438 replies to this topic

[acantelopepope]

I now believe that the regimen I have outlined (including proper rest and assuming no serious medical complications) should be enough to restore piracetam efficacy for the average non-responder. It may take 2 weeks to 2 months; individual results will vary. But if you're interested in seeing piracetam "work", post your course of action to restore aldosterone function here and we'll work towards it together.

Correlation: 10/11= 91%

I want to hear more confirmations of passing the pupil test and users having no trouble with piracetam. We've had one so far.

Edited by acantelopepope, 13 November 2009 - 01:19 AM.

[csrpj]

my pupils began fluctuating immediately.

piracetam used to work wonderfully before... but in last week, it's worked kinda but also left me with bad headache/brainfog an hour or two after taking it. also, taking piracetam or not, been having issues with sleep. the only major change i made is taking wellbutrin twice daily instead of just in the morning.

[John W.]

I want you to do a test for me.

Get a flashlight.
Stand next to a mirror and turn all other lights off.
Shine the flashlight towards your eyes from the side, not directly.
Your pupil should become small.

Over the next 90 seconds, does your pupil remain small, without any variation? Or does it fluctuate, unable to stay small?

This is very important-- I think that I may have discovered what is causing piracetam to work so inconsistently.

Please post your results. 1) Does piracetam "work" for you? (you will know if it does, over a few weeks and taken consistently with a choline source) 2) What were the results of this short pupil reflex test? Did your pupils fluctuate or not?

Thank you.

Ok, I performed the test. For what it's worth this is everything I'm taking:

--6 mg EMSAM patch (aka selegiline, aka deprenyl)
--probably ~ 6 grams piracetam daily. Just started this about a week ago though.
--lecithin or CDP-Choline --- I take a CDP choline (250mg) capsule a day, and try to eyeball out the lecithin to about 75% of each ~2 gram dose of piracetam.
--focus formula (ingredients of note: DMAE bitartate 125 mg; vinpocentine 5 mg, huperzine A 100mcg, Gotu Kola extract 30 mg) [started this last night though]
--pantothenic acid (aka B5) 250 mg daily
--Fishoil 1 gm, 3x daily.

The results were, my irises consistently fluctuated -- VERY dramatically -- the whole 90 seconds. As a baseline I used the same light on my girlfriend, who takes no medicines or supplements, and of course her irises were completely normal.

The only other x factor, as far as I could guess would be that earlier today (about 9 hours earlier...) I had eaten 1/4 bar of 100% cacao bar. I had done this to attempt to test a hypothesis about the PEA in chocolate, which ordinarily gets broken down by MAO-B and thus can't really have the happy/amphetamine effect. I figured as I am on EMSAM, an MAO-B inhibitor, I could test the effect of the PEA/MAOI combo without having to ingest PEA itself (which I am too chicken/have no real desire to try). In any case I really doubt that would be relevant so long after ingestion, but this is my first post and I am new to nootropics; so I decided to err on the side of caution and include.

In any case acantelopepope; thank you very much for the post. It is very disconcerting for the simple fact that it is a very weird and unnerving reaction. I don't think I could clarify myself as a responder or not to Piracetam, given I have only been taking it for a week. I have taken attack doses the first two days (around 9 grams each day) and I definitely feel "different" now when I take the piracetam, but I do not know how to qualify it. I alternate between a significant feeling of energy but sometimes feel very exhausted (in both cases having slept regularly), but I imagine this could be related to my imprecision with choline -- I have just taken more choline with my last piracetam dose of the day, and feel nicely energetic. Since I have taken piracetam, I have noted an 'out of body' kind of feeling sometimes - nothing schizophrenic, but the kind of feeling where you feel slightly less fit to drive than usual. I have had no real objective/quantitative way of testing the cognitive effects of the piracetam though, so if you mean responder strictly in this sense, I would have to say I consider myself a non-responder to unknown.


I am very concerned since the iris thing is not normal, and my knowledge of neurochemistry is negligible. Would anyone be able to put in laymen's terms the risks/consequences suggested by this reaction? And if I understand your point acantelopepope, you're suggesting this reaction essentially would indicate a lack of response to piracetam? If this is the consensus, and since I really need benefits from the piracetam, would there be any strong alternative to making piracetam work than taking pet medicine? I ask because I would feel more comfortable with something more mainstream; and I'm worried I'd get into an even worse state and taking more crap to make the piracetam work.

At any rate thanks everyone for tolerating a noobie with nootropics, and for any of your knowledge you might be able to impart on the these questions.

Edit -- I was looking into pregnenolone because it's really cheap. Upon buying it though I noticed there's a host of steroid warning/cautions: about losing hair, irritability, acne, estrogen serious health effects etc; which makes me uncomfortable. I am comfortable with Maca though, and my brother brought back a bunch from Peru recently. acantelopepope -- could you explain why it was one of your suggestions for a regiment though? I'm drinking some right now and I'll try to serve as a guinea pig in this respect; but the only connection I could find on PubMed of relevance was that Maca actually "reduced or abolished... elevated corticosterone levels". Either way though, it doesn't seem too dangerous, so cheers; and I'll let you know how the Maca works.

Edited by John W., 13 November 2009 - 05:11 AM.

[recitative]

My pupils fluctuated quite a bit.

I responded very well to Piracetam initially. And then after approximately a couple weeks it made me groggy and tired. I did not get any headaches, but my thinking was impaired. I tried taking it with Alpha GPC, CDP choline, DMAE, lecithin, eggs, huperzine-A, etc. The only thing that seemed to work was using it only once every couple weeks.

I started reading this forum to try to figure out what went wrong. The various choline supplements did not help, so I began to doubt that choline was the issue.

