The Travis Corner

Travis

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This makes sense, before I started having hair loss I was supplementing with omega 3,6, and 9 for 7 months. Also I've noticed that even after eating one egg my hairloss excellerates. And I've been eating a lot of potatoes which have a lot of iron. So this was very helpful, thank you!

'Age spots' will go away with time because lipofuscin is diluted through the process of mitosis, in most cells. Yet since neurons rarely divide, if ever, the only way to get rid of neuronal lipofuscin is through fasting. Dietary restriction and fasting activates autophagy, a cascade of events leading to a reconfiguration of the cells' its interior space. Phagosomes are produced in the cytosol that engulf damaged or redundant proteins, and they also contain proteolytic enzymes to recycle them. In this way, the body can maintain life longer with no food using unneeded proteins—i.e. damaged mitochondria—both for energy and new protein synthesis.

Mechanisms of hair loss are less certain, and even the world expert appears clueless (Paus, 1999). Hair loss is a billion dollar industry, so the fact that only a few helpful ideas concerning it exist confirms its perplexing nature. Nonetheless: prostaglandins do appear highly involved and the Koreans, having a very low ω−6 consumption, have the most hair.
 

Mito

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Linoleic acid is perhaps the most prone to peroxidation because it has a bis-allyl hydrogen, and is also the lipid that should be avoided for hormonal reasons.
I had thought linolenic was more prone to peroxidation than linoleic because it has more double bounds?
 
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'Age spots' will go away with time because lipofuscin is diluted through the process of mitosis, in most cells. Yet since neurons rarely divide, if ever, the only way to get rid of neuronal lipofuscin is through fasting. Dietary restriction and fasting activates autophagy, a cascade of events leading to a reconfiguration of the cells' its interior space. Phagosomes are produced in the cytosol that engulf damaged or redundant proteins, and they also contain proteolytic enzymes to recycle them. In this way, the body can maintain life longer with no food using unneeded proteins—i.e. damaged mitochondria—both for energy and new protein synthesis.

Mechanisms of hair loss are less certain, and even the world expert appears clueless (Paus, 1999). Hair loss is a billion dollar industry, so the fact that only a few helpful ideas concerning it exist confirms its perplexing nature. Nonetheless: prostaglandins do appear highly involved and the Koreans, having a very low ω−6 consumption, have the most hair.
Are their certain conditions in which a person shouldn't fast? Like already being too stressed, hypothyroid, bad liver, damaged nervous system, etc? And if I'm trying to reverse my hairloss would fasting not be a good idea?
 

Travis

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I had thought linolenic was more prone to peroxidation than linoleic because it has more double bounds?

I also think that linolenic acid would be more prone to oxidation, both α and γ, but not on account of its' degree of unsaturation. Normal linolenic acid has two bis-allyl hydrogens, yet conjugated linolenic acid is likely more stable than linoleic: The bis-allyl carbon has the most acidic proton found in lipid chains, the one most-easily removed. This means the energy barrier to lipid anion and lipid radical is lower in bis-allyl lipids, and the lipid radical is the first step in lipid peroxidation. The abstraction of a hydrogen (H·) or proton (H⁺) appears to be the first prerequisite for O₂ addition.

Tocotrienols have three double bonds yet no bis-allyl hydrogen; squalene has six, and coenzyme Q₁₀ has ten. Retinol has four double bonds spaced close together, yet close enough to be stabilized through π-conjugation. Docosahexaenoic acid, unfortunately, has the most bis-allyl hydrogens at five. Although DHA is necessary for membranes it certainly appears to be a substantial lipofuscin risk, perhaps explaining why users of this forum report spots after ingesting marine oils. This is a good reason not to take DHA directly but instead synthesize it de novo from α-linolenic acid; this is present in grass-fed milk, grass-fed beef, and leaves. Without DHA, the omega−6 osbond acid sneaks-in is no doubt worse. Osbond acid cannot maintain proper glucose flux, 2-series prostaglandins can form from its precursors, and it still has four bis-allyl hydrogens.
 
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Travis

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Are their certain conditions in which a person shouldn't fast? Like already being too stressed, hypothyroid, bad liver, damaged nervous system, etc? And if I'm trying to reverse my hairloss would fasting not be a good idea?

