The Travis Corner

[CarbAppreciator]

I am fasting right now, and didn't consume anything at all yesterday besides: coffee, water, and (6S)-5-methyltetrahydrofolate. Tonight I will buy more fruit & leaves after just two days of fasting—perhaps not long enough to officially induce autophagy yet I am thin and have a fast metabolism, so maybe.

Nice, i suspect there is at least hepato-autophagy occuring, given the high turnover of liver cells and coffee's targeting of said organ.
Personally, I've been experimenting with time-restricted feeding, averaging about an 8h feeding window starting around 4 pm. I pound coffee all day, and make a nice drink of gin and carbonated water with lime and a few drops of methylene blue on which i sip at 3ish, it's easy to get a buzz in the fasted state.
If nothing else my glycogen storage capacity should be getting larger.

 

[Mito]

I am fasting right now, and didn't consume anything at all yesterday besides: coffee, water, and (6S)-5-methyltetrahydrofolate.

How much (6S)-5-methyltetrahydrofolate are you taking?

 

[Daniel11]

What about nicotine gum?

As a side note, what are your thoughts on the health impacts of nicotine gum vs tobacco? (w/ regards to 5-ar, metabolism, maybe cancer?)

edit: "I think the safest way to use nicotine would probably be by using nicotine-containing gum." -You. Thanks!

Nicotine gum is much better then other options but has preservatives, colorings and other chemicals you will be absorbing directly in to your body sublingually, they gave me a headache, i like nicotine toothpicks they are very clean.

https://pixotine.com

This podcast is good..

“What nicotinic receptors do is they act like gain enhancers. The modulate the gain of a particular neurochemical event. If you stimulate a nicotinic receptor that’s sitting pre-synaptically or sort of in the end of an axon and you get more bang for your buck when a signal comes along. -Dr. Newhouse”

https://blog.bulletproof.com/paul-newhouse/

 

[Travis]

Nice, i suspect there is at least hepato-autophagy occuring, given the high turnover of liver cells and coffee's targeting of said organ.
Personally, I've been experimenting with time-restricted feeding, averaging about an 8h feeding window starting around 4 pm. I pound coffee all day, and make a nice drink of gin and carbonated water with lime and a few drops of methylene blue on which i sip at 3ish, it's easy to get a buzz in the fasted state.
If nothing else my glycogen storage capacity should be getting larger.

That sounds bitchin', and coffee and gin are some of my favourite drinks. I have dabbled with bourbon, green tea, wine, yerba mate, craft beer and the like but nothing competes to gin and coffee (used separately). I also drink quite a bit of coffee per day (~2 liters), and most of it is quite strong because it can sit in the French press for up to two hours. I am fine with this long brew time, and it starts to taste chocolately near the end—albeit tepid. Long-brewed French press coffee is nothing like the burner-scorched Folgers made with a drip maker sold in truck stops, and the 24-hour cold-brew is unparalleled for a summer drink. On hot days, it's good to do an 10-hour room temperature brew during night so you don't have to drink hot coffee in the morning. Chilling room temperature coffee is less ice-demanding, and leads to a less watered-down drink. I think best would be to have three separate French presses in the fridge that you could independently run in 24-hour cold-brew cycles.

 

[Travis]

How much (6S)-5-methyltetrahydrofolate are you taking?

I have over one-hundred 1000·μg capsules of presumed stereochemically-pure (6S)-5-methyltetrahydrofolate containing safe excipients besides (i.e. magnesium stearate). Because my motivation for taking these depends the suspicion of antifolate receptor antibodies, I am attempting to match a descending dose with the supposed antibody decay rate—estimated to be about two months. After the the initial loading period upon receiving the bottle—with special thanks to USPS—I am currently taking about four per day, with another 1000·μg coming from green leaves.

I would like to have some tetrahydrobiopterin as well because brain uptake of this is also blocked by the antifolate receptor antibody. Biopterins and folates are very similar enzymatic cofactors, yet only the latter is a true vitamin; biopterins can be produced within the body via cyclohydrolase working on guanosine triphosphate. Cyclohydrolase can be induced, an enzyme transcribed along with tryptophan pyrrolase upon γ-interferon stimulation. Besides restricting GTP from invading microbes, the tetrahydrobiopterin thus formed becomes a requisite cofactor for nitric oxide synthase—also induced by same cytokine.

