Celnbuterol

Clenbuterol is a β2 agonist with certain structural and pharmacological similarities to ephinphrineand Albuterol, but its effects are more potent and longer-lasting as a stimulant and thermogenic
drug than any other drug in its category. Clen causes an increase in aerobic capacity, central nervous system stimulation, and an increase in blood pressure and oxygen transportation. It increases the rate at which body fat is metabolized while increasing the body’s body’s metabolic rate which basically allows your body to break down macronutrients MUCH EASIER. It is commonly prescribed by doctors it’s for smooth muscle relaxant properties. It used as bronchodilator by people who suffer from breathing disorders like as asthma.  When it comes to beta-2 agonists Like Celn, Albuterol, and ephedrine everyone reacts differently. Half of my article will explain what clenbuterol looks like on paper, in studies, and how it should work and has worked for many people. However Through my many years in dealing with real life people as well as my own experiences I have learned No two people are exactly alike. Everyone reacts differently to different compounds from the side effects they experience to the results they get from them.  I can only explain to you what studies have shown me, what information I have gathered from various literature/resources, what I have learned through my own experiences,  and lastly what I have learned through helping others use these chemicals.  I have used clenbuterol  several different times in several different ways.  I did not get great results with clenbuterol and I did not like the side effects I experienced.  Nonetheless I personally know thousands of people who loved both the results and the experience of using clenbuterol. This may or may not be the right research chemical for you.. My job is to Arm you with as much information as I can so that you can experience clenbuterol for your self. In the safest  possible way and knowing everything there is to know about how your experience may turn out. So that you will be ready for whatever comes your way. So that You can Kill that Sh*t the right way..

What Beta 2 adrenegic agonists?

They promote smooth muscle relaxation, resulting in the dilation of bronchial pathways, vasodilation in liver and muscle, they also cause the relaxation of uterine muscle in women, and the release of insulin where its anabolic properties begin. Beta-adrenergic receptors are stacked together to stimulate G protein. The alpha subunit of the G protein activates adenylyl cyclase, which then catalyzes the production of cyclic adenosine monophosphate  aka cAMP. In the lung, cAMP produces a decrease in the intracellular calcium plasma concentrationd through activation of protein kinase A.  In addition, beta-2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway smooth muscle cells. The combination of decreased intracellular calcium and increased membrane potassium conductance, with decreased myosin light chain kinase activity leads to smooth muscle relaxation and bronchodilation.  This is the reason the body gets so dehydrated and cramped during a Clen run. We will dive into further in a bit.

Clen improves body composition

In this study I came across twenty-three unfit Standard bred mares were divided into four experimental groups. The one group was give 2.4 mcg per kg of clen body weight twice daily plus exercise. The exercise routine was 50 of their max oxygen utilization at three times a week.  Booty fat thickness was measured at 2 week intervals by using B-mode ultrasound, and percent body fat (%fat) was calculated by using previously published methods. Results indicated body fat decreased 9.3% at week 4 and 6.9% at week 6, and fat-free mass) increased by 3.2% at week 8. On the other hand, Clen had significant changes in %fat (-15.4%), fat mass (-14.7%), and FFM (+4.3%) at week 2. ClenEx had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen; however, this group had a different fat free mass response, which significantly increased moer than 4.4% at week 6. That is amazing when you consider this was only a period 8 weeks (2months). Most people are happy if they can lose 2 percent bodyfat in 12 weeks. The fact that fat free mass INCREASED shows that this drug is not only thermogenic but also ANABOLIC. Again this has to be attributed to the fact that Clen increases insulin release, remember insulin is the most anabolic hormone in the body.  (J Appl Physiol. 2001 Nov;91(5):2064-70)

Thought I never would say this, CLen is good for the liver LOL

In a study I came upon, Clenbuterol minimized LPS-induced liver damage, as represented by significantly lowered concentrations of several parameters for liver-failure (AST, ALT, Bilirubin), and improved hepatic tissue morphology. Clenbuterol administration after LPS challenge failed to inhibit TNF alpha-release but reduced liver-damage. Simultaneous use of the beta(2)-AR antagonist propranolol augmented LPS-induced liver failure, suggesting a role of endogenous adrenoceptor-agonists in prevention of organ-failure during systemic inflammation. The results indicate that a selective beta(2)-AR agonist might be used as an additional therapeutic agent in the clinic for the treatment of (acute) systemic inflammatory disorders in order to reduce or prevent subsequent liver failure.  Am I telling you guys to use this as liver protectant on cycle, NOOOOOOOO! All I am getting at is that it’s not liver toxic like others mentioned unless you do not treat your electrolyte levels with care, which can lead other problems besides liver issues, such as heart failure, brain malfunction and so on. (Inflamm Res. 2004 Mar;53(3):93-9. Epub 2004 Feb 16.)

Clen can aid in endurance, well at least for those who have asthma

Already it has been mentioned that Clen aids those with asthma as it breaks of the congested passageways, so that air flows freely. This in turn will allow the individual to do more anaerobic and aerobic activity. In this study, the protective effect of clenbuterol on exercise-induced asthma was studied in 14 patients with a specific bronchial hyperreactivity. The selectivity of clenbuterol for beta 2-receptors was also looked at during this study. Patients were selected according to spirometric criteria: reduced dynamic indexes of respiratory function after exercise and, particularly, forced expiratory volume at 1 s (FEV1) decreased by at least 20% compared with initial values. A polycardiographic study was simultaneously carried out for the evaluation of systolic time intervals and polycardiographic indexes. After the preliminary measurements (C1), oral clenbuterol was taken at 0.02 mg twice a day and measurements were repeated after 30 (CII) and 60 days (CIII) of therapy. During treatment, physical exercise did not significantly influence the indexes of respiratory function (FEV1 decreased by 4.7 +/- 5.8 and 9.8 +/- 10.5% in CII and CIII with respect to initial values). Similarly systolic time intervals and polycardiographic indexes did not change significantly with respect to the initial values. A small increase in heart rate at rest was observed in CII (+ 7%, p less than 0.05): however, no significant changes were recorded in CIII compared with the initial values. Clenbuterol thus seems to offer an effective protection against exercise-induced asthma without the negative effects on the cardiovascular system which may arise from activation of beta 1-adrenergic receptors.  The key is to take the proper dosage with clen, as too much causes respiratory issues which we will dive into. (Respiration. 1987;51(3):205-13.)

