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.
SLEEP is IMPORTANT.
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.
MY THEORY: IT’S A CORTISOL PEAK
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.
CLUES ABOUT THIS PARTICULAR SLEEPING PATTERN
- 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
THEORY: SOMETHING UPSETS THE SYSTEM AFTER FIVE HOURS OF SLEEP. ENOUGH TO MAKE IT PRODUCE CORTISOL, THE ANTI-STRESSHORMONE.
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.
HOW DO RECEPTORS WORK ANYWAY?
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 THE RECEPTOR/G-protein CELL
“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.
HORMONES ARE NEUROTRANSMITTERS
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?
LAYING AWAKE BECAUSE OF CORTISOL
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.
LOOKING AT ACTH PRODUCTION.
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
HYPOTHALAMUS AND ITS CRH
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.
The main question still is: WHAT CAUSES THE SYSTEM TO FREAK OUT AFTER FIVE HOURS OF SLEEP?
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