Acantelopepope, I am very intrigued with your idea. In fact, after now browsing this forum for months this is the first time that I have responded to anything. I several thoughts and questions about this:

1. What is the difference between adrenal fatigue and adrenal insufficiency?

2. Is it strange that this many people seem to have this aldosterone deficiency? The woman in the YouTube video that you posted had a tumor, which is pretty serious, but my pupils were fluctuating as much as hers, and I don't think I have any major health problems.

3. I would like to try some of these supplements that you mentioned but I don't know much about any of them. I read that some of the side effects of Pregnenolone include hair loss and acne. I am a 35 year old man and my full head of hair is one of the few things I have going for me right now, so I don't want to lose it. I think I could live with a few pimples, but the combo of acne and baldness is terrifying. Does anyone out there know how common these side effects are?

4. Iso Cort increases cortisol, but LIB wrote above, "Excess cortisol makes all of your hormones less available at normal levels." So I am confused. (This stuff is way outside my field so please excuse my ignorance.)

5. The wikipedia page for Tribulus Terrestris said that it is supposed to increase testosterone, but it didn't say anything about aldosterone or other hormones.

6. Does the sea salt need to be iodized? I just bought a bunch of salt last week that has no added iodine.

I'll probably think of a few more questions but this is a lot already. Acantelopepope, thanks for your posting.

[JonnyDoowop]

I have very dark eyes so it was hard to tell but from what I saw in the complete dark, my pupils were fluctuating in size and I have lost all piracetam effectiveness after the first two weeks.

[Viscid]

I'm a responder and they fluctuated.

Uh, the pupils seem to fluctuate for almost everyone. This is a pretty BS test.

[Dorho]

The explanation provided here sounds very interesting, but I think there are more factors involved in how a person reacts to piracetam. From what I have read, piracetam's potential effects include, but are not limited to: increased contrast in visual perception, heightened sense of hearing, improved imagination & verbal capabilities, improved working memory, improved recall, improved memory imprinting, a sense of well-being, improved concentration, and increased wakefulness & energy. I doubt a person will get all those effects with simply lifted aldosterone levels.

[Dumbel]

My pupils fluctuate too. I`m on piracetam for 4 days now and think i`m a non-responder. I`m still trying with megadosing (10-20g per day).

I also ordered some pregnenolone and will see if this helps.

Edited by Dumbel, 13 November 2009 - 07:46 AM.

[hyper_ventriloquism]

The pupil fluctuations seem to be the rule rather than the exception for people in this thread. We need to keep in mind that when people preform the test it's likely that they're not holding their head/eyes or light perfectly still. This may influence the tendency for pupil adjustment. BTW, I just started piracetam yesterday, so I'm unsure if I'm a responder at this time.

Edited by hyper_ventriloquism, 13 November 2009 - 02:59 PM.

[nito]

i've started mixing 6 gram with 0.5l water in a bottle and drink it frequently throughout the day, i think i noticed something slightly yesterday. Will update soon!

[John W.]

I'm a responder and they fluctuated.

Uh, the pupils seem to fluctuate for almost everyone. This is a pretty BS test.

I would not say the test is BS. I tested myself and my girlfriend and there was absolutely no doubting the difference, and so I don't think pupils fluctuate for everyone (that is, those not taking piracetam). Hyper_ventriloquism makes a good point though: "The pupil fluctuations seem to be the rule rather than the exception for people in this thread."

We're looking at the correlation of non-responders and out of hand excluding a possible correlation of responders. Another way of looking at the data is that acantelopepope's last count, 10/11 actually just suggests 10/11 people taking piracetam have pupil fluctuation, and actually says nothing about efficacy. Almost everyone seems to have fluctuation, and since the thread title is after all "Piracetam non-responders", it's not surprising that almost everyone taking piracetam and experiencing this appears to be a non-responder. So, inferences about efficacy might be premature. Also, suggest posting it in a thread of something like "Piracetam efficacy"; to generate more input from responders.

On a side note I think more info about everyone's stacks, rather than just piracetam; fluctuation or not, and responder or not is needed.
This could give us a lot more to work with. I for example take DHA (e.g. Fish oil), and I imagine I'm not the only one. I was surprised to find a lot on fish oil and Omega-3 and aldosterone/corticosterone - for example in one study that found "Plasma aldosterone levels were 33% lower in the DHA-fed animals than in controls (22 +/- 3 vs. 33 +/- 3.7 ng/dl, P < 0.05). Plasma levels of corticosterone were 18% lower in animals fed DHA than in controls".

Something else I found is that corticosterone, in this thread one of the thing's we're looking at increasing, can operate like the polar opposite of Huperzine A (increasing function and sensitivity of NDMA as opposed to being an antagonist), and "may adversely affect neuronal viability". Notably though choline seems to help to reduce some of this toxicity.

Keep up the good work everyone, this seems like a very valuable thread.

[lol_k]

I'm a mild-moderate responder to piracetam and been using piracetam for a few months. Both pupils fluctuated when i shined the flashlight into my eyes.

[rainsong]

just did the test, pupils fluctuated moderately. found out that my left pupil is way towards my nose side of the iris :0 - cool. too early to say whether i am a piracetam non-responder but it looks bleakish. will update with developments. thinking i might just need a bit more time off of caffeine/weed to get my systems on kilter. is it possible that so many here have abnormal reflex because they are on piracetam and the strain that piracetam puts on the adrenals? is it possible that caffeine/weed/other drugs could have medium/long-term effects on the relevant mechanisms here? and that maybe the high number of people with a speculatively rare condition is due to their being people with higher incidence of past substance use? is it known whether there are many people which abnormal pupillation that are otherwise asymptomatic?