Clebuterol improves athletic performance?

Unlike inhaled beta 2-agonists, more studies  and human trials need to be performed before the action of systemic beta 2-agonists on athletic performance can be assessed accurately. Experiments in animals with oral clenbuterol have shown growth in muscle bulk across numerous species, but human studies cannot confirm similar muscle mass enlargement in healthy men at the moment. Of course the human studies demonstrate the potential for long-acting systemic beta 2-agonists such as Clen to increase muscle strength in certain muscle fiber types, it is difficult to judge the drugs’ effects on overall athletic performance, because athletic skill is more than strength, speed, and endurance. The effect of oral clenbuterol on athletic performance cannot be evaluated from its actions on muscle strength alone but effects on motor skill/ coordination. However, as evidence stands now, sports regulatory agencies are correct to ban systemic beta 2-agonists until the following 2 points can be proven: (1) oral forms provide a therapeutic benefit that cannot be obtained with aerosol or inhaled forms; and (2) oral forms do not give any unfair advantage to the competitor in muscle strength, power output, or endurance. Provided they are administered as prescribed, aerosol or inhaled beta-agonists do not impart an unfair advantage or enhance athletic performance and can continue to be used in competition by athletes with EIA. However, small studies have shown a small increase in power ouput. I know others such as myself receive a nice initial boost in lifts, for the first few weeks. Part of the reason the strength increase goes away is tolerance, but the other reason is probably tissue receptor saturation, meaning the B 2 receptors desensitized, thus no longer easily stimulated to give that nice pronounced effect. I will disagree with the article in stating that it is not known to whether Beta-2 agonists stimulate brain function, as it is clear that they stimulate the production of cAMP which definitely activates NMDA receptors. NMDA receptors are responsible for hormone production, cathelomine production and even other neurotransmitter production such as DOPAMINE. Both Dopamine and PEA are crucial for motor and coordination skills. Everytime I start taking Clen, I definitely notice more awareness, more MIND MUSCLE CONNECTION and so on.  I would NOT rule out Clen as performance enhancer by any means. For crying out loud, there are still researchers who do not find creatine monohydrate to be a performance enhancer. PFFTTT! (Ann Pharmacother. 1995 Jan;29(1):75-7.)

How to prevent down regulation

As you know Clen starts to lose its potency over a period of an estimated 14 days but I would say more 10 days LOL. Benedryl is one of the anti histamines people use help prevent toldernace. The other anti histamine is Ketofin which again does the same thing. Basically anit histamines inhibit phospholipase which brings the desensitization of beta 2 receptors to a hault. Thus, allowing one to have a longer effective Clen cycle. With these Anithistamines in your system, you can use Clen longer without the typical 1-2 week break in between. Most people will go 2 on and 2 off, but with these anti-histamines you could technically go 4 plus weeks straight. This is of course only one way of doing things and I personally Like a much different method which we will talk about later in my ” Clenbuterol dosage” segment of this write up.

Clenbuterol side effects 

 

Clebuterol depletes taurine from the body

If you want to read the study, I have the citation in paranthesis at the end of this paragraph. I can tell you this, that depletion of taurine can be really unsafe if not monitored. Taurine is responsible for storing electrolytes within their due tissues. Without a proper balance of electrolytes, the body WILL NOT FUNCTION PROPERLY. Be sure to supplement Taurine at least 950mg a day post work out or even as much as 3-6g daily.I recommend taking a dose of just Taurine  in the am, after your second dose of Clen, and post training . The reason Clenbuterol depletes taurine levels in the Liver , is because the body it stops the conversion of T4 to T3 within the Liver.  This is why many chemical using experts will suggest running T3 while on a Clen cycle. Since taurine will aid reducing electrolyte depletion, it will decrease overall cramps. I also recommend taking calcium as mentioned before, all B2 agonist will deplete calcium, so be sure to supplement at 500mg of Calcium while on Clen. Now you will need to supplement magnesium with Clen but it MUST be taken at a different time of the day then Calcium, as magnesium competes with calcium for the same receptors.  Potassium must also be taken during your clen cycle, you could always add some coconut water and bananas to your regime, as they are loaded with potassium and will be absorbed more efficiently than a potassium supplement.   (Adv Exp Med Biol. 1996;403:233-45.)

