Superdrol For Dummies

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    Superdrol For Dummies


    *I think this should be a sticky* Alot of people seem to be in the dark about harsher PH use, with such compounds like superdrol/superdrol clones. I have recommended people search for this thread alot when looking into making a PCT. This is very valuable with alot of good information. It was originally posted by KRZNA at bodybuilding.com, just wanted to give him the recognition he deserves.

    "Superdrol For Dummies"

    I am 18, I have had 4 years plus lifting experience, I feel Ive reached a plateau and want to use superdrol:
    Ive heard this question over and over and would to prevent all those below 21 who want to use superdrol, or any other ph under the age of 21. This is basically inhibiting your bodys natural production of testosterone. Between the ages of 18 thorough 21, males experience the highest test production. If you feel you want to supplement, I would strongly suggest you look for Test boosters, like tribulus and 6oxo. Please note that this has nothing to do with your lack of so called maturity or the feeling that youngsters are careless. This is scientific and numerous studies have been performed in this regard.

    I have just got my superdrol , how do I use it?
    The safest way to use superdrol is to keep the dosage low. Start with a low dose and work your way up if you can handle the sides. All over the boards you can find people using superdrol up to high doses of 40mg. I would suggest the following cycle.

    Week 1 10mg
    Week 2 20mg
    Week 3 - 20mg

    I would personally never recommend over 20mg. 3 week cycles are proven to be safe and effective.

    What times of the day do I take superdrol?
    SD has a low half life, around 6-10 hours therefore make sure you plan your intake every 6-8 hours.
    Different people have different opinions to this question. From what I've seen, the over all consensus is to take the first dose in the morning with an empty stomach with loads of water.
    The next with your preworkout meal with good fats like EFA's , Flax and fish oils, peanut butter. Superdrol takes a heavy toll on your lipid profile. A carb and fat rich meal would somehow help a little bit here. This is my opinion, others differ with it. Preworkout superdrol gives awesome pumps during the workout/weight training routine.

    Does superdrol require a PCT?

    Like every ph on the block SD needs a PCT.

    Give me a sample superdrol PCT.


    wk1: 40mg Nolva, 600 6oxo, 3 fenugreek caps, DHEA 200mg
    wk2: 40mg Nolva, 600 6oxo, 4 fenugreek caps, DHEA 200mg
    wk4: 20mg Nolva, 300 6oxo, 5 fenugreek caps, DHEA 100mg
    wk3: 10mg Nolva, 300 6oxo, 6 fenugreek caps, DHEA 100mg

    Is 6oxo and Rebound XT good enough by itself for a superdrol PCT, most people say it is enough

    No! By no means is 6oxo or Rebound standalone strong enough to restart the test production in your body. You need a SERM! Period!

    Nolvadex is therefore ABSOLUTELY NECESSARY for an superdrolcycle. Please note its Nolvadex not novedex or nolvedex. Please look for Tamoxifen Citrate.
    You can also use Clomid, some users feel this is good as clomid does a lot of good to your lipid profile.

    Sample Clomid PCT

    Day 1- 300mg
    Week 1- 100mg
    Week 2- 75mg
    Week 3- 50mg

    Clomid has worked excellently for me therefore I stop it in 3 weeks. It takes care of any testicular atrophy that may arise on cycle. Please do not use clomid for prolonged periods of time, it is detrimental.
    You can look into combo cycles with both Nolva and Clomid in my PCT thread.

    If budget permits you can also look into NAC.

    Does running milk thistle along side superdrol inhibit gains.
    No, silymarin does not inhibit any gains and does not have any chemical significance. It is purely for the liver. Its effect however is best in the preload and pct.

    What are other good supplements I can run along side superdrol to combat side effects?
    Red Yeast Rice- A fermented rice product, that is our best fighter against negative sides form AAS concerning cardiovascular damage. Comprised of nine different monacolins, which are naturally occurring substances that help regulate cholesterol levels. Along with sterols, and monounsaturated fatty acids, it packs a strong punch.
    Dosage : 1.2g ED

    COQ10- Although this is abundant in food sources, I feel it prudent to put on here. Not only does it show to help cardiac function, but its also imperative to be used with Red Yeast Rice. Can be used in combination with other cholesterol lowering supplements.

    Celery Seed- A powerful anti-oxidant, shown to not only lower blood pressure, but may have cancer fighting properties as well. And there is evidence to show its ability in aiding the liver.

    Hawthorne Berry: Also very useful to lower BP and keep it on check. A great on cycle supplement.
    Dosage 1000mg ed on cycle.

    Policosanol- A blend of fatty alcohols, shows great promise in its use as beneficial to cardiovascular health, to include the maintenance of healthy lipid profiles. There is also some theory to a synergistic affect with EFAs.
    Dosage : 20mg 2x a day

    Saw Palmetto: The prostrate is one delicate part of your system that you do not want to affect under any circumstances.
    SP @ 320mg/day

    Primaforce ProLiver or Liv52.
    Sesathin
    These supplements are very necessary ON cycle as well as in the PCT.

    I took superdrol, its 2 weeks up, I still dont see any change. Why?
    Well, its not superdrols fault, there is some mistake on your part.
    SD will not work if your lipid profile is all haywire.
    Most people underestimate the simple dictum of eating heavy and eating right. Please make sure that your calorics are adjusted to your body weight and height. I do not need to comment on your nutrition, but make sure that you take in 1.7-2g of Protein /lb of body weight.Roughly around week 2.5 through 4 you should start gains of 1lb/day.
    Make sure your carbs and EFAs are at a maximum
    You need to drink @ least 1.5 gallons of water while on superdrol.

    My cycle is over, I have to keep my gains, how do I do it.

    If you want to keep your gains, make sure you take nolvadex. You will lose a little bloat/size due to water retention. Its good to take creatine and nitrous based compounds or cell volumisers at this point to keep your gains. I have not used CEE, but am looking to do so in the near future.

    I had a very satisfying cycle, my pct made me recover fine, I want to get back into another cycle.
    Well,this is something I've seen in many people, the temptation to use m1t and superdrol. Sure it does give good results, but you've gotta understand that you have a life apart from bbing. Imho make sure you give a full two month gap between cycles. After all you've got just one liver to use for a lifetime.



    What are the important things I should know about Research Chemicals?


    15.2 grams of Tamoxifen Citrate equal 10mg of Tamoxifen (nolvadex)
    If a research Liquid manufactuer were unaware of this, and they suspend 10mg of Tamoxifen Citrate in 1 ml of solution and claimed a dosage of 10mg of Tamoxifen/ml then it would be underdosed to the tabs.

    Of course if they claimed 10mg of Tamoxifen and added 15.2 grams of Tamoxifen citrate then they would be giving the correct dose of then 10mg of Tamox/ml relative to the tabs.

    If they say 10mg of Tamoxifen citrate there not lying about the dose, it's jus not as much as the 10mg tabs of nolvadex.

    NOLVADEX_ (tamoxifen citrate) Tablets, a nonsteroidal antiestrogen, are for oral administration. NOLVADEX Tablets are available as:

    10 mg Tablets. Each tablet contains 15.2 mg of tamoxifen citrate which is equivalent to 10 mg of tamoxifen.

    20 mg Tablets. Each tablet contains 30.4 mg of tamoxifen citrate which is equivalent to 20 mg of tamoxifen.

    So whatz the math?
    0.5ml= 7mg tamoxifen
    1.0ml=14mg
    1.5ml=21mg
    2.0ml=28mg
    2.5ml=35mg
    3.0ml=42mg
    3.5ml=49mg
    4.0ml=56mg
    4.5ml=63mg
    5.0ml=70mg

    I am not a doctor and neither do my opinions construe medical advice. These are just my views after using and researching about this product and answering a number of queries from users who were as confused as me when I first started it.




