The Travis Corner

[Travis]

" I had just read the other day that 'prostaglandin E₂ activates Na⁺/K⁺-ATPase,' yet hadn't investigated that finding further. If true, this could perhaps be a mechanism for its carcinogenicity: Although it may seem quaint at first, the intracellular Na⁺/K⁺ ratio is a powerful regulator of growth. This determines the cell membrane potential, influences dNA replication, and is strongly correlated with mitotic index. Certain guanine-rich messenger RNA sequences actually chelate sodium, thereby precipitating into an inactivate state. Sodium has been shown to bind mammalian telomeres, and could influence chromatin condensation. The increased osmotic potential of Na⁺ relative to K⁺ could create the internal osmotic pressure needed for cellular expansion and mitosis."

-This is PROFOUND! and why I do ACV/potassium bicarbonate along with aspirin...keeping membrane potential in the -70 to -80 mV range and high potassium intracellular...

Potassium bicarbonate is the natural choice as it increases the pH of vinegar, yet potassium iodide is also useful. This supplies a different counterion, the iodide ion (I⁻), and although this is pH-neutral it is both a thyroxine precursor and a myeloperoxidase substrate. Potassium ascorbate would also seem helpful for many though you'd probably want to limit yourself to ~3·g/d, or 560·mg K⁺. A scale would be nice for accurately determining mass, both of the potassium and sodium salts ingested. A sodium∶potassium ratio of 1∶10 seems about right, or what is approximately the average of what 99% of mammals consume naturally. I consumed about 1∶16 yesterday.

Although this would be bound to increase aldosterone I don't think it would matter. The Yanomami Tribe does not appear to suffer for it, and nor do most other land mammals. Although aldosterone has a higher affinity for the nuclear mineralocorticoid receptor in vitro—in isolated binding assays—it is the most water-soluble sterol and hence most excluded from the cytosol in vitro. Cortisol can bind and activate the mineralocorticoid receptor nearly as well as aldosterone, and due to both its physiological concentration and inherent solubility you'd almost be forced to assume it's the proper endogenous ligand. Aldosterone works extracellularly on membrane receptors.

 

[Travis]

So now dear and very esteemed Travis discusses bacteria strains that are beingn or at the very least not harmful. Always with the Peat-rational in the background. I personally have long sought this kind of information. The sterile-gut idesl proposed by sind always made me feel uneasy, that’s simply not how human life evolved.
Have I something of worth to contribute here apart from my brabble? Only that Tri-Creatine-Malate, a popular sports supplement, always makes me feel quite good. Very ergogenic even acutely and feels like I can breathe a bit more deeply. Creative and Malate are both mito-respiration enhancing obviously

I am now curious about creatine's mechanism of action: The Wikipedia articles states that its 'main role is to facilitate recycling of adenosine triphosphate (ATP),' yet I find this explanation unrealistic. Adenosine triphosphate recycles itself multiple times per minute, rapidly cycling from cAMP to ATP as it conducts protons from the mitochondria to the cell membrane. As far as I'm concerned: cyclic AMP picks up three protons at the mitochondria thereafter becoming ATP, a molecule repelled from the mitochondria due to its high negative charge. Adenosine triphosphate then becomes hydrolyzed on the membrane by adenylyl cyclase, thereby releasing its protons into the extracellular fluid. This is how cytosolic pH is maintained throughout the glycolytic process, and also why the urine is acidic (and also why fire hydrants in Dalmationville are surrounded by patches of dead grass). Furthermore, the hydroxyl ion that is released via phosphodiester formation neutralizes another proton, making four total:

[1] cAMP⁻ + 2H⁺ ⟶ AMP⁻

[2] AMP⁻ + 2PO₄²⁻ + H⁺ ⟶ ATP⁴⁻ + OH⁻

[3] OH⁻ + H⁺ ⟶ H₂O​

Wikipedia indirectly contradicts itself in the very next paragraph by stating that its production rate is merely '1 gram per day,' certainly not enough to significantly contribute to ATP synthesis. Creatine is an N¹-methylated and N¹-acetylated substituted guanidinium, and as such you might wonder if it's a substrate of nNOS. Yet I can find no evidence of creatine either being a substrate or inhibitor of nNOS, and neither one of these properties could rightly account for its anabolic effects. But on a hunch, I had found these:

Löbner, Jürgen. "Creatine is a scavenger for methylglyoxal under physiological conditions via formation of N-(4-methyl-5-oxo-1-imidazolin-2-yl) sarcosine (MG-HCr)." Journal of agricultural and food chemistry (2015)

