Hepatic Flexure causes lifelong insomnia

I cannot believe that I did not figure this out earlier. It’s so logical, looking back.

Each night I wake up at 3AM. Wide awake. I lie awake for about 1 hour – 1,5 hr. Then I sleep a little but do not wake up rested.
Lying down = right upper bend in the colon gets squished. Matter cannot pass and builds up in the ascending colon. After 4,5 hours my body jolts itself awake from the stress.

4,5 hours being the bare minimum of sleep it needs to get by. Or the amount of time the small intestines need to process everything they’ve got and dump it into the colon.

I’ve had this insomnia as long as I can remember. Even as a child. My parents thought I was afraid of the dark or the house burning down. Every night I woke up. Always have.

Now that I’ve been addressing constipation and slow colonic transit the past couple of weeks I’ve had some succes  in sleeping through the night. Glorious feeling! Getting 6 hours instead of 4,5.

It makes sense now that I think about it: as I lie down the hepatic flexure gets squished (by the liver?) and matter cannot pass into the traverse colon. Stuff builds up in the ascending colon, especially in the 4,5 hours of sleep, and then I jolt awake because of the stress reaction. Lying awake for a good hour tossing and turning (making matter pass the hepatic flexure?). Perhaps I miss the train of the BMM (Body Mass Movement) that occurs every so often and one is every 1,5 hours?

I’m now looking into solutions for keeping that flexure open when I lie to rest. Can’t find a similar problem on the internet but I’m looking for clues at people who have a prolapsed traverse colon (colonic ptosis).

It is very common to have your colon twist and fold, both at the traverse colon (red) and the sigmoid colon (blue):


and these people (children too) all have slow colonic transit.

God knows how mine is twisted at the red part. All I know is when I lie down the traverse colon is no longer accessible. The life long insomnia as a result of this has caused adrenal problems and “ME”. I’ve fixed the latter and when I start sleeping though the night my adrenals will probably need less Hydrocortison as a crutch.

So what can I do? What do people with prolapsed traverse colon or enteroptosis get advised?

  • Surgery is out, not enough succes rate .
  • Defining stomach muscles is advised. (fit20 is an excellent regime for that. As is kettlebelling)
  • As is stomach massage.
  • As is hanging upside down (during sports) to let gravity help.

So what will I do?

  1. I will do more muscle exercising. I already do normal crunches on machines, both at fit20 and the gym. I will incorporate diagonal movements such as standing on a training ball and moving a barbell from left to right. Kayaking movements would be excellent too.
  2. I will do extra sets right before bed. Get as much matter out of the ascending colon as possible. Also massage these parts before going to sleep.
  3. continue mindfulness and supplements to enhance colonic motility (it’s still an issue)
  4. adopt a different sleep posture? It is related to me lying flat. Sleeping on my right or left or stomach does not seem to change much. Perhaps lie with head lower than buttocks? Head higher? Learn to sleep standing up, strapped to the bed?
  5. asking my doctor for advice about what I put into my mouth. Ascending colon specializes in taking out the moisture, perhaps if I can keep matter fluid it passes the hepatic bend easier? Is this where laxatives target? I have not used laxatives ever and I know they are not a lasting solution, if anything they can make matters worse. Usually fiber is advised to make matter moist but fiber works against my colonic inertia and gives too much bulk in the ascending colon at night.
  6. ask my doctor about enemas. Would that be good, cleaning the tubes once a month? My previous GP was against it because my system is so sensitive. He was often right.
  7. ask my doctor about anything else she can think of. Perhaps she thinks it fruitful to talk this over with a GI specialist? I dread going to yet another professional who deals with so many “special snowflakes” and patients who have dr.Google at their fingertips and somehow showing them that I indeed have a weird thing.

We’ll see. I’m meeting my new GP on Thursday. See if that goes better than when I met her replacement. I am preparing a medical dossier for her so she can see my casus in one glance. Everything on just one piece of paper.

PS in addition I still have classic “hepatic flexure” as described by my old GP. A bit of air forms in the colon and cannot pass the flexure. It clogs it up, preventing other mass to pass. I can solve this by lying on my right and letting gravity do its thing: the air squeezes past and rises upwards, into the traverse colon. I then turn on my back. Perhaps do my gymnastics.