    The superdrol checklist :

    Superdrol 10/20/20
    RYR 1.2g ed
    Milkthistle 1000mg
    Hawthorne Berry 1000mg
    CoQ10
    Policosinol- 20mg 2x ed

    PCT:
    SERM :Nolvadex 40/30/20/10
    AI :R-Xt or 6oxo
    Prostrate:Saw Palmetto 325mg

    DHEA 200/200/100/100
    Fenugreek
    Clomid (optional)
    RYR 1.2g ed
    Milkthistle 1000mg
    Hawthorne Berry 1000mg
    CoQ10
    Policosinol- 20mg 2x ed

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    Dude didn't that come from BB?
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    Quote Originally Posted by mathis50262 View Post
    Dude didn't that come from BB?
    traitor...
    •   
       

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    Quote Originally Posted by bigpapa View Post

    Give me a sample superdrol PCT.


    wk1: 40mg Nolva, 600 6oxo, 3 fenugreek caps, DHEA 200mg
    wk2: 40mg Nolva, 600 6oxo, 4 fenugreek caps, DHEA 200mg
    wk4: 20mg Nolva, 300 6oxo, 5 fenugreek caps, DHEA 100mg
    wk3: 10mg Nolva, 300 6oxo, 6 fenugreek caps, DHEA 100mg
    This pct, to me, is a little off. Other than that its a pretty good write up.
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    Quote Originally Posted by nosnmiveins View Post
    traitor...
    No way man!! Never!! I stumbled across it in a google search.
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    very good! Really Informative?
    is there a tren xtreme or phera plex for dummies?
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    Believe its from KRZNA but I could be wrong. Dude knows his stuff
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    where ever this originated from its good stuff!!


    bump
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    yeah i mentioned that in the top of the message. The write up was from KRZNA who i gave credit to if you read it. it is an excellent source. i thought this would save people the trouble of going and googling it, thought it would be better if it was right here. yes it is originally from bb.com...which i left that forum over a year ago and came here cux the people there are ****ing *******s..but you guys are alright lol
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    Quote Originally Posted by bigpapa View Post
    yeah i mentioned that in the top of the message. The write up was from KRZNA who i gave credit to if you read it. it is an excellent source. i thought this would save people the trouble of going and googling it, thought it would be better if it was right here. yes it is originally from bb.com...which i left that forum over a year ago and came here cux the people there are ****ing *******s..but you guys are alright lol


    Lol i wasn't trying to start anything, was just mentioning it. Glad you posted it here.

    BB.com isnt so bad. Any of you guys heard about PHF? Decent collection of PH/DS people...pm me for details if you want
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    Quote Originally Posted by nickrut View Post
    Lol i wasn't trying to start anything, was just mentioning it. Glad you posted it here.

    BB.com isnt so bad. Any of you guys heard about PHF? Decent collection of PH/DS people...pm me for details if you want
    o i know u werent. was just clarifyin if neone missed it. no worries.
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    Be careful,.. he has a gun!!!
    Think training's hard,. try losing!
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    Quote Originally Posted by bonscott View Post
    Be careful,.. he has a gun!!!
    thats right...i used that one when i was a prostitute...thug life.
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    Thumbs up


    Ya I have that saved in my favs..
    Bigpapa, you mind if I add this? It was written by Ryan Smith.. Good diet info to go with SD.

    June 8th, 2005, 01:30 PM
    Below you will find a great article for maximizing gains while on Superdrol. Also if anyone has any specific questions feel free to ask. We also have some amazing products that will be coming out within 60 days.

    Anabolic Nutrition for Growth
    A look into diets to maximize gains while taking SuperdrolTM
    By Ryan Smith

    Let’s face it, you bought this product because you want results, and Superdrol can provide them. As with every great supplement, your body will need proper nutrition to take full advantage of the power of Superdrol. The following recommendations are provided to help you, the consumer, take it to the next level, to get the most out of your Superdrol cycle. With the strongest supplement to hit the stores in years, and an equally effective diet, you will grow beyond what was thought possible.

    A bodybuilding diet is not simple, nor is it something to take lightly if you are serious about massive gains in size and strength. The old ideal of eating everything in sight to gain weight is not the smart way to get big. Will it work? Yes, but this is not the best way to do it. You can gain the LBM (Lean Body Mass) without the unwanted fat. The key is not allowing yourself to go overboard with the amount of food you take in. Eat clean; which means stay away from nutritionally defunct foods like ice cream, and eat plenty of protein along with adequate amounts of complex carbohydrates. To figure out how many calories you need to bulk while taking Superdrol use the following:

    Harris Benedict Formula (Basal Metabolic Rate)
    BMR = 66 + (13.7 X weight in kilos) + (5 X height in cm) - (6.8 X age in years)

    1 inch = 2.54cm
    1 kilogram = 2.2lbs

    To determine your total daily calorie needs, multiply your BMR by the appropriate activity factor, most individuals will have light to moderate activity levels.
    • If you are Sedentary - little or no exercise = BMR X 1.2
    • If you are Lightly Active (light exercise/sports 1-3 days/week) = BMR X 1.375
    • If you are Moderately Active (moderate exercise/sports 3-5 days/week) = BMR X 1.55
    • If you are Very Active = BMR X 1.725 (hard exercise/sports 6-7 days/week) = BMR X 1.725
    • If you are Extra Active (very hard daily exercise/sports & physical job or 2X day training) = BMR X 1.9
    After figuring your BMR add an extra 500 calories a day in complex carbohydrate/protein rich foods.

    An ideal percentage to use for the diet is 40/40/20. That is 40% carbohydrates, 40% protein, and 20% fat. Below is a sample bulking diet for a 6 foot 200 pound male using the formulas provided; with nutritionally dense foods, and adequate amounts of complex carbohydrates, proteins, and fats. Superdrol allows for a higher carbohydrate, and protein rich diet since it is so potent with energy storage. Users have reported that hunger increases almost immediately after starting Superdrol. This diet is based around the use of Superdrol, with key meals in certain places to allow for the best benefits from this supplement.

    Age: 25
    Height: 6 feet
    Weight: 200lbs
    BMR: 3690 total calories
    (66 + (1247) + (915) – (170) = 2058 cal x 1.55 = 3190 cal + 500 cal = 3690 total calories)

    To gain body weight, you must consume more calories than you burn. One pound of body weight is equivalent to 3500 calories, so eating an extra 500 calories per day will allow for gaining one pound a week. If gains stall, DO NOT increase the dose at first, but simply add in another 100 calories per day, and then assess from there. These numbers are not fixed; you should add more calories on days that you are more active, like leg day.
    Daily Bulking Diet

    (You may increase dosages of Superdrol throughout your cycle to find the results that work best for you. Superdrol usually requires additional dosage as you progress through your cycle)

    Meal 1
    10mgs Superdrol
    7 Whole eggs
    1 multigrain bagel
    1 serving of bran cereal
    8oz skim milk
    ¼ cup of low fat cheese

    Meal 2
    1 Chicken Breast
    1 serving or scoop of protein powder
    ¼ cup of low fat cheese
    1 tablespoon flaxseed oil

    Meal 3
    1 can of Tuna (may be substituted with any lean white meat)
    1 cup of Broccoli, raw or steamed
    1 multigrain bagel

    Meal 4
    10mgs Superdrol
    1 serving/scoop protein powder
    1 cup slow cooked oats
    2 servings of turkey chili
    *This is your pre-workout meal, it can be moved to fit your schedule; however, it must be eaten prior to every workout.

    Meal 5
    1 serving/scoop whey protein powder
    1 cup slow cooked oats
    *This is your post-workout meal, it can be moved to fit your schedule; however, it must be eaten after every workout.

    Meal 6
    1 cup of fat free cottage cheese
    ½ cup of lentils
    1 scoop casein/milk isolate protein powder

    Meal 7
    1 serving of some type of white fish, Haddock, Cod
    1 cup broccoli
    1 tablespoon Flaxseed oil

    Totals:

    Calories- 3710

    Fat- 100

    Carbohydrates- 345

    Protein- 362

    Water consumption should accompany every meal, and throughout the day. Try to get at least a gallon in every day, especially around workouts. As you can see the Superdrol is based around your largest protein/carb meals for the day. The second dose is also taken before your workout for the best benefit.

