the cause of my 3AM-5AM insomnia

I have this typical insomnia:

  1. fall asleep easily
  2. wake up at 3AM
  3. lie awake for about two hours, being wide awake, very alert

Upon examination there are a few characteristics to consider:

  • I wake up sweaty, with a heated body. I can’t go back to sleep unless I cool down. This points towards some sort of stress reaction my body is having, causing me to wake up.
  • The mental alertness is ridiculously high. It’s like I have a pinball machine in my head. It’s not anxiety, it’s more a superability and -willingness to solve a problem. This is a dopamine excess.
  • The 3AM is not 3AM. The insomnia occurs pretty much precisely 4,5 hours after I fall asleep.

These three things: stress reaction; dopamine excess and 4,5 hours interval have now led me to the cause of my insomnia. It has to do when the internal workings of the machine trigger the neural wiring which reacts violently.

A small intestinal problem triggers my overexitable neurotransmitters.

It takes 4,5 hours for food to traverse the small intestines. It then enters the colon. There, in my case, it remains. It doens’t travel up the ascending colon because it cannot make the curve near the liver (there’s probably an air bubble blocking the way). Food keeps being piled on and the right vertical part of my colon expands, causing stress, waking me up. Since the enzyme that’s supposed to break down stress hormones is broken in me, the MAO A enzyme, my levels of noradrenaline (=norepinephrine) and dopamine are getting very high. Causing me to lie awake for 1,5 to 2 hours, frantically  writing speeches on Important Subjects. During this time my cortisol is depleted and my growth hormone doesn’t get the time of day (I’m robbed of a significant portion of REM sleep). This is a large tax on the body and leaves me with diminished capacity for getting out of bed the following day and healing properties, especially now that I’m over 25 and my endo-glands can no longer make up for such a plundering.

There we have it. A simple blockage leads to a build up in the right colon which makes my body cry out. Triggering the release of too many excitable neurotransmitters.

Again it’s the imbalance between Sympathetic Nervous System (SNS) and the Parasympathetic Nervous System (PNS), which both have so much to do with the perifere location: the gut.

My balance is skewed in favour of the SNS due to a homozygous mutation of the MAO A  gene and a life time of training to be in Fight or Flight. I can unlearn the latter. I can only influence and work around the former.

Gut motility is mostly governed by PNS. It’s the modus of Rest & Digest in opposition of SNS’s Fight or Flight. Looking at particular neurotransmitters I’ve now learned that as soon as dopamine rises the stomach is reluctant to release its content. This is why a dopamine-antagonist (Domperidone) is prescribed to people with nausea and vomiting (Dutch link). And this is why I have to go lie down about an hour after I have ingested food. The stomach takes 45 minutes to break down the first bites I took and is now ready to release it. I need to make room for PNS to do its thing and the only way I know how to at the moment is to lie down and relax. As soon as I do so my upper GI tract starts gurgling. If I don’t lie down I’ll grow weary and moody as the day progresses and I’ll be devilish in the evening and have hellish insomnia at night.

Motility in the small intestine is dependent upon having enough of the PSN neurotransmitter Acetylcholine and by activating lots of serotonine receptors. Having bad MAO A is a good thing here, serotonine is soaring and there should be one for every receptor. As soon as I lie down at night the small intestine starts happily motoring things along. In 4,5 hours it has emptied all it had into the next portion of the gut via the one way ileocecal valve into the colon. Luckily I have no problems there. For some this valve flutters and lets stuff and bacteria creep back into the small intestine.

We’ve all seen the picture of how the colon lies in the belly:

The colon rises up, all the way to the liver, then bends to the left, traversing in front of the stomach exit to the spleen area. There’s another bend downwards and then it ends in the temporary holding station called Sigmoid Colon.

Which is true for only about 5% of humanity. In most of us the colon is going wherever it wants. Diagonally to the spleen. Bending backwards. Bulging inwards into small intestine territory. So don’t take anything for granted, these idealistic pictures are just theory.
This colon is more likely:
 pic by Glitzy queen00, radiographer in the UK

I don’t know the route my colon lies. I can feel contents at certain places so I have some idea. But I suspect at the Traverse Colon things are iffy. Interfering with the stomach exit and the duodenum, where also the major PNS nerve is located, the Nerves Vagus.

At the right bend, the Hepatic Flexure, its location is probably irritating the liver. I often have a heavy feeling there, bordering on pain. And now I know that something is hindering process in the night. My GP suggested a mechanical issue: an air bubble is trapped in the Hepatic Flexure, preventing passage. He made the analogy with a bottle with air trapped in it: you can’t pour the liquid in a smooth motion.

I can work with mechanical problems. The solution is to lie on the right side. The air travels upwards, into the Traverse Colon. I’m using breathing as a motion device, the expanding and contracting lungs are the main mechanical force on organs, making them move and shift. It’s a natural thing. A good thing.

When I had an echo done of the liver I had to breathe out and hold my breath. The lungs forced the liver to peek out from under the ribcage and the technician could scan it.  It looked so beautiful! Things were moving and fluids were flowing and we saw all kinds of channels. It was such a marvel. Movement through breathing is very good for the internal organs.

