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Wednesday, May 7, 2014

Debunking the Hoax - Testosterone Gel's and Products Causing Cancer

AND Without further or official introductions...that's what I'M CALLING THIS...and that's what I KNOW....and, MOST IMPORTANTLY that's WHAT THIS IS!!
A HOAX, a CAMPAIGN started because of DECEPTION in the industry, and the saddest error of judgement!
 ...A campaign that is partially true, but only because people are MISLED!!!

However I won't let my words alone be the judge. Let's look into this shall we? Follow me.
                                                       ~Read along~
Just keep your bullshit alert on high, because I know in the end you will understand, hopefully.....
For once, I'm sticking up for *(kinda)* the pharmaceuticals....but I also would say this...people NEED TO DO THEIR OWN RESEARCH!!!!!


If you look carefully into public medial journals, where some of these famous groundbreaking and heart shuttling observations were made - there was no specificity nor description of what forms of testosterone were used and if bloodwork was obtained...during and after treatment. It appears not at all in some cases.
In the real-life cases where bloodwork was not obtained and other values were not accounted for, I shame the doctors for that matter. However not all cases are the same - the problem we have is that there has not been ONE study showing that ANDROGENIC hormones; testosterone or DHT have been proven to cause any sort of CANCER themselves, in a setting where the men's estrogen VALUES were also LOW or OPTIMAL. I can say that studies have shown it...but the BIGGER ISSUE - is that ESTROGEN levels are hardly EVER accounted for or examined DURING the course of these studies. ESTROGEN has SIGNIFICANT growth promoting and DOCUMENTED EVIDENCE - of TUMOR PROLIFERATING (growing, replicating) properties!!!!


Well I'll be damned. Prostate Cancer...wanna have a look?
Estrogen action and prostate cancer

Jason L Nelles,1 Wen-Yang Hu,1 and Gail S Prins1,†

In a recent cross-sectional analysis, serum steroid levels were assayed in 1413 matched men of various races and while testosterone levels did not differ, African–American men had significantly higher serum estradiol levels than Caucasian or Mexican–American men, a difference that was most pronounced in early and mid-adulthood[29]. This is highly significant in that African–American men have a twofold higher rate of prostate cancer than Caucasian–American men, as well as a greater prostate cancer risk than Hispanic males. Studies on pre- and peri-natal exposure to estrogens have also raised concerns about their carcinogenic potential. Some authors have suggested that the higher incidence of prostate cancer among African–American men is partly due to in utero exposure to maternal estrogens since African–American women have higher circulating estrogen concentrations during pregnancy than Caucasian women [30,31], although gestational androgen levels are also elevated. Animal models of prostate cancer have demonstrated that, at least in rats, estrogen is a necessary, if not sufficient, condition for prostate carcinogenesis. Although rats do not naturally develop prostate cancer, it can be induced in Noble rats by combined treatment with estradiol and testosterone, with testosterone playing a supportive role since androgen supplementation alone is insufficient to drive carcinogenesis [32–34]. A recent review by Bosland reinforced this notion, citing an incidence of prostate cancer induction in Noble rats of 100% with testosterone and estrogen, but only 40% with testosterone alone.

Also here are the studies on Estrogen and Breast Cancer....
J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):89-96.

Russo J1, Russo IH. 
The role of estrogen in the initiation of breast cancer.