 

Not so good for cardio

Yes I know we discussed how the right amount of Clen could aid in endurance, but aerobic activitiy is a different part of your cardio conditioning, also think of it like this. I know people can lift more reps which requires more oxygen while on a cycle, yet; they cannot run the miles they were able to off of cycle. The difference here is merely aerobic verse anaerobic exercises. Anaerobic activity is based off of short bursts while aerobic activity is geared more the long haul. A power lifter would be a description of an anaerobic athlete, while a triathlon competitor would be a good description of an aerobic athlete. In a study I found, Clen Xdecreased O2max around 6.2% and velocity to O2max decreased 10.0%, whereas both CLENEX and CLEN decreased in time to exhaustion between 4 and 6 percent.  EX alone increased  O2max by more than 6.5%, velocity to O2max over 10.0%, velocity to produces lactate concentration of 4 mmol or plus 13.5%, and time to exhaustion slightly under 15%. Plasma volume was altered in CLENEX below 10% and EX over 27% but not in CLEN. Posttest recovery HR was higher at 2 min post-GXT in the CLENEX, CLEN, and CON compared with their pretest values; RVP remained elevated at 2 min of recovery in the CLEN and CON groups; however, in the EX, recovery HR and RVP had returned to pre-GXT levels by 2 min of recovery. There you notice that with other groups, their heart rate returned to normal, but with the pure clen group heart rate was still elevated, sure they were able to push beyond a normal rate but with the normal healthy body they would have recovered faster. I like to think of this like someone taking ephedrine before a fight, they would gas out in the first round due to such an elevated heart rate, the heart needs to be able to settle so that the body stays hydrated, and adrenaline to cortisol stay at proper levels, no one wants an adrenaline dump during competition, as their performance will suffer greatly.  (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.)

 

 

 

 

Clen can cause Skin Cell Death of the Heart at least in Rats

 

We all know that high doses of Clen cause extremely elevated heart rate levels. But we all thought it was only from the increased metabolic rate, thyroid production, and depletion of potassium. Well in essence, in theory, the depletion of potassium could be the reason for myocyte necrosis within the heart. Of course more research would be warranted to prove this theory but I cannot affor to pay for it. LMAO! In this study, Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. This data shows significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term heart health.

It is my job to tell you the dangers of everything as well as the benefits my friends. Unlike the Media however I will only tell you the truth and not over hyped propaganda with an agenda behind it. No I will explain the side effects and dangers of using a chemical that are “real”..

Celnbuterol

Clenbuterol is a β2 agonist with certain structural and pharmacological similarities to ephinphrineand Albuterol, but its effects are more potent and longer-lasting as a stimulant and thermogenic
drug than any other drug in its category. Clen causes an increase in aerobic capacity, central nervous system stimulation, and an increase in blood pressure and oxygen transportation. It increases the rate at which body fat is metabolized while increasing the body’s body’s metabolic rate which basically allows your body to break down macronutrients MUCH EASIER. It is commonly prescribed by doctors it’s for smooth muscle relaxant properties. It used as bronchodilator by people who suffer from breathing disorders like as asthma.  When it comes to beta-2 agonists Like Celn, Albuterol, and ephedrine everyone reacts differently. Half of my article will explain what clenbuterol looks like on paper, in studies, and how it should work and has worked for many people. However Through my many years in dealing with real life people as well as my own experiences I have learned No two people are exactly alike. Everyone reacts differently to different compounds from the side effects they experience to the results they get from them.  I can only explain to you what studies have shown me, what information I have gathered from various literature/resources, what I have learned through my own experiences,  and lastly what I have learned through helping others use these chemicals.  I have used clenbuterol  several different times in several different ways.  I did not get great results with clenbuterol and I did not like the side effects I experienced.  Nonetheless I personally know thousands of people who loved both the results and the experience of using clenbuterol. This may or may not be the right research chemical for you.. My job is to Arm you with as much information as I can so that you can experience clenbuterol for your self. In the safest  possible way and knowing everything there is to know about how your experience may turn out. So that you will be ready for whatever comes your way. So that You can Kill that Sh*t the right way..

What Beta 2 adrenegic agonists?

They promote smooth muscle relaxation, resulting in the dilation of bronchial pathways, vasodilation in liver and muscle, they also cause the relaxation of uterine muscle in women, and the release of insulin where its anabolic properties begin. Beta-adrenergic receptors are stacked together to stimulate G protein. The alpha subunit of the G protein activates adenylyl cyclase, which then catalyzes the production of cyclic adenosine monophosphate  aka cAMP. In the lung, cAMP produces a decrease in the intracellular calcium plasma concentrationd through activation of protein kinase A.  In addition, beta-2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway smooth muscle cells. The combination of decreased intracellular calcium and increased membrane potassium conductance, with decreased myosin light chain kinase activity leads to smooth muscle relaxation and bronchodilation.  This is the reason the body gets so dehydrated and cramped during a Clen run. We will dive into further in a bit.

Clen improves body composition

In this study I came across twenty-three unfit Standard bred mares were divided into four experimental groups. The one group was give 2.4 mcg per kg of clen body weight twice daily plus exercise. The exercise routine was 50 of their max oxygen utilization at three times a week.  Booty fat thickness was measured at 2 week intervals by using B-mode ultrasound, and percent body fat (%fat) was calculated by using previously published methods. Results indicated body fat decreased 9.3% at week 4 and 6.9% at week 6, and fat-free mass) increased by 3.2% at week 8. On the other hand, Clen had significant changes in %fat (-15.4%), fat mass (-14.7%), and FFM (+4.3%) at week 2. ClenEx had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen; however, this group had a different fat free mass response, which significantly increased moer than 4.4% at week 6. That is amazing when you consider this was only a period 8 weeks (2months). Most people are happy if they can lose 2 percent bodyfat in 12 weeks. The fact that fat free mass INCREASED shows that this drug is not only thermogenic but also ANABOLIC. Again this has to be attributed to the fact that Clen increases insulin release, remember insulin is the most anabolic hormone in the body.  (J Appl Physiol. 2001 Nov;91(5):2064-70)