After 5 to 20 minutes I turn on my back. I now lift my pelvis to the roof, resting on my feet and shoulderblades. This is a trick I learned when I went in for a pap smear and the cervix was not there. Somehow the uterus had shifted or folded back and hidden the cervix out of sight. I was asked to do these gymnastics so it may shift to another position. Mechanics. Everything shifts in there, nothing’s stationary. Organs are lying next to each other and are all able to shift and move.

There’s an excellent system in pace to allow for these movements. It both secures the internal organs to the scaffolding (the skeleton) and it lubricates the surfaces so there’s no chafing. It’s the Mesentry, a thin layer of epithelial cells surrounding all organ parts, like pieces of clingfoil taped to the back wall at various points:

 pic by blumdesign.com

The architectural structure of the mesentries is amazing, with small gutters transporting the fluid all around. Breathing and moving and muscular movements aid this system. Go check out non-profit educational site The Radiology Assistent for excellent images and explanations of many internal organs and structures.

I’m still on my bed, pelvic to the sky. I’m again using my breath to move things along. When breathing out I can manually manipulate the downwards colon on the left side a bit, trying to help it transport the air bubble to the exit. After just a few minutes I’ll feel the need to pass some gas. It’s only a little bit and I cannot believe that this is actually the bubble that was stuck at the Hepatic Flexure. But I have a result and I’m glad with it.

I now do this in the evening, before I go to bed. And during the day, when I take my hour rest. And at night, should I wake up. My insomnia is less severe because of this, there’s less dopamine produced. I still lie awake but now I’m a docile book, not a screeching video game. I have reduced the stress reaction. But I have not eliminated it yet.

 pic by amazon

I’m looking into a better motility of the colon. It’s not only air in the Hepatic Flexure, I’ve also noticed slow transit in the Traverse Colon. Then there’s considerable build up in the Sigmoid Colon to examine. And there’s a lack of neural signalling that I need to go, either #1 or #2.

Then there’s the food I eat that influences bulk, consistency, roughage and gas production. I already know to stay away from onions, beans and whole grains. Also carbohydrates make for a more severe insomnia, especially potato products. Which lead my GP and me to assume glycemic problems almost 15 years ago when I entertainingly mentioned how a potato dinner would keep me more wide awake at night than other dinners. Having been down the whole blood sugar route I can now say this is not an issue. But experiencing an insuline peak during the day does trigger the SNS for which I pay during the night. So sugar is still bad, but for a different -and far more serious- reason. Insulin is a potent poison, it should be engaged very prudently.

There, I’m done for today. There’s a lot to be sorted. Especially learning how/which neurotransmitters dampen the motility. Looking at you, dopamine. How to enhance the numbers for Acetylcholine? There’s a loop into the Methylation Cycle there that complicates things. There are probiotics that can help with signaling for defeacation. And how I can give PNS more time of day? I’m already grumbling that I have to lie down for an hour trice a day. But I gotta keep that pinball machine chilled if I ever want to sleep through the night and reap the benefits of both cortisol and growth hormone the following day.

A few more things to park here for future pick up:

1. Strengthening the gut muscles is a separate avenue to travel. One that works well for a lot of people, including a lot with Irritable Bowl Syndrome (IBS) (this is a link with the best instructional video for swinging a kettlebell). I’ve started kettlebelling which is a fun thing to do. I keep mine in the kitchen and kettle the bell a few times while I wait for the tea water to boil. Nothing on a schedule, no counting, . Keeping it fun. I already notice that there’s a certain pleasure in keeping your body upright using the core muscles, instead of stacking all your organs on top of each other and leaning on them. Sitting upstraight on a chair, like I was a woman from a 100 years ago, is pleasurable. Standing straight too. I’m stacking vertebrae instead of organs.

2. The stretching in the ascending colon activates trigger points causing sympoms. They are the reflex zones of the colon:

reflexzones dikke darm

The symptoms that occur at night in my insomniatic period are all noted in the reflex zones of the ascending colon: irritated and stuffed nose; oversensitive sense of hearing (fear triggering); strained eyes; soar throat and tonsils; extra pain in my right shoulder impingement. I have no issues with the other organs noted in this picture, apart from bladder and uterus which are at the sigmoid end.

These symptoms, especially of the allergy kind in tonsils, throat and nose, have thrown me off scent for the longest time. I kept thinking it was dry air or dust mites that kept me awake at night. But it’s the other way around: only if I wake at night dry air and dust mites become a problem. If I sleep through the night they don’t bother me.

3. pH in gastro tract.

4. osteopatic views on movement in and amongst internal structures. Link in Dutch.

5. the various types of motility in the intestines. one link and link to Flash card notes.

6. duodenic colic reflex makes you want to go #2 when the stomach fills up.