'Daily MG-HCr excretion of non-vegetarians ranged from 0.35 to 3.84 µmol/24 h urine and of vegetarians from 0.11 to 0.31 µmol/24 h urine, indicating that formation of MG-HCr in vivo is influenced by 10 the dietary intake of creatine.' ―Löbner

​

Roy, Soumya Sinha. "Protective effect of creatine against inhibition by methylglyoxal of mitochondrial respiration of cardiac cells." Biochemical Journal (2003)

'Moreover, post-mitochondrial supernatant (PMS) of cardiac cells could almost completely protect the mitochondrial respiration against the inhibitory effect of methylglyoxal. A systematic search indicated that creatine present in cardiac cells is responsible for this protective effect. Glutathione has also some protective effect. However, creatine phosphate, creatinine, urea, glutathione disulphide and β-mercaptoethanol have no protective effect. The inhibitory and protective effects of methylglyoxal and creatine respectively on cardiac mitochondrial respiration were studied with various concentrations of both methylglyoxal and creatine.' ―Roy

The creatine & methylglyoxal product also has a pKa closer to that of water, tending to facilitate proton transport. Imidazoles can enhance carbonic anhydrase activity for this reason, increasing the rate in which protons can be removed from the enzyme. Since carbonic anhydrase has unrestricted access to its two substrates, carbonic dioxide and water, what limits the rate is actually product removal. Enzyme chemists are unanimous in their belief that proton removal is indeed the rate limiting step of carbonic anhydrase.

 

[Travis]

- But ACV (Braggs) is easy to obtain and use as a raw vinegar...

I don't know where you live, but where I live Balsamic vinegar is more readily obtainable. In the grocery stores in my area: raw Balsamic vinegar outnumbers unpasteurized apple cider vinegar about 10∶1, by volume. Balsamic vinegar is also generally about ³⁄₄ the price, although of course it can be considerably more expensive. Apple cider vinegar has the benefit of entirely lacking that bourgeois Italian mystique, effectively fixing its price at $.15–.25 per ounce.

 

[Jon]

I am now curious about creatine's mechanism of action: The Wikipedia articles states that its 'main role is to facilitate recycling of adenosine triphosphate (ATP),' yet I find this explanation unrealistic. Adenosine triphosphate recycles itself multiple times per minute, rapidly cycling from cAMP to ATP as it conducts protons from the mitochondria to the cell membrane. As far as I'm concerned: cyclic AMP picks up three protons at the mitochondria thereafter becoming ATP, a molecule repelled from the mitochondria due to its high negative charge. Adenosine triphosphate then becomes hydrolyzed on the membrane by adenylyl cyclase, thereby releasing its protons into the extracellular fluid. This is how cytosolic pH is maintained throughout the glycolytic process, and also why the urine is acidic (and also why fire hydrants in Dalmationville are surrounded by patches of dead grass). Furthermore, the hydroxyl ion that is released via phosphodiester formation neutralizes another proton, making four total:

[1] cAMP⁻ + 2H⁺ ⟶ AMP⁻

[2] AMP⁻ + 2PO₄²⁻ + H⁺ ⟶ ATP⁴⁻ + OH⁻

[3] OH⁻ + H⁺ ⟶ H₂O​

Wikipedia indirectly contradicts itself in the very next paragraph by stating that its production rate is merely '1 gram per day,' certainly not enough to significantly contribute to ATP synthesis. Creatine is an N¹-methylated and N¹-acetylated substituted guanidinium, and as such you might wonder if it's a substrate of nNOS. Yet I can find no evidence of creatine either being a substrate or inhibitor of nNOS, and neither one of these properties could rightly account for its anabolic effects. But on a hunch, I had found these:

Löbner, Jürgen. "Creatine is a scavenger for methylglyoxal under physiological conditions via formation of N-(4-methyl-5-oxo-1-imidazolin-2-yl) sarcosine (MG-HCr)." Journal of agricultural and food chemistry (2015)

'Daily MG-HCr excretion of non-vegetarians ranged from 0.35 to 3.84 µmol/24 h urine and of vegetarians from 0.11 to 0.31 µmol/24 h urine, indicating that formation of MG-HCr in vivo is influenced by 10 the dietary intake of creatine.' ―Löbner

View attachment 10552 View attachment 10549

​

Roy, Soumya Sinha. "Protective effect of creatine against inhibition by methylglyoxal of mitochondrial respiration of cardiac cells." Biochemical Journal (2003)