Fasting is certainly not indicated for every circumstance, and neuronal lipofuscin tends only to become a problem with age. Centenarians have lipofuscin is their neurons, so it's certainly not fatal, yet people approaching ~60 years of age should become quite interested in this. Even before that point, it could be a good idea for people to attempt to autolyze accumulated neuronal lipofuscin every few years or so.

Lipofuscin can occupy a substantial volume of neurons, perhaps slowing their metabolism and the organisms' thought-speed. And yet, there are a few other inclusion bodies found in the aging brain worth considering: Neurofibrillary tangles are the classic inclusion body found in Alzheimer's disease, a condition originally diagnosed histologically by its presence. Physically, this appears to be an aggregate of aluminum ions (Al³⁺) and highly-phosphorylated tau (τ)—a microtubule-associated protein. The observation that Al³⁺ is most often, if not invariably, found at the center of neurofibrillary tangles has been confirmed by electron dispersive spectroscopy and laser microprobe mass analysis; it has also been shown to bind it directly, as confirmed by electrophoretic gel-shift. There is also substantial epidemiological evidence for aluminum's involvement as well, and injecting rabbits with aluminum replicates the characteristic symptoms of Alzheimer's. Aluminum's trivalent nature—unusual for a biological ion—along with its' natural affinity for phosphates likely account for its' unique τ-aggregating ability.

Beta-amyloid is an extracellular inclusion body formed by chondroitin/heparin sulfate and amyloid-precursor protein. There's a considerable amount of physical data implying that its formation is merely a consequence of low brain sulfate groups. Without sulfate attachments: chondroitin and heparin lose ζ-potential and collapse along with its' associated protein, amyloid-precursor protein, thus becoming the β-amyloid inclusion body. Perhaps the best evidence is epidemiological: Alzheimer's has been strongly-linked to the use of acetaminophen, a molecule that removes sulfate groups through conjugation. I'll cite the below articles as proof, but there's certainly more evidence than this:

[1] Han, X. "Substantial sulfatide deficiency and ceramide elevation in very early Alzheimer's disease: potential role in disease pathogenesis." Journal of neurochemistry (2002)
[2] Kisilevsky, R. "Arresting amyloidosis in vivo using small-molecule anionic sulphonates or sulphates: implications for Alzheimer's disease." Nature medicine (1995)
[3] Heafield, M. "Plasma cysteine and sulphate levels in patients with motor neurone, Parkinson's and Alzheimer's disease." Neuroscience letters (1990)
[4] Schubert, D. "Amyloid beta protein precursor is possibly a heparan sulfate proteoglycan core protein." Science (1988)
[5] Miura, Y. "Inhibition of alzheimer amyloid aggregation with sulfated glycopolymers." Biomacromolecules (2007)

Lafora's disease is characterized by amyloid deposits, an anglicized term deriving from the Latin word for 'starch.' These inclusion bodies stain with iodide solution so were presumed historically to literally be starch. And yet, the much similar glycogen also stains with iodide—the reason why Lugol's is found in microscopy kits. Lafora's disease is now termed a
starch storage disease and its' characteristic amyloid deposits are officially considered 'misfolded glycogen.' Yet, both glycogen and starch—amylopectin in particular—are highly-branched α-linked polyglucose; there is absolutely no chemical difference between them besides their degree and length of branching. I have studies bookmarked indicating that its' more likely to be amylopectin based on the subtle shift in wavelength emitted by the iodide stained polysaccharide. Volkheimer had proved that retrograde dry starch particles, such as those found in toast, can actually travel to the brain

Sidenote: I had just confirmed the fact that it really is a polysaccharide in seaweed that is accountable for its' high iodide content, as previously suspected. Seaweeds of all types have a polysaccharides displaying high iodide-affinity. This particular polysaccharide is characterized by alternating α- and β-linked sulfated galactose units and goes by the name of carrageenan.
 

Travis

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@Travis I notice you advocate supplementing potassium iodide, what are your reservations about Lugols solution?

I think it is too reactive and shouldn't be consumed if iodide is available. Lugol's is initially made by using molecular iodine (I₂) to potassium iodide (KI). The potassium iodide immediately dissociates in water into potassium (K⁺) and iodide (I⁻) ions, both of which are essential minerals. The molecular iodine (I₂) remains as such and also forms poly-iodines (Iₓ) of a few types, such as triiodide (I–I–I⁻). The molecular iodines are oxidants and react spontaneously with lipids and tyrosine, meaning that ingesting Lugol's should lead to iodinated lipids in the intestinal tract. Alternatively, it can be reduced by biological reducing-agents such as ascorbate into two iodide ions (I⁻), perhaps why studies on prisoners show both forms approximately equipotent in preventing goitre.

