/m2 basis) and was associated with severe irritation to the stomach (necrosis, gastritis, ulceration, and hemorrhage).

There is no specific antidote to overdosage and treatment must be symptomatic. In the management of an overdose, consider that multiple agents may have been taken. Vomiting may be induced if the patient is alert. Dialysis may be helpful because ARIMIDEX is not highly protein bound. General supportive care, including frequent monitoring of vital signs and close observation of the patient, is indicated.

CONTRAINDICATIONS

None known.

 

[OMEGA]

Re: HUCKS condensed assesment of benifits of liquidex

Sure buddy.By down-regulating aromitase/estrogen production,one is less likely to be succeptible towards developing those 'stubborn' fatty pockets(love handles,lower pecs,stomach)that plague those of us with a moderate to high level of estradiol production.Estrogen is also pivotal in sub-q regions,where it causes fluid retention and smoothing between the muscle and skin.Then there is the skin itself:Estrogen has a 'thickening' effect on the dermal layers,that is,it increases the cell populations and intracellular volume of the dermal regions.By using an agent such as liquidex,you can actually REVERSE this effect,and what that correalates to is that paper-thin skin that shows off vascularity/cuts like nothing else.As for the hormonal benefits,by blocking off overall E production,the hypothalamus and pituitary compensate by creating more of their catalystic hormones(GnRH,L/H)in hopes that by producing more T,that enzymatic conversion will bring E levels back in line.What these glands don't know however,is that the enzyme responsible for this(aromitase)is being blocked off at the testicular level.So using liquidex actually creates an optimal hormonal environment,one rich in T production and starved in E production.

 

[the UNDERTAKER]

what about male fertility?? or reproductive abnormalities??

 

[DTOX]

It increases LH/FSH... I wouldn't be surprised if it's used to treat male infertility in the future.

what about male fertility?? or reproductive abnormalities??

 

[OMEGA]

then why do people use clomid?


and why have non of you thanked my girlfreind?

 

[macDbol]

i dont talk to inflatable dolls, let alone thank them


j/k,,,good post

 

[shifti]

who the fuck is going to read all of that bullshit

 

[Beach Boy]

omega's question

do we need as much clomid, or clomid at all, if I've been using arimidex?

Thank you omega, spank your girlfriend for me.

 

[OMEGA]

she will be spanked, but if I spank too hard she will deflate

 

[Willyumyum]

she will be spanked, but if I spank too hard she will deflate

YUM

 

[HUCKLEBERRY FINNaplex]

Tell the GF to sign up,and we'll shoot some karma at her...

 

[monkeyballs]

who the fuck is going to read all of that bullshit

Go away and play with your crayons.


Great post. So I'm guessing this is from the pamphlet that comes with a filled script?

Also, with femara and l-dex Clomid is now totally obsolete? Correct?

 

[OMEGA]

YUM

Tell the GF to sign up,and we'll shoot some karma at her...

smooth one

she may she just may

Great post. So I'm guessing this is from the pamphlet that comes with a filled script?

Also, with femara and l-dex Clomid is now totally obsolete? Correct?

I don't know about the clomid femara thing

but as far as the info

she is a master degree student at UCSF medical school and they have online data base access to some pretty interesting stuff
that would cost us money to get

if you got some questions on other stuff drop me a pm and I can post some...info

last time I checked we were in this all together so the more info the merrier

 

[monkeyballs]

Solid.
PM coming your way.

And for what it's worth...some Karma.

 

[OMEGA]

got it

 

[Counterstrike]

dude my eyes are killing me to read so i will ask. is it safe for weight loss and at what dose is effective and till how long? i read a post a while back wher ethis guy had his girl take armin and started losing weight big time so he said but peopel where tellign himto stop it b/c is bad due to estrogen reducing qualities is it safe or not and s it effective?

 

[Counterstrike]

up

 

[OMEGA]

?

 

[OMEGA]

bumpalump

 

[iamcdn]

can i get a summary
i don't even read that much in 4months of university

 

[Punschkrapfen]

i read a post a while back wher ethis guy had his girl take armin and started losing weight big time so he said but peopel where tellign himto stop it b/c is bad due to estrogen reducing qualities is it safe or not and s it effective?

it should not work for pre-meonpausal women because they produce most of their estrogen in the ovaries. Only post-menopausal women produce estrogen like men, of course, very much less because they don't have testes, but the adrenal gland also makes some testosterone. And only the formation of estrogen from testosteorone using the enzyme aromatase can be blocked.

 

[totallyjacked]

CONFUSED

I have a few questions actually, is liquidex just the generic version of armidex? If using liquidex is it not necessary to take clomid anymore? When during or after a cycle should it be taken and at what dose and for how long should it be taken for a 200lb male. If anyone can answer this question that would be great!