My history with...
weed: sporadic, then a period of mostdaily use for a few weeks a year and a half ago, and then a period of mostdaily, but light (<0.5 small bowl) use, lasting 5 months, with odd intervals of a week or so off, lasting hitherto.
caffeine: regular long-term (2.5yr) use, with regular breaks mostly <200mg/day. never more than 500mg for more than a few days in a row. very rarely doses of 1000mg or of 100mg+ insufflated or of 30ish-mg smoked.
speed: a couple of times.

this is all i could find in the way of research on cannabis.
http://www.biomedexp...of_cannabis_use
, but cannabis does seem to cause fatigue. negative cognitive effects of marijuana are supposed to mostly disappear after a month of use. maybe that interval might correspond to that of a possible cannabis effect on the adrenals?
there is plenty on the web about caffeine and adrenal burnout.

should intense exercise be helpful with this? what about diet? lo-carb? also, i read that rhodiola is good for adrenal insufficiency.

thanks for making aware!

[tritium]

I tried progesterone cream today and it was the most productive day I've had in a while! My motivation to do work increased greatly and the fog was almost completely gone. I started with a few dabs under the armpits in the morning. Then, I started to get a little foggy later in the day so I added some more cream, which helped clear the fog.

I also took 1-2mg of yohimbine, but I don't usually get this effect from it. Therefore I think this effect was from the progesterone cream and not the yohimbine.

I hope somebody finds the root cause of this problem, as I don't want to be using progesterone cream forever. Maybe there is a deeper problem which caused the low aldosterone levels?

[John W.]

I tried progesterone cream today and it was the most productive day I've had in a while! My motivation to do work increased greatly and the fog was almost completely gone. I started with a few dabs under the armpits in the morning. Then, I started to get a little foggy later in the day so I added some more cream, which helped clear the fog.

I also took 1-2mg of yohimbine, but I don't usually get this effect from it. Therefore I think this effect was from the progesterone cream and not the yohimbine.

I hope somebody finds the root cause of this problem, as I don't want to be using progesterone cream forever. Maybe there is a deeper problem which caused the low aldosterone levels?

Tritium --- Do you take Omega-3 supplements? I usually do, but I stopped for 2 days (and have been taking Maca root). I did the eye test last night (it had been maybe 6 hours since my last dose of Piracetam though), and the fluctuations were dramatically decreased. The second time I did the test, like 2 minutes later, almost no fluctuations at all. I don't know if it's stopping the Omega 3 or the Maca or both but there is has been a big difference. No idea why the Maca would work, but the Omega-3 would make sense.

[nito]

I tried progesterone cream today and it was the most productive day I've had in a while! My motivation to do work increased greatly and the fog was almost completely gone. I started with a few dabs under the armpits in the morning. Then, I started to get a little foggy later in the day so I added some more cream, which helped clear the fog.

I also took 1-2mg of yohimbine, but I don't usually get this effect from it. Therefore I think this effect was from the progesterone cream and not the yohimbine.

I hope somebody finds the root cause of this problem, as I don't want to be using progesterone cream forever. Maybe there is a deeper problem which caused the low aldosterone levels?

Tritium --- Do you take Omega-3 supplements? I usually do, but I stopped for 2 days (and have been taking Maca root). I did the eye test last night (it had been maybe 6 hours since my last dose of Piracetam though), and the fluctuations were dramatically decreased. The second time I did the test, like 2 minutes later, almost no fluctuations at all. I don't know if it's stopping the Omega 3 or the Maca or both but there is has been a big difference. No idea why the Maca would work, but the Omega-3 would make sense.

So omega 3 interacts with piracetam , or what u saying?

[tritium]

Tritium --- Do you take Omega-3 supplements? I usually do, but I stopped for 2 days (and have been taking Maca root). I did the eye test last night (it had been maybe 6 hours since my last dose of Piracetam though), and the fluctuations were dramatically decreased. The second time I did the test, like 2 minutes later, almost no fluctuations at all. I don't know if it's stopping the Omega 3 or the Maca or both but there is has been a big difference. No idea why the Maca would work, but the Omega-3 would make sense.

No, I don't take any Omega-3. I just take a multivitamin, 3-4 grams piracetam, and 0.2-0.3 grams alpha-gpc. I desperately need to find a solution to make piracetam work again, because my grade are as low as they have ever been this semester.

[John W.]

I tried progesterone cream today and it was the most productive day I've had in a while! My motivation to do work increased greatly and the fog was almost completely gone. I started with a few dabs under the armpits in the morning. Then, I started to get a little foggy later in the day so I added some more cream, which helped clear the fog.

I also took 1-2mg of yohimbine, but I don't usually get this effect from it. Therefore I think this effect was from the progesterone cream and not the yohimbine.

I hope somebody finds the root cause of this problem, as I don't want to be using progesterone cream forever. Maybe there is a deeper problem which caused the low aldosterone levels?

Tritium --- Do you take Omega-3 supplements? I usually do, but I stopped for 2 days (and have been taking Maca root). I did the eye test last night (it had been maybe 6 hours since my last dose of Piracetam though), and the fluctuations were dramatically decreased. The second time I did the test, like 2 minutes later, almost no fluctuations at all. I don't know if it's stopping the Omega 3 or the Maca or both but there is has been a big difference. No idea why the Maca would work, but the Omega-3 would make sense.

So omega 3 interacts with piracetam , or what u saying?

Yeah, well if this thread is correct anyways. The idea behind the thread seems that lower aldosterone or corticosterone levels make non-responders, which is why there's the discussion of supplementing steroids. But Omega 3 (specifically the DHA) seems to lower at least aldosterone if not both aldosterone and corticosterone. The study above found that rats fed DHA had their aldosterone lowered by 33% and corticosterone by 18%.

If acantelopepope is right, and piracetam itself lowers aldosterone and corticosterone, and piracetam works better with these levels normalized, then yes, Omega 3 would get in the way of and negatively impact piracetam.