7. MAO A influencing when it’s already bust. Progesteron; B2; Ginko Biloba. Progesteron!

and to be perfectly clear: for years I’ve researched all the usual suspects for insomnia. Blood sugar; glycogen; sleep hygiene; circadian rhythm; melatonin; dual sleep; Chinese organ clock; you name it I’ve looked into it. It has done nothing. I could have guessed since I’ve had this sleeping pattern all my life, through every stage of health and constitution.

This now is the first approach that ticks all the boxes, explains everything and gives positive preliminary results when I tweak the dials that are involved.

For other people experiencing this type of insomnia I suggest assuming your body too is experiencing some stress reaction and figuring out what causes yours. I doubt it’s the same colonic issue I have but it might be. Especially if your MAO A gene is faulty you’ll recognize the alertness of your insomnia. This is separate from what causes the stress reaction. But if you are homozygous for MAO A then your dopamine is too high and interfering with stomach emptying and colon motility.

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Sleep: progesterone pill works

Here are my sleeping hours of the previous month:
slaapuren jan 2014

Quite a lot of nights I slept through! (compared to my usual sleeping pattern)
In yellow when I took a progesterone pill to bridge the gap from nonREMsleep to REMsleep. I upped the dose as my period drew closer. This did not always work.

And here it’s sorted without taking into account the time the clocks said I went to sleep. Each purple block is 15 minutes of sleep:
slaapuren gecorrigeerd
compared to my record of the previous month, without prog pills:

In yellow is when I took a 100mg Progesterone pill. This is Utrogestan, the bio-identical hormone.

On some nights I didn’t sleep through. There were some causes: I did an earthing experiment around 17th of December. This messed me up, had my brain overexcited for three days afterwards.
The Atlas Profilax treatment may have had something to do with the nightmare I had.
The massage might have released all kinds of toxins.
On Jan 8/9 I took a lot of folinic acid (leucovorin) which releases too much excitement on my brain, I feel. I also forgot to take Valerian.
Then, as my period drew neared even two pills did not have the desired effect.
On Jan 21st I laid awake all night with terrible pains, from the baby carrots I had eaten the day before.

So it is important for me that my intestines are comfortable (foodwise + HCL help); that I take my Valerian each evening; that there are no sounds waking me up (especially deep rumbling sounds) and that I take a progesterone pill right before going to sleep.

Sleep: slept through! Theory to the test.

Last night I took a Progesterone pill and I slept through the night on an unusual day of my cycle (day 13). I woke up refreshed and extremely happy. This supports the theory I’ve cobbled together in the last few days.

The happiness came from high serotonin and noradrenaline, I felt. And of having a good night sleep and perhaps having found another sensible theory!

On a side note:
I have noticed I’m quite excited the last few days.The amount of blog posts is indicative. This is “excited brain” on display. Not a good thing per sé.
And I feel a little sheepish that you all can see it.

I think it comes from the mB12 and Folinic Acid supplementation causing all kinds of waste to come free (akin to Copper Dumps) and raising noradrenaline. (the last week I’ve laid awake for 3 hours or more instead of the usual 1,5-2 hours). Aided by the Atlas Profilax treatment that activates overall my Sympathetic Nervous System is having a good time at the moment.
Luckily I succeed at shutting it up twice a day, when I take my horizontal rests.

The only other thing I know to do is be physically active during the day (I háve to walk outside every day since the AtlasPROfilax) and lessen the mB12 and Folinic Acid. Take a small break from Methylation.

So I’m going to the motions and I know it. I hope to calm down to my regular self in the future.

COPIED POST
The post under this paragraph I wrote this morning for a Spanish guy on the RisingPhoenix.me forums that shares the same sleeping pattern as me. (should that be “as I”?)
It’s full of white space because brain fogged people need their words in small doses.

Hi,
I’ve got a theory for my sleeping 5 hours and then lying wide awake for 2, being very alert. It fits all the symptoms and medical data I have.

SHORT VERSION:
after 5 hours I get excess noradrenaline on the brain. This prevents GABA rising and REMsleep commencing and makes one very alert.

Oral supplementing of the neurotransmitter Progesterone makes me sleep for 7 or 8 hours straight. Maybe because one of its metabolites, Allopregnanolone, dampens neurons firing and promotes GABA. It is as potent as benzo’s and sleepingpills, which is what most people use for this kind of insomnia.

Progesterone is NOT a female sex hormone.

LONGER VERSION:
In the brain a small amount of noradrenaline is needed after the 4,5 hours of nonREMsleep to stop the REM-off neurons from firing and let REM-on neurons start. When REM-on neurons get active GABA will rise and REMsleep will start.

REM sleep depends on high GABA.

Too much noradrenaline makes this impossible. GABA will not rise and insomnia will cause more noradrenaline. Noradrenaline is the neurotransmitter that makes you very very alert.

Reason might be MAO A not breaking down noradrenaline sufficiently due to a mutation.

Another reason might be too low Progesterone (I have this, tested and proven). Progesterone is not a female sex hormone, it is a human hormone. Testosterone is made from it. Cortisol is made from it. And it is a neurotransmitter in the brain.

In the brain Progesterone increases MAO’s activity slightly.

