View Full Version : Fish oil theory and science (split from Fish oil for the treatment of ADHD)


SB_UK
07-21-15, 04:12 PM
If ADHD is cerebral dysfunctional learning based reward activation failure- I can see how dexedrine would work. Not fish oil.

Lunacie
07-21-15, 04:58 PM
If ADHD is cerebral dysfunctional learning based reward activation failure- I can see how dexedrine would work. Not fish oil.

Fatty acids, such as those found in fish and fish oil (omega-3 fatty acids)
and evening primrose oil (omega-6 fatty acids), are "good fats" that play
a key role in normal brain function.

I don't think anyone understands why sometimes meds work for awhile and
then stop working. That happened to my granddaughter on Concerta. Makes
me very happy that fish oil has been working for me for over a decade. :D

SB_UK
07-22-15, 10:47 AM
Fish oil - should be highly volatile.

eg


Marine omega-3 rich oils are used by more than a third of American adults for a wide range of purported benefits including prevention of cardiovascular disease. These oils are highly prone to oxidation to lipid peroxides and other secondary oxidation products. Oxidized oils may have altered biological activity making them ineffective or harmful ... ...

SB_UK
07-22-15, 11:01 AM
Omega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator receptor activator (PPAR)gamma peroxisome

&
mitochondria
Mitochondria and peroxisomes: are the 'big brother' and the 'little sister' closer than assumed?http://www.ncbi.nlm.nih.gov/pubmed/17935214

Mitochondria and peroxisomes are metabolically linked organelles, which are cooperating and cross-talking.

-*-

What does a mitochondria need a peroxisome for ?

Peroxisomes IPA: [pɛɜˈɹɒksɪˌsoʊmz][1] (also called microbodies) are organelles found in virtually all eukaryotic cells.[2] They are involved in the catabolism of very long chain fatty acids, branched chain fatty acids, D-amino acids, and polyamines, reduction of reactive oxygen species - specifically hydrogen peroxideReactive oxygen species are always going to be involved whenever mitochondria are around - and so the peroxisome was recruited to mitigate the damage ?

Lunacie
07-22-15, 11:18 AM
Fish oil - should be highly volatile.

eg

Scare tactics ... totally unnecessary and unwarranted! :umm1:

Fish oil that has been exposed to high heat and oxidation will usually smell
rancid. I've taken a couple of bottles back to the store because of the smell.
If the fish oil smells rancid, don't use it. Simple as that.

Available evidence shows oxidation of fish oil is not a concern in humans.

Lunacie
07-22-15, 11:18 AM
Fish oil - should be highly volatile.

eg

Scare tactics ... totally unnecessary and unwarranted! :umm1:

Fish oil that has been exposed to high heat and oxidation will usually smell
rancid. I've taken a couple of bottles back to the store because of the smell.
If the fish oil smells rancid, don't use it. Simple as that.

Available evidence shows oxidation of fish oil is not a concern in humans.

SB_UK
07-22-15, 12:30 PM
http://www.ncbi.nlm.nih.gov/pubmed/17876199
n-6 Fatty acids reduce insulin resistance, probably by acting as a ligand for peroxisome proliferator-activated receptors-gamma

One of the main problems with PUFAs is that they are chemically really unstable. eg http://paleoleap.com/many-dangers-of-excess-pufa-consumption/

Don't like the idea of n-3 vs n-6 as n-3 are harder to come across than n-6.

Much more attracted to raw vegan [not heated above a certain temperature ie non-oxidized] n-6 fatty acids as Peroxisome proliferators.
Property lost on heating ?

SB_UK
07-22-15, 01:43 PM
The end results of lipid peroxidation are referred to as either AGEs or ALEs, short for advanced lipoxidation end-products.

You may be killing yourself.

SB_UK
07-22-15, 02:00 PM
Surely - taking large amounts of fish oil is as silly as taking any artificial chemical ?
All built on the crazy premise that nature can't do its job, but thankfully we've some profit-driven pharma or herbal 'treatment' salesman who thrives on human suffering (and ignorance) to ?? help us out ??.

SB_UK
07-23-15, 03:08 AM
http://www.nutritionj.com/content/13/1/17

PPAR alpha
The natural ligands of PPARα are omega-3 fatty acids. PPAR gamma

Apart from polyunsaturated fatty acids eg omega-3 fas, phytanic acid is also a natural PPARγ agonist in the human diet that reveals a similar activity to omega-3 PUFA

More interesting - phytanic acid - just because it's easier to access

But - animal-based - not good
Publically accessible animal-derived foods have been compromised by the high drug-based, low quality feed, low living quality conditions that mass production has required.

wikiP/phytanic acid
dairy products, ruminant animal fats, and certain fish.However - ref in wikiP
We provide indirect evidence that great apes, in contrast to humans, derive significant amounts of phytanic acid from the hindgut fermentation of plant materials. This would represent a novel reduction of metabolic activity in humans relative to the great apes.In contrast, great ape species in the wild derive a significant amount of their total daily metabolic energy needs through the fermentation of lower quality plant materials in their hindguts [20 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964658/#B20)-25 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964658/#B25)]. Although hindgut fermentation also occurs in humansWell known connection between food fed and gut biome.
Shift from vegan to animal-product based diet as observed with 'affluence' - the tendency towards eating anmal products appears to occur as communities become more wealthy.
But more healthy ?