    Although Superdrol is best used for bulking, it can be used in a cutting cycle with the proper diet.. Again, what follows is a diet for a 6 foot, 200 pound male on a cutting cycle of Superdrol.

    In order to lose fat while cutting you must consume less calories than you burn. This can be achieved in several different ways; the one I will demonstrate maintains high protein intake, and moderate carbohydrates. This time however, because Superdrol will allow the user some leeway, we will actually drop calories as needed from fat, and very little from the carb/protein meals. You never want to lose over two-three pounds a week, and three is pushing it. When lowering calories, your glycogen storage is depleted. The good news is that while taking Superdrol this depletion can be limited. Superdrol has an immense effect upon the body’s glycogen storage; in fact it is quite incredible how powerful it is at keeping energy stores. Keeping protein levels high is very important in staving off muscle loss. The fact that carbohydrates are kept at a moderate level allow for a much easier way to cut. Again these numbers are not fixed; they should fluctuate from day to day depending on your activity. For example on leg day you may want to have some fruit during your workout for energy, Gatorade is another option. Keep simple carbohydrates intake, like sugar, as low as possible.


    Age: 25
    Height: 6 feet
    Weight: 200lbs
    BMR: 2690 total calories
    (66 + (1247) + (915) – (170) = 2058 cal x 1.55 = 3190 cal – 500 = 2690 total calories)

    Daily Cutting Diet
    (You may increase dosages of Superdrol throughout your cycle to find the results that work best for you. Superdrol usually requires additional dosage as you progress through your cycle)

    Meal 1
    10mgs Superdrol
    7 whole eggs
    1 multigrain bagel
    ¼ cup of low fat cheese

    Meal 2
    1 Chicken Breast
    1 serving or scoop of protein powder
    ¼ cup of low fat cheese

    Meal 3
    1 can of Tuna (may be substituted with any lean white meat)
    1 cup of Broccoli, raw or steamed

    Meal 4
    10mgs Superdrol
    1 serving/scoop protein powder
    ½ cup slow cooked oats
    1 servings of turkey chili
    *This is your pre-workout meal, it can be moved to fit your schedule; however, it must be eaten prior to every workout.

    Meal 5
    1 serving/scoop whey protein powder
    1 cup slow cooked oats
    *This is your post-workout meal, it can be moved to fit your schedule; however, it must be eaten after every workout.

    Meal 6
    ½ cup of fat free cottage cheese
    1 scoop casein/milk isolate protein powder

    Meal 7
    1 serving of some type of white fish, Haddock, Cod
    1 cup broccoli
    1 tablespoon Flaxseed oil

    Totals:

    Calories- 2635

    Fat- 84

    Carbohydrates- 195

    Protein- 288

    Another key player in the fat loss diet is cardiovascular exercise. I know, we all dread it, but it must be done. A simple way to determine the amount of cardio you need to burn fat, while not burning up muscle, is the following formula. This formula is used to determine how many Beats Per Minute (BMR) your heart rate needs to be in for fat loss.

    220 - (Your age) x 65%-75%

    Low-intensity cardiovascular exercise (65-75% max heart rate) for 45-60 minutes per session is ideal. If you choose to do cardio after weight training keep it to 30 minutes. On leg days there is no need for cardio.
    Example of a 6 foot male 200 pounds

    220 – 25 = 195 x .65 = ~127 BPM. At 75% it would be, ~146 BPM

    Target this BPM and duration three – four days a week.

    Some Food Choices

    Protein Sources
    Chicken breast
    Lean Red meats 10% fat or less
    Lean fishes
    Fatty fishes (salmon)
    Whole eggs
    Egg Whites
    Turkey
    Fat Free/Low fat cottage cheese (1-2%)
    Protein powder
    Jerky


    Complex Carbohydrate Substitutions and Choices
    Oatmeal (not instant)
    Yams
    Sweet potatoes
    Brown rice
    Whole grain bread/wraps/bagels/muffins
    Raw/steamed/grilled vegetables
    Fibrous cereals (Fiber One, granola (low sugar) Smart Start, Uncle Sams, All Bran)
    Lentils

    Fat Sources
    Nuts (Raw almonds, walnuts, cashews etc…)
    Flax seeds/ Flax seed oil
    Fish oil
    Primrose oil
    Borage oil
    Olive oil
    Enova oil


    Vegetable Substitutions and Choices
    Asparagus, Broccoli, Brussels Sprouts, Cabbage, Carrots, Cauliflower, Celery, Cucumbers, Green Beans, Kale, Lettuce(all varieties), Mushrooms, Radishes, Spinach, Squash (summer varieties only), Tomato, Water Chestnuts, Zucchini
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    Just to chime in, when it says "whole egss" are they seriously talking about that person should eat 10 whole f'n eggs? I have to think that is a type-o
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    DLM5 add away brother! i hope what happens with this thread is everybody chimes in with their experiences, cycle, pct, diets, training, etc..and this can become sort of a handbook for not only superdrol compounds but any ph, including the harsher ones. hoepfully this thread will become so successful that the mods make it a sticky to sort of make it a one stop shopping for people looking for information.
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    was wondering if anyone can clarify whether the information below regarding SERM's is acurate.


    Clomid & Nolvadex - The Dark Side

    By Eric M. Potratz (Email)

    Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.

    discuss this article in the forum

    Preface - Over the past 15 years, the use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs) has become a staple in the HRT and bodybuilding communities.

    The popularity of these drugs stems from the popular advice to use these drugs for everything from testosterone recovery, bloat reduction, to gyno prevention. In many communities SERMs have become akin to vitamins -- vitamins that can do no wrong and provide seemingly endless benefits.

    This article is not intended to examine the proper use or possible applications of Clomid or Nolvadex. Instead, we will be exploring the historical development of these drugs, the short-term side-effects and long-term consequences.

    As I will illustrate, these drugs are true danger to men’s health.

    Synthetic estrogens, the beginning -

    It was the 1930’s and there was a new age of hormone-dependant pathologies on the rise. Scientists were eager to determine the structural requirements of estrogen for new drug design.

    In 1937 Sir Charles Dodd of the Middlesex Hospital of London found estrogenic activity in a molecule with two benzene rings linked together via a short carbon chain (eg, diphenylethane). (1) Soon thereafter, a synthetic, non-steroidal estrogen known as diethylstilboestrol (DES) was created from this basic molecular backbone. (1) By 1941, DES was an FDA approved drug, and by the 1950’s, DES gained widespread popularity as the drug of choice for menopausal symptoms, cancer treatment, and prevention of miscarriages. (2)

    DES sparked the interest of ambitious drug manufactures that saw this synthetic molecule as a potential “molecular backbone” which could be tailored for estrogenic activity, and patented for maximum profit.

    Within months, a research group from the University of Edinburgh found that the addition of a benzene ring to the original diphenylethane structure created an somewhat of an anti-estrogen known as triphenylethylene. (1) Although it had very weak estrogenic activity, it was called an anti-estrogen because it competed with the body’s more powerful estradiol for the ER receptors.

    Although the complex estrogenic action of triphenylethylene was not fully understood, it was considered the perfect molecular platform for future drug development because of its high oral bioavailability and extended half-life due to its lipophilicity (fat solubility). As it was later discovered, the estrogenic action could be manipulated with structural modifications for more specific agonist/antagonist actions. (3) Despite the lack of understanding for its full physiological effects, triphenylethylene would become the molecular backbone for generations of SERM’s to come.

    By the early 1940’s, the world’s largest chemical manufacturers, including Imperial Chemical Industries (ICI), got word of the triphenylethylene development, and seized the opportunity to expand this new class of compounds. By the 1950’s, the synthesis of new triphenylethylene based molecules had began picking up momentum, as the first FDA approved SERM’s started appearing on the market.

    One of the first was Triparanol, which was sold as a cholesterol lowering SERM, until it was eventually pulled from the market in the 1950’s for causing cataracts in patients. (7) Later, Ethamoxytriphetol (MER-25) was discovered and found to be a reliable contraceptive and anti-cancer agent in rats, but failed in humans due to the drug’s severe toxicity and stimulation of “acute psychotic episodes”. (6)

    Despite these early warning signs, development continued.