Progesterone’s most profound neuronal effect, however, results from its direct effect on the neuronal membrane. Progesterone has an inhibitory effect on neuronal excitation, depressing neuronal firing.

One of its metabolites in the brain is Allopregnanolone. This is a neuroactive steroid that does something with GABA. It has a potency similar to that of the most potent benzodiazepines (Valium etc) and approximately a thousand times higher than pentobarbitals (sleeping pills).

(I still need to check my sources but this one put me onto Allopregnanolone and this one researches REMsleep)

CONTEXT:
Noradrenaline is noradrenergic, meaning to do with the Sympathetic Nervous System.
Onset of REMsleep and GABA is from cholinergic brain input, it is about the Parasympathetic Nervous System. (source here)
The nervous system is not limited to the brain, of course.

REMEDIES:
– stop noradrenaline from rising (how? how? How do I get the Sympathetic Nervous System to shut up?)
– stop REM-off neurons from continious firing (how? by taking benzo’s? by taking Allopregnanolone?)
– raise GABA (how? taking precursors?)

SUPPLEMENTING:
Taking GABA is useless, it cannot go through the blood brain barrier (BBB) because it is too big a molecule, say people on the forums here. If a GABA supplement does have a soothing effect it means your BBB is leaky (search forums on this, Hip and Gestalt say smart things about this)

Progesterone: only take progesterone, no progestins. Be vigilant about this. Read the label.

Take the oral pill, not the cream, someone one the forums here said the pill form is the only form that yields Allopregnonalone. As is my own experience too.

In Europe the (only) correct brand for Progesteron is Utrogestan. It is not over the counter. Your doctor will probably resist and needs to be educated. Both on Progesterone/Progestins and on males needing this basic hormone.

A 100 mg pill gets converted to 10mg active Progestrone (the liver filters out the rest, working hard). This 10mg is the dose a regular human body needs for a regular day, it’s a physiological doses. It is what a normal body produces on its own. Supplementing the full 10mg is too much for a man who -presumably- produces at least some of his own in his adrenals. Problem.

Females need more because they also use Progestrone to balance out Estrogens. Their physiological dose varies every day and can range from 10 to 60mg. (60mg on day 21 of cycle)

Larger Utrogestan pills (200/500mg) are for females in pregnancy. They may need much more than the daily 60mg to keep their baby on board which is where the hormone gets its name: PRO-GESTational-hoRmONE and our association with it being a female sex hormone.

HRT = RISKY
There is no knowing in advance how your body choses to convert the Progesterone. It may raise your Testosterone, your Cortisol, your Aldosterone. Taking too much may numb the receptors or lower your own production.
HRT is risky business. Always start low and go slow.

10 mg Progesterone is excess of what a man needs, I feel. I’d want 20 or 50mg pills to start with but these are not produced. You could cut open a capsule and take only the white liquid, I guess. It looks like paint.

One thing about taking physiological doses is that your body is able to get rid of it within the day. You are not overdosing as is often the case with conventional HRT or other drugs.

ME/CFS people probably have decreased capacity for elimination so should even take less, of any drug or supplement. On a positive note: we notice effects sooner so small doses give us information fast.

MY EXPERIENCE
On some nights I take 100mg Utrogestan pills for my menstrual cycle and then I sleep through the night every time, unless it’s the last week before my period. I was told sleepiness was a symptom of too high a dose. Now I am not so sure. It feels awful during the day and I avoid it. But at night I sleep well and wake up with new vigour. And now I found a plausible explanation for it.

As long as my liver can stand it and I wake up feeling refreshed I am now taking Progesterone at night. The correct thing to do is find out with how low a dose I sleep through. But because my need as a female differs each day and I have CFS I’m not up for cutting up pills and taking notes yet.

For you I have no quick solution, sorry. Only this theory that, to me, makes sense and fits both our symptoms.

UPDATE
I just learned the antibodies to GLUTEN also block conversion from glutamate into GABA.
Leaving ones brain with too much glutamate (*boing! boing!*) and not enough GABA (zzzzz…)

source = http://neuroendoimmune.wordpress.com/2014/06/03/is-gluten-making-you-overstimulated/

Neurotransmitters: progesteron on the brain

Just for funsies I was wondering about the relation between noradrenaline (NA) and progesteron in the brain. Any neurotransmitter interference there?

Boy! Did I hit the jackpot!
It’s only from one source and I haven’t had time to check out the source itself or other sources or research but if this is true it connects a whole lot of dots.

the source: sexualhealthmedicine.com

PROGESTERON AND SEROTONINE
Progesteron and oestrogens claim serotonine receptors in the brain. Oestrogens promote the growth of these receptors, progesteron decreases it. This can account for some of the depressive feelings during PMS (post menstrual syndrome, occurring at least one week before the period, when oestrogens drop and leaves behind a field of serotonine receptors who’ve got nothing to feed upon).

PROGESTERONE AND MAO
Progesterone increases MAO activity, Estrogens decrease its functionality (!!)
Meaning Progesterone promotes excitatory neurotransmitters getting catabolized, broken down, whisked away.

