The Travis Corner

[Hairfedup]

Are you sure it's not an issue with muscles of the pelvic floor? Can the prostate "spasm"? I think you diagnosed yourself online and ended up with cancer. Just so you know I survived 24 (100%) Google-induced cancers.

Oh wow...yeah I guess it really could be the pelvic floor...its just the heaviness in the rectum that made me think prostate. Google can really scare you lol.

 

[Travis]

travis there was a study showing that mice treated with histamine stopped having tic-like behavior, why do you think this is?
Tourette-like tics vanish in mice treated with histamine

I think histamine is a complex neurotransmitter similar to serotonin, so it matters what part of the brain its found in. I am not sure how much the 'excessive grooming' noted in the rats is really analogous to tic‐like behaviour, and it seems somewhat of a stretch to consider it such. Under their model, hundreds of molecules could probably be shown to reduce 'tic‐like behaviour'—or excessive grooming.

 

[Travis]

Do you think it’s because it prevents a buildup of polyamines? Do the studies suggest an optimal frequency?

No, but these were dose‐dependent relationships; so I don't think there's a limit to how much this should work.

 

[BigYellowLemon]

@Travis

So if any PUFA is consumed, it should be a-linolenic acid, EPA/DHA are the only ones out of the Omega-3s that can be metabolized into toxic prostaglandins, yet a-linolenic acid will still up the 3/6 ratio, and whatever DHA we need can be synthesized and used.

And also, two questions about Mead acid:

1: do you think Mead acid can replicate the cholesterol exclusion of DHA? No other PUFA can substitute for DHA in the brain, but Mead acid may be different. See this comment by Tyw: Some Thoughts On Avocadoes

Perhaps in developing humans DHA is needed, but in fully grown humans, Mead acid can sustain whatever white matter structures have been built already. Also with 5mg DHA daily uptake and use in the brain, it'd only be 3 years until all brain DHA is replaced (of course this is assuming it's not just some small pool of DHA within the brain being recycled, with the rest locked away).

With Mead acid replacing DHA, you'd (potentially) have a brain twice as resistant to oxidation as a normal one - or more.

Of course, DHA likely cannot replace functions like rhodopsin, or any other currently unknown functions of DHA in which the incredibly fast molecular motion of DHA is utilized.

2: How potent are the prostaglandins which Mead acid creates? As far as I know, they're just as strong as arachidonic acid metabolites. The only sources I've seen for Mead acid says this, I cannot find anything about Mead acid creating "anti-inflammatory prostaglandins".

If Mead acid doesn't create prostaglandins and similar PUFA metabolites which are weaker then omega-3 metabolites, and if it can't replace the functions of DHA, then I think a small amount of a-linolenic would be better - it creates weak prostaglandins, is likely as oxidatively fragile as Mead acid, yet can fulfill the needs of the brain for DHA.

Also, just so everyone is aware, Birds, Bats, and Naked Mole Rats, and really any animal has mostly the same mitochondrial membrane composition - the main difference is the levels of DHA, which is multitudes more fragile than anything else. B/B/NMR have mitochondria that are pretty standard, except they have low DHA. Humans are actually similar, in fact humans likely have even more DHA depleted membranes than NMR.

Lifespan seems to mainly be correlated with DHA levels, and the smaller the animal, the more DHA is found on membranes, and vice versa. This is because of volume/surface area scaling, in which the larger an animal becomes, the lower the rates of oxidation required. Nothing intrinsic about size, it's more that size favors certain traits which make rates of oxidation much higher, and which also effects lifespan. This is also why the bigger an animal gets, the slower the heart rate becomes.

 

[Travis]

@Travis

So if any PUFA is consumed, it should be a-linolenic acid, EPA/DHA are the only ones out of the Omega-3s that can be metabolized into toxic prostaglandins, yet a-linolenic acid will still up the 3/6 ratio, and whatever DHA we need can be synthesized and used.

