State of the art - August 2014

Essence of somnia/insomnia/(un)consciousness

The best and most actual summary of how sleep AND consciousness work, is this chapter out of a book of Springer 2014, by Nir. This chapter has been made 'open science'. This is the best description in the world, 2014: summary-how-sleep-works-sleep-and-consciousness-Nir-2014 (click PDF)

Unfortunately the writers of above piece (and excellent book: 'Neuroimaging of consciousness', Springer 2014, see http://amazon.co.uk) were not aware of a very important earlier finding: during Slow Wave Sleep, the mPFC (medial PreFrontalCortex, the big brain where all 'calculations' take place) is DECOUPLED from the DMN, Default Mode Network (operating system of the brain). This has been described in 2009 and later articles:

Decoupling of mPFC from DMN during SWS (Slow Wave Sleep) (click PDF)

This is a line ICF researches in 2014 - what is best 'to do with your consciousness' lying awake and trying to sleep? End 2014 an article of us will appear about the subject. 'Counting sheep' is not the best solution, and that can be proven neurobiologically (!).

The essence of falling asleep is that the VLPO within the Hypothalamus releases GABA, a neurotransmitter that 'quietens' neurons by keeping their 'polarization' to the max. This is described by our senior neuroscientist in the following article: 'How sleeping pills exactly work' (click PDF)

In case of insomnia, probably one of the 4 following things fail:

1) release of GABA within the VLPO/hypothalamus
2) the GABA (natural ligands) binding to GABA receptors
(in case 1 or 2 fail, sleeping pills aiming at GABA receptor binding work very well)
3) lack of Orexin A, that ensures stable consciousness states (so: when awake you stay awake, when asleep you stay asleep). People with narcolepsy/cataplexy lack Orexin A. When FDA will FINALLY approve the new sleeping pille 'Suvorexant', enforcing the working of Orexin A, one will be able to make longer sleeping periods within interim awakenings
4) lack of DECOUPLING of mPFC from DMN (see above article, and a line ICF is further pursuing)

Regarding 1): the release of GABA within the hypothalamus is a very complicated issue, because in fact ALL sorts of neurotransmittors affect the hypothalamus. The hypothalamus is evolutionary the eldest part of the brain, the 'boss' of the brain, part of the limbic (emotional) system but also quite 'rudimentary' (it does not 'think' like the Cortex, it reacts intuitively)

Regarding 2), receiving GABA: a) it is very difficult to research where the natural GABA ligands consist of and b) there are many natural problems with GABA receptors and the chloride ion channels they open. The issue of 'chloride channels not working properly' is very detailed, complex and is being studied as 'weakness' underlying many illnesses.

A more extensive article about the possible neurobiological reasons of insomnia is the following (unfortunately forgetting the decoupling again, but for the rest: good article, 2012)

Neurobiology of chronic insomnia (2012) (click PDF)

Quite a lot of physicians are 20-30 years behind in knowledge of working of somnia/insomnia. Neurologists are generally uninterested in the issue, your best chance is to find a psychiatrist who studies neuroscience, especially of somnia/insomnia/(un)consciousness on the side. In case your physician is not up to date, print and bring him/her above articles.

A lot of faire tales and irrelevant research from the pre-neurobiology era exist about somnia and insomnia. Disregard all this outdated and in-exact research and look to research that includes neurobiology.

The main problem with 'prolonged insomnia', certainly when insomnia continues while other life problems have disappeared, is that insomnia generates FEAR of not sleeping well, more insomnia nights create a TRAUMA and that the INSOMNIA TRAUMA reinforces fear and insomnia. It is then not possible to 'break' the insomnia fear, without administering sleeping pills for many years close to the FDA max. Chronic insomnia detoriates job performance and leads to dismissal, job loss, poverty, impossibillity to maintain good relationships and a very suffering life, if not to 'insomnia fatale'. Rodents deprived of sleep die within 2 weeks. The Guiness Book of records mentions 11x24 hours as sleep record. Chronic insomniacs often have 7x24 hours as record, and after that unvoluntary sleep deprivation a good sleeping patterin never returnds. Yearlong irregular nights of 1-4 hours, shaking and cognitive impairmant and suffering characterize life.