I have to do this on top of whatever I have to do to empty the ascending colon.


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.

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.

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 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).

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.

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



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.

Sleep: tracking my hours

I’ve been tracking my hours the last month. Here are the hours I was in my bed asleep, in Elderberry purple:

sleep hours tracking

You see that as a rule I don’t sleep through the night. Most nights I lie awake for a couple of hours. On two nights when I did get a full nights sleep I had had a very short night the previous one.

Now for my next trick…

sleep hours quantity

Hocus Pocus Holy Quantity, Batman!
I forgot about the actual time I went to bed and just lined up the hours I slept.

There’s a clear pattern here. It doesn’t matter at what time I’m going to bed, on most nights I sleep 4,5 hours and then I wake up.

I have had this sleeping pattern all my life. I remember as a child, under the age of 10, calling for my parents. Every night. So this pattern of mine is unrelated to my CFS or ME. It does wreck havoc in my illness as I do not recuperatie sufficiently from the day before.

Lately I’ve been reading up on neurotransmitters that are involved in the various sleep stages. It seems something is happening to me after the last stage of Deep Sleep. Something in the transition makes my body react, seemingly with neuro-exitatory molecules. Could be cortisol (main suspect due to the half time of it that co-incides with my time awake before I can go back to sleep) but it can easily be any other.

I have some info on them, the neuro transmitters, but I’ll come back to that another time.  I also found some other people with this pattern, on the ME forums over at phoenixrising.me. They battle it with sleeping pills and benzo’s and anti-histamines. Which all take effect on neurotransmitters. But I’ll try and sort that out later.

For now I just wanted to park the tracking graphs here.

PS. Elderberry is the plant of Hulda, Frau Holle. Sambucus, full of vit. C.
The juice of the berries will stain your white summer clothes forever! But when you try to dye wool with this rich colours, they will fade in the sun over time.

Thinking myself to sleep. Research notes.

I have a specific sleep pattern that is of no good. I sleep for 5 hours straight and then I wake up. I am wide awake. This lasts for about an hour, maybe two. Then I get back to a light sleep for another hour or two. I have had this all my life. Every night.

This is a specific pattern of insomnia. It is not cured by sleep hygiene. It wrecks havoc on the body. My current fascination is to get to the bottom of it and FIX it.

Here now follow my research notes. I need a place to keep track of my thoughts. I’m not sure this of interest to any of you… I apologize.

dr. Gominak, a neurologists, found that all her patients improve when their sleep is restored. No matter what their neurological symptoms are. She thinks this has to do with specific healing that takes place in Deep Sleep and in REM sleep. For this healing Human Growth Hormone (HGH) is released and the body needs to be in perfect partial paralysis. Too much paralysis and you get sleep apneu (and rise from your deep sleep, preventing healing). Not enough paralysis and you sleep talk or get up to pee. Both patterns are not good because they prevent right paralysis and healing by HGH.

I get those first five hours of sleep. I typically wake up at 3 ‘o clock and lie awake till 5. I do get some Deep Sleep. This means I will not die from this insomnia. I know this because I have not died before. I have slept like this all my life, even as a child. But my adrenals have given out on this pattern.

When I wake after five hours I experience a specific status. My mind is clear and wide awake (if not racing). My body is hot, too hot. I feel this is a cortisol peak. Cortisol has a half time of 1 hour or two. The time it takes me to settle down, cool down and get back into a slumber.

The problem is I needed this cortisol to get me out of bed in the morning, for the Awakening Response. For years my adrenals have gone the extra mile and given me a nightly cortisol peak and a secondary in the morning. Until they gave out. First partially in 2008. Now totally in 2013.
This is what makes this sleeping pattern so dangerously. Apart from the not proper healing in your sleep bit.