And also, two questions about Mead acid:

1: do you think Mead acid can replicate the cholesterol exclusion of DHA? No other PUFA can substitute for DHA in the brain, but Mead acid may be different. See this comment by Tyw: Some Thoughts On Avocadoes

Perhaps in developing humans DHA is needed, but in fully grown humans, Mead acid can sustain whatever white matter structures have been built already. Also with 5mg DHA daily uptake and use in the brain, it'd only be 3 years until all brain DHA is replaced (of course this is assuming it's not just some small pool of DHA within the brain being recycled, with the rest locked away).

With Mead acid replacing DHA, you'd (potentially) have a brain twice as resistant to oxidation as a normal one - or more.

Of course, DHA likely cannot replace functions like rhodopsin, or any other currently unknown functions of DHA in which the incredibly fast molecular motion of DHA is utilized.

2: How potent are the prostaglandins which Mead acid creates? As far as I know, they're just as strong as arachidonic acid metabolites. The only sources I've seen for Mead acid says this, I cannot find anything about Mead acid creating "anti-inflammatory prostaglandins".

If Mead acid doesn't create prostaglandins and similar PUFA metabolites which are weaker then omega-3 metabolites, and if it can't replace the functions of DHA, then I think a small amount of a-linolenic would be better - it creates weak prostaglandins, is likely as oxidatively fragile as Mead acid, yet can fulfill the needs of the brain for DHA.

Also, just so everyone is aware, Birds, Bats, and Naked Mole Rats, and really any animal has mostly the same mitochondrial membrane composition - the main difference is the levels of DHA, which is multitudes more fragile than anything else. B/B/NMR have mitochondria that are pretty standard, except they have low DHA. Humans are actually similar, in fact humans likely have even more DHA depleted membranes than NMR.

Lifespan seems to mainly be correlated with DHA levels, and the smaller the animal, the more DHA is found on membranes, and vice versa. This is because of volume/surface area scaling, in which the larger an animal becomes, the lower the rates of oxidation required. Nothing intrinsic about size, it's more that size favors certain traits which make rates of oxidation much higher, and which also effects lifespan. This is also why the bigger an animal gets, the slower the heart rate becomes.

Nothing can substitute for DHA in the brain, not even DPA which has five double bonds. You can see this during the MRI in Zellweger's and related syndromes: arachidonic acid is less effective than docosapentaenoic acid, which is in turn less effective than docosahexaenoic acid at excluding sterols.

So it appears as though α-linoleneic acid is the only obligatory fatty acid; it also serves as the precursor to eicosapentaenoic acid, which forms the less-active 3-series prostaglandins.

 

[Obi-wan]

Multiple studies[18][19] have shown a relationship between α-linolenic acid and an increased risk of prostate cancer. This risk was found to be irrespective of source of origin (e.g., meat, vegetable oil).[20] However, a large 2006 study found no association between total α-linolenic acid intake and overall risk of prostate cancer;[21] and a 2009 meta-analysis found evidence of publication bias in earlier studies, and concluded that if ALA contributes to increased prostate cancer risk, the increase in risk is quite small.[22] -Wilkipedia

So according to @Travis Linolenic acid forms 2-series prostaglandins and gets into the inside of the cell and causes proliferation
But alpha-linolenic forms 3-series prostaglandins that do not get into the inside of the cell.

Am I on the right page Travis?

 

[Travis]

Multiple studies[18][19] have shown a relationship between α-linolenic acid and an increased risk of prostate cancer. This risk was found to be irrespective of source of origin (e.g., meat, vegetable oil).[20] However, a large 2006 study found no association between total α-linolenic acid intake and overall risk of prostate cancer;[21] and a 2009 meta-analysis found evidence of publication bias in earlier studies, and concluded that if ALA contributes to increased prostate cancer risk, the increase in risk is quite small.[22] -Wilkipedia

So according to @Travis Linolenic acid forms 2-series prostaglandins and gets into the inside of the cell and causes proliferation
But alpha-linolenic forms 3-series prostaglandins that do not get into the inside of the cell.

Am I on the right page Travis?