Insomnia Clients Foundation (ICF) - home on: insomnia.academy

As Insomnia Clients Foundation (founded 2012, Chamber of Commerce Netherlands) we want to maximally speed up the 'transport' of most recent scientific findings towards (chronic) insomnia clients. This is necessary because without 'patient organisation', the
- translation of scientific findings into clinical guidelines may take 10-15 years
- the dissimination of knowledge from clinical guidelines to local GP guidelines may take another 20 years.

When you suffer from insomnia, you do not want to wait 30-35 years until 'finally' GP's catch up with science.

In 2013 in some countries (NL), existence of chronic insomnia is denied by GP's, and the myth is adhered to that sleeping pills may cause dependency. In scientific research however, it has already been proven 20 years ago that - except for diazepam - sleeping pills do not cause physical dependency nor desensitivation. Primary insomnia and chronic insomnia are VERY NORMAL.

ICF has 5 websites, of which is the 'homesite' - http://insomnia.academy

SELF HELP GROUPS FACEBOOK

https://facebook.com/groups/sleepingpills

https://facebook.com/groups/primaryinsomnia

https://www.facebook.com/groups/chronicinsomnia


Furthermore

In order to be able to go into more details on other subjects, we also have the following other 4 sites:

  • Donations: Insomnia Clients Foundation

    IBAN: NL54SNSB0937008613
    BIC:
    SNSBNL2A

    Netherlands

  • http://gaba-receptor.com (important because the gaba-receptor binding is important to let Cl- ions flow in order to 'absorb' incoming current flux (electric signals) and keep the neuron below threshold of firing
  • http://neurophysiology.biz (physiology and electronics of the neurons are crucial)
  • http://electrophysiology.net (one of our specialism is electrophysiology, also outside somnia/insomnia)
  • http://neuroelectronics.org (neuroscience will go from 'biology/physician terrirtory' to the field of exact scientists and electronic engineers, who will take over)
Mail us on info@insomnia.academy. Also, have a look at our menu and other pages. We constantly update this site, but always starting our homepage with 'state of the art' info.


Essence of sleep


VLPO is a nucleus in the midst of the brain, approximately as large as an olive. VLPO stands for 'ventrolateral preoptic nucleus' and in some languages it is simply called the 'sleep brain' or 'sleep nucleus'.

Unfortunately, this VLPO cannot give a 'hard command' to sleep, but it can emmit neurotransmitters of the type 'GABA'. Human brains consist of neurons, that are charged electronically and can pass on electricity to other neurons, and of 'plasma'. There is no blood in the brains.

'Sleep-wake' is a sort of battle between 'quitening neurons', meaning: inhibiting the passing on of electrical pulses ('spiking') and on the other side 'excitation of neurons'. The GABA neurotransmitter, as well as open GABA receptors (we will elaborate on that later) are quietening neurons. That is what we want, suffering from insomnia.

The VLPO emits GABA neurotransmitters to the nuclei around them, and 'hopes' this will lead to a quietening of neurons and sleep.

However, 'enemies' of GABA, the excitatory neurotransmitters as GLU and NE, can hinder the quietening of neurons. GABA can even be metabolized into the 'enemy' GLU = glutamate. Furhtermore, in the adjacent nuclei it is very important that the GABA receptors OPEN their Cl- ion channels, so Cl- ions can flow in, and neurons can go towards their resting potential of appr. - 70 mu Volt.

Summary: the VLPO emits GABA to neighbouring nuclei in order to 'calm down' the neurons of the CNS (Central Nervous System). Expressed in frequency, spiking frequency of neurons is supposed go down from maybe 30-50 Hz in a wake state to 1-2 Hz in the sleep state. Sleeping pills work all the same in the sense that they bind to the GABA receptors in order to open the Cl- ion channels. This is the secret of sleeping! The two central elements in sleep are VLPO and GABA - that is the reason we chose VlpoGaba.com as domain name.