Beware the effects of Anastrazole

[Komo]

Since estrogen ataches to the DNA, how can the affinity for the receptor (ere) change within one single human being?

Do you think that polymorphisms in the estrogen responce element are present in differen tissues of the body??

Either it antagonizes or it doesn`t.....

i can´t see how the liver would detect an estrogen without the route through the estrogen receptor. Do you know any other way? I am very interested in this stuff, so if you got some more info i would be glad to read it!

/Komo

 

[fhg43]

See this post:

Arimidex & Letrozole(Femara)

One thing to keep in mind is that the the natural conversion of test to estradiol is what keeps coronary arterys from becoming suseptible to atherogenesis.

Check out my link. I agree that aromatase inhibitors may be helpful in cycles with high doses of test, but I also think it is used in situations where it isn't needed.

FHG

 

[40butpumpin]

Cholesterol does not "clog arteries." This is verbage that is designed to frighten the uneducated into taking cholesterol lowering drugs and lining the pockets of the phatmaceutical companies.

Cardiovascular disease is a hardening of the arteries. Hardening of the arteries is caused by calcification of the same. Calcification is just that, a build up of calcium along the arterial wall(s). Calcium buildup is caused by a very complex process which has very little, if anything at all, to do with cholesterol. Doctors in Europe have discovered a bacteria called nanobacteria (obviously named for its size), that are setting up camp on our arterial walls and creating an environment there that causes this complex process to start and then continue to accelerate. Homocysteine is a big player in all of this. With it the process continues, without it the process is halted. If you don't catch it early enough and your arteries become calcified you can still get help with chelation therapy. There is a protocol involving EDTA, a powerful chelating agent used for chelating off the calcium deposits on your arteries, and a simple antibiotic for killing the bacteria. Remember what mainstream medicine did to the guy who discoverd that stomache ulcers were/are caused by a bacteria? Disease is big bucks guys, we need to educate ourselves.

 

[Triple J]

Since estrogen ataches to the DNA, how can the affinity for the receptor (ere) change within one single human being?

Do you think that polymorphisms in the estrogen responce element are present in differen tissues of the body??

Either it antagonizes or it doesn`t.....

i can´t see how the liver would detect an estrogen without the route through the estrogen receptor. Do you know any other way? I am very interested in this stuff, so if you got some more info i would be glad to read it!

/Komo

Komo you need to do some basic research, and I do not want to represent myself as an expert, either. But since your statements show a basic misunderstanding of some facts, maybe I can help clarify some points. Like I said I am not an expert either, so take my statements on a conceptual level, and draw your own conclusions. So no flames please.

Families of steroid hormones (like estradiol, estradione, etc) do not attach to the DNA, hormones interact with receptors which then influence transcription behavior in the DNA and RNA, influencing genetic expression, which proteins are produced, etc. And yes different forms of e will have different affinities for different receptors in different locations. This is why nolvadex and clomid are similiar drugs (both estergen mimickers) but with slightly different charactersitics.

As far as the liver goes, this is where most cholesterol is produced in the body. The liver's lipid metabolism is influenced by many factors, many dietary. The liver also metabolizes, or breaks-down, steroid hormones, like T and E. To illustrate, the reason they add the 17aa to the orals is to make them harder to break-down in the liver. The reason injectable test is esterified is so it will be slowly released, cause once released, it is rapidly metabolized by the liver. The metabolic breakdown of these hormones influences the cholesterol metabolism as well. Now if this is also governed by receptor influence within the liver I do not know. I suspect is just a result of metabolic clearance (hypothetically, perhaps e break-down leads to more HDL somehow).

Artherisclosis is an inflammatory condition, poor lipid profiles can make one more susceptable, but factors mentioned in other posts are all valid disease contributors and perhaps more causative. Another factor is the hormonal balance of echonosoids in the blood which influence a wide degree of potential inflammatory conditions. So many factors will influence tendency to develop disease. However, lipid profile is still accepted by most as a basic risk factor as well.

I hope this helps somewhat.