The name linolenic acid is given to 18∶3, but does not specify where the double bonds are—but this matters, so they use Greek lowercase gamma and alpha to denote explicitly the ω−6 and the ω−3 bond position. If α-linolenic acid caused cancer it wouldn't matter, since we'd be dead without it (unless a person ate fish). The γ-linolenic acid is the ω−6 and does everything that linoleic acid does; in fact, linoleic acid becomes γ-linolenic acid before it becomes arachidonic acid:

linoleic acid ⟶ γ-linolenic acid ⟶ arachidonic acid​

I have seen a study with α-linolenic acid and cancer, and perhaps this should be looked at. Sometimes blood cell membrane lipids and/or those on lipoproteins are measured, reflecting recent consumption. But obviously, people diagnosed with cancer often change their diet and small studies like that may not mean much. The Paul Godley study had used a biopsy of adipose tissue and had found a higher risk for γ-linolenic acid than for α-linolenic acid, although that did carry some risk. Perhaps α-linolenic acid also needs to be kept in range, consuming only small amounts for DHA synthesis (?) and avoiding prostaglandins almost entirely—even the 3-series ones?

 

[Obi-wan]

Table 6. Food sources of alpha-linolenic acid (PFA 18:3), listed in descending order by percentages of their contribution to intake, based on data from the National Health and Nutrition Examination Survey 2005-2006


Rank Food item Contribution to intake (%) Cumulative contribution (%)
1 Salad dressing 10.5 10.5
2 Chicken and chicken mixed dishes 6.4 17.0
3 Grain-based desserts 6.1 23.1
4 Pizza 5.8 28.9
5 Yeast breads 5.0 33.9
6 Mayonnaise 4.0 37.9
7 Pasta and pasta dishes 3.5 41.4
8 Quickbreads 3.4 44.9
9 Fried white potatoes 2.8 47.7
10 Mexican mixed dishes 2.7 50.4
11 Nuts/seeds and nut/seed mixed dishes 2.7 53.1
12 Burgers 2.6 55.7
13 Margarine 2.6 58.3
14 Regular cheese 2.6 60.8
15 Dairy desserts 2.2 63.1
16 Whole milk 2.2 65.3
17 Eggs and egg mixed dishes 2.2 67.4
18 Other fish and fish mixed dishes 2.0 69.4

 

[Obi-wan]

Seed oils are the richest sources of α-linolenic acid, notably those of chia, perilla, flaxseed (linseed oil), rapeseed (canola), and soybeans. α-Linolenic acid is also obtained from the thylakoid membranes in the leaves of Pisum sativum (pea leaves).[7] Plant chloroplasts consisting of more than 95 percent of photosynthetic thylakoid membranes are highly fluid due to large abundance of linolenic acid, that shows up as sharp resonances in high resolution carbon-13 NMR spectra, invariably.[8] Some studies state that ALA remains stable during processing and cooking.[9] However, other studies state that ALA might not be suitable for baking, as it will polymerize with itself, a feature exploited in paint with transition metal catalysts. Some ALA may also oxidize at baking temperatures.[10] ALA percentages in the table below refer to the oils extracted from each item.

Common name Alternate name Linnaean name % ALA†(of oil) ref.
Chia chia sage Salvia hispanica 64% [11]
Kiwifruit seeds Chinese gooseberry Actinidia chinensis 62% [11]
Perilla shiso Perilla frutescens 58% [11]
Flax linseed Linum usitatissimum 55% [11]
Lingonberry cowberry Vaccinium vitis-idaea 49% [11]
Camelina camelina Camelina sativa 35-45%
Purslane portulaca Portulaca oleracea 35% [11]
Sea buckthorn seaberry Hippophae rhamnoides L. 32% [12]
Hemp cannabis Cannabis sativa 20% [11]
Walnut English walnut / Persian walnut Juglans regia 10.4% [13]
Rapeseed canola Brassica napus 10% [2]
Soybean soya Glycine max 8% [2]
†average value
-Source Wikipedia

 

[Obi-wan]

If I stay away from foods that are very high in Linoleic acid I also stay away from foods high in alpha- Linolenic acid

 

[Obi-wan]

Another list of foods high in Linoleic Acid from Wikipedia:

Name % LA† ref.
Salicornia oil 75%
Safflower oil 74.62%
Evening Primrose oil 65-80% [19]
Poppyseed oil 70%
Grape seed oil 69.6%
Sunflower oil 65.7%
Prickly Pear seed oil 62.3%
Barbary Fig Seed Oil 65%
Hemp oil 54.3% [20]
Corn oil 59%
Wheat germ oil 55%
Cottonseed oil 54%
Soybean oil 51%
Walnut oil 51%
Sesame oil 45%
Rice bran oil 39%
Argan oil 37%
Pistachio oil 32.7%
Peanut oil 32% [21]
Peach oil 29% [22]
Almonds 24%
Canola oil 21%
Chicken fat 18-23% [23]
Egg yolk 16%
Linseed oil 15%
Lard 10%
Olive oil 10% (3.5 - 21%) [24][25]
Palm oil 10%
Durio graveolens 4.95% [26]
Cocoa butter 3%
Macadamia oil 2%
Butter 2%
Coconut oil 2%
†average val

Travis's dreaded egg stands in at 16%, right below chicken fat. My prostate cancer become more aggressive when I consumed chicken bone broth with egg drop.

 

[Amazoniac]

Salicornia oil 75%

I wasn't aware of this one.
__

Butter 2%
Coconut oil 2%

I wonder if it's good to consume a bit of dairy fat along with coconut fat since you mentioned that there is competition between omega 3 and 6, and coconut fat has no omega 3. Same for cocoa butter.

When Did This Forum Start Complaining About The PUFA In Coconut Oil ?
Apparently tyw doesn't think so:
Omega-3 Fatty Acids Fight Inflammation Via Cannabinoids ?

?

 

[Obi-wan]

And arachidonic acid converts to prostaglandin E2

The derived name blew my mind. From Wikipedia:

The name prostaglandin derives from the prostate gland. When prostaglandin was first isolated from seminal fluid in 1935 by the Swedish physiologist Ulf von Euler,[2] and independently by M.W. Goldblatt,[3] it was believed to be part of the prostatic secretions. In fact, prostaglandins are produced by the seminal vesicles. It was later shown that many other tissues secrete prostaglandins for various functions. The first total syntheses of prostaglandin F2α and prostaglandin E2 were reported by E. J. Corey in 1969,[4] an achievement for which he was awarded the Japan Prize in 1989.

In 1971, it was determined that aspirin-like drugs could inhibit the synthesis of prostaglandins. The biochemists Sune K. Bergström, Bengt I. Samuelsson and John R. Vane jointly received the 1982 Nobel Prize in Physiology or Medicine for their research on prostaglandins.

Another PLUS for aspirin!

 

[Obi-wan]

Aspirin causes several different effects in the body, mainly the reduction of inflammation, analgesia (relief of pain), the prevention of clotting, and the reduction of fever. Much of this is believed to be due to decreased production of prostaglandins and TXA2. Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme.[1] This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors. However, other effects of aspirin, such as uncoupling oxidative phosphorylation in mitochondria, and the modulation of signaling through NF-κB, are also being investigated. Some of its effects are like those of salicylic acid, which is not an acetylating agent.

There are at least two different cyclooxygenase isozymes: COX-1 (PTGS1) and COX-2 (PTGS2). Aspirin is non-selective and irreversibly inhibits both forms[4][better source needed] (but is weakly more selective for COX-1[5]). It does so by acetylating the hydroxyl of a serine residue.[6] Normally COX produces prostaglandins, most of which are pro-inflammatory, and thromboxanes, which promote clotting. Aspirin-modified COX-2 produces lipoxins, most of which are anti-inflammatory.

@Travis, aspirin should also prevent prostaglandin E2...

 

[pimpnamedraypeat]

Hey travis what do you know about ordered water in the living body and, hypothetically, could the process that underlies that ordering take place in other materials and in other contexts?

 

[Travis]

Hey travis what do you know about ordered water in the living body and, hypothetically, could the process that underlies that ordering take place in other materials and in other contexts?

Yes. The ordering of water varies from highly ordered as seen in ice, to the near total disorder seen in vapor—although it could become even further disordered by ionization, and further yet by nuclear fission (although of course it stops being 'water' at this point). If you look at the crystal structure of the idealized pure ice, you'll notice that it's geometrically perfect: corresponding bond angles are parallel to eachother and each oxygen is separated by the same distance(s). The idealized ice only happens at absolute zero, or 0 degrees Kelvin.

