i picked up one like this for about $10 http://www.ebay.ca/i...c6cc2569&_uhb=1
That one doesn't register small mg increments (i.e.you don't know if you have 3 or 6mg).
Edited by Megatrone, 24 May 2013 - 03:35 PM.
Posted 24 May 2013 - 03:35 PM
i picked up one like this for about $10 http://www.ebay.ca/i...c6cc2569&_uhb=1
Edited by Megatrone, 24 May 2013 - 03:35 PM.
Posted 24 May 2013 - 03:40 PM
i picked up one like this for about $10 http://www.ebay.ca/i...c6cc2569&_uhb=1
That one doesn't register small mg increments (i.e.you don't know if you have 3 or 6mg).
Posted 24 May 2013 - 05:13 PM
Posted 24 May 2013 - 08:02 PM
Transitioning to new and better habits is a process that I'm currently working to complete. The night before last I made a terrible decision in staying up very late to study knowing I had to get up early. In the past I've done this without too much backlash, however, this is my first experience while using nootropics and the last two days have been a struggle.
There have been some reports of positive effects when sunifiram consumers sleep slightly less 5-6hours.
Mine is a report of fatigue and lack of focus with a meager ~2.5 hour segment of sleep. I would attribute the slow recovery to my study attempts for finals during the recovery process.
This is likely a symptom of my behavioral patterns combined with nootropics. I have trouble managing a consistently balanced lifestyle. With noots the main issue seems to be finding rest / feeling unstimulated by anything minimally challenging or with purely entertainment based activities. It is especially so for those things that exhibit both of these qualities e.g. a fast paced purely action movie and anything that is blatantly one dimensional.
welp theres my 1.5 weeks into suni update.
Posted 24 May 2013 - 09:19 PM
I think living and expectations (not work and education) put on you in general is pretty hard. Therefore, I live my life by routines, and I cannot understand impulsiveness and spontaneity.Before I do something, everything needs to be well planned.
Posted 24 May 2013 - 11:43 PM
Posted 25 May 2013 - 12:02 AM
Posted 25 May 2013 - 12:23 AM
Posted 25 May 2013 - 12:26 AM
Edited by Isochroma-Reborn, 25 May 2013 - 12:47 AM.
Posted 25 May 2013 - 12:50 AM
Edited by Isochroma-Reborn, 25 May 2013 - 12:54 AM.
Posted 25 May 2013 - 02:47 AM
Posted 25 May 2013 - 07:16 PM
Posted 26 May 2013 - 08:51 PM
Edited by deeptrance, 26 May 2013 - 08:55 PM.
Posted 26 May 2013 - 09:02 PM
As many others have reported, sunifiram has had negative consequences on my sleep cycle and the problem has been getting worse over time. Last night I slept from 3AM to 6:30AM and couldn't go back to sleep. I can lie down all day and drift out of focus but not go to sleep, so napping doesn't work. Given that sleep is so crucial for mental, emotional, and physical health, I think it's likely that I'm an idiot for continuing to take sunifiram
Posted 26 May 2013 - 09:11 PM
Edited by Isochroma-Reborn, 26 May 2013 - 09:11 PM.
Posted 26 May 2013 - 09:12 PM
Posted 26 May 2013 - 09:14 PM
Posted 26 May 2013 - 10:44 PM
Posted 27 May 2013 - 12:31 AM
Posted 27 May 2013 - 09:19 AM
Posted 27 May 2013 - 03:30 PM
Posted 27 May 2013 - 09:48 PM
Posted 27 May 2013 - 10:18 PM
Magnesium, especially magnesium threonate, alone should cancel out some of the excess excitation. Similarly, I expect that potassium, calcium, and low blood glucose will make the excitation stronger. Note that too much brain magnesium will be anti-LTP and pro-apoptosis of neurons; balance it well.I've been doing a lot of research today on the role of glutamate in neurotransmission and various physiological and mental functions. What I've recognized is that I am hypersensitive to glutamate and anything that is glutamatergic.
No such thing. How about the term ampakines?racerams
Edited by Climactic, 27 May 2013 - 10:20 PM.