    Among one of the newer SERM’s to appear in the late 1950’s, was a mixture of two stereoisomers -- zuclomiphene and enclomiphene -- both having unique estrogenic and anti-estrogen actions. This mixture was collectively called clomiphene, and later marketed as Clomid.



    Then, in 1962, ICI synthesized ICI-46474, another mixture of a trans and cis isomers with mixed estrogenic and anti-estrogenic activity. (7) Ultimately, the trans isomer was found to be the predominate anti-estrogen, which was isolated and eventually named tamoxifen, and later marketed as Nolvadex.

    Originally, ICI pushed these new SERM’s to market as a “morning after” contraceptives, which were eventually approved by the FDA. (4) Yet again, the profit hungry and presumptuous drug manufacturer based its findings on rat studies, which would prove to be a mistake upon subsequent human research that showed the SERM’s induced, rather than inhibited ovulation. (4) Needless to say, tamoxifien was withdrawn as a contraceptive.

    And remember DES, the original synthetic estrogen developed back in the 1930’s? As it turned out, DES was found to increase the risk of breast cancer by 50%. Further research linked DES to millions of vaginal and testicular cancers among the children of mothers who took DES during pregnancy. (2,5)

    The light on synthetic anti-estrogens was dim, and by the late 1960’s, there was little enthusiasm to continue R&D with triphenylethylene based SERM’s, especially considering their inherently toxic effects (7, 10)

    It wasn’t until 1971, that tamoxifen would be dug up from the dead and considered as a candidate for cancer treatment.

    Treating cancer with a carcinogen –

    When research is done on anti-cancer drugs (such as SERMs), the aim is to find a drug that prolongs life, with the least amount of acute side-effects. In other words, the goal isn’t so much about finding a cure, as it is finding something that can alleviate the symptoms and/or prolong life.

    For an estrogen dependant cancer, the idea was simple – Block the proliferative action of estrogen with an anti-estrogen and slow the cancer growth. What could be more appropriate than an already available, orally active, patentable synthetic estrogen such as tamoxifen? It was a practical shoo-in.

    Therefore, in 1971, when drug researchers decided to examine all of the historical anti-cancer SERM data, they found that all of the SERM’s showed anti-proliferative activity on estrogen dependant cancer, and all of them demonstrated some extent of toxicity. (10, 37-39) However, the SERM that happened to show the least amount of toxicity was tamoxifen. (clomiphene missed the mark by showing a high rate of cataract formation)

    At the time, Pierre Blais, a well known drug researcher, commented on the finding (5) -

    “Tamoxifen is a garbage drug that made it to the top of the scrap heap. It is a DES in the making."

    In spite of the criticism from a number of researchers, the FDA approved tamoxifen as a cancer treatment in 1977, and in 1985 ICI was awarded a US patent for tamoxifen in the treatment of breast cancer. (5) Soon, tamoxifen would become the most popularity prescribed cancer drug.

    “Its FDA approved for cancer treatment. It must be safe!”

    It’s wrong to assume that an “FDA approved” drug has a proven safety profile. The FDA has continually issued stronger health warnings for tamoxifen over the years. For instance, in 1994 the FDA demanded that the tamoxifen manufacturer Zeneca (an ICI sub-division), issue warning letters to health care practitioners about the increased risk of endometrial and gastro-intestinal cancers with tamoxifen use. Zeneca also reported adverse effects similar to those seen with DES, such as reproductive abnormalities in the animals whose mothers received tamoxifen. (remember, DES was the original synthetic estrogen, and also an analog to tamoxifen)

    A number of cancer researchers have pointed out the health risks too, such as Elwood et al (6) -

    “[Tamoxifen], therefore, is not appropriate for use in the general population because of the known increased risk of endometrial cancer”

    “So why is tamoxifen the most popularly prescribed cancer drug, if it’s so toxic?”

    The answer is simple. Tamoxifen is the lesser of two evils.

    Tamoxifen remains the most popularly prescribed drug because it is one of the few drugs that has shown a “statistically significant” improvement of the survival rate of breast cancer patients.* (Not to mention, tremendous financial motives and intraworking’s from its patent holder Zeneca)

    Remember, the goal in cancer treatment is to prolong life -- even if it means committing to therapy that is potentially cancerous or injurious to future health (as confirmed in long-term follow up’s and close examinations of tamoxifen patients).

    So, perhaps the risks are worthy for the cancer patient, but are they worthy for the health conscious male?

    * Most research has shown tamoxifen to improve the survival rate by 4-14%. For instance, over a 5 year period, 74% of the women survived who used tamoxifen, compared to 70% of the women on placebo. Depending on the type of cancer, this may translate into an extra 2-3 years of life for a cancer patient. (9) Continuing tamoxifen therapy for more than 5 years, results in increased tumor recurrences and serious side effects. (8)

    Translating the science, for men’s health -

    Fast forward 30 years, through hundreds of human and animal trials and we find that the research is quite extensive, and contradicting. (21)

    The damaging evidence from many early rat studies showed severely toxic effects, including the development of cancer in the liver, uterus, or testes upon tamoxifen administration. (30-34,41) However, this evidence was largely disregarded by further test tube studies on human cell-lines which appeared to show a lack of toxic effects. (21)

    This misleading test tube data gave the green flag to perform large scale human studies with tamoxifen in the 80’s and 90’s. Even more misleading, was the majority of the human research described tamoxifen as having a “low incidence of troublesome side effects” and that the “side effects where usually trivial”. (22)

    As science would uncover, the lack of human toxicity reported in original tamoxifen research was a result of insufficient study duration, inability to detect low level DNA damage with insensitive methodologies, and/or misdiagnosis of collateral cancers as metastasis infections from the breast cancer itself. (15, 21, 28-34)

    A word on clomiphene (Clomid) –

    Clomiphene (Clomid) consists of two stereoisomers which possess radically different pharmacodynamics. Zuclomiphene has predominantly estrogenic effects and slow clearance while the enclomiphene isomer has predominately anti-estrogenic effects and quick clearance. (9) This creates a dichotomy between estrogen blockage and estrogen stimulation and an acute imbalance once Clomid administration is discontinued. Bodybuilders will often complain of “estrogenic rebound” after stopping Clomid, which could be attributed to the lingering estrogenic isomer zuclomiphene as the anti-estrogenic enclomiphene has long cleared the system. (Recently, enclomiphene has been isolated by the pharmaceutical company Repros, for use in Androxal™.)

    For all intents and purposes, tamoxifen is a superior SERM, simply for the fact that tamoxifen provides a purely anti-estrogenic isomer, whereas Clomid provides a mix of anti and pro estrogenic effects.

    In regards to the health consequences about to be listed, it can be safely assumed that Clomid will share similar detrimental effects as tamoxifen, since it shares the same triphenylethylene backbone and carcinogenic tendencies. (44,45,57,58)

    Liver cancer -


    Originally, tamoxifen was accepted as being non-toxic to human liver upon finding that tamoxifen did not cause noticeable liver damage (DNA adducts) during short-term test tube studies with human liver cells. (35,36)

    However, it became apparent that test tuberesearch was largely flawed due to the low rate of metabolism in such a superficial environment. (21) It was soon discovered that the hepatotoxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen and N-desmethyltamoxifen metabolites, which would only appear in an in vivo environment. (15) Surely enough, the results from the original rat studies showing dramatic carcinogenic effects on the liver, 30-34,41 soon correlated with human data when researchers found the same type of liver DNA adducts in tamoxifen patients. (15, 28-34)

    More recent human research has reported tamoxifen treated women to have 3x the risk of developing fatty liver disease, which occurs as soon as 3 months into therapy at only 20mg/day. (24-26) In some cases, the disease lasts up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy shows cases of deadly hepatocellular carcinoma. (27-29)

    In 2002, a bizarre study examined the use of tamoxifen for hepatocellular carcinoma treatment in humans. It was assumed that since tamoxifen could inhibit proliferation of breast cancer, it could offer the same benefit for liver cancer. The devastating results could not have been further indicative of tamoxifen’s hepatotoxic nature, as the tamoxifen treatment significantly increased the rate of death, compared to the group not receiving tamoxifen. (14)

    Finally, in a case study reviewing tamoxifen induced liver disease; D.F Moffat et al made a profound statement –


    “hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast.”