With temperature you get movement. Temperature is described as molecular kinetic energy; molecules start bouncing around, vibrating, and bending—sometimes millions of times per second (the IR spectra of a molecule corresponds to intramolecular bending frequencies). So with every degree increase in temperature, you'd expect another unit of deviation from the ideal 'ice' crystal at 0‧K; this can all be mathematically defined. However, there are ways to increase 'order' without changing the temperature: certain ions or certain protein configurations will order water more than you'd expect it to be ordered at that temperature, making the water appear at a lower temperature (kinetically). I think some definitions of temperature—those based on kinetic energy—would even allow you to state that it actually is at a lower temperature, even in the body where you could prove it to be at 98.6°F in other ways. I think a formal definition of water structuring could revolve around free energy, enthalpy, and entropy: ΔG = ΔH − TΔS. Chemically, I think the enthalpy term (ΔH) describes internal bending and internal bond energy; the entropy term (ΔS) would more‐or‐less describe the 'order'—which gets multiplied by temperature. Entropy is somewhat hard to define. The words 'entropy' and 'disorder' are commonly found in the same sentence, but a formal definition of entropy is difficult because its essentially a statistical parameter created in the age of steam engines.

 

[pimpnamedraypeat]

certain ions or certain protein configurations will order water more than you'd expect it to be ordered at that temperature, making the water appear at a lower temperature (kinetically). I think some definitions of temperature—those based on kinetic energy—would even allow you to state that it actually is at a lower temperature, even in the body where you could prove it to be at 98.6°F in other ways.

Interesting. I wonder how these proteins do that. My guess is via an electromagnetic field. This study showed that you can double the water pumped by a protein with an electric field

“Electropumping of Water Through Human Aquaporin 4 by Circularly Polarized Electric Fields: Dramatic Enhancement and Control Revealed by Non-Equilibrium Molecular Dynamics”.

Applying an electric field to water in a naturally occurring protein substantially boosts the flow of the liquid

The research found that applying circularly polarised electric fields to water in human membrane-protein channels, known as aquaporin 4, resulted in “electro-pumping” that doubles the flow of water through the biological channels.

Aquaporins (AQP) are proteins that channel water in all known life forms and are crucial to the regulation of water in organs and cells.

The investigators used a molecular dynamics simulation to study what effect the application of the external force of an electric field would have on the permeability – or flow of water – through an aquaporin.

Circularly polarised (CP) electric fields rotate in a propeller-like manner. The investigators found that when applied to water molecules’ the rotational or propeller-like momentum of the CP field thrusts water into linear or forward momentum.

The application of the electric CP fields resulted in what they described as “electro-pumping”, which doubled the flow of water through the aquaporin.

The analyses also found that salt molecules in salt water are too large to exit the aquaporins, and, as a result, the process also provides a method of desalinating water.

“What is novel [in this study] is our ability to control and manipulate the amount and the speed and rate at which water is permeating through the membrane,” said Professor Niall English.

“We can double the rate of permeability of the water through aquaporins using CP fields.”

The authors concluded that the “electro-pumping” raises the “breakthrough possibility of rotating-field enhancement and control over water permeability in aquaporins, or other biochannels as a potentially viable and competitive water treatment technology”.

Yes indeed, structured water seems to be an electric phenomenon, bar none.

 

[Travis]

This is interesting, and can perhaps be understood geometrically.

Below is shown the aquaporin. What had surprised me was the narrow channel in relation to the water molecule's size, almost as if they have to travel single‐file. This article had been published this year, so these are probably the next generation of molecular models. I have to admit, the one seen below is fairly good though he doesn't tell us what the colors indicate (he actually took the image from a previous article on the exact same thing).

I wish he'd give us details about the electrode which applied the field, but he doesn't—perhaps the other article does. He explains this in a water‐dependent manner, and nothing is said about how the protein itself is affected by the magnetic field.