'Moreover, post-mitochondrial supernatant (PMS) of cardiac cells could almost completely protect the mitochondrial respiration against the inhibitory effect of methylglyoxal. A systematic search indicated that creatine present in cardiac cells is responsible for this protective effect. Glutathione has also some protective effect. However, creatine phosphate, creatinine, urea, glutathione disulphide and β-mercaptoethanol have no protective effect. The inhibitory and protective effects of methylglyoxal and creatine respectively on cardiac mitochondrial respiration were studied with various concentrations of both methylglyoxal and creatine.' ―Roy

View attachment 10550 View attachment 10551

The creatine & methylglyoxal product also has a pKa closer to that of water, tending to facilitate proton transport. Imidazoles can enhance carbonic anhydrase activity for this reason, increasing the rate in which protons can be removed from the enzyme. Since carbonic anhydrase has unrestricted access to its two substrates, carbonic dioxide and water, what limits the rate is actually product removal. Enzyme chemists are unanimous in their belief that proton removal is indeed the rate limiting step of carbonic anhydrase.

So if I'm understanding this, your hypothesis is that creatine is facilitating a higher rate carbonic anhydrase substrate conversion thus a higher rate of glucose oxidation?

If that is what you're saying then that would make sense to me as to why creatine seems to increase serum insulin levels. I always wondered why it did that, but this seems like the best explanation so far. I actually never used it because of this effect but maybe it's not that much of a detriment with adequate fuel?

 

[Travis]

So if I'm understanding this, your hypothesis is that creatine is facilitating a higher rate carbonic anhydrase substrate conversion thus a higher rate of glucose oxidation?

If that is what you're saying then that would make sense to me as to why creatine seems to increase serum insulin levels. I always wondered why it did that, but this seems like the best explanation so far. I actually never used it because of this effect but maybe it's not that much of a detriment with adequate fuel?

I'm not sure if it effects carbonic anhydrase all that much due to its carboyxlate group, though it could, and was just using carbonic anhydrase mostly as an analogy. I think N-(4-methyl-5-oxo-1-imidazolin-2-yl) sarcosine could be dispersed more around the mitochondria, acting to disperse its proton gradient resulting from glucose respiration:

[1] C₆H₁₂O₆ + 6O₂ ⟶ 6H₂O + 6CO₂ + 2560·kJ​

This energy is not released released as heat within the body, and appears to be more-or-less harnessed for electricity. Glycolytic energy production works a bit differently in vivo, and the fist step releases two protons and gains 2 NADH molecules. Electrons are stored on NADH as the hydride ion (∶H⁻).

The NADH molecule is the real prime mover in my opinion, and that of Albert Szent–Györgyi as well. Nicotine adenine dinucleotide transfers its hydride to the mitochondrial complex down the electron transport chain, thereby regenerating NAD⁺. These electrons are removed from hydride by the electron transport chain, forming protons, ultimately going to heme's iron through a long line of CoQ₁₀ and cytochrome C oxidase:

[2] NADH ⟶ NAD⁺ + ∶H⁻​

[3] ∶H⁻ + Fe³⁺ ⟶ H⁺ + Fe⁺​

Oxygen gas it attached to this heme iron, which is then sequentially reduced to water but forms superoxide (¹Ȯ₂⁻) in the process. The phenomenon of nerve conduction—in my opinion—is caused by heme trapping singlet oxygen (¹O₂) fluorescence, thereafter sending the photonic energy down microtubules as Förster resonance. It's well known that glucose oxidation is the reverse of photosynthesis, yet I take it one step further by maintaining that photons enter both equations. Heme and chlorophyll are both porphyrins with a metal ligand.

As far as I'm concerned: adenosine triphosphate is an enzymatic cofactor, magnesium chelator, a pH buffer, and a transporter of protons from the mitochondrial membrane to the cytosol. Adenosine triphosphate is not 'the energy molecule,' an absurd idea started with the observation that ATP induces muscle contraction. The calcium ion (Ca²⁺) more fundamentally induces muscle contraction, and ATP can only do so as well by chelating calcium's muscle relaxing counterion—the magnesium ion (Mg²⁺)—thereby potentiating Ca²⁺ activity.