People with progesterone deficiency have their brain bombarded longer by excitatory neurotransmitters? (it fits the symptoms of Estrogen excess)
How about people with progesterone deficiency AND a faulty MAO A enzyme? oooh boy….

Estrogens numbs the MAO enzyme, allowing the excitatory neurotransmitters to keep bouncing around in your head. People with natural high levels of these neurotransmitters are active, excited and happy (depending on their individual signature of the mix).
People who are low on these neurotransmitters (ADD people perhaps) get depressed when their Estrogen levels drop and Progesterone keeps egging on the break down of the few neurotransmitters they have. They would have very depressive PMS.

But it might be more complex than this. Balancing hormones teaches us that hormones are not like scales: add a little here and it will decrease over there. No, it is more complex.
Having higher levels of a transmitter makes its receptors more numb for it and makes the receptor for its antagonist more hungry. For example, taking more Progesterone enhances the level of Estrogen receptors. Making for more tender breasts during PMS, even though you are supplementing with higher levels of Progesterone than you ever had naturally.

SHORT QUESTION ABOUT HAPPINESS, ENDORPHINES
Might a happy feeling come from Endorphines and not from the mix of high dopamine and progesterone supplementation?
Progesterone correlates to feeling at ease, calm (hello PNS). Not happiness per sé.

PROGESTERONE IN THE BRAIN: SLEEP
Another article from the same source kept me awake last night:

  • Estrogenen increase the serotonergic, noradrenergic and opioidergic activity in the brain. (grrrrr!)
  • Progesterone increases MAO slightly. Progesterone’s most profound neuronal effect, however, results from its direct effect on the neuronal membrane. Progesterone has an inhibitory effect on neuronal excitation, depressing neuronal firing.
  • one of Progesterone’s metabolites is called Allopregnanolone. This is een neuroactive steroid. Allopregnanolone hyperpolarizes neurons by potentiating GABA-mediated synaptic inhibition. It acts at a neurosteroid-specific site on the GABAA receptor to facilitate chloride channel opening and prolong the inhibitory action of GABA on neurons. Allopregnanolone is one of the strongest ligands of GABAA receptors in the CNS, with a potency similar to that of the most potent benzodiazepines (Valium etc) and approximately a thousand times higher than pentobarbitals. (sleeping pills)
  • brain activity of progesterone and allopregnanolone is not dependent solely on ovarian and adrenal production. It is made in the brain itself.

TRANSLATION:

  1. Progesterone depresses neuronal firing.
  2. Its metabolite Allopregnanolone eggs on GABA activity (GABA is needed for REMsleep!)
  3. Allopregnanolone does the same as benzo’s do, the drug so many insomniacs turn to
  4. Allopregnanolone does what sleeping pills do a thousand times better
  5. Progesterone is made in the brain (what if my deficiency is expressed there too? Is it synthesized in the brain from cholesterol? How does this work?)

I
AM
GOING
TO
SCREAM
NOW

Just for a little bit.
It’s all those excited neurotransmitters you see. And not enough progesterone to depress neuronal firing.

I want more (to know about) Allopregnanolone.

 

PS a strong symptom of Progesterone overdose is sleepiness. Allopregnanolone would account for this, as it’s as potent as the strongest sleeping aids.

taking a Progesterone pill (100mg) is the one thing that gets me through the nigh and only during PMS time. Earlier in the cycle and I feel very very groggy the next morning.

PS2 on RisingPhoenix someone says that it’s oral Progesterone that gets converted to this Alloprgnanolone. Not so much the transdermal cream.

Sleep: noradrenaline (2)

I wrote: “I expect the activity in the noradrenaline brain network to change once the sleep waves change. I.e. when the sleep cycle changes so does the activity of the neuron network. I need to go look for studies that tell me wether its activity increases or decreases.
Based on my insomnia I expect it to increase. Leaving me with a surplus of noradrenaline bouncing around my head.”

But I found that noradrenaline falls before we get into REMsleep.

Prof. Mallick is very busy unraveling how noradrenaline and REMsleep are connected. He ties it to illness too. When we are REMsleep deprived, we get ill.

“My working hypothesis is that “one of the functions of REM sleep is to maintain the brain excitability (Mallick et al., 1993, 1994, 1999)” and therefore, REM sleep possibly serves house keeping function of the brain (Mallick and Singh 2011). My lab has been working towards understanding its possible cellular mechanism of action.”
This theory is very popular at the moment. Glia’s and sleep detox and stuff.

Prof. Mallick explains briefly on this page.

He links Glia-activity to Noradrenaline (NA):
“Further, the brain contains neurons as well as glia and both possess NaK ATPase. REM sleep deprivation induced increased NA stimulated neuronal NaK ATPase activity, while the glial enzyme activity was decreased. The opposite actions of NA on neuronal and glial NaK ATPase activity probably help maintain neuronal homeostasis (Baskey et al. 2009) (Fig. 4).”
(NaK ATPase is just the good old Natrium Kalium pump in every cell membrane. Sodium Potassium pump to American friends)

In his scientific research I read about the workings of glia. During sleep the cells of the brain shrink a little bit, giving room to glia and to the intercellular fluids. These two shuttle away debri and cell waste.
It is important that this all happens: the shrinking and the waste elimination.