Thought I never would say this, CLen is good for the liver LOL

In a study I came upon, Clenbuterol minimized LPS-induced liver damage, as represented by significantly lowered concentrations of several parameters for liver-failure (AST, ALT, Bilirubin), and improved hepatic tissue morphology. Clenbuterol administration after LPS challenge failed to inhibit TNF alpha-release but reduced liver-damage. Simultaneous use of the beta(2)-AR antagonist propranolol augmented LPS-induced liver failure, suggesting a role of endogenous adrenoceptor-agonists in prevention of organ-failure during systemic inflammation. The results indicate that a selective beta(2)-AR agonist might be used as an additional therapeutic agent in the clinic for the treatment of (acute) systemic inflammatory disorders in order to reduce or prevent subsequent liver failure.  Am I telling you guys to use this as liver protectant on cycle, NOOOOOOOO! All I am getting at is that it’s not liver toxic like others mentioned unless you do not treat your electrolyte levels with care, which can lead other problems besides liver issues, such as heart failure, brain malfunction and so on. (Inflamm Res. 2004 Mar;53(3):93-9. Epub 2004 Feb 16.)

Clen can aid in endurance, well at least for those who have asthma

Already it has been mentioned that Clen aids those with asthma as it breaks of the congested passageways, so that air flows freely. This in turn will allow the individual to do more anaerobic and aerobic activity. In this study, the protective effect of clenbuterol on exercise-induced asthma was studied in 14 patients with a specific bronchial hyperreactivity. The selectivity of clenbuterol for beta 2-receptors was also looked at during this study. Patients were selected according to spirometric criteria: reduced dynamic indexes of respiratory function after exercise and, particularly, forced expiratory volume at 1 s (FEV1) decreased by at least 20% compared with initial values. A polycardiographic study was simultaneously carried out for the evaluation of systolic time intervals and polycardiographic indexes. After the preliminary measurements (C1), oral clenbuterol was taken at 0.02 mg twice a day and measurements were repeated after 30 (CII) and 60 days (CIII) of therapy. During treatment, physical exercise did not significantly influence the indexes of respiratory function (FEV1 decreased by 4.7 +/- 5.8 and 9.8 +/- 10.5% in CII and CIII with respect to initial values). Similarly systolic time intervals and polycardiographic indexes did not change significantly with respect to the initial values. A small increase in heart rate at rest was observed in CII (+ 7%, p less than 0.05): however, no significant changes were recorded in CIII compared with the initial values. Clenbuterol thus seems to offer an effective protection against exercise-induced asthma without the negative effects on the cardiovascular system which may arise from activation of beta 1-adrenergic receptors.  The key is to take the proper dosage with clen, as too much causes respiratory issues which we will dive into. (Respiration. 1987;51(3):205-13.)

Clebuterol improves athletic performance?

Unlike inhaled beta 2-agonists, more studies  and human trials need to be performed before the action of systemic beta 2-agonists on athletic performance can be assessed accurately. Experiments in animals with oral clenbuterol have shown growth in muscle bulk across numerous species, but human studies cannot confirm similar muscle mass enlargement in healthy men at the moment. Of course the human studies demonstrate the potential for long-acting systemic beta 2-agonists such as Clen to increase muscle strength in certain muscle fiber types, it is difficult to judge the drugs’ effects on overall athletic performance, because athletic skill is more than strength, speed, and endurance. The effect of oral clenbuterol on athletic performance cannot be evaluated from its actions on muscle strength alone but effects on motor skill/ coordination. However, as evidence stands now, sports regulatory agencies are correct to ban systemic beta 2-agonists until the following 2 points can be proven: (1) oral forms provide a therapeutic benefit that cannot be obtained with aerosol or inhaled forms; and (2) oral forms do not give any unfair advantage to the competitor in muscle strength, power output, or endurance. Provided they are administered as prescribed, aerosol or inhaled beta-agonists do not impart an unfair advantage or enhance athletic performance and can continue to be used in competition by athletes with EIA. However, small studies have shown a small increase in power ouput. I know others such as myself receive a nice initial boost in lifts, for the first few weeks. Part of the reason the strength increase goes away is tolerance, but the other reason is probably tissue receptor saturation, meaning the B 2 receptors desensitized, thus no longer easily stimulated to give that nice pronounced effect. I will disagree with the article in stating that it is not known to whether Beta-2 agonists stimulate brain function, as it is clear that they stimulate the production of cAMP which definitely activates NMDA receptors. NMDA receptors are responsible for hormone production, cathelomine production and even other neurotransmitter production such as DOPAMINE. Both Dopamine and PEA are crucial for motor and coordination skills. Everytime I start taking Clen, I definitely notice more awareness, more MIND MUSCLE CONNECTION and so on.  I would NOT rule out Clen as performance enhancer by any means. For crying out loud, there are still researchers who do not find creatine monohydrate to be a performance enhancer. PFFTTT! (Ann Pharmacother. 1995 Jan;29(1):75-7.)

How to prevent down regulation

As you know Clen starts to lose its potency over a period of an estimated 14 days but I would say more 10 days LOL. Benedryl is one of the anti histamines people use help prevent toldernace. The other anti histamine is Ketofin which again does the same thing. Basically anit histamines inhibit phospholipase which brings the desensitization of beta 2 receptors to a hault. Thus, allowing one to have a longer effective Clen cycle. With these Anithistamines in your system, you can use Clen longer without the typical 1-2 week break in between. Most people will go 2 on and 2 off, but with these anti-histamines you could technically go 4 plus weeks straight. This is of course only one way of doing things and I personally Like a much different method which we will talk about later in my ” Clenbuterol dosage” segment of this write up.