Increased processed carbs / animal proteins -> pro-anabolic via insulin/IGF-1 -mediated mechanisms - disease.

-*-

Gut-biome based generation of phytanic acid given gut biome diversification from eating a predominantly plant-based diet ?
Phytanic acid as a natural ligand for peroxisome proliferation.

Supporting white to brown fat conversion - and the formation of a healthy fat which supports metabolic activity ?

-*-

Mechanism I'd prefer - as neater

Mitochondrial superoxide/free radicals drive peroxisome proliferation
- so we have the potential for peroxisome proliferation through animal-derived foods, or plant-derived foods - but they're neither optimal.

It'd be better if in effect chronic aerobic activity was the basis to PPAR activation and peroxisome proliferation.

From publications - forcing the white to brown (healthy) fat transition and supporting the usage of fat in thermogenesis as well as energy generation.

eg
1 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410936/

So - we have all of this fat - but it just doesn't seem to be being used to keep us warm.
Need for brown fat formation.
Forced by omega-3 consumption (not optimal), our own gut microbial transformation (proven in vegan higher primates) ??? or just through prolonged aerobic activity ??? [suggestion]

SB_UK
07-23-15, 03:28 AM
Yay!!

Dana-Farber Cancer Institute researchers have identified a new hormone dubbed irisin that is induced by exercise and triggers the conversion of white fat to brown-like fat in mice
http://www.nature.com/scibx/collections/brownfat/index.html#article4

SB_UK
07-23-15, 03:45 AM
So - the human life-cycle profile will look something like.

[1] Mother's milk <- sole requirement for an animal-derived product ?
[2] Shift from acute anabolic (insulin/IGF-1) anaerobic to chronic aerobic ie the Usain Bolt to Mo Farah transition in food required / physical activity profile ie from protein/carbs to fat to caloric restriction
question ? - why do people favour the anabolic profile of food intake - see primitive reward system - umami/sweet/salt are wired into the primitive reward system - particularly the combination -

umami [protein,glutamate] -> McDonalds burgers with added MSG
sweet [fructose,sucrose] -> McDonalds tomato ketchup and gherkin
salt -> McDonalds salt-laden produce
-- with 'protein power' (Eades and Eades) featuring a table a massive interaction between protein and carb (partic animal protein and high GI carb intake (seen in other publications)) on insulin levels ie far greater an effect on insulin - than either carb or protein alone.

[3] Representing a shift from 'growth' into 'maintenance' (brown fat) phenotype

Until brown fat's dynamic duo of the peroxisome and mitochondria takes the full force of human metabolic (heat and energy) generation.

What's the problem with fatty fish ? (http://www.aquamedia.at/Baltic-Fish-May-be-Too-Toxic-to-be-Sold-in-the-EU.2456.0.html)
The fats preferentially absorb organic carcinogens and heavy metals - many of our own making - which result in net consequences which outweigh any benefit from omega-3 consumption.

http://www.fao.org/docrep/article/agrippa/x9500e04.htm
A wide range of organic and inorganic compounds may occur in feedstuffs, including pesticides, industrial pollutants, radionuclides and heavy metals. Pesticides that may contaminate feeds originate from most of the major groups, including organochlorine, organophosphate and pyrethroid compounds (van Barneveld, 1999).The consumption of fat by its very nature must concentrate organic (hydrophobic) compounds - which're then passed on.

Completely powered by SCFAs (generated by some means) directly into Complex II mitochondria

bypass Complex I

eg

We also provide in vivo and in vitro evidence that DβHB protects not by alleviating MPTP-related complex I inhibition, but by enhancing oxidative phosphorylation via a mechanism dependent on mitochondrial complex II (succinate-ubiquinone oxidoreductase).http://www.ncbi.nlm.nih.gov/pmc/articles/PMC193668/

-*-

The sole question is where do we get our 'fat' from ?

Eating it is so yesterday's news.

SB_UK
07-23-15, 04:05 AM
So - T2D's magical drugs of 'fibrates and TZDs' are simply peroxisomal proliferators which operate as part of a white to brown fat transition - which can be forced by the need for peroxisomes
- need being driven by regulated peroxide generation from regulated constant aerobic exercise ?

Sufficient intensity to drive the need for adaptation.

-*-

So once again (much like the cerebellar story for neurodevelopmental conditions) wholly environmental (the current T2D/obesity) solution in nature.

Core problem - an inflexible society which demands a certain level of mental acuity at a certain age to pass specific exams to gain a job which pays money which permits survival.
Net effect - insufficient time for learning, insufficient time for exercise.

Simply parrot learn (not learn properly) information at school and then spend one's life 365 days a year pursuing pointless, often complex systems (eg the lawyer and legal systems) which fuel primitive reward systems (money, power, sex craving) and do not allow the human lifecycle representing development (to transcend the primitive reward system into free will (enforced moral consistency)) to complete.

SB_UK
07-23-15, 04:26 AM
Particularly like the idea of mitocondria cutting Complex I off and allowing beta-hydroxybutyrate to enter at Complex II - because that symbolically divorces the mitochondria fom glycolysis - the primitive energy generating facility and as stated in 'The Warburg Effect' - the key mechanism at play in cancer.

primitive to higher reward system
->-
Substantia nigra's free dopamine (potentiated by ADHD meds) to polymerized dopamine (neuromelanin) formation.