SLEEP STAGES: REM-OFF AND REM-ON
He found that during nonREMsleep (the first five hours of my nights) there’s a continuous firing of neurons called REM-off.
Once they seize firing another set of neurons start firing, REM-on.
REMsleep commences.

The REM-off/on’s activities are governed by GABA (and Noradrenaline). During REMsleep GABA is high, deactivating the Lucus Coeruleus. PubMed source here.
As long as there’s GABA, there’s REMsleep. Onset is governed by cholinergic input from the Locus Coeruleus. PubMed source here (prof. Mallick)
(cholinergic = Parasympathetic nervous system!)

REM-off neurons are called norepinephrinergic. Meaning they have to do with the SNS.
When a brain is REMsleep deprived it’s NA rises, keeping the REM-off neurons firing, prolonging the REMsleep deprivation. Gaba inhibits those pesky REM-off neurons, giving REM-on a chance. PubMed source here.
Stay away from stress, children.

During a study of blocking adrenoceptors to determine interaction between neurotransmitters and sleep this was quoted:
“Also, a critical level of norepinephrine in the system was required for the generation of REM sleep, however, a higher level may be inhibitory.”
PubMed sourcs, prod.Mallick
So you need a little bit to get to REMsleep. But too much will prevent it.

ME WANTS TO SLEEP
There must be a system governing NA levels in the brain during nonREMsleep. When it’s time to go to REMsleep the NA level will drop/rise (?) to the right level to let REMsleep commence.
In my brain the target is overshot. The NA level rises so much that I don’t get to REMsleep. I get to wake.

I think I’m onto something. I’ll investigate further. What system, what influences it?
In the mean time I’ll make sure I don’t get up while I lie awake. Getting that second stint of sleep is important. Get all the REMsleep you can.

5 hours solid sleep, 2 hours awake, 2 hours of (crappy) REMsleep. It’s the best I can do at the moment.

Sleep theory: noradrenaline

I’m still looking for a sensible theory to account for my weird sleep pattern of insomnia after the 5h non-REM sleep part of the night.

At the moment I’m looking into the excitatory neurotransmitters because I found out the disposal system of these is a bit crooked in me. The enzyme responsible of breaking down (nor)adrenaline, dopamine and serotonin is called MAO A and I have an allele combination that makes it do its work veeeeeery slowly. Making me an upbeat, cheerful person by nature. Going into manic chattering when excited too much:

I found some tidbits I’m going to connect without knowing what I do.

LAST NIGHT
I woke up after 5 hours of sleep. I lay there with my eyes closed, observing, and noticed that although my brain was ON my body was not. My body was heavy, warm, sleepy.
I tried to not get my brain any more excited than it already was (no lights on, no surfing, no worrying, no thinking up clever schemes, no planning). I did resolve to investigate another angle to this insomnia when properly awake: what if it’s not cortisol keeping me awake but something that’s only active in the brain?
Cortisol travels through the blood and should have effect all over the body. Maybe one of the excitatory neurotransmitters keeps its actions restricted to the brain?

NORADRENALINE IN THE BRAIN
Noradrenaline is both a hormone and a neurotransmitter. It’s made in the adrenals (not the same part that makes cortisol though) and released in the blood = hormone. And it’s made in the brain (in sections called Locus Coeruleus, in the brain stem) = neurotransmitter.
As a neurotransmitter it’s active in the central nervous system and sympathetic nervous system. As such it fires up the sympathetic nervous system, elbowing the parasympathetic system into submission.
The actions of norepinephrine are carried out via the binding to adrenergic receptors.

Locus Coeruleus, noradrenaline HQ

Wiki says: “Noradrenergic neurons project bilaterally (send signals to both sides of the brain) from the locus ceruleus along distinct pathways to many locations, including the cerebral cortex, limbic system, and the spinal cord, forming a neurotransmitter system.”
Does it say here that there’s a distinctive network in the brain for this neurotransmitter? Is there a web bringing it’s activity fast and furious into all parts of the brain?
yes it does

This network can be tested. Increase in activity can be measured. Data can be found!
They think this network is involved in decision making and in storing memories. There’s research on it (using rats I believe).

BUILDING NORADRENALINE AND USING IT TO BUILD OTHER STUFF
Noradrenaline (or norepinephrine) is synthesized in 3 steps:

  1. the aminoacid Tyrosine is hydroxylated into L-DOPA (by enzyme/gen Tyrosine Hydroxylase)
  2. L-DOPA is decarboxylated into Dopamine
  3. Dopamine is hydroxylated into Noradrenaline

Wiki: “Noradrenaline is the hormone and neurotransmitter most responsible for vigilant concentration in contrast to its most chemically similar hormone, dopamine, most responsible for cognitive alertness.[4]”

check. check. This is what I have in abundance, especially at night. This is also what places me on the other end of the spectrum from people with ADD, I believe. I wish we could barter and both end up in the middle.