 

[fhg43]

40butpumpin-

Your points are valid. However read the study I posted on that link (I'll just post it below):

Testosterone attenuates expression of vascular cell adhesion molecule-1 by conversion to estradiol by aromatase in endothelial cells: Implications in atherosclerosis

Abstract:
We previously reported that testosterone attenuated atherogenesis in LDLR/ male mice, and that this effect of testosterone was most likely caused by its conversion to estradiol. Estradiol inhibits vascular cell adhesion molecule-1 (VCAM-1) expression, and expression of VCAM-1 is one of the early events in atherogenesis. We assessed the cellular mechanism(s) involved by which testosterone attenuates atherogenesis. We evaluated whether testosterone inhibited TNF-induced VCAM-1 expression via its conversion to estradiol by the enzyme aromatase in human umbilical vein endothelial cells (HUVEC). Aromatase mRNA was dedected by reverse transcription-PCR in these cells. Testosterone (30 nM-1 µM) attenuated VCAM-1 mRNA expression in a concentration-dependent manner. The non aromatizable androgen, dihydrotestosterone, had no effect on VCAM-1 mRNA expression. Testosterone was less effective in attenuating VCAM-1 expression in the presence of anastrozole, an inhibitor of aromatase, indicating that testosterone inhibited VCAM-1 via conversion to estradiol. Estradiol also attenuated VCAM-1 mRNA expression, but this action was not abolished in the presence of anastrozole, indicating that anastrozole itself did not modulate VCAM-1 mRNA expression. The effect of testosterone on VCAM-1 mRNA expression was inhibited in the presence of the estrogen receptor antagonist, ICI-182780. Testosterone also attenuated TNF-induced VCAM-1 protein expression, and this attenuation was abolished in the presence of anastrozole. In conclusion, testosterone inhibited VCAM-1 mRNA and protein expression in HUVEC by its conversion to estradiol via the enzyme aromatase present in the endothelial cells. Results from our study may help explain the mechanism by which testosterone may have beneficial effects on the cardiovascular system.

Test converts to estradiol; "estradiol inhibits vascular cell adhesion molecule-1 (VCAM-1) expression; and expression of VCAM-1 is one of the early events in atherogenesis."

Atherogenesis-according to WebMD: "(ath´´er-o-jen´ê-sis) formation of abnormal fatty or lipid masses in arterial walls."


FHG

 

[Triple J]

The abstract supports the notion that nolva or clomid could have a similiar inflluence, and be beneficial in a manner not associated with liver lipid metabolism

 

[fhg43]

40butpumpin-

Cholesterol does not "clog arteries."

Ummmm.... WebMd isn't the most technical source on the web but they seem to indicate that cholesterol did clog arteries.

Cholesterol
"Low-density lipoprotein cholesterol (LDL). LDL is called the "bad cholesterol" because it can cause cholesterol buildup and blockage of your arteries. (See an illustration of a blocked artery.) LDL is mostly fat and only a small amount of protein. At normal levels, it carries cholesterol from the liver to other parts of the body where it is needed for cell repair and other activities. When LDL cholesterol is elevated, it and other substances build up in the walls of the arteries and form a plaque (atherosclerosis). Over time, plaque may cause the arteries to harden and narrow. Blood flow to the body's tissues and the heart muscle is reduced (ischemia). At times, the plaque may rupture and a blood clot may form in the narrowed artery, blocking blood flow. This ultimately can lead to damage or death of tissues (heart attack or stroke). By lowering LDL cholesterol, you can reduce your risk of atherosclerosis, heart attack, stroke, and other complications.
An LDL level of less than 100 mg/dL (less than 2.6 mmol/L) is considered optimal.
An LDL level of 100 to 129 mg/dL (2.6 to 3.35 mmol/L) is considered near optimal or above optimal.
An LDL level of 130 to 159 mg/dL (3.35 mmol/L to 4.10 mmol/L) is considered borderline high.
An LDL level of 160 to 189 mg/dL (4.12 to 4.88 mmol/L) is considered high.
An LDL level of 190 and above (4.90 mmol/L and greater) is considered very high.
High-density lipoprotein cholesterol (HDL). HDL is sometimes called the "good cholesterol" because it helps prevent cholesterol from building up in your arteries. It is mostly protein and only a small amount of fat. HDL cholesterol helps clear the bad cholesterol from the body by picking up leftover cholesterol from the bloodstream and carrying it back to the liver for disposal. If you are at risk for heart disease, it may be beneficial to raise your HDL cholesterol levels. Low HDL cholesterol increases the risk of coronary artery disease. High levels of HDL appear to help protect against atherosclerosis, heart attack, stroke, and other complications.
An HDL level of 60 mg/dL (1.56 mmol/L) or higher is desirable. An HDL level over 60 mg/dL reduces the risk of heart disease, even if LDL or total cholesterol is high.
An HDL level of 40 to 60 mg/dL (1.04 to 1.56 mmol/L) is considered acceptable.
An HDL level below 40 mg/dL (below 1.04 mmol/L) is considered low. Low HDL is considered a major risk factor for coronary artery disease in people who also have high total cholesterol levels.
Triglycerides/very low-density lipoprotein cholesterol (VLDL). Triglycerides are another type of fat, which is carried in the blood by very low-density lipoproteins. Only a small amount of triglycerides is normally found in the blood; most are stored in fat tissue. VLDL is similar to LDL cholesterol in that it contains mostly fat and not much protein. A high triglyceride level along with a high LDL cholesterol also can increase the risk of heart attack.
A triglyceride level of 150 to 199 mg/dL is considered borderline high.
A triglyceride level of 200 mg/dL is considered high.
What causes high cholesterol?