Clenbuterol side effects 

 

Clebuterol depletes taurine from the body

If you want to read the study, I have the citation in paranthesis at the end of this paragraph. I can tell you this, that depletion of taurine can be really unsafe if not monitored. Taurine is responsible for storing electrolytes within their due tissues. Without a proper balance of electrolytes, the body WILL NOT FUNCTION PROPERLY. Be sure to supplement Taurine at least 950mg a day post work out or even as much as 3-6g daily.I recommend taking a dose of just Taurine  in the am, after your second dose of Clen, and post training . The reason Clenbuterol depletes taurine levels in the Liver , is because the body it stops the conversion of T4 to T3 within the Liver.  This is why many chemical using experts will suggest running T3 while on a Clen cycle. Since taurine will aid reducing electrolyte depletion, it will decrease overall cramps. I also recommend taking calcium as mentioned before, all B2 agonist will deplete calcium, so be sure to supplement at 500mg of Calcium while on Clen. Now you will need to supplement magnesium with Clen but it MUST be taken at a different time of the day then Calcium, as magnesium competes with calcium for the same receptors.  Potassium must also be taken during your clen cycle, you could always add some coconut water and bananas to your regime, as they are loaded with potassium and will be absorbed more efficiently than a potassium supplement.   (Adv Exp Med Biol. 1996;403:233-45.)

 

Not so good for cardio

Yes I know we discussed how the right amount of Clen could aid in endurance, but aerobic activitiy is a different part of your cardio conditioning, also think of it like this. I know people can lift more reps which requires more oxygen while on a cycle, yet; they cannot run the miles they were able to off of cycle. The difference here is merely aerobic verse anaerobic exercises. Anaerobic activity is based off of short bursts while aerobic activity is geared more the long haul. A power lifter would be a description of an anaerobic athlete, while a triathlon competitor would be a good description of an aerobic athlete. In a study I found, Clen Xdecreased O2max around 6.2% and velocity to O2max decreased 10.0%, whereas both CLENEX and CLEN decreased in time to exhaustion between 4 and 6 percent.  EX alone increased  O2max by more than 6.5%, velocity to O2max over 10.0%, velocity to produces lactate concentration of 4 mmol or plus 13.5%, and time to exhaustion slightly under 15%. Plasma volume was altered in CLENEX below 10% and EX over 27% but not in CLEN. Posttest recovery HR was higher at 2 min post-GXT in the CLENEX, CLEN, and CON compared with their pretest values; RVP remained elevated at 2 min of recovery in the CLEN and CON groups; however, in the EX, recovery HR and RVP had returned to pre-GXT levels by 2 min of recovery. There you notice that with other groups, their heart rate returned to normal, but with the pure clen group heart rate was still elevated, sure they were able to push beyond a normal rate but with the normal healthy body they would have recovered faster. I like to think of this like someone taking ephedrine before a fight, they would gas out in the first round due to such an elevated heart rate, the heart needs to be able to settle so that the body stays hydrated, and adrenaline to cortisol stay at proper levels, no one wants an adrenaline dump during competition, as their performance will suffer greatly.  (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.)

 

 

 

 

Clen can cause Skin Cell Death of the Heart at least in Rats

 

We all know that high doses of Clen cause extremely elevated heart rate levels. But we all thought it was only from the increased metabolic rate, thyroid production, and depletion of potassium. Well in essence, in theory, the depletion of potassium could be the reason for myocyte necrosis within the heart. Of course more research would be warranted to prove this theory but I cannot affor to pay for it. LMAO! In this study, Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. This data shows significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term heart health.

It is my job to tell you the dangers of everything as well as the benefits my friends. Unlike the Media however I will only tell you the truth and not over hyped propaganda with an agenda behind it. No I will explain the side effects and dangers of using a chemical that are “real”..

Clenbuterol dosage

When dosing clenbuterol you have several different ways of doing so however we have two main common dosing protocols. The first one being the 4 weeks on 4 weeks off clenbuterol dosage program, and the second being the 2 weeks on 2 weeks off clenbuterol dosage program.  Weather you decide to go with 2 weeks on 2 weeks off or 4 weeks on 4 weeks off the dosing will always start off the same and gradually increase/ramp up the same as well. When starting your clenbuterol program you will want to sart out with 3 20mcg doses a day and move up 20mcg every 2 to 3 days till you reach 140mcg max dosing for a man 100mcg for a woman IMO of course. Always spread the dosing out over 3 doses a day or more if you can and space them a couple of hours apart.  Never go above 140mcg and always only go up 20mcg every 2 to 3 days. You must access tolerance  first moving into clen easy to gauge how your body will react to this compound. Always live on the side of safety my friends.  Once you reach 140mcg stick to that dose for the rest of the time you are on the clen cycle. If you are a smaller person Ie below 175lb then you need not go above 100mcg at most. This should be plenty to see results and always remember that more is not always better. Here is what my dosing looked like over the first 10 days of my last clenbuterol program…

Day.  Morning/noon/night

1. 20mcg/20mcg/20mcg

2. 20mcg/20mcg/20mcg

3. 40mcg/20mcg/20mcg

4. 40mcg/20mcg/20mcg

5. 40mcg/40mcg/20mcg

6. 40mcg/40mcg/20mcg

7. 40mcg/40mcg/40mcg

8. 40mcg/40mcg/40mcg

9. 40mcg/40mcg/40mcg

10. 60mcg/40mcg/40mcg

 

 

 

A recently published study has examined the effects of overeating (1,000 extra calories per day) on fat mass accumulation and lean mass accumulation, while on a low, moderate, or high protein diet. This isn’t going to be a surprise to bodybuilders anywhere, but although each group managed to gain quite a bit of fat (they weren’t training), the high protein group gained about 7 lbs of lean mass. Not too bad without any training huh?