 

[Mito]

Methionine synthase lowers homocysteine by methylating it, and the cofactors (6S)-tetrahydrofolate and cobalamin are both required for this enzyme to function. The natural (6S)-5-methyltetrahydrofolate even comes pre-loaded with a methyl group and can enter the brain through the choroid plexus. The B-vitamins having subscripts in multiples of three are involved in homocysteine metabolism: pyridoxal (B₆), folate (B₉), and cobalamin (B₁₂) all lower it while niacin (B₃) can increase it.

Can adenosylcobalamin and hydroxycobalamin be cofactors for methionine synthase or does it have to be methylcobalamin or cyanocobalamin?

 

[Travis]

Can adenosylcobalamin and hydroxycobalamin be cofactors for methionine synthase or does it have to be methylcobalamin or cyanocobalamin?

I think any one will do, and whatever comes bound to the cobalt atom will be dissociated within the body.

Like heme and its iron atom, the cobalamin macrocycle will also bind many small molecule gasses at its central cobalt. Heme has been shown to ligate nitric oxide, dioxygen, and carbon monoxide and cobalamin can bind methane and nitrous oxide. It's well-known among anesthesiologists that nitrous oxide will bind & inactivate vitamin B₁₂, and of course this short list is of course not inclusive. Why cobalamin is often found complexed with cyanide I have no idea, but it could have something to do with its extraction procedure. Although the entire macrocycle can be synthesized, this is no small task and I'd assume that most B₁₂ today comes from genetically-engineered bacteria.

 

[Amazoniac]

I was in this adrift-with-a-wasser-bottle dillema: I want to (share) but it's better to wait because we don't know how tomorrow is going to be. We never know the length of the hiatus. Here are more classes:

'The pterins, neopterin and biopterin, occur naturally in body fluids including urine. It is well established that increased neopterin levels are associated with activation of the cellular immune system and that reduced biopterins are essential for neurotransmitter synthesis.' ―S. Messahela​

As like The Steinbeck, most good authors take pains to avoid constructs like that above. When writing articles on certain molecular topics the word 'reduced' can become ambiguous: It can either assume its general meaning or indicate a molecular species reduced electronically (+2e⁻)—with the ionic charge being the noun reduced in the latter latter sense and not denoting the absolute number or summed mass of said molecules, as in the former.

'The pterins, neopterin and biopterin, occur naturally in body fluids including urine. It is well established that increased neopterin levels are associated with activation of the cellular immune system and that reduced biopterins are essential for neurotransmitter synthesis.' ―S. Messahela​

These two different meanings of the same word necessarily have two different antonyms. The word 'reduced' in the general sense is antonymeric with the word 'increased,' while the term 'oxidized'—confusingly having little to do with oxygen—represents the diametrical and most often reversible opposition of the latter meaning: The removal of two electrons (−2e⁻).

'...well established that increased neopterin levels are associated with activation [...] and that reduced biopterins are essential for neurotransmitter synthesis.' ―S. Messahela​

He means of course that electronically-reduced biopterins are essential for serotonin and dopamine synthesis, via hydroxylation, yet his use of the word 'increased' in direct contradistinction to biopterins 'reduced' would be bound to leave an inaccurate impression on a person not familiar with aromatic amino acid hydroxylase (AAAH).

To avoid this ambiguity and potential source of confusion, I propose that the adverb 'electronically' should preface the term 'oxidized' in such otherwise ambiguous cases—or perhaps other grammatical modifications serving to reduce confusion over reduced biopterins could be applied.

Yesterday I had realized that the word 'antoymeric' wasn't found in any dictionary, despite there being a great necessity for such a word. Yet today—perhaps on account of enhanced cognition after finally receiving my (6S)-5-methyltetrahydrofolate in the mail—I had immediately realized that the proper word must actually be 'antonymous' by analogy to the others. Look what happens when I run these words forwards & backwards through my patented bidirectional noun–adjective transformer (⇌™):

synonym ⇌™ synonymous

antonym ⇌™ antonymous

anonynym ⇌™ anonymous
​

Yet this leads to yet another word not found any dictionary, one synonymous with 'pseudonym.' While the word 'anonynym' does appear in some text, this is more-or-less restricted to online screen-names and informal chat—roughly about as prevalent as 'quasinym.'