[acantelopepope]

Hey everyone. I haven't had much time to respond to individual questions here, but the dialogue seems to be progressing regardless.

I found this description of Aldosterone particularly useful and thought to share it with you. It was taken from http://www.tuberose....nal_Glands.html

Regulation and Actions of Aldosterone

Adrenal Fatigue and Craving for Salt

As mentioned in the “Anatomy” section, aldosterone is manufactured in the zona glomerulosa of the adrenal cortex. Like cortisol, aldosterone follows a diurnal pattern of secretion with its major peak at around 8:00 AM and major low between midnight and 4:00 AM. Also like cortisol, its production and secretion increases and decreases in response to stimulation of the adrenal cortex by ACTH. This means that aldosterone levels generally rise in stressful situations. However, aldosterone is not part of the negative feedback loop controlling its release. Instead, it depends on the negative feedback loop in which cortisol levels trigger ACTH activity. This means that cortisol determines the amount of ACTH which controls production of both cortisol and aldosterone with aldosterone having no say in the matter.

The only thing the cells that produce aldosterone can do to regulate production is to alter their sensitivity to ACTH. Therefore, after about 24 hours, the adrenal cells of the zona glomerulosa become less sensitive to the demands of ACTH and stop manufacturing more aldosterone. The amount of circulating aldosterone then begins to decrease, even though the ACTH levels are high and the need for increased amounts of aldosterone may continue. This decreased production continues until the cells of the zona glomerulosa recover their sensitivity to ACTH, but in the meantime the decreased aldosterone leads to many of the symptoms of adrenal fatigue.

Aldosterone is the most important mineralocorticoid, but corticosterone and desoxycorticosterone are also included in this category. The effects of aldosterone depletion can be observed in a large number of hypoadrenic persons. Aldosterone depletion may create one or more different symptoms which are specifically related to the diminished mineralocorticoid levels.

In the chronically stressed person, the levels of sodium and chlorides in the urine should be measured as well as the specific gravity in the urine. Chlorides in the urine are measured by Koenisburg’s test. This test also provides information of the sodium levels being excreted in the urine. Excessive sodium in the urine is one of the first clues that a person has a hypoadrenic problem.

Aldosterone is responsible for the maintenance of fluid (water) and the concentration of certain minerals (sodium, potassium, magnesium and chloride) in the blood, the interstitial fluid (area between the cells) and inside the cells. Working with other hormones such as anti-diuretic hormone from the pituitary and rennin and angiotensin I and II from the kidneys, aldosterone keeps the fluid balance and salt concentration intact, in roughly the same concentration as sea water. In the blood and interstitial fluid, sodium is the most dominant of the four minerals. Inside the cells, potassium has the highest concentration. These four minerals are called electrolytes because they carry minute electrical charges. These electrolytes are very important for proper cell function and fluid properties and they must remain in a relatively constant ratio to each other and to the body fluids. Small deviations in their ratios to each other, or to their concentration in the body fluids, means alterations in the properties of the fluid, the cell membrane and the biochemical reactions within the cell. In fact, most of the physiological reactions in the body depend in some way on the flow or concentration of electrolytes.

Aldosterone, in times of stress is the major director of these relationships by its influence on sodium and water concentrations. Although this interaction is somewhat complex, the overall process is easy to understand if you just keep an eye on the sodium in relation to aldosterone. As the concentration of aldosterone rises, the concentration of sodium rises in the blood and interstitial fluid. Wherever sodium goes, so follows water.

In adrenal fatigue, the craving for salt is a direct result of the lack of adequate aldosterone. As mentioned above, aldosterone controls sodium, potassium and fluid volumes in your body. When aldosterone secretions are normal, potassium, sodium and fluid levels are also normal. When aldosterone is high, sodium is kept high in the fluids circulating in your body.

However, as circulating aldosterone levels fall, sodium is removed from your bloodstream as it passes through the kidneys and is excreted in the urine. When sodium is excreted it takes water with it. Initially, there is some loss of volume of your body fluids but it does not become severe unless the condition worsens. Once your circulating sodium level drops to about 50% of its original concentration in body fluids, even a small loss of sodium or sodium restriction in your diet begins to have severe consequences. Tiny fluctuations in blood sodium concentration have a significant effect o blood volume when sodium is depleted to this level.

When the sodium supply of the blood is not replenished by eating salt-containing foods or liquids, sodium and water is pulled from your interstitial fluids into the blood to keep your blood sodium levels and water volume from getting too low. If too much salt or fluid is pulled from the interstitial fluids, the small amount of sodium in the cells begins to migrate out of the cells into the interstitial fluid.

The cell does not have a great reserve of sodium because it needs to maintain its 15:1 ratio of potassium to sodium. As the sodium is pulled from the cell, water follows the sodium out.

This leaves the cell dehydrated as well as sodium deficient. In addition, in order to keep the sodium/potassium ratio inside the cell constant, potassium then begins to migrate out in small quantities. However, each cell has minimum requirements for the absolute amounts of sodium, potassium and water necessary for its proper function. When these requirements are not met, cell function suffers, even if the proper ratio is maintained.

If you are suffering from moderately severe adrenal fatigue, you must be careful how you re-hydrate yourself. Drinking much water or liquid without adequate sodium replacement will make you feel worse because it will dilute the amount of sodium in your blood even further. Also, your cells need salt to absorb fluids because sufficient sodium must be inside the cell before water can be pulled back across the membrane into the cell.

When you are already low on body fluids and electrolytes, as you are in this situation, you should always add salt to your water. Do not drink soft drinks or electrolyte-rich sports drinks, like Gatorade, because they are high in potassium and low in sodium, the opposite of what someone with low cortisol levels who is dehydrated needs. Commercial electrolyte replacement drinks are designed for people who produce an excess of cortisol when exercising, not people who are low on cortisol and aldosterone. Instead, yo are much better off having a glass of water with ¼ - 1 teaspoon salt in it, or eating something salty with water to help replenish both sodium and fluid volume.