 

Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating

A Randomized Controlled Trial

Abstract

Context The role of diet composition in response to overeating and energy dissipation in humans is unclear.

Objective To evaluate the effects of overconsumption of low, normal, and high protein diets on weight gain, energy expenditure, and body composition.

Design, Setting, and Participants A single-blind, randomized controlled trial of 25 US healthy, weight-stable male and female volunteers, aged 18 to 35 years with a body mass index between 19 and 30. The first participant was admitted to the inpatient metabolic unit in June 2005 and the last in October 2007.

Intervention After consuming a weight-stabilizing diet for 13 to 25 days, participants were randomized to diets containing 5% of energy from protein (low protein), 15% (normal protein), or 25% (high protein), which they were overfed during the last 8 weeks of their 10- to 12-week stay in the inpatient metabolic unit. Compared with energy intake during the weight stabilization period, the protein diets provided approximately 40% more energy intake, which corresponds to 954 kcal/d (95% CI, 884-1022 kcal/d).

Main Outcome Measures Body composition was measured by dual-energy x-ray absorptiometry biweekly, resting energy expenditure was measured weekly by ventilated hood, and total energy expenditure by doubly labeled water prior to the overeating and weight stabilization periods and at weeks 7 to 8.

Results Overeating produced significantly less weight gain in the low protein diet group (3.16 kg; 95% CI, 1.88-4.44 kg) compared with the normal protein diet group (6.05 kg; 95% CI, 4.84-7.26 kg) or the high protein diet group (6.51 kg; 95% CI, 5.23-7.79 kg) (P = .002). Body fat increased similarly in all 3 protein diet groups and represented 50% to more than 90% of the excess stored calories. Resting energy expenditure, total energy expenditure, and body protein did not increase during overfeeding with the low protein diet. In contrast, resting energy expenditure (normal protein diet: 160 kcal/d [95% CI, 102-218 kcal/d]; high protein diet: 227 kcal/d [95% CI, 165-289 kcal/d]) and body protein (lean body mass) (normal protein diet: 2.87 kg [95% CI, 2.11-3.62 kg]; high protein diet: 3.18 kg [95% CI, 2.37-3.98 kg]) increased significantly with the normal and high protein diets.

Conclusions Among persons living in a controlled setting, calories alone account for the increase in fat; protein affected energy expenditure and storage of lean body mass, but not body fat storage.

If you remember the name Craig Titus, you probably remember that he was an IFBB professional who got sentenced to prison for a very long time after killing a woman who’d been his assistant. Well, it appears that he is now back on the market, although still a resident of the Nevada Correctionals System.

Hello,

I’m really happy you’re taking the time out of your day to read my bio.  Never in a million years did I dream I’d be placing myself on an inmate web site to find companionship, but here I am.

If you’re interested in who I am, or what I was all about, then Google me; I’m all over the internet.  Do not believe everything you read; some is true and some is not.  I used to be a professional athlete and now I’m in prison…it’s a long story and if you get to know me I’ll share it with you.  Just know that I’m a loyal Capricorn looking for a true friend in every sense of the word.

I work out five days a week to keep myself in shape.  I keep up on all current events.  I enjoy reading novels and listen to all types of music.

Please make sure to include your address when you write to me.  I cannot email you, you can only email me.  If you’d like to write me direct my current address is below.

I’m looking forward to hearing from you! (smile)

GW-501516 

 

 

GW-501516 is a PPARδ modulator compound is currently being investigated for drug use by GlaxoSmithKline. It activates the same pathways activated through exercise, including PPARδ and AMP-activated protein kinase. It is being trialed as a potential treatment for a few conditions consisting mainly of obesity, diabetes, dyslipidemia and heart disease. GW-501516 has a synergistic effect when combined with the AMP-K agonist AICAR: the combination has been shown to significantly increase exercise endurance in animal studies more than 40%. And from My own experience yes it works my friends.

GW-50156 regulates fat burning through a number of different pathways which includes exercise mimetic effects.  It increases glycogen retention in skeletal muscle tissue while increasing muscle gene expression. This shift changes the body’s metabolism to allow for more fat burning and for energy instead of carbohydrates or protein as the source of fuel. This is why the main reason why it’s being looked into as a treatment for diabetes.  As it will not allow the patients to endure and overly catabolic state, thus allowing energy levels and health to be stable at all times. GW-501516 clearly demonstrates that it increases muscle mass while keeping glucose from touching the adipose tissue sort of like Need2Slin but need2slin does much more then just this. Treatments with GW-501516 have been shown to increase HDL cholesterol by up to 79% and the compound is now undergoing Phase II trials to improve HDL cholesterol in humans. We dive into its attributes further later in the article But again let me speak from personal experience. I did a test with this drug and Winstrol. I know for my self when I take wonstrol it always kills my cholesterol levels. Last time I took it I ended up with an HDL of ten and a LDL over two hundred and it only took less then 2 weeks for this to happen. So knowing this I took wintrol for 4 weeks and also took GW-501516 along with it and I was amazed at the results. My cholesterol levels were BETTER at the end of the 4 week trial. So if cholesterol is of concern for you then you need to get some of this stuff my friend because trust me it works.

