purplehaze

Welcome...PH

Got submitted in the first round last night...

Welcome to AB

Welcome to AB

I have read so many different things about T3, Its hard to weed through what is good info and what is poor info. I also know everyone reacts differently. I have never done t3, but Many years ago I had a Great hook up for anything mexican, so I have done plenty of spiropent, both tabs and liquid. This time around I am using clen from Lion, and GP t3, along with Oxide Var. I will be running these compounds for 6-8 weeks depending how well they work, and how many sides I get. My goal is simply to lower my fat% while not losing any muscle. I plan on a Test based cycle when my body fat in down. I am currently at about 20-21% fat. I know, I'm a fat ass, I was at 30% 8 months ago. My diet is pretty good, I would say its an 8 out of 10, ten being perfect.

 

Week 1: T3-50mcg Ed, Clen-40mcg Ed working my way up 20mcg per day, checking my temp, and reactions to find the sweet spot. Var-50mg Ed

Week 2: T3-75Ed, Clen-100 Ed, Var-50 Ed

Week 3: T3-75 75 75 100 100 100 100, Clen Off, Var-50 Ed

Week 4: T3-75 Ed, Clen Off, Var-50 Ed

Week 5: T3-50 Ed, Clen 100-120 Ed, Var-50 Ed

Week 6: T3-50 50 25 25 25 25 25, Clen 120-150 Ed, Var 50 Ed

Week 7: T3- 12.5 Ed, Clen Off, Var 50 Ed

Week 8: Start Test, D-bol, and Deca or Eq cycle

Weeks 1-7, I also will be taking 1g L-carnitine Ed, and 500mg Taurine

I am open to any and all suggestions.

Thanks

 

Yesterday was my first day, and I did not take the T3, because it was well into the afternoon, and I was unsure of the empty stomach thing. I did 40mcg clen, and had no increase in temp, and no noticible sides.

..

Most of this, I am sure you have read or know already, but diet is key..T-3 is not the magic drug that people sometimes hope it will be..What is your cardio going to be like and what kind of training will you do while on? I see you would like to lose body fat and not muscle,,but you will have to accept some muscle loss esp since you are starting test at week 8..JMO...

When I am on it I find that it works best for (ME) to split the dosage up throughout the day...However, you will see 100s of posts about taking the whole dosage in the morning on an empty stomach....Also, you will see several hundred others contradicting each other on the need to ramp or not...Dont quote me, but I believe leaflets by manufactures claim the half life of t-3 is approximately 2 days...Personally, when I take 75 to 100mcgs of t-3, I like to spread it out...You will have to see what works for you...Btw, you can find the article here by Nandi on T-3..http://anabolicboard.com/forum/showthread.php?t=25952&highlight=nandi

Here are a few posts by Nandi of studies he found that support his thread/article...

(First one by Nandi)

In (1) subjects were put on a month long T3 cycle: 50 mcg/day week 1; 75/day week 2; then 100/day weeks 3 & 4, then stopped abruptly. Six days after withdrawal TSH was back in the normal range; 8 days after withdrawal it had returned to baseline and then spiked above baseline until dropping back to baseline by day 42. The point being TSH recovery is very fast.

As for thyroid hormone levels, after going cold turkey T3 dropped to only 22% below baseline and had returned to normal within 2 weeks. The 22% drop in T3 compared to a 60% drop in T4 represents the "thermostat" upregulating conversion of T4 to T3 in a state of thyroid suppression.

Your thyroid will come back quickly after only a minor suppression of T3 (22%) during a relatively heavy cycle (100 mcg/day). I would not even worry about trying to speed recovery.

(1) J Clin Invest. 1984 Feb;73(2):570-5.

Peripheral tissue mechanism for maintenance of serum triiodothyronine values in a thyroxine-deficient state in man.

Lum SM, Nicoloff JT, Spencer CA, Kaptein EM.

__________________

split your dosage up throughout the day

I agree...How many mcgs of t-3 are you going to take and for how long etc?? I prefer to take it 3 times a day as it seems to work better for me that way...Post the cycle and let us know how you were going to run it..PH

Is it just me or does Lady GAGA look manlyish at times..

No, not safe or deep enough. Use 25G x 1". Also don't risk having that 29G needle breaking-off in one of your muscles.

I agree...

Haha, Well, I've always been a Lindsay Lohan fan, had her up as my avatar for years now! LOL!

Both Skanks these days.... Not really sure right now, as it changes about weekly..Use to have a thing for Jessica Beil but now it Bar Rafaeli

I like Umphreys Mcgee alot. Going to see them in Raleigh in Aug. Seen Phish about 3 or 4 times. Was going to see them in Charlotte on July 2nd but cant. Went to the Further show in Atlanta super bowl weekend and it was really good. But Umphreys is my fav.

Yeah,,,seen them a few times...

New here. Just wanted to say hi.

 

Little bit of background... I'm 30ish. Was a fat kid (300lbs in highschool) and picked up lifting 6 years or so ago to help control the weight. I hover around 200lbs. My ultimate goal one day would be around 225 12% body fat but we'll see if I ever get there.

 

Any way just wanted to introduce.