In a nation of people suffering from adrenal fatigue, the fast food restaurants come to the rescue. Such restaurants use an excessive amount of salt in their foods; a custom left-over from the old road houses where lots of salt was used in the food to stimulate appetites and whet the thirst (for alcohol, the biggest profit item). Although not a good solution, it supplies “emergency” rations daily to people living in marginal health. It averts the crisis and replenishes their supplies for another few hours.

When your aldosterone levels are low and you are dehydrated and sodium deficient, you may also crave potassium because your body is sending you the message that your cells are low on potassium as well as sodium and water. However, after consuming only a small amount of potassium containing foods or beverages (fruit, fruit juice, sodas and commercial electrolyte replacement drinks), you will probably feel worse because the potassium/sodium ration will be further disrupted.

What you really need in this situation is a combination of all three, water, salt and potassium in the right proportions. One of the easiest ways to accomplish this is to drink small repeated doses of water accompanied by a little food sprinkled with kelp powder. Kelp powder contains both potassium and sodium in an easily assimilated form. Depending upon taste and symptoms, extra salt can be added. Sea salt is a better choice than regular refined table salt, because it contains trace amounts of other minerals in addition to the sodium. Another choice is to drink a vegetable juice blend containing some celery and chard and diluted with purified water.

Usually, within 24-48 hours, your hydration and electrolyte balance will have stabilized enough that you can proceed to an adrenal-supporting diet. You must continue to be careful to drink salted water or vegetable juices 2-4 times during the day, varying the amount of salt according to your taste, and you should avoid potassium-containing foods in the morning when your cortisol and aldosterone levels are low. Never eat or drink electrolyte-depleting or diuretic foods and beverages such as alcohol and coffee, especially if you have been out in the sun or are otherwise dehydrated. One of the problems people with adrenal fatigue constantly deal with is a mild dehydration and sodium depletion.

When there is inadequate aldosterone, the kidney allows sodium, chlorides and water to spill into the urine, and maintains ionic balance by retaining, rather than excreting, potassium. Some of these low aldosterone persons present with symptoms of dehydration. The appearance of the tongue is one of the easily monitored indicators of dehydration. Normally, one should feel considerable slickness when running a finger down the protruded tongue of a person. It should slide easily across the tongue like a cube of ice across a wet piece of waxed paper. If the tongue is rough like sandpaper, or if you feel friction, with your finger catching or sticking to the tongue’s surface, it is an indication of inadequate tissue hydration. The person needs more water intake.

The person may report excessive urination, up to 15 or 20 times daily. Likewise, due to the effect of aldosterone on the sweat glands, the person may report excessive perspiration or perspiration with little or no physical activity. The common factor in all of these persons is a weakness of sartorius, gracilis, posterior tibialis, gastrocnemius, or soleus, and a background of some type of stress.

A person with lowered aldosterone may also demonstrate other symptoms. For a nervous system action potential to take place there must be an adequate supply of sodium on the outside of the cell membrane and an adequate supply of potassium inside the cell. They must be balanced. If this balance is undermined by a loss of sodium and retention of potassium, the nervous system will find it difficult to propagate normal action potentials and maintain itself at a good functional level. This may result in a wide variety of symptoms, including muscle twitches and even cardiac arrhythmias (heart palpitations).

With a chronic sodium-potassium imbalance, the person will show the sign of a paradoxical pupillary reflex. Normally, shining a light into a person’s eye will cause the pupil to constrict. This papillary constriction to light should be able to maintain itself for at least 30 seconds. In the hypoadrenic person (especially in the exhaustion stage of the GAS) you will find one of three things:

1. The pupil will fluctuate opened and closed in response to light.

2. The pupil will fluctuate opened and closed in response to light. (This is a deliberate opening and closing, not the minor flutter or twitch of the normally encountered hippus activity.)

3. The pupil will initially constrict to light, but it will dilate paradoxically with continued light stimulation of less than 30 seconds. This patient will frequently complain of eyes that are sensitive to light (such as when going from indoors to outside on a sunny day) or will be seen wearing sunglasses whenever outdoors or even indoors under bright light.

Another problem related to lowered mineralocorticoid levels in hypoadrenia is a paradoxical, non-pitting edema of the extremities. When the patient with hypoadrenia spills sodium and water into the urine and perspiration, and has a tendency to be dehydrated, we would hardly expect him to show signs of holding water, such as edema. But that is exactly what we do see in some hypoadrenic patients.

With the body spilling large amounts of extracellular sodium and likewise retaining intercellular potassium, we can see how an osmotic differential could develop in the patient’s tissues. If the osmotic difference (created by the increased potassium seeking its intercellular position and the lowered extracellular sodium levels) is severe enough, the body will most often attempt to correct this osmotic imbalance by allowing extracellular fluid to enter the cells. (It is also possible that the body could kick the potassium out of the cell and into the extracellular fluids, and although this occasionally occurs, we rarely see signs of this in the blood potassium levels.) The body is trying to dilute the potassium in the cell with water, to bring the system into osmotic equilibrium. The cells take on water, and the patient has swelling.

Often, these patients are placed on a diuretic by an unenlightened physician whose only basis for this prescription is the patient’s symptoms. The diuretic in these patients rarely helps the condition and often aggravates the tendency toward dehydration. Further, many diuretics act as adrenal (aldosterone) inhibitors, adding even more stress to the adrenals and tending to make the patient worse in the long run.