Since I now have a bidirectional noun–adjective transformer (⇌™) on hand—which came free with my flux capacitor (lol, not really*)—let me see what else it can do:

Raw Kale ⇌™ healthy

Coffee & Figs ⇌™ delicious

George Bush ⇌™ disingenuous

Travis ⇌™ HTTP error 403
​

Interesting, I never would have thought that it would agree with me about kale.

[*] Nothing ever comes free with those.​

--
Travisord, Evernote's Clearly (reader) was an excellent browser extension. Do you use something similar? I find the native one in Firing at the Foxes limited in comparison, for example.

 

[Travis]

I was in this adrift-with-a-wasser-bottle dillema: I want to (share) but it's better to wait because we don't know how tomorrow is going to be. We never know the length of the hiatus. Here are more classes:


--
Travisord, Evernote's Clearly (reader) was an excellent browser extension. Do you use something similar?

No I don't, but I will do a search to find this program you speak of.

 

[Amazoniac]

No I don't, but I will do a search to find this program you speak of.

Here. It was quite simple but neat.

 

[Travis]

Here. It was quite simple but neat.

I have tons of bookmarks and multi-tab bookmarks, but also try to retain enough in memory to make everything I'd previously read easily researchable (that is: easily re-findable).

But this is a good point, yes? The word 'reduced' is common in biochemistry to talk about changes in protein or mRNA levels, yet when talking about redox chemistry the same word acquires a new meaning. When talking or writing about reduced transcription/expression levels and redox chemistry—such as in the case of reduced NF-κB activity consequent of the elecronic-reduction of H₂O₂ by glutathione peroxidase—one must take extra precautions to avoid antonymous confoundment. This is something Messahela did not do, but on the contrary: It had actually appeared as if Messahela had taken great pains to construct a sentence intended to confuse the more naïve readers, perhaps as a scientific shibboleth of sorts.

 

[Amazoniac]

I have tons of bookmarks and multi-tab bookmarks, but also try to retain enough in memory to make everything I'd previously read easily researchable (that is: easily re-findable).

But this is a good point, yes? The word 'reduced' is common in biochemistry to talk about changes in protein or mRNA levels, yet when talking about redox chemistry the same word acquires a new meaning. When talking or writing about reduced transcription/expression levels and redox chemistry—such as in the case of reduced NF-κB activity consequent of the elecronic-reduction of H₂O₂ by glutathione peroxidase—one must take extra precautions to avoid antonymous confoundment. This is something Messahela did not do, but on the contrary: It had actually appeared as if Messahela had taken great pains to construct a sentence intended to confuse the more naïve readers, perhaps as a scientific shibboleth of sorts.

https://www.researchgate.net/publication/26629805_Methods_Acronyms_-_The_Witty_Side_of_Science (Yes, dumped a link like a Neanderthal)

 

[Hairfedup]

Hey Travis, what would be the optimal way to ingest turmeric / mix with turmeric in order to inhibit prostaglandin production?

 

[Travis]

https://www.researchgate.net/publication/26629805_Methods_Acronyms_-_The_Witty_Side_of_Science (Yes, dumped a link like a Neanderthal)

He failed to mention the SALSA study, an acronym denoting: 'The Sacramento Area Latino Study on Aging.' I see this as somewhat insensitive, and perhaps even borderline offensive, because the acronym formed is identical to one certain food that happens to be highly-stereotypical of the very minority population under study. This is nearly tantamount to traveling to Georgia, forming a small study group composed of racist pineal scientists, and painfully-constructing a study entitled: 'The West Atlanta trans-Epithelial Route-delivered Melatonin on Negroes Study,' just so you can it The WATERMELON Study.

 

[Travis]

Hey Travis, what would be the optimal way to ingest turmeric / mix with turmeric in order to inhibit prostaglandin production?

Best way to inhibit the 2-series prostaglandins is to avoid ingesting linoleic acid. The only two precursors of arachidonic acid, or proto-2-prostaglandin, are linoleic- (18∶2ω−6) and less-ubiquitous γ-linolenic (18∶3ω−6) acids.