Estrogens are considered to play a major role in promoting the proliferation of both the normal and the neoplastic breast epithelium. Their role as breast carcinogens has long been suspected and recently confirmed by epidemiological studies. Three major mechanisms are postulated to be involved in their carcinogenic effects: stimulation of cellular proliferation through their receptor-mediated hormonal activity, direct genotoxic effects by increasing mutation rates through a cytochrome P450-mediated metabolic activation, and induction of aneuploidy. Recently it has been fully demonstrated that estrogens are carcinogenic in the human breast by testing in an experimental system the natural estrogen 17beta-estradiol (E(2)) by itself or its metabolites 2-hydroxy, 4-hydroxy, and 16-a-hydroxy-estradiol (2-OH-E(2), 4-OH-E(2), and 16-alpha-OH E(2)), respectively, by inducing neoplastic transformation of human breast epithelial cells (HBEC) MCF-10F in vitro to a degree at least similar to that induced by the chemical carcinogen benz(a)pyrene (BP). Neither Tamoxyfen (TAM) nor ICI-182,780 abrogated the transforming efficiency of estrogen or its metabolites. The E(2) induced expression of anchorage independent growth, loss of ductulogenesis in collagen, invasiveness in Matrigel, is associated with the loss of 9p11-13 and only invasive cells that exhibited a 4p15.3-16 deletion were tumorigenic. Tumors were poorly differentiated ER-alpha and progesterone receptor negative adenocarcinomas that expressed keratins, EMA and E-cadherin. The E(2) induced tumors and tumor-derived cell lines exhibited loss of chromosome 4, deletions in chromosomes 3p12.3-13, 8p11.1-21, 9p21-qter, and 18q, and gains in 1p, and 5q15-qter. The induction of complete transformation of the human breast epithelial cell MCF-10F in vitro confirms the carcinogenicity of E(2), supporting the concept that this hormone could act as an initiator of breast cancer in women. This model provides a unique system for understanding the genomic changes that intervene for leading normal cells to tumorigenesis and for testing the functional role of specific genomic events taking place during neoplastic transformation.

It's interesting, but I'm not the only one to say this. Recently Abraham Morgentaler, MD and his associates had published a VERY SIGNIFICANT article regarding these very studies and MORE!

For decades, the storyline was that lowering testosterone levels caused prostate cancer to shrink away and raising testosterone levels caused it grow. The second part of this story was now seriously in doubt, yet the first part was obviously correct. In my own practice, I had seen the beneficial effects of lowering testosterone levels many times over in men with advanced prostate cancer. This part of Dr. Huggins’s work was indisputable. But if lowering testosterone levels caused these cancers to shrink, how was it possible that raising testosterone levels did not cause the cancers to grow? This was a paradox that needed to be solved if physicians were to accept the possibility that testosterone therapy may not increase the risk of prostate cancer.

The Paradox Resolved

The answer turns out to be not all that complicated. All the reports of testosterone causing rapid growth of prostate cancer occurred in men who already had extremely low testosterone levels, due to castration or estrogen treatment. Once we get beyond the near-castrate range, it is hard to find any evidence that changes in T concentrations matter at all to prostate cancer. This is essentially what Drs. Fowler and Whitmore described in their 1981 article when they suggested that “near maximal” growth of prostate cancer is provided by naturally occurring T concentrations. The experimental proof of this concept was provided by a landmark article published in 2006 using much more sophisticated means. In this study by Leonard Marks and colleagues, men with low testosterone received injections of testosterone or a placebo every two weeks for a total of six months. At the beginning and end of the study, measurements of testosterone and DHT (the more active form of testosterone within prostate tissue) were obtained from the blood and also from the prostate itself. The results showed that although blood concentrations of testosterone and DHT rose substantially in the T injection group, as expected, the concentration of testosterone and DHT within the prostate itself did not change at all and was similar to the group that received placebo injections. In addition, biochemical markers of prostate cell growth also did not change with T injections. This study showed in elegant fashion that raising testosterone levels in the blood did not raise testosterone levels within the prostate. It is as if once the prostate has been exposed to enough testosterone, any additional testosterone is treated as excess and does not accumulate in the prostate. In technical terms, we say the prostate has been saturated with regard to testosterone. And it is this saturation that resolves the paradox of testosterone and prostate cancer. Saturation explains the paradox in this way. At very low levels of T, near the castrate range, prostate growth is very sensitive to changes in T concentration. Thus, severely lowering testosterone will definitely cause prostate cancer to shrink; adding testosterone back will cause the cancer to regrow. However, once we get above the point where the prostate is saturated with testosterone, adding more testosterone will have little, if any, further impact on prostate cancer growth. Experimental studies suggest the concentration at which this saturation occurs is quite low. In other words, the old analogy I learned in training was false. Testosterone is not like food for a hungry tumor. Instead, a much better analogy is, “Testosterone is like water for a thirsty tumor.” Once the thirst has been satisfied, prostate tumors have no use for additional testosterone. And the vast majority of men with low testosterone appear to have prostates that are not particularly thirsty.