-----

Also, a few quick comments:
1. In statistics, there is a term known as "sampling bias". Basically, when a certain population is elicited, the statistics that are derived from it will be skewed.The title of this thread and the startling nature of failing the pupil test dictate that those who fail the test will post, thus skewing the results. However, just because we have seen around 15 people fail the test, does not NEARLY indicate that it is average to fail the test. I.e., this test is not baloney, as was suggested by one individual.
2. Aldosterone deficiency is almost guaranteed to be concomitant with a larger problem of the adrenals or HPA axis in general.
3. It will do immensely more for your energy and focus to address these adrenal issues than using something like Piracetam ever will. Being healthy should be your primary concern, before looking to obscure drugs and vitamins.
4. If you failed the pupil reflex test, it would be a big mistake to brush it off as non-consequential. Please educate yourself and pursue the issue.

Edited by acantelopepope, 15 November 2009 - 07:50 AM.

[meursault]

This is a slight aside from the current discussion on this thread, but...

Many people supplement choline with piracetam because piracetam modulates cholinergic neurotransmission. However, piracetam also modulates glutamatergic pathways.
It might be worth experimenting with glutamic acid supplementation and piracetam.

[Dumbel]

It might be worth experimenting with glutamic acid supplementation and piracetam.

I did glutamic acid for about 2 weeks before i started with piracetam (for about 1 week now with ~15g per day). I didn`t have any benefits or negative effects from piracetam yet - and so does my girlfriend, absolutely nothing yet.

But soon my pregnenolone arrives. I will give it a try then.

[Peterlau]

Hi there,

FYI, I just did the test and I find my pupil fluctuates during the test.

I am a non-responder of piracetam.

Do you need more information of my supplement intake?

[cheesycow5]

Maybe change the title to "Piracetam responders"? Or start a new thread.

[John W.]

Maybe change the title to "Piracetam responders"? Or start a new thread.

Agreed, otherwise there is a sampling bias, or at least something of an assumption we're making about responders from no posts by them. It seems most likely this pupil thing is probably not an average response, even for those taking piracetam, but the thread would definitely be more persuasive with more responder posts.




Also, something else to consider - 5-HT (se. Speaking of the pupil response we are all having, an English Doctor noted (and this seems to be standard medical opinion now) the following:

"Dr. James concluded the abnormal pupil response is a result of some kind of interference in the transfer of impulses from the brain to the eye.

He believes ME is the result of a deficiency of a neuro-transmitter called 5HT, whose job is to pass impulses through nerves to cells. The eyes of ME sufferers treated with 5HT behave normally.

"I do not yet know how the ME virus causes abnormalities in 5HT transmission but it does inhibit its function," says Dr. James. By administering drugs to stimulate levels of 5HT together with treatment aimed at fighting postviral disease, Dr. James believes ME sufferers can be cured.
...
Many sufferers are perfectionists who take on a mammoth work load. They cannot switch off. If they are laid low by a virus, they do not recover from it properly and there is where the problems start."


Also, if you just google 5-HT and CFS or ME (chronic fatigue syndrome) there is a ton of discussion of 5-HT. What I'm unsure of is which comes first -- 5-HT deficiency and then chronic fatigue syndrome (or the pupil test we've failed), or if its vice versa. 5-HT is incredibly involved in the same processes of piracetam, and 5-HT receptors also modulate the release of GABA and acetylcholine. What I'm saying then is that the pupil fluctuations actually suggests seratonin deficiency, as the above Dr. was noting (and this could be either secondary to, or somehow culminating in CFS or adrenal fatigue) If piracetam is rough on our seratonin, this could explain some brain fog (given seratonin's role in neurotransmission), and the fact that some of us don't respond -- if seratonin takes a hit by piracetam, then we wouldn't feel beneficial cognitive effects with low seratonin. Moreover, it could explain how some people take it and have some benefits at first, but then have less as time goes on (eg seratonin dwindles as they take piracetam, until it is low enough that the piracetam is no longer effective). It could also explain why some people report depression from piracetam.

Towards this interpretation, I saw a study the abstract of which concluded "The contents of NE, DA, and 5-HT and their metabolites in the brain were significantly decreased after piracetam administration". I also found several other studies backing this up, the most interesting of which was a comparison (here) between piracetam and aniracetam through analyzing their actions on 5-HTP.


This is a lot to process for me right now so I'm basically just throwing info out there without assimilating it. One thing I wouldn't understand given the 5-HT connection is why I am a non responder and fail the pupil test - given that I am on an MAOI. Could be that I just started it, I don't know.

Given the risk of seratonin syndrome, I shouldn't take 5-HTP. However, if low seratonin is what is causing people to be non responders to piracetam, and to fail the pupil test, 5-HTP might be able to fix this, so would anyone be willing to try 5-HTP for a while and share their experience?

I am also curious about more info regarding seratonin and us non-responders -- so if anyone could add any info about seratonin and you, as a non responder (do you feel depressed? Are you on an anti-depressant? Has anyone ever noticed piracetam worked for them after their anti-depressants began to kick in? etc.) it might help us out here.

[acantelopepope]

Maybe change the title to "Piracetam responders"? Or start a new thread.

Agreed, otherwise there is a sampling bias, or at least something of an assumption we're making about responders from no posts by them. It seems most likely this pupil thing is probably not an average response, even for those taking piracetam, but the thread would definitely be more persuasive with more responder posts.




Also, something else to consider - 5-HT (se. Speaking of the pupil response we are all having, an English Doctor noted (and this seems to be standard medical opinion now) the following:

"Dr. James concluded the abnormal pupil response is a result of some kind of interference in the transfer of impulses from the brain to the eye.

He believes ME is the result of a deficiency of a neuro-transmitter called 5HT, whose job is to pass impulses through nerves to cells. The eyes of ME sufferers treated with 5HT behave normally.