    In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as an infection from the breast cancer itself. (28)

    Although tamoxifen induced liver cancer may take years to manifest in a healthy male, its damaging effects could easily be exaggerated by other popular hepatotoxic drugs, such as 17aa oral steroids. (15)

    Prostate cancer -

    In 1996, the International Agency for Research on Cancer (IARC) concluded that tamoxifen clearly promotes uterine cancer in humans – at a standard 20mg/day dose. (16,23,42) This is due to tamoxifen acting as an estrogen agonist in the uterus, presumably from the 4-hydroxytamoxifen metabolite, which triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts. (33, 40)

    Contrary to popular thought, these implications are quite scary for a male when we realize the male equivalent to the uterus is the prostate – which differentiates from the same embryonic cell line, shares the same oncogene, Bcl-2, and high concentration of estrogen receptors. In fact, there is no reason to assume that tamoxifen would not initiate the same cancerous growth in the prostate. (60-62) It is no wonder that tamoxifen failed as a treatment for prostate carcinoma. (43)

    Note: This same risk would be applicable to Clomid, which has also been linked to uterine cancer and ovarian hyper-stimulation. (18, 19, 57, 59)

    Libido reduction & erectile dysfunction -

    Erectile dysfunction, low libido, and general impotence are typical complaints from men recently discontinuing steroids or HRT therapy, which is often combated by Clomid or Nolvadex, paradoxically so.

    Regardless of any positive effects on fertility or testosterone levels, Clomid and Nolvadex use is highly correlated with erectile dysfunction, libido suppression, and even emotional disorders. (10,47)

    Research with male breast cancer patients has also reported decreased libido, and thrombosis associated with tamoxifen use. (47) The thrombotic effect (blood vessel clogging) could explain the mechanism by which SERM’s may inhibit erectile function, by reducing circulation to erectile tissue. (47, 52)


    Increased susceptibility to gyno -

    Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.

    This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developming gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting upon the progesterone receptor).

    It is interesting to speculate. Is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?


    Ocular toxicity –

    Another possible side effect associated with SERMs is visual cloudiness, loss of vision and even cataract formation. Although this tends to be a more common side effect from high dosed SERM therapy, standard 20mg/day tamoxifen regimes have been reported to cause these symptoms of ocular toxicity. (17, 46)

    Newer SERM’s -

    As the medical community became more aware of the side-effects associated with tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is a closely related analog of tamoxifen, so it also carries many of the related genotoxic effects. (48,49)

    Raloxifene is a newer SERM based off a benzothiophene structure, which appears to make it less toxic in the liver, uterus or prostate. (50-52) Unfortunately, Raloxifene has been associated with a higher incidence of thromboembolism (52), and also has very low oral absorption, making it an expensive alternative at a typical dose (120mg/day). (53) Still, Raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects. (53)

    Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further. (further enumerating the evidence of toxicity with the tamoxifen generation of SERM’s)



    What to do now?

    Firstly, it should become a priority to create awareness about the possible side effects of SERMs. Once educated, users will be able to start reducing their requirements of these drugs, and begin adopting healthier, more responsible alternatives.

    Carefully planned cycles, and the proper use of aromatase inhibitors (AIs) must pursue over haphazard combinations of excessively dosed aromatizing AAS’s -- which require high doses of SERM’s to reduce possible side-effects. Whereas avoiding SERM’s in HRT will involve the natural clearance and management of endogenous estrogens.

    It will be important to maintain testicular function during cycle for a quick and efficient recovery of natural testosterone production for PCT – negating the need for high dose 2-3 month SERM based PCT’s. (For more information on the proper use of hCG during cycle, visit here)

    Thus, abolishing the bad habit of SERMing will involve community wide enlightenment with careful, comprehensive planning of worthy alternatives.

    discuss this article in the forum
  18. Registered User
    KGUNZ101's Avatar
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    Mainly in reference to the bolded sections thanks

    Quote Originally Posted by KGUNZ101 View Post
    was wondering if anyone can clarify whether the information below regarding SERM's is acurate.


    Clomid & Nolvadex - The Dark Side

    By Eric M. Potratz (Email)

    Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.

    discuss this article in the forum

    Preface - Over the past 15 years, the use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs) has become a staple in the HRT and bodybuilding communities.

    The popularity of these drugs stems from the popular advice to use these drugs for everything from testosterone recovery, bloat reduction, to gyno prevention. In many communities SERMs have become akin to vitamins -- vitamins that can do no wrong and provide seemingly endless benefits.

    This article is not intended to examine the proper use or possible applications of Clomid or Nolvadex. Instead, we will be exploring the historical development of these drugs, the short-term side-effects and long-term consequences.

    As I will illustrate, these drugs are true danger to men’s health.

    Synthetic estrogens, the beginning -

    It was the 1930’s and there was a new age of hormone-dependant pathologies on the rise. Scientists were eager to determine the structural requirements of estrogen for new drug design.

    In 1937 Sir Charles Dodd of the Middlesex Hospital of London found estrogenic activity in a molecule with two benzene rings linked together via a short carbon chain (eg, diphenylethane). (1) Soon thereafter, a synthetic, non-steroidal estrogen known as diethylstilboestrol (DES) was created from this basic molecular backbone. (1) By 1941, DES was an FDA approved drug, and by the 1950’s, DES gained widespread popularity as the drug of choice for menopausal symptoms, cancer treatment, and prevention of miscarriages. (2)

    DES sparked the interest of ambitious drug manufactures that saw this synthetic molecule as a potential “molecular backbone” which could be tailored for estrogenic activity, and patented for maximum profit.

    Within months, a research group from the University of Edinburgh found that the addition of a benzene ring to the original diphenylethane structure created an somewhat of an anti-estrogen known as triphenylethylene. (1) Although it had very weak estrogenic activity, it was called an anti-estrogen because it competed with the body’s more powerful estradiol for the ER receptors.

    Although the complex estrogenic action of triphenylethylene was not fully understood, it was considered the perfect molecular platform for future drug development because of its high oral bioavailability and extended half-life due to its lipophilicity (fat solubility). As it was later discovered, the estrogenic action could be manipulated with structural modifications for more specific agonist/antagonist actions. (3) Despite the lack of understanding for its full physiological effects, triphenylethylene would become the molecular backbone for generations of SERM’s to come.

    By the early 1940’s, the world’s largest chemical manufacturers, including Imperial Chemical Industries (ICI), got word of the triphenylethylene development, and seized the opportunity to expand this new class of compounds. By the 1950’s, the synthesis of new triphenylethylene based molecules had began picking up momentum, as the first FDA approved SERM’s started appearing on the market.

    One of the first was Triparanol, which was sold as a cholesterol lowering SERM, until it was eventually pulled from the market in the 1950’s for causing cataracts in patients. (7) Later, Ethamoxytriphetol (MER-25) was discovered and found to be a reliable contraceptive and anti-cancer agent in rats, but failed in humans due to the drug’s severe toxicity and stimulation of “acute psychotic episodes”. (6)

    Despite these early warning signs, development continued.

    Among one of the newer SERM’s to appear in the late 1950’s, was a mixture of two stereoisomers -- zuclomiphene and enclomiphene -- both having unique estrogenic and anti-estrogen actions. This mixture was collectively called clomiphene, and later marketed as Clomid.



    Then, in 1962, ICI synthesized ICI-46474, another mixture of a trans and cis isomers with mixed estrogenic and anti-estrogenic activity. (7) Ultimately, the trans isomer was found to be the predominate anti-estrogen, which was isolated and eventually named tamoxifen, and later marketed as Nolvadex.

    Originally, ICI pushed these new SERM’s to market as a “morning after” contraceptives, which were eventually approved by the FDA. (4) Yet again, the profit hungry and presumptuous drug manufacturer based its findings on rat studies, which would prove to be a mistake upon subsequent human research that showed the SERM’s induced, rather than inhibited ovulation. (4) Needless to say, tamoxifien was withdrawn as a contraceptive.

    And remember DES, the original synthetic estrogen developed back in the 1930’s? As it turned out, DES was found to increase the risk of breast cancer by 50%. Further research linked DES to millions of vaginal and testicular cancers among the children of mothers who took DES during pregnancy. (2,5)

    The light on synthetic anti-estrogens was dim, and by the late 1960’s, there was little enthusiasm to continue R&D with triphenylethylene based SERM’s, especially considering their inherently toxic effects (7, 10)

    It wasn’t until 1971, that tamoxifen would be dug up from the dead and considered as a candidate for cancer treatment.

    Treating cancer with a carcinogen –

    When research is done on anti-cancer drugs (such as SERMs), the aim is to find a drug that prolongs life, with the least amount of acute side-effects. In other words, the goal isn’t so much about finding a cure, as it is finding something that can alleviate the symptoms and/or prolong life.

    For an estrogen dependant cancer, the idea was simple – Block the proliferative action of estrogen with an anti-estrogen and slow the cancer growth. What could be more appropriate than an already available, orally active, patentable synthetic estrogen such as tamoxifen? It was a practical shoo-in.

    Therefore, in 1971, when drug researchers decided to examine all of the historical anti-cancer SERM data, they found that all of the SERM’s showed anti-proliferative activity on estrogen dependant cancer, and all of them demonstrated some extent of toxicity. (10, 37-39) However, the SERM that happened to show the least amount of toxicity was tamoxifen. (clomiphene missed the mark by showing a high rate of cataract formation)

    At the time, Pierre Blais, a well known drug researcher, commented on the finding (5) -

    “Tamoxifen is a garbage drug that made it to the top of the scrap heap. It is a DES in the making."

    In spite of the criticism from a number of researchers, the FDA approved tamoxifen as a cancer treatment in 1977, and in 1985 ICI was awarded a US patent for tamoxifen in the treatment of breast cancer. (5) Soon, tamoxifen would become the most popularity prescribed cancer drug.

    “Its FDA approved for cancer treatment. It must be safe!”

    It’s wrong to assume that an “FDA approved” drug has a proven safety profile. The FDA has continually issued stronger health warnings for tamoxifen over the years. For instance, in 1994 the FDA demanded that the tamoxifen manufacturer Zeneca (an ICI sub-division), issue warning letters to health care practitioners about the increased risk of endometrial and gastro-intestinal cancers with tamoxifen use. Zeneca also reported adverse effects similar to those seen with DES, such as reproductive abnormalities in the animals whose mothers received tamoxifen. (remember, DES was the original synthetic estrogen, and also an analog to tamoxifen)

    A number of cancer researchers have pointed out the health risks too, such as Elwood et al (6) -

    “[Tamoxifen], therefore, is not appropriate for use in the general population because of the known increased risk of endometrial cancer”

    “So why is tamoxifen the most popularly prescribed cancer drug, if it’s so toxic?”

    The answer is simple. Tamoxifen is the lesser of two evils.

    Tamoxifen remains the most popularly prescribed drug because it is one of the few drugs that has shown a “statistically significant” improvement of the survival rate of breast cancer patients.* (Not to mention, tremendous financial motives and intraworking’s from its patent holder Zeneca)

    Remember, the goal in cancer treatment is to prolong life -- even if it means committing to therapy that is potentially cancerous or injurious to future health (as confirmed in long-term follow up’s and close examinations of tamoxifen patients).

    So, perhaps the risks are worthy for the cancer patient, but are they worthy for the health conscious male?

    * Most research has shown tamoxifen to improve the survival rate by 4-14%. For instance, over a 5 year period, 74% of the women survived who used tamoxifen, compared to 70% of the women on placebo. Depending on the type of cancer, this may translate into an extra 2-3 years of life for a cancer patient. (9) Continuing tamoxifen therapy for more than 5 years, results in increased tumor recurrences and serious side effects. (8)

    Translating the science, for men’s health -

    Fast forward 30 years, through hundreds of human and animal trials and we find that the research is quite extensive, and contradicting. (21)

    The damaging evidence from many early rat studies showed severely toxic effects, including the development of cancer in the liver, uterus, or testes upon tamoxifen administration. (30-34,41) However, this evidence was largely disregarded by further test tube studies on human cell-lines which appeared to show a lack of toxic effects. (21)

    This misleading test tube data gave the green flag to perform large scale human studies with tamoxifen in the 80’s and 90’s. Even more misleading, was the majority of the human research described tamoxifen as having a “low incidence of troublesome side effects” and that the “side effects where usually trivial”. (22)

    As science would uncover, the lack of human toxicity reported in original tamoxifen research was a result of insufficient study duration, inability to detect low level DNA damage with insensitive methodologies, and/or misdiagnosis of collateral cancers as metastasis infections from the breast cancer itself. (15, 21, 28-34)

    A word on clomiphene (Clomid) –

    Clomiphene (Clomid) consists of two stereoisomers which possess radically different pharmacodynamics. Zuclomiphene has predominantly estrogenic effects and slow clearance while the enclomiphene isomer has predominately anti-estrogenic effects and quick clearance. (9) This creates a dichotomy between estrogen blockage and estrogen stimulation and an acute imbalance once Clomid administration is discontinued. Bodybuilders will often complain of “estrogenic rebound” after stopping Clomid, which could be attributed to the lingering estrogenic isomer zuclomiphene as the anti-estrogenic enclomiphene has long cleared the system. (Recently, enclomiphene has been isolated by the pharmaceutical company Repros, for use in Androxal™.)

    For all intents and purposes, tamoxifen is a superior SERM, simply for the fact that tamoxifen provides a purely anti-estrogenic isomer, whereas Clomid provides a mix of anti and pro estrogenic effects.

    In regards to the health consequences about to be listed, it can be safely assumed that Clomid will share similar detrimental effects as tamoxifen, since it shares the same triphenylethylene backbone and carcinogenic tendencies. (44,45,57,58)

    Liver cancer -


    Originally, tamoxifen was accepted as being non-toxic to human liver upon finding that tamoxifen did not cause noticeable liver damage (DNA adducts) during short-term test tube studies with human liver cells. (35,36)

    However, it became apparent that test tuberesearch was largely flawed due to the low rate of metabolism in such a superficial environment. (21) It was soon discovered that the hepatotoxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen and N-desmethyltamoxifen metabolites, which would only appear in an in vivo environment. (15) Surely enough, the results from the original rat studies showing dramatic carcinogenic effects on the liver, 30-34,41 soon correlated with human data when researchers found the same type of liver DNA adducts in tamoxifen patients. (15, 28-34)

    More recent human research has reported tamoxifen treated women to have 3x the risk of developing fatty liver disease, which occurs as soon as 3 months into therapy at only 20mg/day. (24-26) In some cases, the disease lasts up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy shows cases of deadly hepatocellular carcinoma. (27-29)

    In 2002, a bizarre study examined the use of tamoxifen for hepatocellular carcinoma treatment in humans. It was assumed that since tamoxifen could inhibit proliferation of breast cancer, it could offer the same benefit for liver cancer. The devastating results could not have been further indicative of tamoxifen’s hepatotoxic nature, as the tamoxifen treatment significantly increased the rate of death, compared to the group not receiving tamoxifen. (14)

    Finally, in a case study reviewing tamoxifen induced liver disease; D.F Moffat et al made a profound statement –


    “hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast.”