A New Concern: Prostate Cancer and Low testosterone

I no longer fear that giving a man testosterone therapy will make a hidden prostate cancer grow or put him at increased risk of developing prostate cancer down the road. My real concern now is that men with low testosterone are at an increased risk of already having prostate cancer. When my colleagues and I published our results in 1996 from prostate biopsies in men with low testosterone and PSA of 4.0 ng/mL or less, the 14 percent cancer rate was several times higher than any published series of men with normal PSA. In 2006, Dr. Rhoden and I published a larger study of prostate biopsies performed in 345 men. The cancer rate of 15 percent in this group was very similar to the first study. But whereas the cancer rate in 1996 was much higher than anything published to that date in men with PSA of 4.0 ng/mL or less, in 2006 the perspective had changed due to an important study called the Prostate Cancer Prevention Trial. A New Concern: Prostate Cancer and Low Testosterone In that study, the cancer rate among men with a PSA of 4.0 ng/mL or less was also 15 percent. Because this value is identical to what we had found in our patients with low testosterone, it was suggested that the cancer rate in men with low testosterone is the same as the normal population—neither higher nor lower. However, the average age of men in our study was a decade younger than the men studied in the Prostate Cancer Prevention Trial (fifty-nine versus sixty-nine years). Almost half the men in the other study were seventy years or older, and age is the greatest risk factor we know for prostate cancer. The way I look at these numbers is that men with low testosterone have a cancer rate as high as men with normal T who are a decade older. More importantly, in our study of 345 men, we found that the degree of testosterone deficiency correlated with the degree of cancer risk. Men whose testosterone levels were in the bottom third of the group were twice as likely to have cancer diagnosed on biopsy as men in the upper third. This finding adds to the concern that low testosterone is a risk factor for prostate cancer. There is now additional data from around the world associating low testosterone and worrisome features of prostate cancer. For example, low testosterone is associated with more aggressive tumors.

In addition, men with low testosterone appear to have a more advanced stage of disease at the time of surgical treatment. Whereas I originally began to perform prostate biopsies in men with low testosterone because I was worried that treatment might cause a hidden cancer to grow, I now perform biopsies in these men because I am concerned they might have an increased risk of cancer. This risk is approximately one in seven for men with PSA values less than 4 ng/mL. Because prostate cancer tends to be curable when caught early, I feel I’ve done these men a service by finding their cancers before they have an abnormal PSA or DRE. With today’s ability to monitor men with prostate cancer, not all of these men will necessarily require treatment. But the ones who have evidence of more aggressive tumors should definitely have an advantage by having their diagnosis made early. The Evidence as it Now Stands For over sixty-five years, there has been a fear that testosterone therapy will cause new prostate cancers to arise or hidden ones to grow. Although no large-scale studies have yet been performed to provide a definitive verdict on the safety of testosterone therapy, it is quite remarkable to discover that the long-standing fear about testosterone and prostate cancer has little scientific support. The old concepts, taken as gospel, do not stand up to critical examination. I believe the best summary about the risk of prostate cancer from testosterone therapy, based on published evidence at the time this book is written, is as follows: Low blood levels of testosterone do not protect against prostate cancer and, indeed, may increase the risk.