 

[Fractality]

Potassium bicarbonate is the natural choice as it increases the pH of vinegar, yet potassium iodide is also useful. This supplies a different counterion, the iodide ion (I⁻), and although this is pH-neutral it is both a thyroxine precursor and a myeloperoxidase substrate. Potassium ascorbate would also seem helpful for many though you'd probably want to limit yourself to ~3·g/d, or 560·mg K⁺. A scale would be nice for accurately determining mass, both of the potassium and sodium salts ingested. A sodium∶potassium ratio of 1∶10 seems about right, or what is approximately the average of what 99% of mammals consume naturally. I consumed about 1∶16 yesterday.

Although this would be bound to increase aldosterone I don't think it would matter. The Yanomami Tribe does not appear to suffer for it, and nor do most other land mammals. Although aldosterone has a higher affinity for the nuclear mineralocorticoid receptor in vitro—in isolated binding assays—it is the most water-soluble sterol and hence most excluded from the cytosol in vitro. Cortisol can bind and activate the mineralocorticoid receptor nearly as well as aldosterone, and due to both its physiological concentration and inherent solubility you'd almost be forced to assume it's the proper endogenous ligand. Aldosterone works extracellularly on membrane receptors.

What about sodium bicarbonate/baking soda and raw vinegar? @Obi-wan

 

[Obi-wan]

What about sodium bicarbonate/baking soda and raw vinegar? @Obi-wan

Sodium bicarbonate is baking soda

 

[Jon]

What about sodium bicarbonate/baking soda and raw vinegar? @Obi-wan

Doesn't that make sodium acetate?

Sodium bicarbonate is baking soda

The two together make sodium acetate, yes?

 

[Fractality]

Yes but does sodium acetate have the complete opposite effect(s) as potassium acetate?

 

[Jon]

Wow that was odd, I didn't mean to respond to both of you? Sorry about that.

 

[Obi-wan]

Doesn't that make sodium acetate?


The two together make sodium acetate, yes?

Yes and acetate and Co enzyme A is what is used in the Krebs cycle as acetyl CoA

 

[Obi-wan]

Yes but does sodium acetate have the complete opposite effect(s) as potassium acetate?

Same effect as acetyl CaA going into the Krebs cycle but different minerals. Inner potassium keeps a high potential in a cell so as Travis said keep a higher potassium to sodium ratio. Plus I feel a difference with potassium bicarbonate where sodium bicarbonate just gives me more energy

 

[Jon]

I'm not sure if it effects carbonic anhydrase all that much due to its carboyxlate group, though it could, and was just using carbonic anhydrase mostly as an analogy. I think N-(4-methyl-5-oxo-1-imidazolin-2-yl) sarcosine could be dispersed more around the mitochondria, acting to disperse its proton gradient resulting from glucose respiration:

[1] C₆H₁₂O₆ + 6O₂ ⟶ 6H₂O + 6CO₂ + 2560·kJ​

This energy is not released released as heat within the body, and appears to be more-or-less harnessed for electricity. Glycolytic energy production works a bit differently in vivo, and the fist step releases two protons and gains 2 NADH molecules. Electrons are stored on NADH as the hydride ion (∶H⁻).

The NADH molecule is the real prime mover in my opinion, and that of Albert Szent–Györgyi as well. Nicotine adenine dinucleotide transfers its hydride to the mitochondrial complex down the electron transport chain, thereby regenerating NAD⁺. These electrons are removed from hydride by the electron transport chain, forming protons, ultimately going to heme's iron through a long line of CoQ₁₀ and cytochrome C oxidase:

[2] NADH ⟶ NAD⁺ + ∶H⁻​

[3] ∶H⁻ + Fe³⁺ ⟶ H⁺ + Fe⁺​

Oxygen gas it attached to this heme iron, which is then sequentially reduced to water but forms superoxide (¹Ȯ₂⁻) in the process. The phenomenon of nerve conduction—in my opinion—is caused by heme trapping singlet oxygen (¹O₂) fluorescence, thereafter sending the photonic energy down microtubules as Förster resonance. It's well known that glucose oxidation is the reverse of photosynthesis, yet I take it one step further by maintaining that photons enter both equations. Heme and chlorophyll are both porphyrins with a metal ligand.

As far as I'm concerned: adenosine triphosphate is an enzymatic cofactor, magnesium chelator, a pH buffer, and a transporter of protons from the mitochondrial membrane to the cytosol. Adenosine triphosphate is not 'the energy molecule,' an absurd idea started with the observation that ATP induces muscle contraction. The calcium ion (Ca²⁺) more fundamentally induces muscle contraction, and ATP can only do so as well by chelating calcium's muscle relaxing counterion—the magnesium ion (Mg²⁺)—thereby potentiating Ca²⁺ activity.