"I do not yet know how the ME virus causes abnormalities in 5HT transmission but it does inhibit its function," says Dr. James. By administering drugs to stimulate levels of 5HT together with treatment aimed at fighting postviral disease, Dr. James believes ME sufferers can be cured.
...
Many sufferers are perfectionists who take on a mammoth work load. They cannot switch off. If they are laid low by a virus, they do not recover from it properly and there is where the problems start."


Also, if you just google 5-HT and CFS or ME (chronic fatigue syndrome) there is a ton of discussion of 5-HT. What I'm unsure of is which comes first -- 5-HT deficiency and then chronic fatigue syndrome (or the pupil test we've failed), or if its vice versa. 5-HT is incredibly involved in the same processes of piracetam, and 5-HT receptors also modulate the release of GABA and acetylcholine. What I'm saying then is that the pupil fluctuations actually suggests seratonin deficiency, as the above Dr. was noting (and this could be either secondary to, or somehow culminating in CFS or adrenal fatigue) If piracetam is rough on our seratonin, this could explain some brain fog (given seratonin's role in neurotransmission), and the fact that some of us don't respond -- if seratonin takes a hit by piracetam, then we wouldn't feel beneficial cognitive effects with low seratonin. Moreover, it could explain how some people take it and have some benefits at first, but then have less as time goes on (eg seratonin dwindles as they take piracetam, until it is low enough that the piracetam is no longer effective). It could also explain why some people report depression from piracetam.

Towards this interpretation, I saw a study the abstract of which concluded "The contents of NE, DA, and 5-HT and their metabolites in the brain were significantly decreased after piracetam administration". I also found several other studies backing this up, the most interesting of which was a comparison (here) between piracetam and aniracetam through analyzing their actions on 5-HTP.


This is a lot to process for me right now so I'm basically just throwing info out there without assimilating it. One thing I wouldn't understand given the 5-HT connection is why I am a non responder and fail the pupil test - given that I am on an MAOI. Could be that I just started it, I don't know.

Given the risk of seratonin syndrome, I shouldn't take 5-HTP. However, if low seratonin is what is causing people to be non responders to piracetam, and to fail the pupil test, 5-HTP might be able to fix this, so would anyone be willing to try 5-HTP for a while and share their experience?

I am also curious about more info regarding seratonin and us non-responders -- so if anyone could add any info about seratonin and you, as a non responder (do you feel depressed? Are you on an anti-depressant? Has anyone ever noticed piracetam worked for them after their anti-depressants began to kick in? etc.) it might help us out here.

This is a much different direction than I originally anticipated, but the ideas are intriguing. I might post more details later, but here's the short story: I began taking piracetam in November '08, just about a year ago, after being put on Wellbutrin 100mg SR since early October for Major Depression. I was feeling better on the Wellbutrin and other supplements I was taking like Rhodiola and L-Tyrosine, but my cognition was still not anywhere near the level I deemed acceptable. I had a hard time following lectures, participating in discussions, etc. About 4-5 days after I started taking 1fast400 Piracetam this all began to change. By early December, I was ecstatic at my verbal dexterity and extremely improved sociability. This only got better all the way until February of '09. It wasn't until the middle of March that these effects really began to wane, and I started feeling extremely tired, irritable, cynical, and "depressed". I grasped at everything I could think of to bring back piracetam/aniracetam's positive effects, but I only felt worse and worse, until I hit rock bottom from June 1st to early August. It wasn't until I completely cut out piracetam/aniracetam/choline that I began to feel even somewhat good again. I have been grappling with the cause of my continued lethargy and depression issues since then, and until I began taking an Iodine and Adrenal supplement, I was losing hope. Now, I have been diagnosed hypothyroid, and I am working out a plan to help my thyroid and adrenals recover. Once those are restored, then I believe piracetam will again have its positive effects on me. I look forward to that.

My pupils fluctuate a lot less now, and I attribute it primarily to the 1-2tsp iodized sea salt I take daily. This is NOT restoring aldosterone levels, but it is correcting the electrolyte imbalance caused by a faulty potassium/sodium ratio (see my last post). They still are not nearly "normal," but they are a lot better, and seeing this improvement is very encouraging. I recommend everyone begin taking iodized sea salt daily.

[Viscid]

Guys, pupil oscillations are completely normal. It is not a result of any deficiency.

Here's a book on it.

http://books.google....d=0CDcQ6AEwCTgK

This is a dumb test and a dumb thread with no relevance whatsoever to piracetam's effectiveness.

Oh and it's spelt "Serotonin"

[John W.]

Guys, pupil oscillations are completely normal. It is not a result of any deficiency.

Here's a book on it.

http://books.google....d=0CDcQ6AEwCTgK

This is a dumb test and a dumb thread with no relevance whatsoever to piracetam's effectiveness.

Oh and it's spelt "Serotonin"

Thanks for the the heads up on having misspelled serotonin. However it is easier to avoid misspelling when your entire reason for posting is only to criticize other people, and not actually add anything useful or constructive. So don't judge me too harshly...

Secondly, I suggest you actually read the test you posted rather than acting like a 13 year old "dumb test, dumb thread". I apologize if you actually are 13. But yes, let me try to explain the one page you cited, since apparently even the pictures weren't obvious enough for you. In the PCT, a small slit of light is shined SOLELY AT THE VERY BOTTOM EDGE the pupil -- ergo when the pupil contracts to avoid taking in the light, it has time to expand to take in more light, and when it expands large enough to become stimulated by the small slit at the bottom, it repeats the process. And these cycles, between constriction and expansion, are the basis for testing. Of course this is common.

