Valdoxane and Melatonin

Valdoxane .
Andre Willers
6 Oct 2011

Synopsis :
A mild selective stasis generator.Good for anti-depressants .

Discussion :
See http://andreswhy.blogspot.com “Melatonin and dinosaurs” Jun 2011
Repeated in Appendix A for ease of reference.

Valdoxane is simply melatonin crippled in very specific ways .The limitation on possible receptor sites enhances some effects like anti-depressants .

Remember , melatonin is the Great Disruptor of feedback effects . That is it's function .

Valdoxane does this , but more effectively .

Rather ho-hum .

Andre

xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
Melatonin  and Dinosaurs .
Andre Willers
14 Jun 2011
 
"Sleep that knits up the ravell'd sleave of care " Shakespeare
 
Synopsis :
Melatonin ended up in various evolutionary roles because of it's powerful , terminal antioxidant effect . Many neurotransmitters (especially NO classes) can be seen as free radicals . (See Appendix A)
Melatonin is Nature's Terminator . (See Appendix C)
 
Discussion:
A handy Terminator got roped into being the Enforcer for various feedback systems that had to be kept from repeating  .
 
Examples :
 
1.Cancers (eg breast , prostate cancers)
Interruption of signaling molecules .
 
2.Circadian rhythms of the brain (sleep)
Dismantling runaway feedback systems before they corrupt long-term memory irreparably (sense of self) See Appendix C
 
3.Gut rhythms :
A separate system Melatonin excretion by various cells and bacteria .
 
4.Bile :
Funnily enough , a separate system . Why ?
Tied to the energy system and things like diabetes .
 
5.Mitochondria :
A sophisticated auto-governor on rates of activity relative to intra-cell position .
Really simple . Really cool . (Think a steam engine's governor) See Appendix B.
 
6.Skin
As expected , such a powerful terminal antioxidant will also be on the ramparts against foreign invaders (like in the gut)
 
7 Immune system
Basically a memory system , with potentially unlimited feedback .
Melatonin will terminate this as well , especially in localized , concentrated doses .
But note the correlation between blue-light and HIV .
Very high-intensity pulses of blue light (484 nanometers) or UV should disable the HIV virus .
 
Contradictions :
This is only seven usages  .There are probably more . The same concentrations of melatonin cannot serve all .
Hence , melatonin receptors evolved to meter and control cellular responses .
As well as dopsin receptors in the visual systems .
 
Loss of UV Dopsins
About 100 MYA for mammals . Remnants (melanopsins) are still responsible for nervous system entrainment , but some biological adaptability (ie getting melatonin from diet) was lost .
It also means that humans are especially vulnerable to depression of melatonin production by light in the Blue Wavelengths (484 nanometers) . CFL and LED lights .
This means that you should only use blue lights if you want to be alert . The effect is very strong (about 100 times) .
Interesting , this should be able to be hyperreal . Diffraction patterns (as with insect , bird and reptile scales) could give blue-to UV light that the mammalian optical systems will interpret as hyperreal .And hyperactive .
 
Speculation :
Mammalian loss of these dopsins are thought to be the result of low level of light on the forest floor .
But what if the scaly animals had evolved to use Blue and UV as a weapon ?
It would have reduced melatonin production even in darkness .
 
Imagine huge , impregnable Dinosaur behemoths with a skin ecology of luminescent bacteria , the light diffracting from their scales into the blue and UV .
A magnificent sight !
 
Remnants :
Birds with brilliant UV plumages should have DNA of the lumenifages in suppressed state . Or you can do it the hard way from the skins of late-stage dinosaurs .
 
Light-flash Extinction :
An amusing thought . The extremely bright flashes of the meteors would have burned out the skin ecology of the dinosaurs , the subsequent darkness sending them into a terminal melatonin deep sleep . See FireFall .
This can be tested . Since melatonin is a terminal antioxidant , the breakdown products should be measurable even after 65 MY .
 