'CP-field-induced roto-translational coupling of nanoscale-confined water molecules in asymmetric environments, via coupling of their spin angular momentum to their linear momentum to induce positive net flow—“electropumping”, as it were...' ―Burnham​

Not sure about his explanation: The spin angular momentum (quantum mechanical) is not permanently oriented along the long axis of the water molecule, but exists on all electrons in a random orientation. The only things permanently related to the water molecule as a whole is the center of gravity and the dipole moment, which exists perpendicular to the long axis and can be effected by a magnetic field. The spin angular momentum can be aligned with the field but this alone probably wouldn't reorient the water molecule like the dipole moment will (1.85‧D)—which is substantial for water. I don't you'd be able to align nonpolar molecules, like liquid propane (0.132‧D), as you can align water. Perhaps he's trying to make this sound more sophisticated and hip than it is, I don't know; but at least he doesn't use the word 'quantum' anywhere in the article. He does, however, say this:

'...tantalizing possibility of using “propeller-like” circularly polarized (CP), rotating electric fields to boost “electro-osmotic” water flow more substantially in confined nanochannels’ milieux.' ―Burnham​

Not sure about the propeller analogy; I mean, I get it: It's spinning and it's moving, yet it has nothing to push against. An actual propeller is much larger than the surrounding air/water that propels it through the medium; tiny water molecules have none of this—they are the medium, and have nothing to push against besides the vacuum or a few other water molecules at most. I know that not all analogies are perfect, but they should be when you're trying to conceptualize these effects. I think it's enough to say that the circularly‐polarized electromagnetic field aligns the water molecules axially through their dipole moments while giving them rotational inertia along same axis. The lowering of the cross section presented to the pore would lower the electrostatic interactions with said protein and its induced spin would do likewise—further increasing the flow rate. Perhaps it would be interesting to see how the other author explains it, of who's 2011 article that molecular model (above) was lifted:

Garate, J-A. "Human aquaporin 4 gating dynamics in dc and ac electric fields: a molecular dynamics study." The Journal of chemical physics (2011)​

Okay, the original article has more realistic language despite having one of the same authors listed. This one focuses a bit on the protein and even hypothesizes a 'gating mechanism' involved, one involving the histidine²⁰¹ and arginine²¹⁶ side chains.

'Nevertheless, the “signature” dipole rotation in the C.R. does necessarily take place to a greater or lesser extent in all cases, to allow water passage through the AQPs.' ―Garate

'Although we relate this primarily to the high side-chain (gating) dynamics of H²⁰¹, water orientation dynamics are also an important factor. This is confirmed with static efz water orientations where the dipole orientation distribution P₁(z) is shifted to lower values, meaning that water molecules are trying to align with the field applied in the –z direction, thus presenting a more defined dipolar orientation which is correlated with an increase in permeabilities.' ―Garate

'We observed that lower permeabilities coincide with greater variability in, and disruption to, water dipolar orientation; especially for the static efz case, the dipole alignment enhances water incorporation inside C.R.' ―Garate

'The torsional angles of the side-chain of H²⁰¹ exist in at least two transient states, designated up and down; the former configuration enhances water conduction due to an increment in the pore radius at the S.F. region, although we have found that rapid “up/down” transitions also serve to increase permeabilities. It has been observed that the fields alter the side-chain dynamics of both residues in the S.F., confirming that H²⁰¹ torsional dynamics is highly relevant for human aquaporin water conductivity.' ―Garate

'DC and ac fields alter water dynamics within the lumen of the pores. One particular effect is the disruption of the well-defined water dipolar orientation. This is expected, as the principal effect of the electric fields is dipolar reorientation (especially for static electric or low-frequency fields). It was found that the less well defined the dipolar orientation, the lower the magnitude of the permeabilities. An interesting point is the case of a static electric field applied in the −z direction. As we have shown previously, electric fields applied along the axis of (5,5) single-walled carbon nanotubes enhance water fluxes therein by a shift in dipolar orientation of the water molecules; a similar effect occurs in human aquaporin.' ―Garate

'...while the very well-conserved asparagine–proline–alanine (NPA) motif serves as the other, in which a finely defined water dipole rotation take place during passage.' ―Garate

'...as stated above, a fine electrostatic tuning of the water molecules’ dipoles is achieved by aquaporins.' ―Garate​

I'm getting the impression that he thinks histidine²⁰¹ imparts a spin and aligns water molecules down he pore, catalyzing flow more than you'd expect from diffusion alone in in its absence (the football spiral analogy; human aquaporin var. Eli Manning).