Was this how any of us did the test? I for one did not use a slit lamp or horizontal beam of light shined directly below my pupil. When we did the test with a light to the side, light fell upon the whole area of our eye, and there were fluctuations. This is completely different because there is no reason for fluctuation, since the light source hits the whole eye -- not the pupil until it constricts, at which point the pupil naturally would expand again until its hit. This fluttering of the pupil is not to be expected, and is not the norm. I don't know how to spell this out any clearer, and I don't know if this will mean anything to you since four very simple drawings apparently weren't enough.

If you're going to post, think before you do, and avoid simply attacking the thread and its posters. It just makes you look dumb.

Edited by John W., 18 November 2009 - 02:59 AM.

[acantelopepope]

Guys, pupil oscillations are completely normal. It is not a result of any deficiency.

Here's a book on it.

http://books.google....d=0CDcQ6AEwCTgK

This is a dumb test and a dumb thread with no relevance whatsoever to piracetam's effectiveness.

Oh and it's spelt "Serotonin"

The section you referenced is referring to the specific application of a "slit lamp" -- a beam of light .5mm in thickness (not your average flashlight, to put things lightly) to the very bottom portion of the pupil. The pupil constricts, removing it from the beam of light, at which time it expands again, placing it back in the tiny beam of light... and the cycle of oscillations continue.

Needless to say, nobody here was using a beam of light half of a millimeter thick aimed with mechanical preciseness at the bottom-most portion of their pupil.

When a beam of light covers the ENTIRE AREA OF THE EYE, the pupil's job is to constrict. When it fails to remain constricted, this indicates an abnormality.

Here's three graduate researchers and a scientific review journal's assent to the vailidity of the aldosterone/pupil reflex connection, in case you were too dense to understand the link that you just erroneously posted.

A Pilot Study of Some Physiological
and Psychological Effects of Caffeine
Sanford Bolton, Ph.D.1
Martin Feldman, M.D.2, Gary Null, M.S.3
Emanuel Revici, M.D.3 and Linda Stumper, B.S.1
from the Journal of Orthomolecular Psychiatry, Vol. 13, #1

Pasted from <http://www.garynull.....htm#Footnote2>


The pupil in the normal subject reacts briskly and remains constricted as long as the light beam is present. If the body is severely sodium depleted, the pupilary constriction does not "hold" and the pupil oscillates. It may even fail to constrict at all. Although salt depletion may occur as a result of many abnormal physiologic processes, the most common is diminished adrenal function and diminished aldosterone and the subsequent chronic loss of sodium and chloride into the urine (Feldman).


Pasted from <http://www.garynull....feineStudy.htm>


Think about it. What good would the pupil reflex to sunlight be at protecting humans (and most animals with eyes) from excess UV rays if after constricting, they just dilated again--flooding your eyes with extreme brightness? It wouldn't be useful at all, and if it were normal, we'd all have much worse vision. Clearly the inability to sustain constriction is abnormal.

Oh, and nobody cares about spelling except your middle school English teacher. Save your ignorant slander for grade school.

[hyper_ventriloquism]

With a chronic sodium-potassium imbalance, the person will show the sign of a paradoxical pupillary reflex. Normally, shining a light into a person’s eye will cause the pupil to constrict. This papillary constriction to light should be able to maintain itself for at least 30 seconds. In the hypoadrenic person (especially in the exhaustion stage of the GAS) you will find one of three things:

1. The pupil will fluctuate opened and closed in response to light.

2. The pupil will fluctuate opened and closed in response to light. (This is a deliberate opening and closing, not the minor flutter or twitch of the normally encountered hippus activity.)

3. The pupil will initially constrict to light, but it will dilate paradoxically with continued light stimulation of less than 30 seconds. This patient will frequently complain of eyes that are sensitive to light (such as when going from indoors to outside on a sunny day) or will be seen wearing sunglasses whenever outdoors or even indoors under bright light.

I think we can shorten this to two symptoms, since #1 and 2 are the same, ha. Also, note that in #2 minor flutter is said to be normal. I interpret this to mean that repeated slight dialation and constriction is normal as long as the pupil stays small. What is not normal is when the pupil fails to stay constricted in response to the light. This is how I interpret the above quote.

My pupils stay very constricted overall, but fluctuate slightly. I think this is normal. I started piracetam three days ago at 1 gram three times per day, no attack dosing. I've noticed some nice effects so far. Tomorrow, I'll add choline to the mix.

[acantelopepope]

With a chronic sodium-potassium imbalance, the person will show the sign of a paradoxical pupillary reflex. Normally, shining a light into a person’s eye will cause the pupil to constrict. This papillary constriction to light should be able to maintain itself for at least 30 seconds. In the hypoadrenic person (especially in the exhaustion stage of the GAS) you will find one of three things:

1. The pupil will fluctuate opened and closed in response to light.

2. The pupil will fluctuate opened and closed in response to light. (This is a deliberate opening and closing, not the minor flutter or twitch of the normally encountered hippus activity.)

3. The pupil will initially constrict to light, but it will dilate paradoxically with continued light stimulation of less than 30 seconds. This patient will frequently complain of eyes that are sensitive to light (such as when going from indoors to outside on a sunny day) or will be seen wearing sunglasses whenever outdoors or even indoors under bright light.

I think we can shorten this to two symptoms, since #1 and 2 are the same, ha. Also, note that in #2 minor flutter is said to be normal. I interpret this to mean that repeated slight dialation and constriction is normal as long as the pupil stays small. What is not normal is when the pupil fails to stay constricted in response to the light. This is how I interpret the above quote.

My pupils stay very constricted overall, but fluctuate slightly. I think this is normal. I started piracetam three days ago at 1 gram three times per day, no attack dosing. I've noticed some nice effects so far. Tomorrow, I'll add choline to the mix.

You're misinterpreting "response to light". The authors here mean that the pupil will "close" when light is shone directly upon it, and it will "open" when that light becomes absent. Therefore, it will open and close "in response to light"-- but it should not close then open and stay open under a beam of light.