Chickens and flu's
The diseases can be seen as stripped-down versions of skin-symbiotes of the old dinosaurs . The worst thing you can do is subject them to UV  Like in brooders . Self-assembly of old sequences will follow . A very old revenge .
 
What is a poor mammal to do ?
Because of the very many uses of melatonin , there is no single solution .
Sometimes you need more , sometimes less . The trick is to know when .
Also , the sources depend on light (especially blue light or UV) , gut , immune system , brain , pills(slow release or fast release) etc .
 
The basic principle is that it stops things dead . Slowly or quickly .
There is a tie-in with the sulfur mechanism that is responsible for the immobilization of all molecular cellular activity (concentrations of H2S about 80 ppm)
Melatonin stops the H2S blockage  . At extremely low concentrations .
Look at the molecule  .
 
This is a typical life-system . Blockages of blockages of blockages leading to a system with graduated responses .
 
Too little melatonin , and H2S is not sufficiently blocked and the organism goes into stasis . Sleep .
 
Evolved into hibernation . The long light periods led to depletion of melatonin , leading to H2S hibernation . Neat .
 
SAD is a direct consequence . Too much melatonin leads to neurotransmitter depletion (especially serotonin)
A berserker has to generate high levels of neurotransmitters internally .
 
Take a pill !
As seen above , the system has many variants . Endo- and exo- just to start with . There are adjuvants (valerian is one) . Epigenetic variants are possible , but this system is so basic that I think adjuvants would give better results .
 
So , take a pill with timing and accompanying chemicals .
Each one should target a separate system .
 
Ageing
The H2S system freezes things . The melatonin system unfreezes it .Pulsing the system enables living and repairing . Sleep with very carefully metered SO2 will enable a very long life for those interested .
 
Who wants to live forever ?
 
Andre
 
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
Appendix A
 
http://en.wikipedia.org/wiki/Melatonin
"Antioxidant
Besides its function as synchronizer of the biological clock, melatonin also exerts a powerful antioxidant activity. The discovery of melatonin as an antioxidant was made in 1993.[85] In many less complex life forms, this is its only known function.[86] Melatonin is an antioxidantthat can easily cross cell membranes and the blood-brain barrier.[6] Melatonin is a direct scavenger of OH, O2−, and NO.[87] Unlike other antioxidants, melatonin does not undergoredox cycling, the ability of a molecule to undergo reduction and oxidation repeatedly. Redox cycling may allow other antioxidants (such as vitamin C) to act as pro-oxidants, counterintuitively promoting free radical formation. Melatonin, on the other hand, once oxidized, cannot be reduced to its former state because it forms several stable end-products upon reacting with free radicals. Therefore, it has been referred to as a terminal (or suicidal) antioxidant.[88]  "
 
Appendix B
" A potential mechanism is that melatonin promotes the recruitment of brown adipose tissue (BAT) as well as enhances its activity.[48] This effect would raise the basal metabolic rate by stimulating thermogenesis, heat generation through uncoupling oxidative phosphorylation in mitochondria."
 
Appendix C
http://en.wikipedia.org/wiki/Phase_response_curve#Melatonin_PRC
 
"PRC in neurons
Phase response curve analysis can be used to understand the intrinsic properties and oscillatory behavior of regular-spiking neurons.[8] The neuronal PRCs can be classified as being purely positive (PRC type I) or as having negative parts (PRC type II). Importantly, the PRC type exhibited by a neuron is indicative of its input–output function (excitability) as well as synchronization behavior: networks of PRC type II neurons can synchronize their activity via mutual excitatory connections, but those of PRC type I can not.[9]
Experimental estimation of PRC in living, regular-spiking neurons involves measuring the changes in inter-spike interval in response to a small perturbation, such as a transient pulse of current. Notably, the PRC of a neuron is not fixed but may change when firing frequency[10] or neuromodulatory state of the neuron[11] is changed."
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx