Best Affiliate Programs For Fast Money Online (and Explaining Affiliate Programs for Beginner's)

Today I am going to show you one way you can make money online, I know there are already several articles like this - however, most of them fail to mention specific techniques that are NECESSARY while "Affiliate Marketing", and they fail to point out some of the less-known but ideal affiliate programs for beginners.

First of all, let's explain an affiliate program.

(SKIP TO RECOMMENDED AFFILIATE PROGRAMS HERE)

An "affiliate program" is not a site where you spend time filling out surveys, or referring people to merely click on links. An affiliate program is a program where you get paid a certain percentage (commisssion) of a product's total cost, in exchange for referring new customer's to that company's (or site's) products. For example, if you are using Amazon's affiliate program, and you link someone to an iPhone being sold on Amazon, then that person buys the product, you will get approximately 10-15% of the cost of that product, paid to you after total's are calculated at the beginning of the next month.

So if you ask, "what is the goal when working for an Affiliate Program?" - it's simply to get as many people possible to buy as many of whatever product you are linkng them to. With virtually every affiliate program,  you will have your own "Tracker Link" which is used to identify you as the person who referred them to the product, this then allows the company to pay you for doing that.

For example, on Amazon's affiliate program - say you are referring people to an Apple iPhone 16GB (Gold) - the link you build to refer people off of will look like this.

http://www.amazon.com/gp/product/B00F3J4E5U/ref=as_li_tl?ie=UTF8&camp=1789&creative=9325&creativeASIN=B00F3J4E5U&linkCode=as2&tag=usernamehere-xx&linkId=O6XSX3VZATGGJ2L2

The part highlighted in black is your user name built into the link, so you can get credit for referring the person to the specific product - in red is the link, identifying product ID - which is Apple iPhone in this case. 

So this is how most affiliate programs work.
You can use multiple methods to support your success when using Affiliate Program's - the best method, is building a blog like mine here, or a full-blown website; domain registered and all. The goal is to get a lot of traffic to your site, then you just need to figure out a way to get people to click your affiliate links.


In order to effectively convince people, you should be a big fan of innovation. You should be interested in targeting new products that have just been released, or products that have yet to be reviewed, that way you can ensure top results on google and other search engines (providing you have placed the proper tags in your article or advertisement). What I mean by tags, are placing relevant keywords that you believe people will search. In relevance to the iPhone - you can write a review on it, and use a title like "is Apple iPhone worth it", since many people will search it in more subtle/casual terms.  Somewhere in the review, you can also write other keywords - like why a particular version is better than another. These are just examples, if your blog or site has a lot of traffic, you are likely to make ALOT of money !!!!

You simply have to be strategic, and know your audience.

Ok so now I have explained an affiliate program. Now am I going to tell you what (in my opinion) are some of the best affiliate programs to use. 

Let's start with an easy affiliate program that you can make quick (and big) money off of. It's a program promoting the drugs Viagra, Cialis, Levitra and a form of Testosterone Gel - known as Andractim. Andractim is actually DHT - if you have read my other articles(1)(2), you will already know what this is. The benefit of promoting such products, is the diversity of customer's, and though you may not think it at first, people use these drugs for other purposes than just treating Erectile Dysfunction, and other related problems. 

For example, this class of E.D drugs (PDE-5 Inhibitors), which work by increasing blood flow to peripheral organs, are also used by Bodybuilders to get a better pump when lifting. Similar to how "Nitric Oxide" products work, and PDE-5 inhibitors can even enhance the effect of all "Pre-Workout" and "N.O Supplement's", therefore they are used as synergist's and amplifier's of other supplements. As these effects become apparent (more blood flow, vasodilation), vascularity (the appearance of veins in muscles) also increases. Therefore some* bodybuilders may use (in combination with other products) these drugs as a pre-contest "enhancement". 

PDE-5 Inhibitors also can treat or cure Premature Ejaculation, many reports have supported this(3)(4). Therefore they can be used for this purpose as well, and this once again broadens the audience and customer line for these products.

The ALL SAINTs Affiliate Program
(Promoting ED drugs and Male Hormone Replacement Product's (TRT))

To sign up, simply click the title in blue above, then go to "Affiliate Program" and click it, it will begin a page that looks like this. 