High blood levels of testosterone do not increase the risk of prostate cancer. Treatment with testosterone does not increase the risk of prostate cancer, even among men who are already at high risk for it. In men who do have metastatic prostate cancer and who have been given treatment that drops their blood levels of testosterone to near zero, starting treatment with testosterone (or stopping treatment that has lowered their testosterone to near zero) might increase the risk that residual cancer will again start to grow. Prostate cancer with infiltration into bladder, lymph nodes, and urethra. Prostate cancer with infiltration into bladder, lymph nodes, and urethra. One of the most important and reassuring studies regarding testosterone and prostate cancer was an article published in the Journal of the National Cancer Institute in 2008, in which the authors of eighteen separate studies from around the world pooled their data regarding the likelihood of developing prostate cancer based on concentrations of various hormones, including testosterone. This enormous study included more than 3,000 men with prostate cancer and more than 6,000 men without prostate cancer, who served as controls in the study. No relationship was found between prostate cancer and any of the hormones studied, including total testosterone, free testosterone, or other minor androgens. In an accompanying editorial, Dr. Carpenter and colleagues from the University of North Carolina School of Public Health suggest scientists finally move beyond the long-believed but unsupported view that high testosterone is a risk for prostate cancer. More and more physicians are coming around to recognize that testosterone therapy is not a true risk for prostate cancer, but it can take many years to alter established beliefs. Don’t be surprised if your own doctor still raises this issue with you if you are considering testosterone therapy. If he objects to treating you for that reason, you should refer him to the article above, or one of the other review articles listed in the References at the back of this book. Even better, have him read this chapter!

Q. I’m fifty-three years old and I’ve been on testosterone therapy for two years, with good results. However, my father was diagnosed with prostate cancer at age seventy-five. Does this mean I need to stop testosterone?

A. There is a familial form of prostate cancer, but only in families in which prostate cancer occurs at age sixty-five or younger. Even in those families where a family member develops cancer at a young age, this does not necessarily mean that every other male in the family will develop cancer. Men with a family history of prostate cancer should be sure to have a yearly PSA and prostate exam. There is no need to discontinue testosterone treatment.

Q. My physician started me on testosterone, but I never had a prostate biopsy. I am sixty-four years old. Was this a mistake?

A. Because there is no evidence that testosterone treatment increases the risk of prostate cancer, it is fine to begin therapy as long as your PSA and DRE are normal. My own practice is to recommend prostate biopsy in men with low testosterone because our published data indicate there is an increased risk that cancer is already present in men with low testosterone, but this is by no means a standard recommendation yet among physicians.

Q. Why do you perform prostate biopsies on men with low testosterone if you don’t feel that testosterone treatment will make a hidden cancer grow?

A. Because so many men with prostate cancer will not die from it, even without treatment, there is a fair amount of controversy over how aggressive to be in making the diagnosis. My perspective is that it is worth knowing the diagnosis, whether or not one chooses to be treated immediately. And because low testosterone seems to represent a small but definite increased risk, I feel that biopsy in men over fifty with low testosterone is worthwhile.

Q. A man in my bowling league was started on testosterone treatment and then developed prostate cancer one year later. Doesn’t that show that testosterone is risky for prostate cancer?

A. If the wife of this man had switched to a new type of laundry detergent before the cancer was diagnosed, would we assume the cancer was caused by the detergent? Of course not. But we are predisposed to believe that testosterone therapy causes prostate cancer, so it is easy to hear a story like this and assume that testosterone therapy caused the cancer. Prostate cancer and testosterone therapy are both common in the United States, and both tend to occur in the same age range, so there will always be stories of men developing cancer some time after beginning testosterone therapy. If testosterone really made prostate cancers grow, then we should see high rates of cancer among men who start testosterone therapy. But we don’t. It’s false logic.

Q. Isn’t it true that all men would eventually get prostate cancer if they lived long enough? If so, why does it even matter if testosterone were to increase the risk of something that is inevitable anyway?

A. Men do get prostate cancer at an increasingly high rate as they age. And it is true that most men diagnosed with prostate cancer would never have a moment’s trouble from it, even if it were left untreated, because most of these cancers grow so slowly that other medical conditions eventually become more troublesome. Yet for those with more aggressive forms of prostate cancer, the danger is very real. The challenge is to identify men at risk, because even high-grade prostate cancer is curable when caught early.

Q. It took more than thirty years for scientists to learn that hormones were dangerous for women and caused breast cancer. Isn’t it possible we’ll eventually find out the same is true for testosterone and prostate cancer?

:::Abraham Morgentaler, MD Abraham Morgentaler, MD A::::

The fear that hormone therapy is dangerous in women is currently being reevaluated, and it appears to not be as dangerous as was originally proclaimed. More to the point, it is critical to understand that men are not women and that testosterone is not estrogen. Anyone, particularly a scientist, must always allow for the possibility that new information will one day change current views. But after so much research over so many decades, there is little reason to believe that testosterone therapy poses a major risk for prostate cancer. As a medical student once said to me, “If testosterone is really so dangerous for prostate cancer, why is it so hard to show it?”