This all makes so much sense! That you :). I drew a conclusion you were mentioning carbonic anhydrase due to creatine' ability of increasing intracellular and extracellular water concentrations and so figured maybe you were saying creating acted by facilitating substrate conversion.

If it's any consolation/compliment to you and others I ask these ignorant questions, I have always been the stupid but quiet kid in class. unfortunately for you and the others I bother, I'm not afraid to fly my ignorance shamelessly as I always get a very satisfying answer, or a further ingriguing topic to ponder. So thanks for that :)

 

[Travis]

Yes but does sodium acetate have the complete opposite effect(s) as potassium acetate?

And acetate ion complexes more strongly with K⁺ than with Na⁺. I personally use sodium bicarbonate because this is all I have at the moment, yet I do have potassium iodide to counter it. My salt mix has about 25% KI and 75% NaCl and I barely use it besides. Ever since I had started taking some potassium iodide my salt tolerance has dropped like a lead zeppelin: I can eat sauerkraut on a salad yet I do have to soak it in water first to 'desalt' it. Since I consume all fruit and plants having a Na⁺∶K⁺ ratio of about 12∶1, I don't mind consuming some extra sodium since this is balanced: (1) by the food, and also by (2) the potassium iodide. Most people consume more potassium than sodium, yet some inner city dwellers are recorded as consuming a ratio of unity or even inverted. This is no bueno for blood pressure and high membrane potential, and I certainly think Obi-Wan has the right idea.

 

[Hans]

dropped like a lead zeppelin

LOL! Love your humor Travis.

 

[Travis]

This all makes so much sense! That you :). I drew a conclusion you were mentioning carbonic anhydrase due to creatine' ability of increasing intracellular and extracellular water concentrations and so figured maybe you were saying creating acted by facilitating substrate conversion.

If it's any consolation/compliment to you and others I ask these ignorant questions, I have always been the stupid but quiet kid in class. unfortunately for you and the others I bother, I'm not afraid to fly my ignorance shamelessly as I always get a very satisfying answer, or a further ingriguing topic to ponder. So thanks for that :)

I am just now getting over a short bout of mental confusion, which seems on all accounts to have been caused by oleamide. At the Amish grocery store last week I had bought some red palm oil, which is about 42% oleic acid on average, and I had used about 1 ounce over the course of a few days. I don't normally eat fat and when I do: I eat coconuts.

Oleamide is the only thing about as serotonergic as serotonin itself, capable of doubling its response on 5-HT₂ at only 10 nM concentrations. The mean concentration of oleamide detected in a small sample of Americans on the Mason–Dixon line (Memphis, TN) in 1989 had been 31.7 μg/ml, which corresponds to 112 μM after doing the requisite calculations. Oleamide has also been shown to modulate other serotonin receptors—e.g. 5-HT₁ and 5-HT₇—in similarly low concentrations, binding allosterically while potentiating serotonin's response. Although I do like to be facetious when talking about oleamide, anyone who considers these studies would likely agree that it's quite serotonergic in very low concentrations:

[1] Arafat, E. S. "Identification of fatty acid amides in human plasma." Life Sciences (1989)

[2] Thomas, E. "The endogenous lipid oleamide activates serotonin 5‐HT₇ neurons in mouse thalamus and hypothalamus." Journal of neurochemistry (1999)

[3] Thomas, E. "Unique allosteric regulation of 5-hydroxytryptamine receptor-mediated signal transduction by oleamide." Proceedings of the National Academy of Sciences (1997)

[4] Boger, D. "Structural requirements for 5-HT₂ and 5-HT₁ serotonin receptor potentiation by the biologically active lipid oleamide." Proceedings of the National Academy of Sciences (1998)

Fatty acid amides are neutral lipids, and as such their brain uptake should occur more readily than their corresponding carboxylates. In the brain: oleamide could cause a high-serotonin condition that I've termed Sicilian encephalopathy, which is more commonly known as 'Italian Brain.' This condition is characterized by hyperemotionality, authoritarianism, irrational behaviour, reduced cognition, Christianity, and a total disregard for most things civilized. Just look at what happens to these Italians who'd just consumed olive oil in decagram amounts: here, here, and here.

 

[Jon]

I am just now getting over a short bout of mental confusion, which seems on all accounts to have been caused by oleamide. At the Amish grocery store last week I had bought some red palm oil, which is about 42% oleic acid on average, and I had used about 1 ounce over the course of a few days. I don't normally eat fat and when I do: I eat coconuts.