    In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as an infection from the breast cancer itself. (28)

    Although tamoxifen induced liver cancer may take years to manifest in a healthy male, its damaging effects could easily be exaggerated by other popular hepatotoxic drugs, such as 17aa oral steroids. (15)

    Prostate cancer -

    In 1996, the International Agency for Research on Cancer (IARC) concluded that tamoxifen clearly promotes uterine cancer in humans – at a standard 20mg/day dose. (16,23,42) This is due to tamoxifen acting as an estrogen agonist in the uterus, presumably from the 4-hydroxytamoxifen metabolite, which triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts. (33, 40)

    Contrary to popular thought, these implications are quite scary for a male when we realize the male equivalent to the uterus is the prostate – which differentiates from the same embryonic cell line, shares the same oncogene, Bcl-2, and high concentration of estrogen receptors. In fact, there is no reason to assume that tamoxifen would not initiate the same cancerous growth in the prostate. (60-62) It is no wonder that tamoxifen failed as a treatment for prostate carcinoma. (43)

    Note: This same risk would be applicable to Clomid, which has also been linked to uterine cancer and ovarian hyper-stimulation. (18, 19, 57, 59)

    Libido reduction & erectile dysfunction -

    Erectile dysfunction, low libido, and general impotence are typical complaints from men recently discontinuing steroids or HRT therapy, which is often combated by Clomid or Nolvadex, paradoxically so.

    Regardless of any positive effects on fertility or testosterone levels, Clomid and Nolvadex use is highly correlated with erectile dysfunction, libido suppression, and even emotional disorders. (10,47)

    Research with male breast cancer patients has also reported decreased libido, and thrombosis associated with tamoxifen use. (47) The thrombotic effect (blood vessel clogging) could explain the mechanism by which SERM’s may inhibit erectile function, by reducing circulation to erectile tissue. (47, 52)


    Increased susceptibility to gyno -

    Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.

    This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developming gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting upon the progesterone receptor).

    It is interesting to speculate. Is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?


    Ocular toxicity –

    Another possible side effect associated with SERMs is visual cloudiness, loss of vision and even cataract formation. Although this tends to be a more common side effect from high dosed SERM therapy, standard 20mg/day tamoxifen regimes have been reported to cause these symptoms of ocular toxicity. (17, 46)

    Newer SERM’s -

    As the medical community became more aware of the side-effects associated with tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is a closely related analog of tamoxifen, so it also carries many of the related genotoxic effects. (48,49)

    Raloxifene is a newer SERM based off a benzothiophene structure, which appears to make it less toxic in the liver, uterus or prostate. (50-52) Unfortunately, Raloxifene has been associated with a higher incidence of thromboembolism (52), and also has very low oral absorption, making it an expensive alternative at a typical dose (120mg/day). (53) Still, Raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects. (53)

    Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further. (further enumerating the evidence of toxicity with the tamoxifen generation of SERM’s)



    What to do now?

    Firstly, it should become a priority to create awareness about the possible side effects of SERMs. Once educated, users will be able to start reducing their requirements of these drugs, and begin adopting healthier, more responsible alternatives.

    Carefully planned cycles, and the proper use of aromatase inhibitors (AIs) must pursue over haphazard combinations of excessively dosed aromatizing AAS’s -- which require high doses of SERM’s to reduce possible side-effects. Whereas avoiding SERM’s in HRT will involve the natural clearance and management of endogenous estrogens.

    It will be important to maintain testicular function during cycle for a quick and efficient recovery of natural testosterone production for PCT – negating the need for high dose 2-3 month SERM based PCT’s. (For more information on the proper use of hCG during cycle, visit here)

    Thus, abolishing the bad habit of SERMing will involve community wide enlightenment with careful, comprehensive planning of worthy alternatives.

    discuss this article in the forum
  19. Registered User
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    Quote Originally Posted by KGUNZ101 View Post
    Mainly in reference to the bolded sections thanks
    Thats crazy, what now.
  20. Registered User
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    Quote Originally Posted by futurepilot View Post
    This pct, to me, is a little off. Other than that its a pretty good write up.
    What would you recommend?
  21. Registered User
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    Ok Ive expressed my situation a dozen times and still have no clear cut answer. Im hoping you superdrol experts will have some words of advice, because clearly Im no expert. Its been 2 months since my superdrol cycle. When I finished my sexdrive/libido was literally gone completely. I went to an endocrinologist and they confirmed my testosterone was on the low-side of normal. She recommended I let myself naturally recover over the upcoming months.

    Its been 2 months now and my libido has improved significantly, but is still weaker than Id like. I was thinking a natural test booster would do me well to speed up the recovery process... am I right on this one?



    My 2nd concern... Ive read above that not only does SD squash test production, but it also squashes estrogen (which can lead to low libido). And not only did I take superdrol, but I stacked with an AI (because Im dumb apparently).

    So if a test booster (e.g. T-Bomb) recovers my testosterone level to normal, will the AI found in my most nattys only crush my estrogen even more???

    And if I take a testbooster without an AI, that will only risk the chance of gyno?




    Sorry, I had a few questions here that I wanted some knowledge on. I know Im stupid, I know Im f*cked up. Please help me and don't crucify me with you're words even more :P

    Let me know some advice if possible and if Im even seeing the big picture correctly here. Because Im not even positive if I remotely know what Im talking about here.

    Thanks,
    - The kid who messed himself up with Superdrol and just wants random erections again.
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    Quote Originally Posted by MadeInCanada View Post
    Ok Ive expressed my situation a dozen times and still have no clear cut answer. Im hoping you superdrol experts will have some words of advice, because clearly Im no expert. Its been 2 months since my superdrol cycle. When I finished my sexdrive/libido was literally gone completely. I went to an endocrinologist and they confirmed my testosterone was on the low-side of normal. She recommended I let myself naturally recover over the upcoming months.

    Its been 2 months now and my libido has improved significantly, but is still weaker than Id like. I was thinking a natural test booster would do me well to speed up the recovery process... am I right on this one?



    My 2nd concern... Ive read above that not only does SD squash test production, but it also squashes estrogen (which can lead to low libido). And not only did I take superdrol, but I stacked with an AI (because Im dumb apparently).

    So if a test booster (e.g. T-Bomb) recovers my testosterone level to normal, will the AI found in my most nattys only crush my estrogen even more???

    And if I take a testbooster without an AI, that will only risk the chance of gyno?




    Sorry, I had a few questions here that I wanted some knowledge on. I know Im stupid, I know Im f*cked up. Please help me and don't crucify me with you're words even more :P

    Let me know some advice if possible and if Im even seeing the big picture correctly here. Because Im not even positive if I remotely know what Im talking about here.

    Thanks,
    - The kid who messed himself up with Superdrol and just wants random erections again.

    Bump guys, someone help a brother out please.
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    Quote Originally Posted by MadeInCanada View Post
    I was thinking a natural test booster would do me well to speed up the recovery process... am I right on this one?
    Yes, you are "right on this one". go to you local sup shop, and purchase "animal stak".



    Quote Originally Posted by MadeInCanada View Post
    my 2nd concern... Ive read above that not only does SD squash test production, but it also squashes estrogen (which can lead to low libido). And not only did I take superdrol, but I stacked with an AI (because Im dumb apparently).
    no you aren't dumb, just new.

    Quote Originally Posted by MadeInCanada View Post
    So if a test booster (e.g. T-Bomb) recovers my testosterone level to normal, will the AI found in my most nattys only crush my estrogen even more???
    yes, and could possibly cause rebound gyno. like I said, pick up animal stak

    Quote Originally Posted by MadeInCanada View Post
    And if I take a testbooster without an AI, that will only risk the chance of gyno?
    this is why you should research more before beggining a steroid cycle, and not to be mean, but it is consumers like you that have the fda back at it again.

    take the nat test booster with nolvadex. and research more on post cycle therapy. try pct for dummies, just google post cycle therapy guide, etc.
    ----------------------

    the people at bb.com and phf are all homo's. well, maybe not all of them, but most. I cant stand to be in those forums for too long, it's like being around a bunch of b*tchy sorority chicks.
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    Quote Originally Posted by ChrisSanderso View Post
    Bump guys, someone help a brother out please.
    Much appreciation bud
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    Quote Originally Posted by jbryand101b View Post
    Yes, you are "right on this one". go to you local sup shop, and purchase "animal stak".





    no you aren't dumb, just new.



    yes, and could possibly cause rebound gyno. like I said, pick up animal stak



    this is why you should research more before beggining a steroid cycle, and not to be mean, but it is consumers like you that have the fda back at it again.