Doctor Brownstein never tires in telling people that 'we need both forms,' claiming that the breast has special affinity for molecular iodine (I₂). He cites in vitro evidence of diiodine (I₂) slowing the proliferation of breast carcinoma cells in support of his statements. However, I find it extremely doubtful that diiodine can circumvent all vitamin C and lipid molecules on it's way from his patented Iodoral™ tablets to the breast—whether male or female this does seems improbable. Thus, I take Dr. Brownstein to be somewhat of a charlatan whether he's sincere or not. If he honestly believes this does happen, I would them accuse him of unintentional charlatanry.

'There are a few things to consider when looking for a supplement to get iodine. Does the product contain both iodine and iodide? The body needs both forms. Different parts of the body look for one of the specific forms. For instance the breasts look for iodine [she serious?] and the thyroid needs iodide [we know].'― Stephanie Buist

I think the reduced proliferation observed in the Brownstein-cited in vitro cancer cells had likely been on account of lipid iodination. Molecular iodine (I₂) of course adds to double bonds found on lipids, a process that happens so reliably that all oils used in soapmaking have a reported iodine value. The iodine value is an accurate index of unsaturation. Since the double bond is obliterated by added iodine atoms, the lipids' geometry shifts from sp²- to the sp³-hybridization and straightens. Iodinated lipids are more like saturated lipids than unsaturated ones, and can be viewed as being 'saturated by iodine' and not hydrogen—or partially-saturated by both. This newfound pseudo-saturation would increase membrane rigidity and should lower glucose flux. Yet on account of the low amount of iodine that'd been used, more realistic* could be that arachidonic acid had been iodinated to 5,6-diiodo-8,11,14-eicosatrienoic acid—or the 8,9-diiodo, 11,12-diiodo, 14,15-diiodo congeners—and lose its' cyclooxygenase specificity. The iodination of arachidonic acid should completely abrogate its' potential to become prostaglandin E₂.

[*] The iodination of the double bond between carbons 5–6, in particular, would seem the more likely occurrence on account of its' close proximity to the water phase when occupying its' assumed position in lipid bilayer of carcinoma cell membrane.
 
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Dobbler

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I havent read past 20 pages but doesn't beef have very good SAFA to PUFA ratio? My organic beef is 65% SAFA, so im assuming its probably 0,5g PUFA per 100g which is low compared to even dairy
 

Ras

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I think it is too reactive and shouldn't be consumed if iodide is available. Lugol's is initially made by using molecular iodine (I₂) to potassium iodide (KI). The potassium iodide immediately dissociates in water into potassium (K⁺) and iodide (I⁻) ions, both of which are essential minerals. The molecular iodine (I₂) remains as such and also forms poly-iodines (Iₓ) of a few types, such as triiodide (I–I–I⁻). The molecular iodines are oxidants and react spontaneously with lipids and tyrosine, meaning that ingesting Lugol's should lead to iodinated lipids in the intestinal tract. Alternatively, it can be reduced by biological reducing-agents such as ascorbate into two iodide ions (I⁻), perhaps why studies on prisoners show both forms approximately equipotent in preventing goitre.

Doctor Brownstein never tires in telling people that 'we need both forms,' claiming that the breast has special affinity for molecular iodine (I₂). He cites in vitro evidence of diiodine (I₂) slowing the proliferation of breast carcinoma cells in support of his statements. However, I find it extremely doubtful that diiodine can circumvent all vitamin C and lipid molecules on it's way from his patented Iodoral™ tablets to the breast—whether male or female this does seems improbable. Thus, I take Dr. Brownstein to be somewhat of a charlatan whether he's sincere or not. If he honestly believes this does happen, I would them accuse him of unintentional charlatanry.