Note as I highlighted important parts.

Now after signing up, you will receive an e-mail about 24 hours later (or less), unless it is a weekend, and this e-mail will contain your login link (to view your stats and commissions), and the link you will give to others when promoting the products.

The e-mail will look like this.

NOTE : I've talked to some people (referred to this program) who have said it took 3 days to get their initial e-mail. So don't be surprised if this happens, generally it's pretty quick though.

NOW.

When you receive that e-mail, you can start marketing with the first link, be VERY CAREFUL to not give anyone the *second link* in that e-mail, because then they will have access to your personal information as well as your stats.

Hyperlinking is your best friend. Wherever you decide to advertise, don't just use your link in plain form, e.g 

http://www.secure-sales.org.uk/clinic/page.cgi?id=user name here

Instead, mask your link with a shortener - such as Bit.ly, depending on the setting you are advertising in, or you can hyper link it like this...

Buy E.D Drugs and Testosterone Gel Here (No-Prescription Required)

There you have it.

Now you just have to be tactical, and figure out your audience, and how to make your page different from the average person marketing these drugs. 

Try using a site like Fiverr.com, where you can pay someone 5$ to post your link on their Twitter or Facebook (typically having hundreds of thousands of followers).

Other suggestions, are emphasizing that this site does not require a prescription for the order, and also that it isn't "off-brand Indian garbage" as I always say.


It's always a good thing to promote high-quality products, and you want to be sort of honest (but not 100%). Think how marketing really works. Company's and representatives always exaggerate, though perhaps in a very covert way most of the time.


I also suspect there isn't a whole lot of lying you can do in regards to these specific products, as the information as to WHAT they do, is EVERYWHERE. But you can certainly notate certain descriptors as I do.

                                  ...... When you receive Commissions (as people click your link and buy the products) from this program, you will receive e-mails about them during the "pay-period" of the month, All Saints does this at different times but generally during the beginning of the month.

This is where it gets exciting...



Once those e-mails appear, your balance will be updated on your stats page and will look something like this....

As you can see, they pay in Euro's, but it will be appropriately converted to USD when they pay you, if you live in the USA.



The second affiliate program I recommend - is AMAZON AFFILIATE PROGRAM (made reference before as well).

SIGN UP HERE FOR AMAZON AFFILIATE PROGRAM


Why is amazon so special?

Well for a number of reasons. First and foremost. Diversity. You have a huge selection of product's throughout every single category - giving you leeway and allowing for maximal customization on your site.

Amazon also gives you bonuses for reaching a certain amount of referrals per month. This is where they really shine. Between the vast selection of products to refer on, the pre-loaded graphic designs (for the products) and the bonuses - amazon is a brilliant affiliate program that is also easy to newbie's and can generate a great amount of income for you and your business.

It's free to sign up, as most affiliate programs are.

Here is an example of an Amazon affiliate link with an Image.

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.....
....That the ONLY BULLSHIT IS COMING FROM PEOPLE LAUNCHING THE CAMPAIGNS.
For once, I'm sticking up for *(kinda)* the pharmaceuticals....but I also would say this...people NEED TO DO THEIR OWN RESEARCH!!!!!

TESTOSTERONE ITSELF DOES NOT CAUSE ANY CANCER, PERIOD. 

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 mean...you 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!!!!

Estrogen excess is ALREADY implicated in BREAST CANCER, UTERINE CANCER, OVARIAN CANCER AND......  PROSTATE CANCER???

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.

Abstract

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???

THAT IT IS ESTROGEN THAT CAUSES AND MUTATES CANCER 


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

LINK TO BOOK

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"!!!!

KEEPING TESTOSTERONE HIGH, AND ESTROGEN REASONABLY LOW - WILL CERTAINLY ELIMINATE YOUR RISK OF DEVELOPING CANCER....


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.

CLICK HERE

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.