 

 pic by Paul Turnbull

There’s a fourth step when fiddling with noradrenaline:

4. Noradrenaline is made into Adrenaline via methylation of its amino group.

It takes methylation to get rid of noradrenaline! Does this get hindered by the same dna-oopsies I have hindering the Methylation Cycle? This would account for huge amounts of noradrenaline lingering in the system, firing up the brain.

Although: would I want to trade noradrenaline for adrenaline in the middle of the night? I don’t think so.

GETTING RID OF NORADRENALINE
Here’s the wiki link on how it is terminated or degraded. Need to read it myself and use its terms to dig through scientific papers.

On first scan I see I shouldn’t take cocaine since it inhibits uptake of noradrenaline. That’s good to know, I’ll inform my dealer.

What facilitates degradation in mammals? What is the usual half time?

“α-Methyltyrosine is a substance that intervenes in norepinephrine synthesis by substituting tyrosine for tyrosine hydroxylase, and blocking this enzyme.”
what’s this? can I buy this? cook it up myself?

“Vesicular transport modulators[edit]
This transportation can be inhibited by reserpine and tetrabenazine.[33]”
are these drugs?

A few inhibitors to the release of noradrenaline are named. And a few that stimulate it. Adrenaline causes noradrenaline. Stay away from stress, children.
This does explain a lot of my own experiences.

Tyrosine is found in eggs, nuts, meat and cheese. And we make it ourselves from Phenylalanine.
Cutting down on any of these food stuffs won’t do much good as the body choses how much it converts. It’s not particularly dependent on intake. Unless you really stop eating these as hard core veganists do. And they might well be happier and more zen because of it too.

 pic by Penny Mathews

 

NORADRENALINE AND SLEEP

They suspect that the network of noradrenaline in the brain is used to store memories.
They also found that in the nonREMsleep this network’s activity coincides with the waves that are visible on EEG. When the wave goes up, so does the activity in the noradrenaline network. When the wave goes down, so does the firing frequency. They suspect this is how mammals store memories during sleep.
Here’s the link to the study (rats).

To me it says that during nonREMsleep the system pulsates, in the same slow way as the sleep waves do. I expect this to change once the sleep waves change. I.e. when the sleep cycle changes so does the activity of the neuron network. I need to go look for studies that tell me wether its activity increases or decreases.
Based on my insomnia I expect it to increase. Leaving me with a surplus of noradrenaline bouncing around my head.

If I can pinpoint why it stays active I can experiment. Or I can start experimenting and use the outcomes to focus the theory better.
It might be that methylation into adrenaline doesn’t work properly or that the MAO A clean up crew is working with two hands tied behind its back. Or the degrading system doesn’t work very well. I’m going to investigate further the subjects I touched upon above.

Or I might figure out why the surplus noradrenaline becomes active in the first place. If I can decrease its release (by taking away the cause or by taking surpressing drugs) I might sleep through the night. It would illustrate that it’s indeed noradrenaline waking me up and keeping me awake.

Well, I’m still just theorizing here. But in theory it all makes sense and it all coincides with my own symptoms and data.

If this becomes a credible, logical train of thought I plan to test it out. (no idea how to test, yet)
At night I want to sleep, from nonREM to REM. So I can wake up and be cheerful all day.

Brain chem: double shot of MAO A, cream, no sugar.


There’s this enzyme called MAO A. It takes a neurotransmitter and slices it up for parts. The neurotransmitters it typically likes are the excitable ones: adrenaline, noradrenaline, dopamine and serotonine.

I have a faulty gene coding for this enzyme. One of the basepairs is double mutated. G codes for higher activity of this enzyme, T for lower. I have two T’s, my enzyme doesn’t work as well as it could.

Now before everyone runs over to dr.Wiki and starts talking about Brunner Syndrome and oversexed violent people, that research is about one family (albeit Dutch) and about a specific mutation that put the whole gene out of commission. My mutation involves a base pair that (I suspect) downregulates the gene and is actually quite common.

But I need to read loads more about it. I did some earlier today and got really excited. But now I’m too fogged to put it all together in a sensible way.
I’m going to put some things here anyway, just for funsies, and hope to come back to it later and sort it out.

 pic by David Schauer

FAULTY MAO A:
Epinephrine doesn’t get cleared away at a normal rate. It pools up and as it’s an excitatory neurotransmitter, it bounces around in my synapses, making my head resemble a pin ball machine. This is actually how I have described my mental state and capacity for many years.

TOO MUCH ADRENALINE:
You know what’s that like, right?

 pic by Eziquel (zick) Boita

You’re wired, sharp, ready to move a mountain, fight a lion and kick some ass. Yeah baby! You are ALIVE!
It’s very akin to being over-caffeinated. Caffeine does indeed raise adrenaline.

This is what I felt like for 35 years. Apart from feeling ALIVE this is also Fight or Flight. This is feeling smart and on top of the world but at the same time wrecking the body because there’s no time or room for slow, healing processes.

