Thread: Clen headaches
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09-22-2012, 06:54 PM #41
[QUOTE=scottroxx;6175155]Hey guys.. You both sound like very intelligent individuals. I do not have the knowledge or experience to doubt or contradict either of you but I must say... this was one of the best posts in actually solving a problem and some theory behind the issue at hand that I have seen out here. Please let's not make an awesome post into another yelling fest!!! Just saying!!
On a better note, I have not had a headache since starting the taurine and increased water intake and as soon as I can get my blood pressure verified ( and I will!! ). I will post the findings as well... Peace guyz, we all f'n rock!!![/QUOTE]
Well I sure as fvck do lol!!!
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09-22-2012, 07:01 PM #42Banned
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I feel your pain brother, I am on a low dose of clen right now and I get them too. Asprin man, lots of water and asprin. One other thing if possible, wake up before you actually wake up for the day, and take the clen drink half liter of water and go back to sleep. I notice much of the sides I have slept off by the time I wake up. And make sure you are staying on the taurine as well 3000-5000mg ED.
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09-22-2012, 07:06 PM #43Banned
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One other thing, I notice if I use 100-150mcg of T4 with the clen I can get just as good results not going to 120mcg of clen provided Im lowering carbs and raising protein. Even for me I just feel its too much for a person and there body. Take care and let me know how you are doing later on.
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09-22-2012, 08:32 PM #44
Get some Taurine and Hawthorn Berry
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09-22-2012, 08:40 PM #45
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09-24-2012, 02:25 PM #47
Because as I have stated several times, the beta-1 stimulation (increased hr and contractile force) far outweighs the vasodilatory effect of its beta 2 actions in humans. Again, instead of making up your own theories, just try using it and tell us how it affects your vitals.
Last edited by Bonaparte; 09-24-2012 at 02:43 PM.
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^ Increaed Hr and such is not BP.
http://onlinelibrary.wiley.com/doi/1...10.00754.x/pdf
That paper states very differently. That clen is primarily a beta 2 agonist and doesnt have near the affinity at beta 1 does.
and ur statement is to try it and see how it works is the defination of bro-science.
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09-24-2012, 06:39 PM #49
i am pretty rusty, in contrast. the last time i touch a physio book was 20yrs ago. thats why i like wiki, its written by smart people like you, and easily edited by other smart people if there is any inaccuracy:
Beta-2 adrenergic receptor
From Wikipedia, the free encyclopedia
Function
Actions of the β2 receptor include:
Circulatory system
Heart muscle contraction
Increase cardiac output (minor degree compared to β1).
Increase heart rate [11] in sinoatrial node (SA node) (chronotropic effect).
Increase atrial cardiac muscle contractility. (inotropic effect).
Increases contractility and automaticity[11] of ventricular cardiac muscle.
Dilate hepatic artery.
Dilate arteries to skeletal muscle.
http://en.wikipedia.org/wiki/Beta-2_adrenergic_receptor
and you already agreed that it increases contractility.
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^ Learn something new every day.
U are right, there are beta 2 receptors in the SA node which increases HR directly. ( the wiki source that it had i couldnt find, but i found some papers on it anyways).
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09-24-2012, 06:46 PM #51
thanks for agreeing. peace?
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Peace
I still stand with my original statement on how it should lower BP. ( granted it may raise due to an increase in volume b/c of the RAAS system... but still lowers BP)
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09-24-2012, 07:00 PM #53
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09-25-2012, 03:46 AM #54
I could come up with plenty of possible reasons why Clen's stimulant effects outweigh its vasodilatory effects despite a higher binding affinity for B2. Has it ever occurred to you that the effects in vivo of these two receptors are not equal and opposite on BP numbers?
How is an objective test, measured with a blood pressure machine "bro-science"? An automated BP cuff does not have an opinion or bias (so long as you don't deliberately do anything to alter the results).
How is that different from any study, apart from sample size and control group? (which really aren't needed when you're looking at a potentially massive jump within a matter of hours that only an idiot could misinterpret as statistically insignificant). It's a simple test that you won't do, because you know that your theories don't hold any water.
Maybe next time I'm working in the ER, I should let all the docs know that treating a hypertensive patient's blood pressure numbers with drugs that are known to work in real life is bro-science, and that the only thing that matters is some potentially flawed study on pubmed dealing with receptor binding affinities which can be optimistically translated into real world results through a MENTAL DETACHMENT FROM REALITY.
You're the one trying to prove a theory here, since everyone else in the world will tell you that clen increases blood pressure. Just try a large dose of Clen and log your BP, or drop the damn subject. You're becoming a real nuisance.Last edited by Bonaparte; 09-25-2012 at 04:25 AM.
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09-25-2012, 07:01 AM #55
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I know its a pain when people argue ...but when its intelligent people I learn so much from it. LOL....
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Why are you getting so angry? isnt 'broscience' taking a compound and stating how it affected the individual and trying to apply it to everyone? and then go on a rant, completely off topic which does nothing to the discussion.
and my theories are based on physiology, and trying to find out why its not how i am thinking, but instead, have a attack towards me, then have the nerve to include that bit about treating HTN with drugs is broscience?! there are plenty of articles out there with the information similar to the article i posted which help construct those treatment methods in the first place. then concluding with a 'mental detachment from reality' because i cite a pubmed article that has the most basic information that helps show where i am coming from... Wow..
anyways... since noone has really explained how BP can go up with a vasodilator.. I got a few thoughts if ya wanna comment
The issue about the increase in contractility, so are you saying that there is a decreased end systolic volume in the heart which increases stroke volume; therefore the heart is pushing out more blood each pump resulting in a higher BP?
--- what about the vasodilator effects? its not a beta 1 agonist, so its not primarily due to the beta 1 aspects, therefore there has to be some vasodilation ( esp when thats what it does) so there has to be more vasodilator (B2) effects compared to beta1 effects.
I refer back to the paper i posted the link to earlier, about the affinities towards beta receptors. this is done with human cell receptors, and the 2nd messanger was measured. and it was clearly shown that it has a primary beta 2 agonist action [efficacy ratio = 1.28], with a less effect as beta 3 agonist (Efficacy ratio = 0.84) and last as beta 1 agonist ( Efficacy ratio = 0.67) --- Efficacy ratio were intrinsic efficacy ratios (KD/EC50) and expressed in LOG format.
Therefore its hard for me to believe that its due to an increased beta 1 action(greater than the beta 2) by clen
What about a superimposed state of hypovolemic shock? with the vasodilation of the arterioles, the afterload resistance drops immensely to a point that the body thinks its blood volume is way to low ( at the carotid body which is the primary control sensory center for these reactions by the body), which kicks on the RAAS system. Then the following compensations lead to the increased BP via A1 and A2 activation, along with ADH secretion which all vasoconstrict and venoconstrict (so block all but the direct activation of beta 2 via clen) and the increase in fluid retention in the kidneys increases the blood volume along with blood osmolarity which all result in increased BP which is greater than the vasodilation done by the beta 2 agonism, along with the venoconstriction done which also increases the blood volume in circulation (instead of being in the vein reservoir)
Then, back to the headaches, the increased BP results in an increase in intracranial pressure, but the pressure increase in is a fixed space which can result in headaches. Then the fact that Taurine helps, which helps keep osmotic balance in the cells, in a hyperosmolarity state which was induced by the 'superimposed hypovolemic state') and the increase in drinking water helps also, to reduce the osmolarity of the blood bringing it back to a stable level ( similar to before clen usage). which helps restabilize the RAAS system and ADH secretion, therefore reducing the fluid retention and lowering the vasoconstriction amount which was helping cause the headache anyways. then with a restabalization of the BP to a stable level. *which can truthfully never be fully achieved because of continued use of clen and its agonistic properties.
also, question.. when on clen, is there an increase in respiratory rate? do people notice themselves breathing faster/ more often? - if so that can also play a part in enhancing the response by the carotid body (due to the decrease in p02 and increase in pCO2; which enhances the response similar to hypoxia and hypovolemic shock
And if you do have any responses, please refrain from pure attacks; and lets talk physio.. thanks
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10-03-2012, 08:28 AM #57
Is the vasodilation effect of beta2 agonist equally felt by all vessels? All arteries? All arterioles? All venules? And all veins?
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10-03-2012, 08:36 AM #58
Vasodilation can only cause a drop in pressure. What ever subsequent responses, either by carotid sinus baroreceptors or renin angiotensin aldosterone system only works towards restoring normotensive state. Once that is reached, the triggers for these responses are gone. There is no way the pressure can be overcorrected over a sustained period, and end up with increased pressure instead.
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Mainly on the arterioles ( i was mistaken in an earlier post), thats where primarily the beta 2 receptors are located
correct, i was aiming towards clen puts the body in the artificial state of hypovolemia, which then the response mechanism kicked in. Ultimately its due to the increase in blood volume(in response to the initial 'shock' of hypovolemia, which was due to the decrease in afterload resistance; sensed by the carotid body as decreased stretch), and the beta 2 activation in the kidney which increases the release of renin, which continues to increase blood volume.
Then headaches were caused by the hyperosmolarity of the plasma, but when that restabalized they went away which lowered the ADH secretion, which slowed fluid retention (via ADH) but the RAAS is still going due to the renin release
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10-03-2012, 08:59 AM #60
I dont think beta2 vasodilation affects all arterioles equally. It mainly works to prepare the body for fight or flight. So blood flow is increased to the coronaries, skeletal muscles and hepatic vessels only. Non essential systems like the bowels and messenteric vessels are shut down till further notice. This decrease in circulation counteracts the abovementioned increase in circulation. Overall effect is no change in blood pressure from the selective vasodilation. However, beta2 can increase heart rate and contractility directly( not through beta1). That is how pressure goes up. Not from overcompensation of nonselective vasodilation.
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I agree with that, however the alpha receptors dominate the mesentaric arteries in the gut, also its regulated by 'functional hyperemia'. so when theres food, the blood flow increases. in the sympathetic response, the alpha receptor is hit mainly which causes the vasoconstriction. there are some beta 2 receptors in the gut, so it will vasodilate but not to the extent that skeletal muscle, coronaries do. They have more beta 2 receptors which will result in a greater effect of a beta 2 agonist.
in the state of 'fight or flight', the flow is increased to those areas and shunted from the gut. but since clen is a drug that affects the receptor that is used, it causes dilation w/o the 'fight or flight' stimuli. The arterioles going to the skeletal muscles have massive capacity to decrease resistance via dilation ( due to the metabolic need of the muscles they require during that "f or f" stimuli) but since that stimuli is absent, the gut arteries are not constricted to conserve blood flow but rather dilated minimally ( b/c of the smaller amount of beta 2 receptors) and the skeletal muscle arterioles are dilated to a greater amount which decreases the resistance in a series fashion. this allows more blood to be in the skeletal muscle arteries which decreases the afterload of the heart enough to mimick the hypovolemic state i mentioned earlier which would result in what ive previously mentioned.
and its never 'overcompensation', its an altered state of hemodynamics which results in compensatory changes.Last edited by Lemonada8; 10-03-2012 at 09:27 AM.
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10-03-2012, 09:36 AM #62
If you also agree that there is no overcompensation, then how can vasodilation raise pressure above normal? All the responses from a lowered pressure due to vasodilation only works towards normal bp. Once that is reached, there is no more stimulus, and the bp wont rise any further from a direct effect of vasodilation. All the mechanisms that work to increase bp in response to vasodilation stops working when bp goes towards normal.
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10-03-2012, 09:41 AM #63
Which means any high bp that you see in clen cannot be a direct effect from vasodilation. It can only be due to beta2's other effects directly on the heart. That it directly increases heart rate and contractility. That is how bp goes up, above normal. Not via vasodilation and the subsequent responses.
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Increased blood volume will cause high blood pressure, which is basically what I'm saying
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10-03-2012, 10:11 AM #65Originally Posted by Lemonada8
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10-03-2012, 10:17 AM #66
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Sometimes it really is just the obvious. ie: Increased contractile force and heart rate.
Just sayin ...
carry on ....
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10-03-2012, 10:17 AM #67
If this were the case, it would occur with low dose cialis and ACE inbitors as well (but it doesn't). Oh, and blood pressure rises acutely when using clen , not chronically or after discontinuation.
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its not overcompensation. its compensation due to the decreased afterload ( pressure required to push blood throughout the heart) which came from the vasodilation ( which decreases resistance in a Series fashion, esp in the skeletal muscle arterioles), that coupled without the constriction of the mesentaric arteries but actually a smaller amount of vasodilation in those arteries, decreasing resistance in a parallel fashion ( by adding the mesentaric arteries which then further decrease resistance within themselves), the total body vasodilation ( yes some to a greater degree than others, but still there), the body senses this as a "low volume state", so it enacts compensatory mechanisms to counteract the 'low volume state' by increasing the total blood volume. its not overcompensation, its just plain ole compensation b/c its induced by a drug ( clen , beta 2 agonist). That coupled with the increased release of Renin ( via Beta 2 in kidney) there is still an increase in blood volume.
Am i not making sense or what? I feel that i am repeating myself?
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No it wouldnt. Cialis is a PDE inhibitor, so it slows the breakdown of cGMP ( which is increased during stimulation, its a 2nd messanger.. so it makes the original 'message' stay longer) which is activated by Nitric Oxide. So it doesnt ever originate a stimulus, it only prolongs the duration it stays. Clen originates the stimulus, because it works on the receptor directly.
an AceI wouldnt increase blood volume either, its a diuretic. It inhibits the conversion of ACE1 to ACE2, which will actually lower blood volume which lowers blood pressure.
