Synaptamide, Neuron Growth, DHA

Kingpinguin

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schultz

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I'd be interested in hearing what he thinks as well. I glanced through the study, and another similar paper, and it appears to be protective, but I am no expert (obviously) and am unable to critique it properly. I wonder if it acts similar to other ethanolamines like diphenhydramine? There was also some protection against LPS.
 
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Kingpinguin

Kingpinguin

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Synaptamide, endocannabinoid-like derivative of docosahexaenoic acid with cannabinoid-independent function. - PubMed - NCBI

The brain synaptamide content is dependent on the dietary DHA intake, suggesting an endogenous mechanism whereby diets containing adequate amounts of omega-3 fatty acids improve synaptogenesis in addition to well-recognized anti-inflammatory effects.

A synaptogenic amide N-docosahexaenoylethanolamide promotes hippocampal development. - PubMed - NCBI

This is supported by the observation that DHA is converted to DEA by fetal mouse hippocampal neuron cultures and a hippocampal homogenate, and DEA is present endogenously in the mouse hippocampus. Furthermore, DEA stimulates neurite growth and synaptogenesis at substantially lower concentrations than DHA, and it enhances glutamatergic synaptic activities with concomitant increases in synapsin and glutamate receptor subunit expression in the hippocampal neurons. These findings suggest that DEA, an ethanolamide derivative of DHA, is a synaptogenic factor, and therefore we suggest utilizing the term 'synaptamide'.

as suggested for years DHA has been known to boost brain function and neuron growth. There similair studies where they see combination of DHA and uridine improves this even more than any of them alone. Guess the mechanics of this well documented effects of DHA are now being brought to light.
Would also explain why DHA content is higher in areas of the body with lots of neurons/nerves like the brain and retina

like to add that I did notice my memory was declining since starting peating 2 years ago and recently I started eating more fatty fish and I noticed a quite significant improvement. Maybe its connected since the hippocampus is responsible for memories. The first part of the brain to shutdown during alcohol intoxication is the hippocampus. Thats why you seem to black out but you still do crazy stuff. You just cant make those memories and it just seems like you never did experience them.
 
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Sativa

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Needed for brain development it seems.
This seems like a stretched assumption.
The endogenously produced mead acid forms perfectly viable endocannabinoids, which activate the cannabinoid system on par with anandamide (which is a top class endocannabinoid)

Consuming external pufa's, which can directly fuel endocannabinoid synthesis & creation, would consequently flood, and alter the fluid dynamic of the bodies endocannainoid system - this is totally not desirable. PUFA consumption also likely desensitizes the endocannabinoid system, in the mid-long term - not cool.
 
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Kingpinguin

Kingpinguin

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This seems like a stretched assumption.
The endogenously produced mead acid forms perfectly viable endocannabinoids, which activate the cannabinoid system on par with anandamide (which is a top class endocannabinoid)

Consuming external pufa's, which can directly fuel endocannabinoid synthesis & creation, would consequently flood, and alter the fluid dynamic of the bodies endocannainoid system - this is totally not desirable. PUFA consumption also likely desensitizes the endocannabinoid system, in the mid-long term - not cool.

anandamide and synaptamide does not have same functions so mead acid cant really do what DHA can.
 

Sativa

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DHA converts to n-Docosahexaenoylethanolamine an endocannabinoid metabolite also called synaptamide
anandamide and synaptamide does not have same functions so mead acid cant really do what DHA can.

anandamide & synaptamide are both endocannabinoids which stimulate the bodies CB1/2 receptors (including the GPR cannabinoid receptors eg GPR55, GPR119 etc)
Mead acid is a precursor for a potent endocannabinoid -
Mead ethanolamide, a novel eicosanoid, is an agonist for the central (CB1) and peripheral (CB2) cannabinoid receptors.

EPA, DHA, Mead acid - are all precursors for potent cannabinoids, at least as equipotent to the endogenous cannabinoid anandamide.

EPA & DHA are only different from mead acid in that they possess neuro-toxic structural issues, which relates to their anti-metabolic effects.
 
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Kingpinguin

Kingpinguin

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anandamide & synaptamide are both endocannabinoids which stimulate the bodies CB1/2 receptors (including the GPR cannabinoid receptors eg GPR55, GPR119 etc)
Mead acid is a precursor for a potent endocannabinoid -
Mead ethanolamide, a novel eicosanoid, is an agonist for the central (CB1) and peripheral (CB2) cannabinoid receptors.

EPA, DHA, Mead acid - are all precursors for potent cannabinoids, at least as equipotent to the endogenous cannabinoid anandamide.

EPA & DHA are only different from mead acid in that they possess neuro-toxic structural issues, which relates to their anti-metabolic effects.

doesnt matter. They call it synaptamide for a reason. In studies it has been shown to increase synaptic growth factors like the other endocannabinoid was not able to do in the same way. So obviously it has its own pharmacology.
 

Sativa

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That might be so, but as far as i'm concerned, any o3/o6 pufa's are irrelevant.
If you really want to increase neuronal growth factors, there are far more strategic & efficient ways, that require far less toxic/questionable substances.

btw, the factors are called BDNF, GDNF & NGF; there are countless non-PUFA ways of stimulating their production.
The mere presence of O3/O6 pufa's would imply loss of neuronal coherence & integrity anyway (since it is a pufa implying it promotes tissues/cell damage) - it's surprising that despite your high intellect & deductive abilities, you have not realised this.

aside - I decided to call the extract i create from my faeces "neuronal-boost", but it still comes from faeces, and the impressive superficial name shouldn't fool someone as smart as you.
 
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Sativa

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You mean the trophic factors Peat speaks so highly about? Like GH or IGF-1?
no I was referring to Neurotrophins - a family of proteins that induce the survival, development, and function of neurons. They belong to a class of growth factors.
All the main 5-HT2A serotonin psychedelics promote BDNF, as do various cannabinoids.
BDNF = neurogenesis.
 
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Kingpinguin

Kingpinguin

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no I was referring to Neurotrophins - a family of proteins that induce the survival, development, and function of neurons. They belong to a class of growth factors.
All the main 5-HT2A serotonin psychedelics promote BDNF, as do various cannabinoids.
BDNF = neurogenesis.

Many thing stimulate BDNF its not mainly serotonin driven.
Honey
Progesterone
Pregnenolone
DHEA
Niacin
Magnesium
Caffeine
Theanine
Uridine

uridine is interesting coz it also alone increases synaptic growth and neural communication. Just like synaptamide. Anandamide doesnt do that. And mead acid endocannabinoid dont either.
 
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