                                           

Where to get PURE Pharmaceutical (Not just "Pharma-Grade") Yohimbine

PURE PHARMACEUTICAL YOHIMBINE 5mg/Tabs

I've had a lot of people e-mailing me and asking me about Pure Pharmaceutical Yohimbine...not just the Yohimbine that is sold by SNS and Primaforce - the thing is, there's not much difference, just that the supplement manufacturers sell in 2.5 mg capsules - while most "pure" pharmaceutical equivalents are in 5 mg "Tabs". However on request, and since I do such a great job "digging around", I've found a such place.


             

                                                         

                                                           Yohimbine HCL                                                       

 Also I'm not going to go on one of my usual rant's about such precautions immediately, I figure you've already done most of the research yourself, hence why you are looking this up.

I will however tell you if you scroll down a bit (chuckle).  



PRECAUTIONS

As Yohimbine HCL is a sympathetic nervous system "Probe" and "Stimulant"... it can ACCELERATE the heart rate and cause a rise in Blood Pressure!
Be careful and start with a small dose - 5 mg - 10 mg / day to start with!



USES
- Burning Fat/ Aiding in the Treatment of Gynecomastia (Male Breast Growth)
-Toning up, Showing more Muscle Definiton and Vasculature (Pre-Contest)
-Improving Libido / Erectile Function
-Increasing Sympathetic Nervous System Activity








How do you re-boot your Central Nervous System?
How do you increase Sympathetic Nervous System Activity?
How do you restore or "probe" adrenaline production?
(How to reboot CNS)


Yohimbine HCL

[Area-1255] The High DHT/Low Estrogen PhenoType

The High/DHT Low Estrogen PhenoType
Defining the Chemical Map of Such Person's.
________________________________________
This is a highly intricate article, and you should know some degree of
NeuroChemistry / NeuroBiology - but I will make it as simple as possible.
_________________________________________
This article aims to define....

• Why High DHT/Low E2 Type's frequently have High B.P
• What other physical traits/symptoms would this Phenotype have
• What Behavioral/Personality Tendencies may Develop from this.
• How to reduce the negative traits / symptoms without affecting hormones.

Previously I had written an article on DHT's effects on the Brain/Nervous System. This article aims to expand on a certain phenotype (composite of someone with said "hormonal values", with a lot of the same manifestations you would see described in the DHT article.

Now on various bodybuilding forums you will see people who complain about low estrogen symptoms, "too high DHT", and the barrage of speculations that ensue on such a topic. Without any real information / sources much of the time, people try to narrow down on this stuff, but often lack in common sense to draw the real connection. I am not saying all do this, but quite a few - and so I aim to make it easier to define the "Why" and the "How" for all things "High DHT AND Low Estrogen" (occurring at the same time). Some of these will also be reminiscent of just plain low estrogen state (since DHT values aren't often accounted for in bloodwork). 

Let's get one thing straight, High DHT does NOT have to be a bad thing, in fact, it is the reflection of the True Man, the embodiment of pure masculinity, true primal thoughts and actions, it's also not terrible to have low estrogen*, but it may well be for some people who do not know what may manifest.

Frequently, I often hear about "E.D (erectile dysfunction) resulting from "low estrogen", this is all over bodybuilding/steroid forums and even in the so-called grey hat medical community. To understand why this happens, you have to understand the chemical changes that take place when estrogen is lowered to near deficient states.  First, estrogen is a major stimulator of Nitric Oxide synthesis - specifically neuronal Nitric Oxide Synthase(1)(2)(3), when converted from Testosterone. The low estrogen state in the male often stems from either using too high of a dosage of an AI (Aromatase Inhibitor), or from a natural (genetic) aromatase deficiency. Aromatase is the enzyme that converts our testosterone to estrogen, especially in the brain(4).

Now nitric oxide is a vasodilator, so by lowering estrogen excessively, overall systemic (throughout the body) nitric oxide may also be lowered, and the nerves that normally inspire sexual functions may wither away(5)(6).

Second to that though, are the indirect/downstream changes to the entire hormonal profile of someone with low estrogen. For example, lowering estrogen also lowers the levels of a carrier protein (literally carries hormones) called SHBG (Sex Hormone Binding Globulin)(7)(8). Testosterone can be bound by this protein and also rendered inactive, when there is less of it, Testosterone is free to bind to it's own receptor, and you end up getting more DHT this way as well (more androgen receptors to bind to).  

Now as described in my other article, there are some relative changes that come with DHT elevations, DHT generally has a positive impact on erectile functions(9), however, in the face of overall Nitric Oxide deficiency, and given that DHT has the capacity to stimulate or increase Alpha-1-Adrenergic receptors(10), you may end up getting too much vasoconstriction by this mechanism.

Too little nitric oxide and and too much alpha-1-adrenergic (adrenaline) stimulation can also lead to hostile and aggressive mindsets. Which we will get to next.



 HIGH DHT / Low Estrogen - Effect on Anxiety and Aggression

I do not believe testosterone (nor does ANY chemical) cause people to be aggressive, people *choose* to act on certain impulses, this is life.

However, the High-DHT/Low Estrogen state may actually have a real "behavioral type" and a strong premise to follow. This type consists of a higher impulsive state, and negative reactions(strong tendencies).

As stated before, estrogen has a strong effect on serotonin and their receptors, DHT tends to increase alpha-1-adrenergic activity, and this can lead to increases in 5-HT1A (serotonin receptor TYPE 1-A) activity. Estrogen's primary effects are on the densities of 5-H2A/2C(increase)(11),5-HT3 (antagonize)(12), and 5-HT4 (increase prolactin)(13). Most of the receptors estrogen acts on (as far as serotonin) are STIMULATORY. However, the 5-HT1A receptor inhibits serotonin release but also acts on many other peripheral zones and increases the release of endorphins(14).

*Serotonin can be calming, and inhibitory*

This means that merely the High DHT and low Estrogen state leads to much lower serotonin activity in general, something that can't be fully reversed by SSRI's or any similar drug. This doesn't even take into account other factors leading to low serotonin, and thus the effect can be compounded in people who have already had lower serotonin levels or have genetic deficiencies in serotonin or it's receptors. 

This induced lack of serotonin, combined with Alpha-1-activity increases, is what leads to nervous system overstimulation by DHT and by Low Estrogen.
This can lead to impatience, high-impulsivity, and aggression. The low serotonin but combined endorphin release from the 5-HT1A receptor can lead to a relative lack of emotions(15)(16)(17)!
This same combination of effects can lead to anxiety. However, because 5-HT1A receptor activation can help social anxiety(18), it is more feasible to say that the anxiety's experienced would be of anticipatory nature (anticipation, waiting for things). 
Many studies have documented the effects of low-estrogen and resultant obsessive-compulsive behavior(19).
Thus another result of High DHT and Low Estrogen would be obsessive compulsive personalities. 

Because DHT increases GABA to an extent, it is likely the person will retain their sanity (at least parts of it), but they will still apply many of their OCD-behaviors - possibly subliminally.

You can actually qwell some of these stimulatory effects by taking an Alpha-1-blocker such as Doxasozin. (20)

This would also help alleviate any other vascular issues resulting from High DHT / Low Estrogen. 

However if your low estrogen problem ISN'T genetic, I suggest fixin that first (namely by supplementing with boron, and stop using/overdosing on AI's).


EXTREME MALE DOMINANCE
...or the behavior of having to assert yourself over the next person. Is highly associated with the serotonin / adrenaline changes induced by the above said balance.


That's no surprise, medical science has been documenting for years the effects of Testosterone on dominance behavior(!)(!), but it is what makes us as men - WHOLE. It's not necessarily a bad thing, unless it gets out of control.
Low Estrogen and High DHT induced impulsivity though, may lead to radical dominance behavior and the blunted emotional response may lead to lack of empathy.  NOT ALWAYS. However very likely.


This does not excuse a lack of willpower in the matter.

People can control themselves, and HAVE, many times with the said "imbalance", but again, it comes down to being in touch with your own mind, and if you decide to realize these things - then you make your own damn choice.  It does not mean that Testosterone, the High-DHT - Low-Estrogen state CAUSES you to act, YOU do that solely, the imbalance simply creates impulsive and aggressive, and domineering tendencies.

PARANOIA

Once again, the lack of serotonin and increases in alpha-1-adrenergic activity can directly lead to paranoia in affected individuals(21).


Does it mean they will become a paranoid "schizophrenic" - NO. It just means a resonating/subtle trait of paranoia may emerge; how potent this effect is depends on many other factors. Such as stimulant use, and previously residing conditions. Keep in mind certain medical conditions may actually cause an estrogen deficiency (like adrenal fatigue, adrenal abnormalties).



ADDICTIONS

Traditionally it has been shown that low serotonin itself can lead to drug addiction and other addictions, considering the high DHT-low Estrogen type leads to significant changes in serotonin receptor distribution/density, and lowers the blood level of serotonin, while increasing adrenaline (see above). This will likely lead to two scenario's; increased alcohol dependancy / addiction (to calm nervous system), or - ironically - stimulant abuse (due to adrenal fatigue).


.This again can be mostly resolved with an Alpha-1 blocker.

PHYSICAL MANIFESTATIONS OF HIGH-DHT LOW -ESTROGEN STATE

Low estrogen is often associated with Joint Problems, Bone density decreases and Joint Clicking / Cracking.....
(DISCUSSION 1)
(DISCUSSION 2)
(SOURCE 1)
(SOURCE 2)

Also lower aromatase/estrogen individuals tend to be taller, and have longer limbs, but possibly less width and / or bone mass(1)(2)(3).

It leaves a skinny/lean or sometimes even frail build, although with high DHT you are likely to be a lean guy but has trouble gaining significant amounts of mass. You won't retain much water, if at all, your cheekbones will show, and your veins will likely be VERY pronounced.(4)(5)



Thus in addition and near Totality, the Symptoms and Effects of the HIGH DHT - Low Estrogen State include.

• High Blood Pressure; resultant anxiety, aggression
• Impulsivity
• Paranoia
• Loss of Normal Erectile Function (*possible*)
• Low Libido/Compulsive Sexual Acts 
• Possible Joint Problems
• Lean / Small Build - Trouble Gaining Weight
• Much Body Hair / Facial Hair**
• Over Time - Increased Height, Long Arms / Fingers
• Pessimism / Hostility - Dominance Behavior's
• Low Water Retention - Pronounced Veins
• Altered Endogenous Opiate Levels (also contributing to increased BP)
• Sodium Retention***

OTHER SOURCES

Oestrogen modulates vascular adrenergic reactivity of the spontaneously hypertensive rat

Abstract

BACKGROUND:

Male spontaneously hypertensive rats (SHRs) show an increased vascular neurogenic response compared with normotensive Wistar-Kyoto (WKY) control rats.

OBJECTIVE:

To study the vascular adrenergic response in hypertensive and normotensive female rats, with a focus on the influence of oestrogen.

METHODS:

Female SHRs and WKY rats were allocated randomly to a control group or to groups to undergo ovariectomy or ovariectomy combined with oestrogen supplementation (17beta-oestradiol 150 microg/kg per day) for either 1 day (group 1E2) or 10 days (group 10E2). Mean arterial pressure (MAP) was recorded and small mesenteric arteries were mounted in a Multi Myograph 610M. Vascular reactivities to transmural nerve stimulation (TNS), exogenous noradrenaline and acetylcholine were analysed.

RESULTS:

MAP was significantly greater in SHRs than in WKY rats in all groups studied. Sensitivity to cumulative TNS (0.12-32 Hz) did not differ between vessels from control SHRs and WKY rats, expressed as the frequency giving 50% of maximal neurogenic response (Ef(50): 4.1 +/- 1.1 and 4.0 +/- 1.6 Hz, respectively). However, there was a greater reactivity to TNS in ovariectomized SHRs than in ovariectomized WKY rats (Ef(50) 1.8 +/- 0.7 and 6.8 +/- 2.2 Hz, respectively; P < 0.05). Oestradiol treatment significantly decreased the sensitivity to TNS in ovariectomized SHRs (P < 0.05), and after 10 days the frequency-response curves were almost identical (Ef(50) 6.3 +/- 1.9 Hz for group 10E2 SHRs and 5.6 +/- 0.8 Hz for group 10E2 WKY rats). The increased adrenergic reactivity in ovariectomized SHRs was inhibited by prazosin, an alpha(1)-adrenergic antagonist, and could not be explained by differences in endothelial function or sensitivity to applied noradrenaline.

CONCLUSION:

Increased adrenergic reactivity is not present in small arteries from female SHRs. The findings of this study suggest that oestrogenacts on prejunctional mechanisms, reducing full expression of hypertension and peripheral vascular pathology.

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.
The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.

The effects of 17β-oestradiol on increased α(1)-adrenergic vascular reactivity induced by prolonged ovarian hormone deprivation: the role of voltage-dependent L-type Ca channels.

Valencia-Hernández I1, Reyes-Ramírez JA, Urquiza-Marín H, Nateras-Marín B, Villegas-Bedolla JC, Godínez-Hernández D.

The present study investigated the hypothesis that the duration of ovarian hormone deprivation before reintroduction of oestrogen affects the role ofoestrogen as a mediator of the contractile function of α(1)-adrenergic receptors. Rats underwent ovariectomy (OVX) or were sham-operated, and the OVX rats were treated with vehicle (corn oil) or 17β-oestradiol (E(2)) for 5 days either 10, 28 or 60 days after OVX. The OVX increased phenylephrine- and Ca(2+)-induced contractions. Interestingly, the phenylephrine-induced contractions were increased at each of the three time points, whereas the Ca(2+)-induced contractions were only increased in the 60-day group. E(2) had biphasic effects on phenylephrine- and Ca(2+)-induced contractility. Indeed, E(2) increased contractions in the 10-day group and diminished contractions in the other groups (the increased contractions were avoided by verapamil). These results indicate that E(2) controls α(1)-adrenergic receptor-mediated contractility through effects on L-type Ca(2+) channels in a way that depends on the timing in which the treatment with E(2) is initiated.

Copyright © 2012 S. Karger AG, Basel.

PMID:

23037569

[PubMed - indexed for MEDLINE]

[Supplement Review] AnaBeta Elite {New Formula 2014}

If it is difficult to read this review Based on the Colors or Fonts, CLICK HERE to go to the Easy-to-Read "LightPortal Version".

ANABETA ELITE (NEW FORMULA 2014)
REVIEW/LOG
_____________________________________________________________________
SUMMARY
______________________________________________________________________

• This new version of ABE is a much stronger stimulant.
• Noticeable changes in heart rate; probably due to Eluethero Extract
• Got much hungrier on this product.
• Gained about 6 lbs of solid muscle, it was used Alone with a High-Protein Diet.
• 4 week Cycle
• Don't take it at night time.
• Vascularity Increased Dramatically
• Endurance is already High, with this it feels UNLIMITED.
• Mild Amphetamine Like Effect if you Take it With Caffeine.
• 4.5/5 STARS - WORTH IT.

Before I get to the log I am going to define the ingredients, quickly and painlessly. 

The first ingredient - Lodhra Bark (Extract) - Symplocos Racemosa Extract

Symplocus Racemosa is a flowering shrub from South Asia. It grows in cold-moderate climates. Research has shown that it contains natural PDE-1 inhibitors. PDE (Phosphodiestearase) is an enzyme that breaks down chemicals like cAMP and cGMP in the body. These chemicals (cAMP and cGMP) have beneficial effects on heart health, metabolism, energy production, sexual function etc.
By stopping the Breakdown of these Chemicals; Which this Extract does, the function of the corresponding Organs are increased.

PDE-1 in specific, of which is the main target by this herb, is mainly located in the brain, and is targeted by some novel anti-depressants and in research for the effects in cognitive dysfunction.
REFERENCE 1
REFERENCE 2






Here also is a Forum Discussion of the Same Research




Second Ingredient

Anacyclus Pyrethrum D.C. (Root) Extract (AnaCycle) 
This ingredient seems to be raved about as their "Gold-Mine" of ingredients. What is it though?

It's a perennial herb much like Chamomile in appearance, and in habitat, one of it's nicknames is actually Spanish Chamomile!
It seems to have multiple unique mechanisms of action.
One study shows that it increases fertility and Testosterone levels pretty significantly.

It also has an Anti-Depressant effect, and AntiConvulsant effects.
ANACYCLUS - ANTI-DEPRESSANT EFFECT

ANACYCLUS - ANTI-CONVULSANT ACTIVITY (ROCK II INHIBITION)


There is some pretty decent research on it's anabolic activity as well(1). It seems it can cause vasodilation by means of that testosterone increase, and also by inhibiting the enzyme RHO-KINASE II (ROCK II). This would bring a better pump for sure. 




THIRD INGREDIENT
Eluethero Root (EXTRACT)I traditionally do not really like this herb. It causes me to have trouble sleeping normally, but it's placed third, and there is a decent amount in there, but not a hefty dose it seems.


Eleuthero is an adaptogen; it helps the body adapt to various stressors.
This one is tested and studied on endurance in particular, most are immobility time studies.

REFERENCE (1)
REFERENCE (2)


Eleuthero is able to increase epinephrine and dopamine levels, it also prevented cortisol increases during strenuous excersise, but increased it at high doses(3)(4).




THE LAST INGREDIENT

A simple and well-heard of one. FORSKOLIN.
Forskolin is a cAMP analogue, and is very synergistic with chemicals that inhibit PDE-1/PDE enzymes.
By activating adenylyl cyclase, it promotes cAMP accumulation, and enhances thermogenesis (body heat - leading to fat burning).


Forskolin also can increase Testosterone production, and can help preserve lean mass.

REFERENCE 1
REFERENCE 2


__________________________________________________________________________

WHERE TO BUY ANABETA ELITE
!! BEST SALE DON'T GET RIPPED OFF !!
_________________________________________________________________________
LOG
_________________________________________________________________________

WEEK ONE, Day One
Hit the bench press today, did get a very noticeable pump (no N.O sups either).
Pushed a few extra reps, I ate a little more today.

WEEK ONE, Day Three
Definite Pump today! Did legs and I felt my legs were engorged, surging with blood.
Powerful Stuff!
Also eating like crazy, appetite increases THIS fast!!???
Having intense bacon cravings.


WEEK ONE, Day FIVE.
Vascularity is increasing noticeably (even when doing nothing), a little sick to my stomach upon dosing today, but not enough to interfere with my workout. Will update later.

EVENING, WEEK ONE, Day FIVE.Great Arms/Chest workout today! Pump's are INSANE!
Calories well above 3000!
I love this shit!

Rest DAYS x2 
Slept like a baby both of these days....
Still eatin a lot, cut down a couple hundred calories on Sunday.


WEEK TWO, Day One



Began lifts again this week. Feeling great, appetite is up.
Chest Press, Shoulder Press, Curls, Pull-Ups, hit them all today. Every muscle group except legs.

WEEK TWO, DAY TWO

Nothin much more noticeable, just an extreme thermal effect, heat and blood pulsating through body. 


WEEK TWO, DAY THREE
Highlighted this one differently. HUGE pumps, and one big thing I noticed.
Objects and places seemed just, different today. I walked into the gym today, everything and everyone felt shorter.


WEEK TWO, Day Four

All stretching, cardio, calaesthenics today. Also some MMA training.

WEEK TWO, Day FIVE

Massive workout today, every body part hit, Core workouts, got a little paranoid at the end of my last set for some reason. Guess just Nervous System stimulation.


WEEK TWO, Day's SIX AND SEVEN.

.........REST DAYS..........


WEEK THREE, DAY ONEWorkouts were productive once again, reached higher Reps on the Bench and also maxed out +10lbs.
Pretty Impressive Stuff.

WEEK THREE, Day Two.
Felt that thermal effect x5 today, massive heat / almost burning feeling in my veins, really liking this! Appetite was down a little today for some reason. Hmmm.


WEEK THREE, Day THREE.

Another productive day, Leg day today, felt the pumps, feeling swole. 
Strength is in over drive, seriousness, and energy at max.
Lovin this product.

WEEK Three, Day FOUR.
Final day this week, definitely made some gains, gained 4.5 lbs so far.
Amazing. Feeling strong as an OX!!!!





ABE NEW VERSION, NEW FORMULA, 2014, THE REVIEW OF. YES.