Several things can cause high cholesterol. Risk factors for high cholesterol can be broken down into those you can control and those you cannot. There are also secondary causes of high cholesterol, such as medications and medical conditions.

Controllable risk factors include some medical conditions, such as diabetes, and diet. Being overweight, smoking, not exercising, and eating a diet high in saturated fat and cholesterol can cause high LDL, low HDL, and increased triglycerides.
Uncontrollable risk factors include a genetic condition called a lipid disorder, which can cause very high cholesterol levels in your blood. Your age and gender are other risk factors you cannot control. After age 20, cholesterol levels naturally begin to rise. Men have higher cholesterol levels than women until women reach age 50 or so and their cholesterol levels rise.
After puberty, women have higher levels of HDL than men."

This is verbage that is designed to frighten the uneducated into taking cholesterol lowering drugs and lining the pockets of the phatmaceutical companies.

I think that yes the pharmaceutical companies are robbing us, however I think uneducated doctors are worse. I can believe how little I know about anatomy/physiology/biology/medecine/etc... and when a person says to me "yeah, X hurts or I injured X and I went to the doctor and he gave me X to take or told me to stop doing X and I'd be fine" I think WTF! that just covers it up, it doesn't help resolve the issue.

IMO the big problem with medecine is that doctors are less concerned with healing and more concerned with covering pain and discomfort.

FHG

 

[BBBodie]

Restoring your Lipid profile to normal

This is from my ND....so as a doc, she knows her stuff and is a competitor as well. We found my profile was whacked, (duh) and she embarked on a threefold approach to reduction:

First - Cardio 5x a week for at least 40 minutes each, the effects of cardio on your lipid profile are well documented, nuff said there.

Second - Add garlic (powdered) to your diet 500mg each morning

Third - Fish (salmon first and foremost) All of these are well documented to do the job, you do it all, and you normalize your system post cycle in a normal fashion (non-drug induced).

Bottom line - you have to expect the swing of the pendulum on the other side, just because you push it up one side, doesn't mean it won't come back...when it does you have to deal with it in a non-invasive way so your body can normalize and you won't lose your gains.

Bo

 

[Komo]

Triple J!

I am in fact an expert! Steroid hormones DO attach to response elements on the DNA=their receptor..... Maybe u need to do some basic research.


I am a civil engineer in molecular biology, so I know what I am talking about....

/Komo

 

[Triple J]

Triple J!

I am in fact an expert! Steroid hormones DO attach to response elements on the DNA=their receptor..... Maybe u need to do some basic research.


I am a civil engineer in molecular biology, so I know what I am talking about....

/Komo

If you are an expert do us a favor and contribute something meaningful to the thread!! and stop calling me out.