The tripartite association of prostaglandin D₂, prostaglandin D synthase, and hair loss is very strong. The hair loss gradient perfectly matches the prostaglandin D₂ gradient, and also that that of the eponymous enzyme that isomerizes it's formation. Since cortisol is what transcribes for prostaglandin D synthase, you might be tempted to think the hair loss gradient is also synonymous with the cortisol gradient.

I used to think that prostaglandin D₂ was the downstream factor, yet am beginning to have a few doubts. I am going to look into this again pretty soon and I do intend on writing an article about it. To actually completely solve the puzzle of hair loss would be quite the task, but some new science has made great contributions and I have a few new leads.

Aspirin, selenomethionine, and γ-tocopherol are three other great choices for reducing prostaglandin D₂ formation. These are of course safe to take internally, yet one should be on the lookout for added titanium dioxide nanoparticles and aluminum when choosing aspirin brands.

 

[Blossom]

Hey Travis, I was curious if you had any thoughts on this prostaglandin analogue:
Bimatoprost - Wikipedia
It's a glaucoma drug that many people use to grow longer eyelashes and some people are now using it off labels for hair loss. I got the impression from listening to a Peat interview that prostaglandin analogues aren't an optimal choice but I'm interested in what you think if you have the time. No rush, and I greatly appreciate you sharing your knowledge with us all.

 

[Travis]

Hey Travis, I was curious if you had any thoughts on this prostaglandin analogue:

A person cannot indiscriminately hate on all prostaglandins, even under a Peat paradigm, because even in the complete absence of all dietary ω−6 fatty acids prostaglandins are still formed. In this event: our endogenous Δ⁹-desaturase and elongase enzymes will form Mead acid (20∶3ω−9) to replace some eicosanoids not produced—via arachidonate (20∶4ω−6) and dihomo-γ-linoleate (20∶3ω−6) under normal ω−6 intakes—and our desaturase & elongase enzymes will continue to elongate the essential ω−3 fatty acids. Since each prostaglandin series is named on account of the number of double bonds it contains, and also the fact that two are lost upon cyclicization, a person might think that Mead acid (20∶3ω−9) is the precursor for prostaglandin E₁. This is not the case, however, and it's the other 20∶3 fatty acid that produces the 1-series prostaglandins: dihomo-γ-linoleic acid (20∶3ω−6).

Mead acid forms leukotriene B₃, a chemotactic eicosanoid similar in function to the ω−6-created leukotriene B₄ yet having about threefold less potency. Leukotriene B₅, the EPA (20∶5ω−3) product, is roughly 5,000 less potent than leukotriene B₄.

Since both the 1 & 2-series prostaglandins are formed via elongase/desaturase products of ω−6 fatty acids, the prostaglandins found in our natural tropical environment would have predominately been of the 3-series. Members of this class are formed via eicosapentaenoic acid (20∶5ω−3), yet there is little data on their comparative potency vs the more-studied 2-series prostaglandins; this seems to be on account of: (1) their increased potency, (2) the near-universal consumption of ω−6 fatty acids in North America and Europe, and also (3) the incorrect assumption that they are actually 'essential.' Prostaglandin E₂ is the most studied prostaglandin by far, perhaps why prostaglandin E₃ is the only studied 3-series prostaglandin. The few studies which have analyzed them both have estimated that prostaglandin E₃ has about fourfold lower activity than prostaglandin E₂.

Since I'm having a very hard time finding data on comparative receptor affinities of prostaglandins D₃ vs D₂, the second-most studied prostaglandin, I would imagine that you could count the studies published on the more tangential prostaglandin F₃ using just one hand . . . or perhaps even less than just one hand (penguins can count up to two using their flippers).