And with the acuteness issue, thats why i said 'hypovolemic SHOCK' where the body enacts compensatory mechanisms to counteract the 'artificial' sense of hypovolemia, by vasoconstricting ( it would hit everything else but that which was directly activated by the clen), and alpha 1 & 2 activation, and venoconstriction (which decreases the amount of blood that is 'stored' in the veins and put more into circulation to help minimize the 'hypovolemia.)
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10-03-2012, 11:09 AM #70Originally Posted by Lemonada8
But you're saying this goes on happening even after normal bp is reached. Such that bp is raised above normal. Such that we now have high bp. Thats overcompensation. That doesnt happen.
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10-03-2012, 11:10 AM #71Originally Posted by jimmyinkedup
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10-03-2012, 11:12 AM #72
And my post count is going overcompensated just with this one thread...
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So, what does clen do in the body? its a beta 2 agonist right? beta 2 receptors are on the arterioles, and cause them to dilate..
The body doesnt sense blood pressure, it senses stretch on the wall. with decreased resistance, flow increases, which decreases transmural pressure (which is what is sensed by the baroreceptors)
then with the compensatory response to increase blood volume ( via vasoconstriction * everywhere thats not already directly activated via clen*, venoconstriction * to increase cardiac return, a temporary increase in circulating blood volume, and ADH secretion * another potent vasoconstrictor) this will increase the volume and resistance to 'normal'. however in this case, with the use of a beta 2 agonist, the resistance cant increase nearly as much so this so the flow has to increase (conductance = 1/resistance) to maintain adequate perfusion. this results in an increased volume, increased linear flow in the vessel; which requires an increased transmural pressure to achieve the same amount of stretch.
I have a OSCE in an hour, so ill have to get back to this.... ill get some physiology equations to help explain
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10-03-2012, 02:08 PM #74
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Hell of a lot of trouble just so you dont have to be wrong.
Ive seen it before (in all of places another clen thread in fact).
Wouldnt it be easier just to say , yeah it probably is because the heart is contracting with more force and more rapidly.
Just sayin ...christ ....
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well considering that inotropisim and chronotropism are seperate from BP, yes they play a part; but still seperate. and the fact that noone can comment on the other compensatory changes that i mentioned... i guess yall dont realy wanna discuss physio.
and increased contractility and HR DOES NOT increase BP when there is vasodilation ( bcuz its a beta 2 agonist), that would be 'over-compensation' wouldnt it? too high of a BP compared to normal... which doesnt happen right?!
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10-03-2012, 03:54 PM #76
Once again when your pointed out as wrong, you go banging on about "what if" and come up with ridiculous theory's.
Admit your incorrect. Its getting f*cking boring Marc.
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10-03-2012, 04:09 PM #77
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Does anyone know if clen was one of the substances zyzz was abusing
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10-03-2012, 04:15 PM #78
I read he used a lot of stims, rec's, steroids , stim. supplements. No wonder his heart gave in to it all.
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Originally Posted by Swifto
Funny thing is that I never resorted to just saying your wrong and stopping at that, which several did.
Truth prolly y'all prolly don't have a clue of what I'm saying and the mechanisms I'm mentioning.
All everyone is doing (xcept Asian to a degree) is repeating themselves while never actually addressing what I said.
I admit when I'm mistaken and have done so before, but that's when I was replied with an actual retort to what I was saying. Pretty sure I actually did so previously in this discussion/debate.
But all I get is the "cash back baby" just repeating "no" time after time.
Please point out what I have said that is physiologically incorrect. Please do so. And while your at it, please point out where what I have said doesn't apply to the topic at hand. Tell u what I'll start for ya. "it takes about 3 days for kidney compensation to really take effect so for a acute BP increase after taking clen can't be due to a kidney issue." (then I would argue that it has a part in chronic Bp increase while using clen)
A "ridiculous theory" that is based on factual physiological knowledge really isn't that ridiculous because it's based on facts.
And funny how noone can really state how a vasodilator will INCREASE BP, when dilation of vessels typically results in a decrease in BP (ie taking Viagra and nitro, both vasodilators which decrease BP, and when taking together can cause a dangerous drop in BP)
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10-03-2012, 06:28 PM #80
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Christ I wasnt gonna , but I cant help it. It can when there is an increase in contractile force and heart rate. Just like when you exercise there einstein. vasodilation occurs...but there is an increase in heart rate and contractile force therefore an increase in BP. Now please STOP!
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