  • My mother has this pattern too, albeit more mild. She wakes up with a soar throat. An ionisator has helped her. This machine makes dust particles in the air settle down.
  • My brother has it, as severe as I have. His adrenals seem to cope, he is nearly 40 and healthy. As long as he doesn’t hold a job that requires getting up before 8 ‘o clock.
  • I’ve found a few others on RisingPhoenix.me who have the same pattern. These people have fatigue. They knock themselves out with anti-histamines and they sleep (somewhat).
  • a few years ago I started to sleep through the night once and again. Co-factors are: destressing, clean bed sheets, valerian, anti-dustmite, earplugs, no cat shananigans in the night, no drinking after 7 o clock in the evening, enough progesterone, no insuline or cortisol peak during the day, no gluten, no cheese, woolen bed and blankets, keeping throat warm, feeling safe. But these give no guarantees whatsoever, it’s a tombola every night.
  • things that didn’t work were: eating before bed, camomille tea, dark room, whale sounds, different bed times, segmented sleep, no tv/screen, use room for only sleep, melatonine, age, location


What causes the system to freak out? Can I prevent it?

Since anti-histamines and dustmites came up I’m wrapping my brain around this first. Here now follows the research I already did. It’s my thought process, it may not be very interesting for anyone else… In cursive are quotes from Wikipedia. In bold thoughts I want to park and get back to at a later time.

A histamine antagonist (commonly called an antihistamine) is a pharmaceutical drug that inhibits the action of histamine by either blocking its attachment to histamine receptors, or inhibiting the enzymatic activity of histidine decarboxylase; catalyzing the transformation of histidine into histamine (atypical antihistaminics). It is commonly used for the relief of allergies caused by intolerance of proteins.

Antihistamine mainly blocks the mucus reaction that cells give, which reaction leads to the annoying allergy symptoms of sneezing and loosing water from all sides of the head.
This is a symptom-approach. I’m more interested in the cause of the allergic reaction and dampening that response.

What now if you don’t produce mucus and sneezing but do reach the stage right before that, where you do get the freaking but not the sneezing? That would make a body make cortisol, I’d think. So: how does the arousal of the allergy initiate?

Key: intolerance of certain proteins. (intolerance to other things too? Dustparticles? )

There are four kinds of Histamine-receptors, see Wiki. They have various functions some of which are interesting to someone looking for sleep.
H1 for example also modulates circadian rythm (!)
And H2 is a system-activator, just like cortisol.

Btw H1 couples via its G mechanism to Vassopressin, het gotta-pee-repressing hormone.

A receptor sits in the cel membrane. With its head outside and its feet dangling on the inside of the cel. A primary messenger bonks into the head, this usually is a hormone. This makes the lights go on in a parking garage called G protein that’s located at the feet of the receptor molecule, on the inside of the cell. One of the cars gets a tank full GTP, the alfa no less! This car leaves the parking garage and drives along the inside of the membrane until it bonks into the soft belly of a protein, the primary effector.
It’s this protein that starts to produce molecules that will influence the cells functioning: the secondary messengers.

This system is called the Second Messenger System and it shows exactly where the various G proteins are that various anti-histamine medicines target.

Secondary messengers can influence the cell insides directly or first activate a secondary effector in the cell membrane.
The alfa-car, a little enzyme in itself, has used up its petrol. All GTP is decreased into GDP. It drifts back to a parking garage at the feet of a receptor cell.

Sometimes this system doesn’t work. The head, the feet, the Parking garage, the car, all and any can malfunction.

pic by Erik Hutters

“Malfunction of GPCR [G Protein-Coupled Receptor] signaling pathways are involved in many diseases, such as diabetes, blindness, allergies, depression, cardiovascular defects, and certain forms of cancer. It is estimated that about 30% of the modern drugs’ cellular targets are GPCRs.”

The human genome encodes roughly 800 G protein-coupled receptors, which detect photons (light), hormones, growth factors, drugs, and other endogenous ligands. Approximately 150 of the GPCRs found in the human genome have unknown functions.

There are about 800 kind of receptors. They use all kinds of things to bonk themselves with in the head (neurotransmitters, hormones, food additives, cocaine, GABA, Calcium ions). Things going wrong leads to all kinds of system wide illnesses such as diabetes, allergies, depression, cancer.