He uses the dipole moment to describe all of this and speaks of spin angular momentum not once. He even presents a simple equation describing the cross section of the water molecule presented to aquaporin:

'C. Water orientation The water molecules’ orientation inside the constriction region is described by

P₁(x) = cos(θ)ₓ
​

...where θ is the angle between the dipole moment of water and the z axis, the position along the pore axis.' ―Garate​

So I'm on board with this guy, and think the axial alignment of the water molecules are the primary effect (dependent on the electric field acting on the dipole moment and not the electrons' spin angular momentum.)

'This may be explained by the very tight and narrow pore present in h-AQP4 which hinders water rotation.' ―Garate​

 

[Hairfedup]

And arachidonic acid converts to prostaglandin E2

The derived name blew my mind. From Wikipedia:

The name prostaglandin derives from the prostate gland. When prostaglandin was first isolated from seminal fluid in 1935 by the Swedish physiologist Ulf von Euler,[2] and independently by M.W. Goldblatt,[3] it was believed to be part of the prostatic secretions. In fact, prostaglandins are produced by the seminal vesicles. It was later shown that many other tissues secrete prostaglandins for various functions. The first total syntheses of prostaglandin F2α and prostaglandin E2 were reported by E. J. Corey in 1969,[4] an achievement for which he was awarded the Japan Prize in 1989.

In 1971, it was determined that aspirin-like drugs could inhibit the synthesis of prostaglandins. The biochemists Sune K. Bergström, Bengt I. Samuelsson and John R. Vane jointly received the 1982 Nobel Prize in Physiology or Medicine for their research on prostaglandins.

Another PLUS for aspirin!

I know it sounds crazy, but could excessive ejaculation increase production of PGD2 in the seminal vesicles....

 

[pimpnamedraypeat]

This is interesting, and can perhaps be understood geometrically.

Below is shown the aquaporin. What had surprised me was the narrow channel in relation to the water molecule's size, almost as if they have to travel single‐file. This article had been published this year, so these are probably the next generation of molecular models. I have to admit, the one seen below is fairly good though he doesn't tell us what the colors indicate (he actually took the image from a previous article on the exact same thing).

View attachment 8371

I wish he'd give us details about the electrode which applied the field, but he doesn't—perhaps the other article does. He explains this in a water‐dependent manner, and nothing is said about how the protein itself is affected by the magnetic field.

'CP-field-induced roto-translational coupling of nanoscale-confined water molecules in asymmetric environments, via coupling of their spin angular momentum to their linear momentum to induce positive net flow—“electropumping”, as it were...' ―Burnham​

Not sure about his explanation: The spin angular momentum (quantum mechanical) is not permanently oriented along the long axis of the water molecule, but exists on all electrons in a random orientation. The only things permanently related to the water molecule as a whole is the center of gravity and the dipole moment, which exists perpendicular to the long axis and can be effected by a magnetic field. The spin angular momentum can be aligned with the field but this alone probably wouldn't reorient the water molecule like the dipole moment will (1.85‧D)—which is substantial for water. I don't you'd be able to align nonpolar molecules, like liquid propane (0.132‧D), as you can align water. Perhaps he's trying to make this sound more sophisticated and hip than it is, I don't know; but at least he doesn't use the word 'quantum' anywhere in the article. He does, however, say this:

'...tantalizing possibility of using “propeller-like” circularly polarized (CP), rotating electric fields to boost “electro-osmotic” water flow more substantially in confined nanochannels’ milieux.' ―Burnham​