    take the nat test booster with nolvadex. and research more on post cycle therapy. try pct for dummies, just google post cycle therapy guide, etc.
    ----------------------

    the people at bb.com and phf are all homo's. well, maybe not all of them, but most. I cant stand to be in those forums for too long, it's like being around a bunch of b*tchy sorority chicks.
    Thanks for the advice. I thought of buying animal stak, but I think Animal Stak has an AI in it? (which is something I need to avoid) right?
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    Quote Originally Posted by MadeInCanada View Post
    Thanks for the advice. I thought of buying animal stak, but I think Animal Stak has an AI in it? (which is something I need to avoid) right?
    nope, animal stack has an all natural aromatase inhibitor, which is really weak, I forget the name, starts with a c, but it isn't powerful enough to really do anything. animal stak is 100% nat, and includes all you will need.
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    Quote Originally Posted by jbryand101b View Post
    nope, animal stack has an all natural aromatase inhibitor, which is really weak, I forget the name, starts with a c, but it isn't powerful enough to really do anything. animal stak is 100% nat, and includes all you will need.
    If your that confident this will speed my recovery, then this is the best advice Ive received
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    this is a great thread and expresses very clearly my confusion, and apparently many others in regards to running SERMs. this isnt the first time i have read the dangers of using them, and it almost seems that the dangers of using are higher than the danger of not using. yes to serm... more prone to gyno, cancer, destroyed natural test production
    no to serm... gyno, destroyed natural test again, no cancer (hopefully)... etc..
    see what i am saying people...
    *I do, however, plan on running a low dose SERM in my upcoming superdrol cycle... im not sure if i feel good about it yet, but everyone seems to insist.. i just never see anyone comment on the greater negatives of using one.. Is it simply because you retain more of the gains from a cycle that everyone leans towards SERM use? either way... great thread, ill be watching this one like a hawk!
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    Quote Originally Posted by dustin06MR View Post
    this is a great thread and expresses very clearly my confusion, and apparently many others in regards to running SERMs. this isnt the first time i have read the dangers of using them, and it almost seems that the dangers of using are higher than the danger of not using. yes to serm... more prone to gyno, cancer, destroyed natural test production
    no to serm... gyno, destroyed natural test again, no cancer (hopefully)... etc..
    see what i am saying people...
    *I do, however, plan on running a low dose SERM in my upcoming superdrol cycle... im not sure if i feel good about it yet, but everyone seems to insist.. i just never see anyone comment on the greater negatives of using one.. Is it simply because you retain more of the gains from a cycle that everyone leans towards SERM use? either way... great thread, ill be watching this one like a hawk!

    What would be the safest natural pct then? Or is there one. I say we start a thread and get the big guns in to help guys like Holy, Dr , PPump, I haven't heard from Pantera in a while , he practically saved my skin about 2 yrs ago when I didn't even know what a serm was. Sad I know, but I have to say guys AM is the absolute best site out there for knowledge, some of the **** I hear on other sites is absolute rubbish. Cheers to AM
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    Quote Originally Posted by ChrisSanderso View Post
    What would be the safest natural pct then? Or is there one. I say we start a thread and get the big guns in to help guys like Holy, Dr , PPump, I haven't heard from Pantera in a while , he practically saved my skin about 2 yrs ago when I didn't even know what a serm was. Sad I know, but I have to say guys AM is the absolute best site out there for knowledge, some of the **** I hear on other sites is absolute rubbish. Cheers to AM
    Safest OTC PCT, well that just brings me back to my confusion again really. I am currently using BBS complete PCT after Havoc and i have had no sides, or anything, although Havoc is mild. I agree though, with all the supposed end all threads for PCT, there really is NO definitive information in regards to SERM's and OTC PCT, besides people swearing up and down to use them, and on the other side, people saying they may do more hgarm than good. All i know is i am fine now, and i would hate to take a SERM and become gyno prone due to the SERM! We do need some SOLID threads for this, that get stickied and are there for new people to read and follow. things like that will prevent ignorant mistakes, at least with the users from this forum. IMO
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    What about major stomach bloat on m-drol, anybody have any ideas. My stomach hurts and I am bloated like a preg chick. WTF
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    Quote Originally Posted by MadeInCanada View Post
    If your that confident this will speed my recovery, then this is the best advice Ive received
    That would be a decent stack or Primordial's Testosterone Recovery Stack. They have mild natural AI's....Resveratrol and 7,8 Benzo. Either way, they are both natural testosterone boosting stacks.
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    Quote Originally Posted by vpower View Post
    That would be a decent stack or Primordial's Testosterone Recovery Stack. They have mild natural AI's....Resveratrol and 7,8 Benzo. Either way, they are both natural testosterone boosting stacks.
    This thread is old. I went with the Animal Stak, and within 2 weeks I noticed a change. I went back to the Endo to get my blood work changed.

    And my total test went from 240 to over 600.
    Free test improved significantly as well.
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    Quote Originally Posted by ChrisSanderso View Post
    What about major stomach bloat on m-drol, anybody have any ideas. My stomach hurts and I am bloated like a preg chick. WTF

    you eating a lot of carbs? if so decrease the carb intake and sodium as well. that might take care of it
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    ok i kno this thread is pretty much dead n gone but i got my hands on m-drol one of the more popular clones and the only thing i have in way of post cycle is PCT by ADS which i planned on stacking with tribulis but both are OTC to begin with so my faith in these products are lacking. Im 22 wit no previous use of any kind of ph's or juice but have an older brother who i've witness go up in down in muscle size repeatedly due to poor pct and plenty of friends who ignored any use of AI's or anti-e's all together leaving them wit gyno. my dilemna is that im not enthused about using nolva or arimidex etc so can anyone suggest specific estrogen regulation and a proper pct product besides the aforementioned? please help i've been spending hours researching this everynight for weeks now. and yes i will be takin support supps like milk thistle hawthorne berry and nac but im jus concerned wit not gettin bitch tits and keeping my gains afterwards bottomline. any advice would be greatly appreciated im startin to feel like im chasing a ghost and i dont want to take a chance wit mediocre products
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    Quote Originally Posted by tater27 View Post
    ok i kno this thread is pretty much dead n gone but i got my hands on m-drol one of the more popular clones and the only thing i have in way of post cycle is PCT by ADS which i planned on stacking with tribulis but both are OTC to begin with so my faith in these products are lacking. Im 22 wit no previous use of any kind of ph's or juice but have an older brother who i've witness go up in down in muscle size repeatedly due to poor pct and plenty of friends who ignored any use of AI's or anti-e's all together leaving them wit gyno. my dilemna is that im not enthused about using nolva or arimidex etc so can anyone suggest specific estrogen regulation and a proper pct product besides the aforementioned? please help i've been spending hours researching this everynight for weeks now. and yes i will be takin support supps like milk thistle hawthorne berry and nac but im jus concerned wit not gettin bitch tits and keeping my gains afterwards bottomline. any advice would be greatly appreciated im startin to feel like im chasing a ghost and i dont want to take a chance wit mediocre products

    Well, you better get enthused about it because a SERM is the thing you should be taking during m-drol PCT. Over the counter pct will give you a nice rack and loss of the muscle you'll gain.

    How old are you? and if you're 165 then you shouldn't use this stuff for a good while.
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    22 but whys the wieght an issue to wait? thought i was actually in the clear age wise from previous threads, this is a lose lose situation haha. is it fairly safe to assume that the neg sides associated wit serms would be minimal with only one time use, i kno this is hopeful sounding even in theory... idk man this is depressing im gonna be ****ting out major organs by the time im done wit this cycle
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    Only one question. If a guy takes tamox, or clomid for a month a year, during a PCT cycle. Just how likly is he to develop any probs.???? We ar not taking the stuff to combat breast cancer!
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    point taken
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    ok wait so since mdrol is a progestrin or however u spell it nolva will cause or further irritate existing gyno i'd have to do clomid with an ai like aromasin right? agree disagree tell me im a fool idc jus want feedback thanx
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