Oleamide is the only thing about as serotonergic as serotonin itself, capable of doubling its response on 5-HT₂ at only 10 nM concentrations. The mean concentration of oleamide detected in a small sample of Americans on the Mason–Dixon line (Memphis, TN) in 1989 had been 31.7 μg/ml, which corresponds to 112 μM after doing the requisite calculations. Oleamide has also been shown to modulate other serotonin receptors—e.g. 5-HT₁ and 5-HT₇—in similarly low concentrations, binding allosterically while potentiating serotonin's response. Although I do like to be facetious when talking about oleamide, anyone who considers these studies would likely agree that it's quite serotonergic in very low concentrations:

[1] Arafat, E. S. "Identification of fatty acid amides in human plasma." Life Sciences (1989)

[2] Thomas, E. "The endogenous lipid oleamide activates serotonin 5‐HT₇ neurons in mouse thalamus and hypothalamus." Journal of neurochemistry (1999)

[3] Thomas, E. "Unique allosteric regulation of 5-hydroxytryptamine receptor-mediated signal transduction by oleamide." Proceedings of the National Academy of Sciences (1997)

[4] Boger, D. "Structural requirements for 5-HT₂ and 5-HT₁ serotonin receptor potentiation by the biologically active lipid oleamide." Proceedings of the National Academy of Sciences (1998)

Fatty acid amides are neutral lipids, and as such their brain uptake should occur more readily than their corresponding carboxylates. In the brain: oleamide could cause a high-serotonin condition that I've termed Sicilian encephalopathy, which is more commonly known as 'Italian Brain.' This condition is characterized by hyperemotionality, authoritarianism, irrational behaviour, reduced cognition, Christianity, and a total disregard for most things civilized. Just look at what happens to these Italians who'd just consumed olive oil in decagram amounts: here, here, and here.

Very interesting. I have a good feeling that posturing, enthusiastic hand gestures, and establishment of cohorts and admirers are also side effects of oleamide as demonstrated here:

I actually found a video detailing Travis's consciousness trying to teach and save my left brain hemisphere from years of public school doctrine, while the right tries to help. The other psyches observing are equally amazed and impressed with Travis, sadly none quite understand exactly what he's saying. If you scroll to 19:27 and watch until 28:04 you can observe our amazing journey together:

 

[Ulysses]

public school

I'm triggered.

 

[Jon]

I'm triggered.

Haha how so?

 

[Travis]

Very interesting. I have a good feeling that posturing, enthusiastic hand gestures, and establishment of cohorts and admirers are also side effects of oleamide as demonstrated here:

Agreed, you can almost feel the oleamide watching that man gesticulate. I had heard once that Benito Mussolini had sent Adolf Hitler a bottle of the best Italian olive oil in 1942, a move that had led to the loss of the 6th Army in a fit of oleamide-inspired overconfidence. Hitler had then sent the last ¹⁄₇th of the bottle back with a note stating:

'Thanks Benito, but this olive oil is a bit too serotonergic for my taste. All I can do after consuming it is draw puppies, rainbows, and clouds with Eva Braun and Albert Speer using wax crayons. I have since taken-up amphetamines instead, and consider this a far safer habit considering my responsibilities as fuhrer. I have also resumed cooking with the Jew tallow Heinrich Himmler sends me. ―Adolf Hitler ​

I have given-up using small sub-capful-sized doses of free olive, macadamia, and palm oils on salads. Oil makes the grated garlic taste better, and although coconut oil will always be king yet I need one that is liquid at 64.379 °F: the average temperature of vegetables after I'm done cutting them. Perhaps I'll mix coconut oil with just enough perilla oil to lower the melting point while contributing only 14% oleic acid and an ω−6/ω−3 ratio of .222. An oil blend containing 20% perilla and 80% coconut oil would contain:

• 7.76% oleic acid (18∶1ω−9)
• 4.06% linolenic acid (18∶2ω−6)
• 12.6% α-linolenic acid (18∶3ω−3)

With of course the remaining 75.58% being saturated. This would ensure proper DHA (22∶6ω−3) synthesis—via α-linolenic acid elongation/desaturation—in one of the safest ways imaginable, far safer than consumed oxidized DHA directly. Members of this forum attest that preformed DHA is a lipofuscin hazard, which is certainly believable considering its degree of saturation and lipofuscin's mechanism of formation. Brunk & Terman have made lipofuscin in vitro using oxygen, heat, and polyunsaturated fatty acids.

But I'll probably just stick to fat-free salads until I buy more coconuts, which can be shredded and used directly.