any ideas for bad blood test results

[bigbaldbulldog]

got my results back for my blood work...everything was great excpet my cholesterol , it was waaaay off..my good was 13 should be 40 and my bad was 200 and should be 120....i am only 3 weeks into a cycle and i am only doing 750 mgs test a week 300 mgs tren and ....my diet is pretty sound and i am not sure what i can do to get my numbers half way right...any ideas short of stopping my cycle ?

[rugbythug]

What about your ant-e's that can hurt them pretty bad. Mine was bad but better than yours. I think I was using a lot of femera when I got mine. Look into exemestan if you are real nervous

[bigbaldbulldog]

well i had just strted talking them 5 days before and it was letrozole...2.5 mgs a day...i have bad shit like that in my family so i need to be acferful of the cholesterol levels...

[jipped genes]

policosanol is a supplement that has helped me drop my LDL 45 points in 1 month and raised HDL 12 while that dosnt solve the problem it did help and i have changed nothing in my diet so i would say its the policosanol. check this link out

http://www.myplanet.net/bpgroup/about_policosanol.html

[SuperSport]

there is some debate about cholesterol levels.....some of the research I have read put forth by Dr. William Campbell Douglass, MD, and Dr. Robert Jay Rowen, MD, is pretty convincing that cholesterol is not the evil that modern medicine claims it to be.

Doglass has referred to an article published in the British Medical Journal (the Lancet I suppose) that indicates cholesterol screening is useless....I will try to dig up that study/research. I have been curious about it myself.

However, homocystiene levels are an excellent indicator of cardiovascular disease....men with high levels of homo have 3x as many heart attacks as men that have low levels. Seems like oxysterols are the root cause of elevated homo levels. B-vitamins are excellent in lowering homo levels. Douglass has said.."Homocystiene corrodes the vessels".

I will try to find this cholesterol news from thses MD's (and others) and I will post it when I track the info down.

[bigbaldbulldog]

great..thanks guys..glad to be back home..got inches of snow last night....no golfing here...

[SuperSport]

here is some info...didn't get to check all of it out...but basically saying screening tests are not accurate in predicting disease...I will look further in the next few days...

British Medical Journal april 28, 2001

Type that into a search on google, some info will come back.

[xcelbeyond]

Synthergine by Synthetek has worked wonders for many to get liver values better.

I've read lots where letrozole will f*ck your lipid profile, esp LDL. How much are you taking? I went from from 1 tab ED to 1/2 tab ED to 1/2 tab EOD and that's on 1g test + other goodies (I'm VERY prone to e-related gyno).

xcel

[Heckman]

Originally posted by SuperSport
here is some info...didn't get to check all of it out...but basically saying screening tests are not accurate in predicting disease...I will look further in the next few days...

British Medical Journal april 28, 2001

Type that into a search on google, some info will come back.

Kind of makes you wonder how much more mis-information the medical community tries to get us to believe!
Once you figure out who educates most of our Doc's, you will then know where all of this hocus pocus comes from...
Oh, he mumbled...."could it be the the pharmaceutical cartel?"

[bigbaldbulldog]

taking 1 1/4 mgs liquid letrozole ED....i will contact them asap to get things back on track ...thanks

[Bilter]

[
However, homocystiene levels are an excellent indicator of cardiovascular disease....men with high levels of homo have 3x as many heart attacks as men that have low levels. Seems like oxysterols are the root cause of elevated homo levels. B-vitamins are excellent in lowering homo levels. Douglass has said.."Homocystiene corrodes the vessels".

My dad had a heart attack about 10 years ago. Everything checked out normal EXCEPT his homocystiene levels were very high. He ahd to go a on 3 months (If I remember correct) cycle of B12 shots .

[Magic]

I alsolo have bad cholsterol levels- probably due to all the gear plus the anti-es. I've just started using a product that is a mix of gugguls, niacin and policosanol to prevent it- after 3months the results are impressive.

Someone above said to look into using exemestane instead of letrozole? So it's not the actual action of the anti-e that stuffs LDL levels? I mean, how is exemestane any better than letrozole? Cos you can take it less often?

[Magic]

Found these:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11506958

and this in another one:

"ENDOCRINE PATHWAY REVEALS "ACHILLES' HEEL": Like other steroid hormones, the two circulating estrogens-estrone and estradiol-are produced from cholesterol. Inhibiting the enzymes that are involved at earlier steps in the branching pathway of steroidogenesis could have an undesirable impact on the production of other physiologically important hormones such as aldosterone and cortisol. Since aromatase catalyzes the last step in estrogen production, it makes an ideal target for the development of selective and potent inhibitors "

Maybe this is why it increases LDL- without the aromatase little cholesterol is broken down to make any oestrogen/testosterone.... so if that was true, exemestane would also have a negative effect on lipids....still reading.....

and this:

[Early phase II dose-finding study of exemestane in postmenopausal patients with advanced/recurrent breast cancer]

[Article in Japanese]

Tabei T, Ogita M, Hirata K, Satomi S, Kimura M, Abe R, Morishita Y, Kimura M, Andou J, Higashi Y, Yoshino K, Tominaga K, Kajiwara T, Kitajima M, Koyanagi Y, Watanabe T, Yamaguchi S, Watanabe M, Toyama K, Kanda K, Kashiki Y, Miura S, Kobayashi Z, Aoyama H, Miyazaki I, Oka T, Koyama H, Kinoshita H, Monden M, Takai S, Yayoi E, Kobayashi T, Takatsuka Y, Kajiwara T, Sonoo H, Toge T, Takashima S, Nomura Y, Nagao K, Fujita Y.

Saitama Cancer Center.