Not sure about the propeller analogy; I mean, I get it: It's spinning and it's moving, yet it has nothing to push against. An actual propeller is much larger than the surrounding air/water that propels it through the medium; tiny water molecules have none of this—they are the medium, and have nothing to push against besides the vacuum or a few other water molecules at most. I know that not all analogies are perfect, but they should be when you're trying to conceptualize these effects. I think it's enough to say that the circularly‐polarized electromagnetic field aligns the water molecules axially through their dipole moments while giving them rotational inertia along same axis. The lowering of the cross section presented to the pore would lower the electrostatic interactions with said protein and its induced spin would do likewise—further increasing the flow rate. Perhaps it would be interesting to see how the other author explains it, of who's 2011 article that molecular model (above) was lifted:

Garate, J-A. "Human aquaporin 4 gating dynamics in dc and ac electric fields: a molecular dynamics study." The Journal of chemical physics (2011)​

Okay, the original article has more realistic language despite having one of the same authors listed. This one focuses a bit on the protein and even hypothesizes a 'gating mechanism' involved, one involving the histidine²⁰¹ and arginine²¹⁶ side chains.

'Nevertheless, the “signature” dipole rotation in the C.R. does necessarily take place to a greater or lesser extent in all cases, to allow water passage through the AQPs.' ―Garate

'Although we relate this primarily to the high side-chain (gating) dynamics of H²⁰¹, water orientation dynamics are also an important factor. This is confirmed with static efz water orientations where the dipole orientation distribution P₁(z) is shifted to lower values, meaning that water molecules are trying to align with the field applied in the –z direction, thus presenting a more defined dipolar orientation which is correlated with an increase in permeabilities.' ―Garate

'We observed that lower permeabilities coincide with greater variability in, and disruption to, water dipolar orientation; especially for the static efz case, the dipole alignment enhances water incorporation inside C.R.' ―Garate

'The torsional angles of the side-chain of H²⁰¹ exist in at least two transient states, designated up and down; the former configuration enhances water conduction due to an increment in the pore radius at the S.F. region, although we have found that rapid “up/down” transitions also serve to increase permeabilities. It has been observed that the fields alter the side-chain dynamics of both residues in the S.F., confirming that H²⁰¹ torsional dynamics is highly relevant for human aquaporin water conductivity.' ―Garate

'DC and ac fields alter water dynamics within the lumen of the pores. One particular effect is the disruption of the well-defined water dipolar orientation. This is expected, as the principal effect of the electric fields is dipolar reorientation (especially for static electric or low-frequency fields). It was found that the less well defined the dipolar orientation, the lower the magnitude of the permeabilities. An interesting point is the case of a static electric field applied in the −z direction. As we have shown previously, electric fields applied along the axis of (5,5) single-walled carbon nanotubes enhance water fluxes therein by a shift in dipolar orientation of the water molecules; a similar effect occurs in human aquaporin.' ―Garate

'...while the very well-conserved asparagine–proline–alanine (NPA) motif serves as the other, in which a finely defined water dipole rotation take place during passage.' ―Garate

'...as stated above, a fine electrostatic tuning of the water molecules’ dipoles is achieved by aquaporins.' ―Garate​

I'm getting the impression that he thinks histidine²⁰¹ imparts a spin and aligns water molecules down he pore, catalyzing flow more than you'd expect from diffusion alone in in its absence (the football spiral analogy; human aquaporin var. Eli Manning).

He uses the dipole moment to describe all of this and speaks of spin angular momentum not once. He even presents a simple equation describing the cross section of the water molecule presented to aquaporin:

'C. Water orientation The water molecules’ orientation inside the constriction region is described by

P₁(x) = cos(θ)ₓ
​

...where θ is the angle between the dipole moment of water and the z axis, the position along the pore axis.' ―Garate​

So I'm on board with this guy, and think the axial alignment of the water molecules are the primary effect (dependent on the electric field acting on the dipole moment and not the electrons' spin angular momentum.)

'This may be explained by the very tight and narrow pore present in h-AQP4 which hinders water rotation.' ―Garate​

That's a bit disappointing I thought the elctric field was acting like a fan or propeller and pushing the water.

But alignment works too. I reckon it works better actually. Structured water is aligned water. If electric fields can align water with the proteins so it goes thought at 2x the rate I reckon the can align water ao it's structured.

I tagged you in haiduts thread aboit gravity. I wanted to see what thoughts you had on the charge seperation found in a bucket of flour shaken back and forth.