MOODSWINGS:
While the (nor)epinephrine builds up and pools because the clean up crew is working with one hand tied behind their back, the body shuts down production of NE because there’s just too much. Then, when the NE eventually does get cleared away, there’s a gross shortage of the stuff.

Having your MAO A not work properly causes you to have all kinds of peaks and lows other people have not. In your mood. Mood swings!
I had noticed that my feelings had a more wide amplitude than those of my friends, classmates and mates at university. Also, they could swing really fast.

pic by Samuel Ascaso Piqueras

ADHD and RITALIN SHED SOME LIGHT:
“Because the nerve circuits in the prefrontal brain regions, which are normally involved in attention, require high levels of dopamine and noradrenaline stimulation, reduced levels of these two neurotransmitters could potentially lead to the weakened regulation of attention and behavior observed in ADHD .”

“Methylphenidate, the active ingredients in Ritalin®, acts like a weak form of cocaine to increase dopamine and noradrenaline levels but tends to do it all over the brain sometimes resulting in unwanted side-effects such as nervousness, drowsiness, insomnia, suspicion and paranoia.”

LINK TO SYMPATHETIC NERVOUS SYSTEM
“Norepinephrine, which is closely related to dopamine, is the main chemical messenger of the sympathetic nervous system. The sympathetic nervous system controls many automatic functions of the body, such as heart rate and blood pressure. The loss of norepinephrine might help explain several of the non-movement features of Parkinson’s, such as fatigue, irregular blood pressure, decreased gastric motility or movement of food through the digestive tract, and postural hypotension. ”

MY NEW FRIENDS:
At the forums of PhoenixRising.me I found a few others with this mutation and hearing how they live their lives makes all kinds of sense to me. They thrive on flat blood sugar levels. They too only need a morsel of a drug or supplement to notice its effect. They know about coffee.

It’s so nice to recognize! I have much to learn from them.

RIDICULOUSLY SENSITIVE:
This mutation offers a sensible explanation for my sensitivity. Any jump in adrenaline has an after effect long after the event.

Because of the delayed decrease and pooling of the neurotransmitters it’s good to have an uneventful day. It also explains why the band of comfort with supplements and drugs is very narrow. Basically it explains why I am so ridiculously sensitive to things. The sensitivity my doctor compares to autistic sensitivity.

RELATION WITH CORTISOL AND SLEEP
It seems cortisol has a balancing effect on (nor)epinephrine?

“The other two neurotransmitters that have been implicated as playing an important role in sleep are norepinephrine (NE) and serotonin (5-HT).”It might be that high NE invites a rise in cortisol. If Deep Sleep causes NE to rise and in my case uncomfortably high, cortisol might kick in to try and dampen it. But it’s too much and I wake up and lie awake, waiting for the cortisol to leave the system.

I read a piece about how at night the body plays pretend-inflammation because it needs to do certain things for which it needs the higher temperature. I do know brain temp rises. It isn’t actual inflamation. But an overly dramatic imune system might think so, causing cortisol to rise.

I have to reread it and try and understand but at the moment: brain fog.

MOA A RUNS IN THE FAMILY
A little more about MAO A. It sits on the X-chromosome. I have two faulty alleles. So my mother AND my father(‘s mother) gave me a faulty allele.

This means that my father has the same disfunction that I have, a homozygote, him having only one X-chromosome. And so does my brother. They must have the same peaks and lows in their adrenaline.

Well…..we ARE a family that comes across as being over-cafeïnated….
My whole family from father’s side does. We are smart, fast, ALIVE, intense, quick silvery. We’re the people you want to be close to in a crisis, we will get you out. It may be this one allele causing it all.

pic by michelle kwajafa

MODERN SOCIETY
Of course, the whole of modern society is overcafeinated. We LOVE quick, smart, fast and extravert. So it might be that my inborn tendency (the mutation) was exagareted by the time and society I live in.

AT EASE
I have not had the pin ball machine head for a few years now… Also, the “inner pounding” (roaring, ‘daveren’ in Dutch) has been gone for a while now.
Both since I started progesterone. And Valerian.

(Valerian does something with some neurotransmitters…. need to refind.. GABA, it interacts with GABA. It’s an agonist, a promotor.

“GABA does not penetrate the blood–brain barrier; it is synthesized in the brain. It is synthesized from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate (which is the active form of vitamin B6) as a cofactor. GABA is converted back to glutamate by a metabolic pathway called the GABA shunt. This process converts glutamate, the principal excitatory neurotransmitter, into the principal inhibitory neurotransmitter (GABA).
It gets transformed and it used as fuel for the citric acid cycle”
Need to read up on GABA and glutamate and wether all enzymes for their pathways are good in me.)

LOST THE PLTO
Now I’ve lost the plot. But I’m very interested. It ties together the pinball machine, the constant Fight or Flight, the sensitivity, the parasympathethic nervous system and the mutation. Above all: it ties together some particular characteristics I have noticed in me compared to other people. I’ll go to sleep now, talk to you later.
pic by Florin Garoi