Prostaglandins E & D exert effects on cell membranes expressing their receptors by either increasing or decreasing cyclic AMP. Changes is cAMP are always associated with Ca²⁺ influx/efflux, perhaps on account of the adenosine phosphates of different lengths also having differing affinities for Ca²⁺/Mg²⁺. Prostaglandin D has two membrane receptors, DP1 and DP2, and these work in opposite directions. This is by no means unusual, as melatonin receptors and two prostaglandin E receptors directly oppose eachother. This means that the exact ratio of DP1∶DP2 receptors, or the expression of either one alone, can determine how prostaglandin D effects the cell. Two prostaglandin E receptors oppose eachother in the same way, through cAMP & Ca²⁺, yet I have yet to read about the functions of the other two. Since prostaglandin F and its analogues have a peculiar affinity for lengthening eyelashes, I'd guess that follicles in that location express prostaglandin F receptors coupled to Gα protein.

Among G protein-coupled receptors, it is the specific G protein that determines the second messenger system while the receptor part determines what activates it. The Gα protein in particular is coupled to adenylate cyclase, the enzyme responsible for synthesizing cAMP. Increased cyclic AMP increases the metabolic rate of the cell, and this could increase the hair growth rate.

The initial function of prostaglandins could simply have been the detoxification excessive superoxide (Ȯ₂⁻). The most defining characteristic of prostaglandin H, which generates all the others, is its endoperoxide bridge. The creation of this cyclic dioxygen bridge is carried-out by cyclooxgygenase, and it needs both a lipid and superoxide (Ȯ₂⁻) for this to occur. Prostaglandin H has a half life of about five minutes, after which it spontaneously decomposes to either prostaglandin E or prostaglandin D.

Prostaglandins are only made pathological to the extent that our natural 3-series prostaglandins have been supplanted by the 1 & 2-series prostaglandins. The progressive ingestion of ω−6 fatty acids that had necessarily accompanied our escalating supra-tropical migration had created this problem, and this process had occurred faster than humans could evolutionarily adapt to.

I think it's easy to understand why the ω−6-generated leukotriene B₄ is more powerful than both leukotriene B₃ and leukotriene B₅, the respective natural products of ω−9 and ω−3: Humans have neither a ω−6-desaturase or a Δ¹²-desaturase so they cannot form ω−6 fatty acids, yet helminths and fungi freely make and excrete them. Since leukotriene B's classic function is to act as a chemotactic molecule for neutrophils and natural killer cells, you'd have to assume that this increased selectivity is intentional. However, I cannot begin to think why 2-series prostaglandins would be more powerful than those of the 3-series; there could be some reason for this, or perhaps it could simply be some incidental molecular property of the prostaglandin receptors (perhaps a valine, otherwise harmless in the absence of linoleic acid, had been used where an isoleucine would have been more fortuitous).

 

[Blossom]

Thanks @Travis.
ETA: There are two threads where people inquired about this substance. If you don't mind I'd like to link your quote in response?

 

[Blossom]

stereochemically-pure (6S)-5-methyltetrahydrofolate

Is that the same thing as Deplin?

 

[Amazoniac]

He failed to mention the SALSA study, an acronym denoting: 'The Sacramento Area Latino Study on Aging.' I see this as somewhat insensitive, and perhaps even borderline offensive, because the acronym formed is identical to one certain food that happens to be highly-stereotypical of the very minority population under study. This is nearly tantamount to traveling to Georgia, forming a small study group composed of racist pineal scientists, and painfully-constructing a study entitled: 'The West Atlanta trans-Epithelial Route-delivered Melatonin on Negroes Study,' just so you can it The WATERMELON Study.

So you want to know what the 'K' in 'vitamin K' stands for, the confusing nomenclature that has mislead the public since its definition? At first you would expect that it only stands for koagulation, yet! It actually also stands for kognition:

- Vitamin K and the Nervous System: An Overview of its Actions | Advances in Nutrition | Oxford Academic
- Vitamin K, an emerging nutrient in brain function
- Vitamin K Antagonists and Cognitive Decline in Older Adults: A 24-Month Follow-Up
- Thieme E-Journals - Seminars in Thrombosis and Hemostasis / Abstract​

..as they say, 'the devil is in the details.' Should you be now thinking: 'But Travasoniac, how could that be if I was never able to find it there?' To that I would reply, slightly grateful from the hint for a paid promotion: 'It was never there indeed and you wouldn't be able spot it no matter how much you tried. But a good starting place to look for it would be in milk.¹'

[1] Woodford, Keith. "The devil in the milk." No one cares (2009)​