Concerns had been raised right before the 2008 Beijing Olympics that GW-501516 could be used by athletes as a performance enhancing drug which was not detectable nor tested for during the doping test. The main reason why athletes would use it is because of the increase in endurance through the increase of glycogen storage leading to increased muscular endurance, again ring a bell. Need2Slin does THE SAME THING! GW-501516 has yet to be label a controlled or banned substance by any national drug enforcement agency including Wada. Obviously no one will test positive for this drug, so if I were an Olympic athlete looking for a boost; this would be at the top of the list considering its much outweighed pros over cons. Any Athletes looking for a edge can use this drug and never have to worry about popping hot. They can not test for it my friends so you are golden. Some new testing is coming out in the next 3-5 years that will allow them to basically test your DNA to see if your bosy as been drug altered in anyway but this is years in the making. For now you are safe to take GW-501516 and not have to worry about popping hot.

Injecting GW501516 is like injecting a cardio session LOL

The benefits of endurance exercise on general health make it desirable to identify orally active agents that would mimic or potentiate the effects of exercise to treat metabolic diseases. Although certain natural compounds, such as reseveratrol, have endurance-enhancing activities, their exact metabolic targets remain elusive. We therefore tested the effect of pathway-specific drugs on endurance capacities of mice in a treadmill running test. Researchers found that PPARbeta/delta agonist and exercise training synergistically increase oxidative myofibers and running endurance in adult mice. Because training activates AMPK and PGC1alpha, they then tested whether the orally active AMPK agonist AICAR might be sufficient to overcome the exercise requirement. Unexpectedly, even in sedentary mice, 4 weeks of AICAR treatment alone induced metabolic genes and enhanced running endurance by 44%. These results demonstrate that AMPK-PPARdelta pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.  Now how does this peptide cause mice to lose weight without activity? Simple, the Activation of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, β-oxidation, cholesterol efflux, and energy uncoupling. In addition, the treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPARγ induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Overall the peptide GW501516 (PPARβ/δ agonists) would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARβ/δ may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12): 2477).. However I would advice only using this drug orally IMO..

 

Proof that GW5010516 increases insulin sensitivity

Elevated plasma free fatty acids cause insulin resistance in skeletal muscle through the activation of a constant chronic inflammatory process. This process involves nuclear factor (NF)-kappaB activation as a result of diacylglycerol (DAG) accumulation and following protein kinase Ctheta (PKCtheta) phosphorylation. At present, it is unknown whether peroxisome proliferator-activated receptor-delta (PPARdelta) activation prevents fatty acid-induced inflammation and insulin resistance in skeletal muscle cells. In C2C12 skeletal muscle cells, the PPARdelta agonist GW501516 prevented phosphorylation of insulin receptor substrate-1 at Ser(307) and the inhibition of insulin-stimulated Akt phosphorylation caused by exposure to the saturated fatty acid palmitate. This latter effect was reversed by the PPARdelta antagonist GSK0660. Treatment with the PPARdelta agonist enhanced the expression of two well known PPARdelta target genes involved in fatty acid oxidation, carnitine palmitoyltransferase-1 and pyruvate dehydrogenase kinase 4 and increased the phosphorylation of AMP-activated protein kinase, preventing the reduction in fatty acid oxidation caused by palmitate exposure. In agreement with these changes, GW501516 treatment reversed the increase in DAG and PKCtheta activation caused by palmitate. Consistent with these findings, PPARdelta activation by GW501516 blocked palmitate-induced NF-kappaB DNA-binding activity. These findings indicate that PPARdelta attenuates fatty acid-induced NF-kappaB activation and the subsequent development of insulin resistance in skeletal muscle cells by reducing DAG accumulation. The results of the study clearly demonstrate that PPARdelta activation is a pharmacological target to prevent insulin resistance. (Endocrinology 2010 Apr; 151(4) :1560-9.)

 

The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells. (Volume 343, Numbers 1-2, 249-256, DOI: 10.1007/s11010-010-0520-8) As you can see this peptide has a profound effect on the liver and pancreas resulting in lower blood sugar and controlled insulin output.

GW501516 prevents brain aging.

 

 

Brain inflammation plays a central role in numerous brain pathologies, including multiple sclerosis (MS). Microglial cells and astrocytes are the effector cells of neuroinflammation. They can be activated also by agents such as interferon-γ (IFN-γ) and lipopolysaccharide (LPS). Peroxisome proliferator-associated receptor (PPAR) pathways are involved in the control of the inflammatory processes, and PPAR-β seems to play an important role in the regulation of central inflammation. In addition, PPAR-β agonists were shown to have trophic effects on oligodendrocytes in vitro, and to give partial protection in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. In the present work, a three-dimensional brain cell culture system was used as in vitro model to study antibody-induced demyelination and inflammatory responses. GW 501516 is a specific PPAR-β agonist that researchers chose to  examine for its capacity to protect from antibody-mediated demyelination and to prevent inflammatory responses induced by IFN-γ and LPS. GW 501516 decreased the IFN-γ-induced up-regulation of TNF-α and iNOS in accord with the proposed anti-inflammatory effects of this PPAR-β agonist. However, it increased IL-6 m-RNA expression. In demyelinating cultures, reactivity of both microglial cells and astrocytes was observed, while the expression of the inflammatory cytokines and iNOS remained unaffected. Furthermore, GW 501516 did not protect against the demyelination-induced changes in gene expression.  This suggests that the protective effects of PPAR-β agonists observed in vivo can be attributed to their anti-inflammatory properties rather than to a direct protective or trophic effect on oligodendrocytes.  We all know that both alzheimer’s and Dementia are caused by chronic inflammation within the brain. Further research is still needed but this peptide displays promise in preventing the aging of the brain. (Journal of Neuroinflammation 2009, 6:15 doi:10.1186/1742-2094-6-15)