Abraham Morgentaler, MD, is an associate clinical professor of urology at Harvard Medical School, and is the founder of Men’s Health Boston, a center focusing on sexual and reproductive health for men. He is the author of a number of popular books including The Male Body and The Viagra Myth. Excerpted with permission from Testosterone for Life: Recharge Your Sex Drive, Muscle Mass, Energy and Overall Health by Abraham Morgentaler, MD, FACS. Published by McGraw-Hill.

Therefore as you can see, I have a reason for arguments, they are VALID ARGUMENTS!

Excerpts such as this one...

You can clearly see the Doc was wrong for not performing the proper tests...however, it's the INACCURACY and lack of specification, and a lack of knowledge in the area that leads to false campaigns. The problem is - a simple fact, such as that Estrogen is MADE FROM TESTOSTERONE, is never considered in all of these accusations against testosterone...and Ya know, there ARE pharmaceutical drugs, that have gone through rigorous and extensive trials - called Aromatase Inhibitors, that do indeed, decrease or STOP conversion of Testosterone to Estrogen, which JUST SO HAPPEN to also prevent prostatic carcinoma's and cause apoptosis to human prostatic carcinoma. Thus...what does that say???


Another study shows that Aromatase Knockout (estrogen deficient) mice do not develop prostate cancer.

Indeed, aromatase knockout mice, which are estrogen deficient but have increased levels of androgens, do not develop prostate cancer [90].

So in reality, there is an overwhelming body of evidence, when looked at correctly, and not in the deluded minds of Campaign artists - who's main goal is to make money, that ESTROGEN is the MAJOR FACTOR in PROSTATE CANCER.

Though I do agree that the victims who have fallen prey SHOULD be compensated, and that the Doctors who had not performed the proper testing (including bloodwork) should be corrected, what really needs to be done, is EVERY MAN ON TESTOSTERONE REPLACEMENT THERAPY, SHOULD HAVE THEIR ESTROGEN LEVELS CHECKED!!!!
If they turn out HIGH, or moderately elevated (ESPECIALLY, if you have GENETIC predispositions to Prostate Cancer), then you should proceed to ask your doctor for an "Aromatase Inhibitor"!!!!


So there you have it....
The answer is NOT to PERSECUTE testosterone therapist's, Medical Doctor's (in most cases), or the manufacturer's of Testosterone Replacement Products, but to inform everyone, and anyone on these therapies, to DEMAND they get their estrogen level's checked, and to proceed when necessary, to request the appropriate counter-therapies for bad estrogen:testosterone RATIOS.

AGAIN...the "Victims" should be compensated - if their condition is severe, or even moderate...but that's not the ABSOLUTE answer...or the Preventative One.
The answer is keeping people INFORMED and using aromatase inhibitors when necessary.

If your doctor will not give you a script for (for some stupid reason) an aromatase inhibitor drug, there are places you can buy them online.

The best place to find aromatase inhibitor drugs online, and also where you can buy letro (letrozole) (most powerful aromatase inhibitor) online....
Well.. look below, best prices as well. You don't need to put up with that from your doc!!!

You can buy 20 tablets of Letrozole (the best AI) for 29 $  - HERE AT THIS SITE
On the same site you can find over a dozen other AI's.

Also for a High Quality Testosterone Replacement Gel that DOES NOT convert To Estrogen.

THIS will stop the conversion of Testosterone to Estrogen and thus effectively prevent Prostate and other Cancer's as well as stop any growth in it's tracks. Be sure to also eat healthy and consult your doctor about this regimen.


click here now


  1. totally true! grate article, very Agressive style!

  2. Thumbs up. more people should talk about this.

  3. Agreed brother! i always hated seeing those campaign commericals!

  4. Great article ....

  5. excellent article. and vouch for the sites mentioned! all are legit! guy knows what he's talkin about!

  6. excellent article. people rly need to study their hoarmones! e2 levels particularly.


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