Posted 27 May 2013 - 10:30 PM
Posted 27 May 2013 - 11:04 PM
Posted 28 May 2013 - 03:26 AM
Magnesium, especially magnesium threonate, alone should cancel out some of the excess excitation. Similarly, I expect that potassium, calcium, and low blood glucose will make the excitation stronger. Note that too much brain magnesium will be anti-LTP and pro-apoptosis of neurons; balance it well.I've been doing a lot of research today on the role of glutamate in neurotransmission and various physiological and mental functions. What I've recognized is that I am hypersensitive to glutamate and anything that is glutamatergic.
No such thing. How about the term ampakines?racerams
Posted 28 May 2013 - 04:07 AM
Correct, you can get the required omega-3 oil from concentrated oils with fewer grams.
I'm cheap & poor so I eat 213g cans of Pacific Wild Salmon - two per day.
According to the label each can contains 16g fish oil.
As for sleep, wow!
I'm waking up at 5.5 hours but I can easily go back to sleep and reach 8 hours.
The dreams are stunningly real and my memory is working to a degree thought impossible mere months ago.
When I close my eyes during the day I get hyperrreal recall and visualization of images.
My memory has improved to the point where I am remembering everything, including the names of thousands of MP3 files - just looking at the file causes the music to start playing in my mind. It was a shocker so yesterday I assembled a new CD with 67 tracks (in ISO/Romeo file mode). It was enormously fun and a bit more to listen to those tracks and hear so much fresh new detail.
Somone turned the World on again for me. Something - Sunifiram.
Edited by alecnevsky, 28 May 2013 - 04:11 AM.
Posted 28 May 2013 - 04:17 AM
Not sure why you would take a mutagenic form (orotate) of magnesium when there are other good forms available.Could your reference too much magnesium on LTP claim? I am taking 1g a day of orotate
Mg++ blocks N-methyl-d-aspartate (NMDA) glutamate receptor ion channels, preventing ion flow at typical neuronal resting potentials.10 Divalent cations, including Mg++ at mM concentrations, decrease the activation of voltage-gated channels through surface charge screening effects,11, 12, 13, 14 thereby reducing neuronal excitability. Mg++ at high extracellular concentrations also blocks Ca++ influx and diminishes synaptic transmission.15
Recent evidence suggests that relief from long-term Mg++-induced inhibition might result in homeostatic increases in long-term potentiation and plasticity.20
Chronic incubation of neurons with elevated concentrations of KCl in the culture medium has been shown to protect neurons from apoptotic cell death resulting from over-inhibition and from neurotrophic factor deprivation.23, 28, 29, 30, 31 KCl depolarization is thought to prevent apoptosis by moderately increasing intracellular Ca2+ concentration.30 If Mg++ acts by decreasing neuronal activity, we would hypothesize that treatment with KCl would counteract the effect of Mg++.
We found that KCl significantly protected against both spontaneous neuronal death and against cell death induced by MgSO4 (Figure 2d).
Although Mg++ has complex effects on cellular excitability, including both excitatory and inhibitory influences, our data indicate that the overall inhibitory influence of Mg++ accounts for decreased neuronal survival with prolonged exposure. In spite of a surprising depolarization of resting potential, the net effect of Mg++ is inhibitory, as shown by recordings of network activity. Decreased excitability triggers neuronal death, and depolarization with potassium protects against death.
Endogenous magnesium maintains cell function, integrity, and energy production, and extracellular Mg++ modulates a variety of different ion channels and receptors, including NMDA receptors,10 Ca++ channels,36 GABAA receptors17 and voltage-gated channels.11, 12, 32 Manipulation of each of these channel types has been shown to affect cell survival during developmental synaptogenesis, when many neurons undergo physiological cell death.31, 34 The common theme with apoptotic neuroactive agents, including Mg++, is that neuronal activity is strongly suppressed. In susceptible, developing neurons activity suppression activates an apoptotic ‘trigger’. This common trigger could be reduced intracellular Ca++,30 but the trigger set-point can be influenced by environmental factors.29
developing neurons and neuronal networks require an appropriate level of active input for proper development and survival. Clinically relevant Mg++ concentrations kill neurons at this stage by dampening excitability and increasing apoptosis.
Edited by Climactic, 28 May 2013 - 04:26 AM.
Posted 28 May 2013 - 04:19 AM
Edited by Isochroma-Reborn, 28 May 2013 - 04:39 AM.
Posted 28 May 2013 - 04:52 AM
Edited by Isochroma-Reborn, 28 May 2013 - 04:54 AM.
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