GW501516 helps prevent the onset of Diabetes

In contrast to the well-established roles of PPARgamma and PPARalpha in lipid metabolism, little is known for PPARdelta in this process. We show here that targeted activation of PPARdelta in adipose tissue specifically induces expression of genes required for fatty acid oxidation and energy dissipation, which in turn leads to improved lipid profiles and reduced adiposity. Importantly, these animals are completely resistant to both high-fat diet-induced and genetically predisposed (Lepr(db/db)) obesity. As predicted, acute treatment of Lepr(db/db) mice with a PPARdelta agonist depletes lipid accumulation. In parallel, PPARdelta-deficient mice challenged with high-fat diet show reduced energy uncoupling and are prone to obesity. In vitro, activation of PPARdelta in adipocytes and skeletal muscle cells promotes fatty acid oxidation and utilization. Our findings suggest that PPARdelta serves as a widespread regulator of fat burning and identify PPARdelta as a potential target in treatment of obesity and its associated disorders. (Cell. 2003 Apr 18;113(2):159-70. PMID:12705865)

PPAR Agonist help prevent Dyslipidemia

In vitro and in vivo genetic and pharmacological studies have demonstrated PPARα regulates lipid catabolism. In contrast, PPARγ regulates the conflicting process of lipid storage. However, relatively little is known about PPARβ/δ in the context of target tissues, target genes, lipid homeostasis, and functional overlap with PPARα and -γ. PPARβ/δ, a very low-density lipoprotein sensor, is abundantly expressed in skeletal muscle, a major mass peripheral tissue that accounts for approximately 40% of total body weight. Skeletal muscle is a metabolically active tissue, and a primary site of glucose metabolism, fatty acid oxidation, and cholesterol efflux. Surprisingly, the role of PPARβ/δ in skeletal muscle has not been investigated. We utilize selective PPARα, -β/δ, -γ, and liver X receptor agonists in skeletal muscle cells to understand the functional role of PPARβ/δ, and the complementary and/or contrasting roles of PPARs in this major mass peripheral tissue. Activation of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, β-oxidation, cholesterol efflux, and energy uncoupling. Furthermore, we show that treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPARγ induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Moreover, we surmise that PPARβ/δ agonists would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARβ/δ may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12): 2477)

 

GW5015016 decreases chances of Heart Disease

The peroxisome proliferator-activated receptors (PPARs) are dietary lipid sensors that regulate fatty acid and carbohydrate metabolism. The hypolipidemic effects of the fibrate drugs and the antidiabetic effects of the glitazone drugs in humans are due to activation of the alpha (NR1C1) and gamma (NR1C3) subtypes, respectively. In macrophages, fibroblasts, and intestinal cells, GW501516 increases expression of the reverse cholesterol transporter ATP-binding cassette A1 and induces apolipoprotein A1-specific cholesterol efflux. When dosed to insulin-resistant middle-aged obese rhesus monkeys, GW501516 causes a dramatic dose-dependent rise in serum high density lipoprotein cholesterol while lowering the levels of small-dense low density lipoprotein, fasting triglycerides, and fasting insulin. These results suggest that PPARdelta agonists may be effective drugs to increase reverse cholesterol transport and decrease cardiovascular disease which is typically associated with the metabolic syndrome X. (Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5306-11. Epub 2001 Apr 17. PMID:11309497)

 

As for as dosing is concerned, I recommend 5-20mgs once a day, and research on HUMANS has clearly shown that 5mg is sufficient to elicit its intended effects. I really don’t understand why this peptide is not as common as it should be. Its exercise in a vial LMAO.

Now onto the fun stuff guys. Dosing, stacking and uses for this drug. Many people would start out at a 5mg a day dose and I think this is fine but I would also add in another 5mg dose pre work out as well on work out days at the very least if not just run it 10mg every day IMO. IMO one could use this during pct allow you to keep calories high and not gain to much fat which is often what happens. I think its also great in combo with Sarms S4 as a bridge between cycles but I am against using S4 during pct. SO only use it after pct and you are sure you have recovered. Now here is the best part GW-501516 can be used with Drugs like winstrol, Beastdrol, and other orals that would cause problems with cholesterol and this would help keep the numbers to a minimum. High blood pressure, nose bleeds and high cholesterol is common with a lot of oral steroids and this drug will help in the sense that it will lower cholesterol levels..

 

That is all for now my friend. Always remember to Keep Killing that sh*t!!!!!

 

 

 

Hey guys – when you have a great product, you don’t need to resort to illegal hacking and other dirty tactics to sell it. Here’s a Fox News article about Progenex: a protein powder marketed towards the Crossfit community, that got caught using a hacker to make themselves look better online, and remove negative comments about them from the ‘net.

“Consider the case of Darren Meade, who in 2010 was working as interim CEO at a California-based company. In an effort to address a number of negative comments (about both himself and his company [Progenex]) posted online…he discovered the company wanted to sell illegal hacker code to scrub negative comments from the web…”

Excerpt – this part is especially heinous and disgusting – it’s Adam Zuckerman, the owner of Progenex, talking about how he wants to use his hacking program to extort parents:

“I would love to run an underground campaign that says, ‘Google is trying to destroy your reputation,’” an executive on the call is heard saying. “I like the idea of, ‘the more popular you are, the more dangerous it is,’ and giving people the scare tactic of, ‘the more exposure you have … the faster it is for your enemies to attack you.’”

“I think there’s a whole other campaign where we can break the parents,” the executive continued. “Send them a picture of their kid with a gun in his mouth — Google did it. ‘Little Johnny is going to commit Google-cide. Can you stop it?’”