 

[ROAD DOG]

what about the bad cholesterol issue with liquidex,how common is it to mess up someone's cholesterol levels while using liquidex?

 

[Punschkrapfen]

some posts on this board indicate that people are already replacing clomid with aromatase inhibitors post cycle.
there are 2 negative feedback loops on the HPTA - testosterone and estrogen. it is possible that the pituitary gland does not produce LH even if no testosterone is present, but estrogen is. to keep estrogen away from the hypothalamus, you can either block the receptors there or eliminate estrogen from the body altogether. Clomid and Nolvadex do the first thing (SERM - selective estrogen receptor modulator), aromatase inhibitors do the second thing.
Whether one approach is better than the other remains open, because i don't know how well Clomifen does bind to the estrogen receptors. Its definately not 100%, because both Nolvadex and Clomid fight with estrogen to bind.

and, yes, liquidex contains anastrozole, the same ingredient as in Arimidex. read: http://www.mesomorphosis.com/steroid-photographs/anastrozole/
Femara (letrozole) and Aromasin (exemestane) are stronger though.
Arimidex can eliminate some 80%, Femara 90% and Aromasin up to 98% of aromatase produced estrogen. Best and safest approach to cycle recovery would be to combine one aromatase inhibitor with a SERM.

 

[emptywallet]

some posts on this board indicate that people are already replacing clomid with aromatase inhibitors post cycle.
there are 2 negative feedback loops on the HPTA - testosterone and estrogen. it is possible that the pituitary gland does not produce LH even if no testosterone is present, but estrogen is. to keep estrogen away from the hypothalamus, you can either block the receptors there or eliminate estrogen from the body altogether. Clomid and Nolvadex do the first thing (SERM - selective estrogen receptor modulator), aromatase inhibitors do the second thing.
Whether one approach is better than the other remains open, because i don't know how well Clomifen does bind to the estrogen receptors. Its definately not 100%, because both Nolvadex and Clomid fight with estrogen to bind.

and, yes, liquidex contains anastrozole, the same ingredient as in Arimidex. read: http://www.mesomorphosis.com/steroid-photographs/anastrozole/
Femara (letrozole) and Aromasin (exemestane) are stronger though.
Arimidex can eliminate some 80%, Femara 90% and Aromasin up to 98% of aromatase produced estrogen. Best and safest approach to cycle recovery would be to combine one aromatase inhibitor with a SERM.

So if your taking liquidex with clomid, it would be useless as the clomid would have no estrogen to bind to? That doesnt sound right for some reason......

 

[FOZY]

So if your taking liquidex with clomid, it would be useless as the clomid would have no estrogen to bind to? That doesnt sound right for some reason......

Clomid binds not to acruall estrogen but to estrogen RECEPTOR sites in the pituitary gland. When the sights are blocked estrogen cant fill them.....Nolvadex does the same thing but uses different sites ( mostly the breast ) but has the same function as clomid........................So arimi and clomid ot Nolva togeather seams like a good combo..elimate estrogen and what does get through has no wehre to go since clomid / nolva are filling the sited


Hope this helped

 

[Golfer18--old]

It amazes me that some of you will ask questions when the information is right in front of you because you don't want to become educated on the subject.

 

[Golfer18--old]

Oh yeah, great post OMEGA.

 

[emptywallet]

It amazes me that some of you will ask questions when the information is right in front of you because you don't want to become educated on the subject.

It takes me a little bit to get some things. I am unsure of my ability to understand things sometimes. I was curious to if I was reading it correctly, apparently I was not, so I'm glad I asked the question. Sorry if I am inconviencing (sp) you in some way.

 

[RRR]

Sorry but I'm not fully comprehending all this
Can someone explain this an easier way. I read it 3x's and still confused This seems like it is a good post if you could understand it. No flames please, bet you not everyone understands all this medical talk. Thanks

 

[OMEGA]

Oh yeah, great post OMEGA.

thanks mang

 

[emptywallet]

Clomid binds not to acruall estrogen but to estrogen RECEPTOR sites in the pituitary gland. When the sights are blocked estrogen cant fill them.....Nolvadex does the same thing but uses different sites ( mostly the breast ) but has the same function as clomid........................So arimi and clomid ot Nolva togeather seams like a good combo..elimate estrogen and what does get through has no wehre to go since clomid / nolva are filling the sited


Hope this helped

Thank you for the reply. I understand it now. I appreciate you helping me with it. RRR, better watch asking questions bro, Golfer might come by and start swingin at you with one of his clubs if you ask questions ......

 

[RRR]

Thank you for the reply. I understand it now. I appreciate you helping me with it. RRR, better watch asking questions bro, Golfer might come by and start swingin at you with one of his clubs if you ask questions ......

LOL......Golfer, please don't come after me with a 9 iron

 

[Golfer18--old]

LOL bro I'm not coming at you with a nine iron....