Welcome to AB......PH

Welcome to AB...PH

I saw 7 of the Dead reunion shows last year in 6 cities. I try to make one festi a year, this year I'm doing All Good in WV, its not too far away. I am a silver smith, and I make alot of dead jewelry. When I was playing ball in college, I worked for a security company that contracted to the Dead and others. I got to meet Jerry in 93. I was lost to the scene back then, and my only words to him were "Don't worry I won't let anyone Fuck With You". I was a big Phish fan in the late 90s, I did get to see a show last year at Bonnaroo, it was good, but not the same as when I was doing tour with my now ex-wife. Peace, Billy

You sound similar to me my man..I thought about doing the all good this year, but we went to Wannee instead and we are trekking to see a few other bands this year too..String cheese namely .....Have a good time my man..That lineup looks really good this year..PH

Welcome back......PH

Isn't clen two weeks on two weeks off , and the T3 u need to b careful since it will Fck up ur tyroid if takein to high of a dose & for to long of a period. I dnt knw about the E.C.A. But I knw clen & t3 together wrk really good for fatloss or cutting.

I have read a good deal of studies that suggest that you can safely take t-3 for extended periods and at relatively high dosages with little or no long term side effects...Here is a good read for those that have time..It is by Nandi and his work is based on several studies conducted and posted on pubmed...

This article written by Nandi

Thyroid Hormone for Weight Loss:

Physiologic and Metabolic Effects

by Nandi

Introduction

It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.

Thyroid Function and Physiology

Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer's classic paper from a later author:

"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.

Increased Oxidative Energy Metabolism

Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.

Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)

Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)

Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)

Mitochondrial Uncoupling

As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.

Andregenic Receptor Modulation

Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine Ketotifen concurrently with the clenbuterol. Studies have shown that Ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that Ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.

Decreased Phosphodiesterase Expression

In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.

Increased Growth Hormone Secretion

In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.

Decreased Insulin Secretion

Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.

The Future

As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Haycock in Muscle Monthly:

All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.

Summary

We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.

__________________

Obama had nothing to do with the explosion on the rig.

 

His blame comes from denying Gov Jindal of his request to put up oil barrier reefs, which would have contained the oil spill off shore, thus saving the regions wild life, and sparing much of their fishing industries.

 

Obama didn't even visit the region until roughly 20 days (his words were "I was there a month ago to talk to experts"). He said this 50 days after the disaster that killed 11 Americans. So obviously he didn't give a shit until it became politically necessary to make an appearance.

 

I guess he's to busy vacationing, smoking fags, and hosting rock bands to care about dead American workers.

He couldn't even tear himself away from his vacation to honor our dead war hero's on Memorial Day.

At least he's consistent. Doesn't care about dead American workers, or our fallen American military personal.

 

Obama has claimed (correctly) it is his responsibility to manage this crisis. Yet hasn't managed to do anything except to make idle threats (to kick some ass - his words), but he hasn't figured out who's ass to kick.

Being that he has quoted Harry Truman's "The buck stops here", he can start with his own.

 

This temporary occupant of the White House has claimed BP is the best group to handle the problem - which obviously they're not!!!

 

You're the same kind of person that blamed Bush for his Katrina response (Bush took 4 days to visit the disaster), and sent in the bumbling FEMA on the first day. Failed effort > no effort, so stop being a hypocrite...

 

Lastly; I don't hate my President. I respect and admire the office of the Presidency. I do hate the mental midgets who voted someone with no executive experience into the world's most important job.

We are getting what we deserve - the worst President since Jimmy Carter...

Well,,most of our politicians are douche baggy and worthless anyway....I really don't get too caught up in the Political races because they are all lies and and say whatever to get elected..

No idea bro, nobody talks about them.

 

I think sublingual delivery is bunk.

I agree with Jay.....I haven't heard anything good about those tabs..

So all the hype surrounding the USA v England match and the game ends with a 1-1 tie. WTF? I don't get it, no team won and nothing was accomplished. 90 minutes of nothing.

 

Below are some pics of great soccer legends

 

 

http://www.soccersucks.net/soccer_perversion.html

For the USA, that was a win..PH

Sweet...Chuck needs to retire.

Strangefolk is a New England jamband from Vermont. I like gov. mule too. Was listening to them this past weekend. They do an awesome cover of "Soulshine".

Yeah,,it is Warren Haynes Song...

They actually do a lot of covers..I have seen them cover stuff from all over the music spectrum..I once saw them cover Temple of the Dog Hunger Strike...They cover old classics like Cortez,a few Zep Songs but they will cover weirder things like newer shit...They are pretty good..

Well,,SEC fan here...I believe the SEC will remain pretty much the same...I believe we may pick up a Texas AM

I cant get it...I have tryed,,but its not for me.,.PH

I am glad...They should have done it when Cry Baby Pete was still there...P

Had some computer issues but Im back- so too bad LOL!!

 

I bet y'all were hoping.:007:

What are you guys' thoughts on this:

 

If a person was taking 50mg a day is it better to spread them out say 25 in the morning and 25 before your workout or take all 50 say at lunch time everyday? Just wodering? thanks.

Divide it up....