Exemestane was administered orally to postmenopausal women with advanced/recurrent breast cancer at a dose of 10 mg/day or 25 mg/day once daily for more than 8 weeks in order to evaluate the drug's anti-tumor effects and safety in a dose-finding study. The response rate (CR + PR) in the 10 mg and 25 mg group was 25.0% (8/32) and 31.4% (11/35), respectively, demonstrating no significant differences between the two groups, yet a higher efficacy rate was observed in 25 mg group. The efficacy rate in hormone-treatment-resistant patients within the 10 mg and 25 mg groups was 14.3% (3/21) and 26.1% (6/23), respectively, demonstrating more than a 20% response rate in 25 mg group. Incidences of the adverse events of which relevance to the drug could not be excluded were 30.6% (11/36) in the 10 mg group. 13.9% (5/36) in the 25 mg group and 22.2% (16/72) in the total group. The major adverse events were, hot flashes, numbness of the limbs, nausea, headache etc. Abnormal findings in clinical laboratory tests were as follows: ALP increase; GOT increase; GPT increase; gamma-GTP increase; total cholesterol increase; urinary sediment present. Abnormal findings in endocrine function were as follows: aldosterone decrease; testosterone.cortisol.DHEA-S decrease. .
total cholesterol increase

but then there is this one- good and bad:

"During dose escalation with the aromatase inhibitor exemestane, the methylene line width seemed to decrease (31.9 vs 38.8 Hz, at 12 weeks and baseline, respectively). Significant decreases in total (13%) and HDL (32%) cholesterol, apo A1 (25%), and total triglyceride (16%) levels were found during the same interval." Breast Cancer Res Treat. 1995;36(3):287-97.

and then, so I'm totally confused:

" In OVX animals, EXE resulted in a 28% reduction of serum cholesterol (P<0.0001) and reduced LDL by 64% compared with OVX controls (P<0.0001). The positive results of EXE on bone and lipid metabolism in the OVX rat model merit further investigation of the effects of EXE in postmenopausal women." Bone. 2004 Mar;34(3):384-92.

BUT to finalise off, and this one I believe because it was written very recently in a peer-reviewed cancer journal....

Ann Oncol. 2004 Feb;15(2):211-7. Related Articles, Links


The effect of exemestane on serum lipid profile in postmenopausal women with metastatic breast cancer: a companion study to EORTC Trial 10951, 'Randomized phase II study in first line hormonal treatment for metastatic breast cancer with exemestane or tamoxifen in postmenopausal patients'.

Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C, Cufer T, Lobelle JP, Mattiaci MR, Piccart M, Paridaens R.

Jules Bordet Institute, Brussels, Belgium.

BACKGROUND: The impact of aromatase inhibitors (AIs) on non-cancer-related outcomes, which are known to be affected by oestrogens, has become increasingly important in postmenopausal women with hormone-dependent breast cancer. So far, data related to the effect of AIs on lipid profile in postmenopausal women is scarce. This study, as a companion substudy of an EORTC phase II trial (10951), evaluated the impact of exemestane, a steroidal aromatase inactivator, on the lipid profile of postmenopausal metastatic breast cancer (MBC) patients. PATIENTS AND METHODS: The EORTC trial 10951 randomised 122 postmenopausal breast cancer patients to exemestane (E) 25 mg (n = 62) or tamoxifen (T) 20 mg (n = 60) once daily as a first-line treatment in the metastatic setting. Exemestane showed promising results in all the primary efficacy end points of the trial (response rate, clinical benefit rate and response duration), and it was well tolerated with low incidence of serious toxicity. As a secondary end point of this phase II trial, serum triglycerides (TRG), high-density lipoprotein cholesterol (HDL), total cholesterol (TC), lipoprotein a (Lip a), and apolipoproteins (Apo) B and A1 were measured at baseline and while on therapy (at 8, 24 and 48 weeks) to assess the impact of exemestane and tamoxifen on serum lipid profiles. Of the 122 randomised patients, those who had baseline and at least one other lipid assessment are included in the present analysis. The patients who received concomitant drugs that could affect lipid profile are included only if these drugs were administered throughout the study treatment. Increase or decrease in lipid parameters within 20% of baseline were considered as non-significant and thus unchanged. RESULTS: Seventy-two patients (36 in both arms) were included in the statistical analysis. The majority of patients had abnormal TC and normal TRG, HDL, Apo A1, Apo B and Lip a levels at baseline. Neither exemestane nor tamoxifen had adverse effects on TC, HDL, Apo A1, Apo B or Lip a levels at 8, 24 and 48 weeks of treatment. Exemestane and tamoxifen had opposite effects on TRG levels: exemestane lowered while tamoxifen increased TRG levels over time. There were too few patients with normal baseline TC and abnormal TRG, HDL, Apo A1, Apo B and Lip a levels to allow for assessment of E's impact on these subsets. The atherogenic risk determined by Apo A1:Apo B and TC:HDL ratios remained unchanged throughout the treatment period in both the E and T arms. CONCLUSIONS: Overall, exemestane has no detrimental effect on cholesterol levels and the atherogenic indices, which are well-known risk factors for coronary artery disease. In addition, it has a beneficial effect on TRG levels. These data, coupled with E's excellent efficacy and tolerability, support further exploration of its potential in the metastatic, adjuvant and chemopreventive setting."

Moral of the story.....results are all over the shop but it seems promising that exemestane is actually better for serum Cholesterol levels than letrozole and tamoxifen.

[BiggerStronger]

Either take exemestane or take 1.25mg of letrozole EOD with 10-20mg of Nolva ED. Nolva acts as a estrogen in the liver thus making cholesterol levels better. Estrogen has a big part in cholestrol regulation.