The hormone ACTH is the neurotransmitter that floods the whole body and is picked up specifically by the receptors in the adrenal cells. Through the Second Messenger System mentioned above, it activates these cells to produce cortisol. http://en.wikipedia.org/wiki/CAMP-dependent_pathway
Another hormone, Glucagon, is picked up by receptors in the liver and activates glycogen breakdown
Another hormone, ADH vassopressin, makes blood vessels contract, ignoring your pee pressure. (Supposed to be high during the night. If you wake up to pee it isn’t)(perhaps it’s high all day in me?)

So Hormone Replace Therapy (HRT) is basically neurotransmitter therapy. Bonking around the heads of 800 kind of receptors in your body. Better be careful what kind of neurotransmitters you put in there.

This includes vitD3 which is a hormone and not a vitamin. All hormones are made from cholesterol so does supplementing leave you with high cholesterol?

ACTH is produced, adrenal cells make cortisol, I wake up. Because the system downstream gives the right results I can assume the adrenal cels work properly (the receptor receives ACTH, the alfa car drives, the cortisol is made). Looking in that place for a cause of my cortisol peak seems not logical right now.
The production of cortisol by a cell could be inhibited my crippling the G protein with a particular anti histamine however. Effective. But not solving the cause.

It’s the anterior pituitary gland in my head that produces the hormone ACTH. I can therefor conclude I have not primaire Addison’s. The gland functions.
The pituitary gland does so in response to the hormone corticotropin-releasing hormone (CRH) released by the hypothalamus, another piece of brain.
Gaat pituitary gland op eigen houtje aan de acth produktie of is het i o v de hypothalamus?

There’s a lot involved in regulating the levels of ACTH. There are feedback loops coming from the adrenals themselves, for instance. These feedback come in fast loops and in slow loops.

In order to regulate the secretion of ACTH, many substances secreted within this axis exhibit slow/intermediate and fast feedback-loop activity. Glucocorticoids secreted from the adrenal cortex work to inhibit CRH secretion by the hypothalamus, which in turn decreases anterior pituitary secretion of ACTH. Glucocorticoids may also inhibit the rates of POMC gene transcription and peptide synthesis. The latter is an example of a slow feedback loop, which works on the order of hours to days, whereas the former works on the order of minutes.
(The half-life of ACTH in human blood is about ten minutes.)

“Hours to days”!?
Might these slow loop feedbacks be connected in any way to the circadian rythme or sleep cycles? Can there be something awry in the slow loop feed back making me release cortisol in the middle of the night?

There are ACTH receptors outside of the adrenal glands. They are in the bone producing cells.
Also: ACTH is a cleavage product of the pro-hormone, proopiomelanocortin, which also produces other hormones including melatonin.

Can inappropiately timed ACTH rob the body of the pro-hormone needed to make the sleep hormone melatonin?

Of course, a real elevated production of ACTH is the illness Cushing. I don’t have that. But the knowledge about Cushing disease might shed a light on these nightly cortisol peaks.
Also, the ACTH producing enzyme in the pituitary may be of the same sort as my busted MRT: a brake that slips. The gene to check for mutations might be POMC.

pic by andre leme

Pituitary gland takes its cue from the Hypothalamus. The hypothalamus is the grand concert director in your head. It oversees all kinds of information coming in, both from the inside and the outside of the body. It sends out all kinds of signals to make various body parts do things.

Because of the hypothalamus people can influence and calm their adrenals by practizing mental zen and active destressing and behavourial therapy and (re)training the Central Nervous System.
But the hypothalamus also reacts to:
– Neurally transmitted information arising in particular from the heart, the stomach, and the reproductive tract
– Autonomic inputs
– Blood-borne stimuli, including leptin, ghrelin, angiotensin, insulin, pituitary hormones, cytokines, plasma concentrations of glucose and osmolarity etc.

Is it one of these that triggers my system after 5 hours of sleep?

Well, this concludes the thinking I’ve done when lying awake last night and two hours of reading this morning. I will look into the bold sections.

Other questions to ask about this are:
What happens to the body in those 5 hours? Do the glucose reserves in the liver get depleted? Have all the toxins build up during sleep healing and not find a way out (due to genetic mutations)? Has our food digested by that time and is energy not properly stored away, causing blood sugar to spike? Has all the progesterone gone, crippling basis processes?

 pic by John Evans