'There are a few things to consider when looking for a supplement to get iodine. Does the product contain both iodine and iodide? The body needs both forms. Different parts of the body look for one of the specific forms. For instance the breasts look for iodine [she serious?] and the thyroid needs iodide [we know].'― Stephanie Buist

I think the reduced proliferation observed in the Brownstein-cited in vitro cancer cells had likely been on account of lipid iodination. Molecular iodine (I₂) of course adds to double bonds found on lipids, a process that happens so reliably that all oils used in soapmaking have a reported iodine value. The iodine value is an accurate index of unsaturation. Since the double bond is obliterated by added iodine atoms, the lipids' geometry shifts from sp²- to the sp³-hybridization and straightens. Iodinated lipids are more like saturated lipids than unsaturated ones, and can be viewed as being 'saturated by iodine' and not hydrogen—or partially-saturated by both. This newfound pseudo-saturation would increase membrane rigidity and should lower glucose flux. Yet on account of the low amount of iodine that'd been used, more realistic* could be that arachidonic acid had been iodinated to 5,6-diiodo-8,11,14-eicosatrienoic acid—or the 8,9-diiodo, 11,12-diiodo, 14,15-diiodo congeners—and lose its' cyclooxygenase specificity. The iodination of arachidonic acid should completely abrogate its' potential to become prostaglandin E₂.

[*] The iodination of the double bond between carbons 5–6, in particular, would seem the more likely occurrence on account of its' close proximity to the water phase when occupying its' assumed position in lipid bilayer of carcinoma cell membrane.
What is your opinion on Dr. Abraham's iodine loading protocol: 50 mg per day for three months, then 12.5 mg per day thereafter forever?
 

Travis

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What is your opinion on Dr. Abraham's iodine loading protocol: 50 mg per day for three months, then 12.5 mg per day thereafter forever?

Those doses levels don't appear particularly well thought out, and do sound suspiciously similar to multiples of Iodoral™ (which he does make money on). Iodoral™ contains molecular iodine, which I;d consider merely an unnecessarily-reactive source of iodide (I⁻). The doses are actually quite tame: potassium iodide has been used clinically in gram-sized doses, and with few side effects reported. The Wolf-Chaikoff effect apparently does not occur in humans because that would requires and i.v. injection, as used by Chaikoff & Wolf. The body really does have iodide stores, proven by loading doses, and this body compartment prevents plasma from reaching Wolf-Chaikoff levels. Based on glycogen's well-known affinity for iodide ions, a person could realistically suppose that most body I⁻ exists in the extracellular space.
 

Fractality

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I havent read past 20 pages but doesn't beef have very good SAFA to PUFA ratio? My organic beef is 65% SAFA, so im assuming its probably 0,5g PUFA per 100g which is low compared to even dairy

Is that beef also grass fed/pasture raised?
 

Travis

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I havent read past 20 pages but doesn't beef have very good SAFA to PUFA ratio? My organic beef is 65% SAFA, so im assuming its probably 0,5g PUFA per 100g which is low compared to even dairy
Well not all polyunsaturated fatty acids are created equal, and there's some indication that a higher ω−3/ω−6 is desirable. For this reason, the best beef should come from grass-fed cows—and especially those who'd lived in warm climates for increased lipid saturation. I am aware that most packaging does not indicate cow provenance, yet I don't buy beef so perhaps some do. [?] I think I'll look at cow autopsy data and their' diets pretty soon to see how significant these lipid grass∶grain ratios really are, a important factor in deciding if grass-fed is worth the higher cost.
 
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@Travis so from what I've read in your writing, you recommend plenty of iodine for thyroid production and selenium for t3 conversion. I remember you writing that vegetables have higher amounts of selenium than what's estimated. What vegetables are the best sources of Selenium? I believe you wrote that Broccoli was one if I'm not mistaken, what other ones would be good to consume? Thanks
 

Hairfedup

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Hey Travis, as per your recommendation I thought I'd let you know I've got my hands on some Cyclosporine. Currently being tested at my local university lab, but I'm confident it will pass quality control. Olive oil is my chosen carrier, with a 5% solution. A part of me was thinking starting low with a 2.5% solution but I'm not sure. As I don't have access to the entire papers where they used such a solution, I'm not sure how long to leave the solution on my scalp. A few hours? All night? In terms of application I was probably thinking every day or maybe 5 on 2 off. Would really appreciate some feedback.
 

Travis

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@Travis any idea how long methylxanthines block b-casomorphin for? A few hours perhaps? Surely not 12+ hours
Probably not that long. A pedantic answer could be the dissociation rate, which doesn't appear to have been quantified for caffeoyl quinide. Yet, the dissociation constant is 2.19 nM; this makes it as powerful as naloxone and a veritable antiopiate drug. This is more water-soluble than naloxone and thus should leave the body more quickly, so even though they have similar binding affinities towards μ-opiate receptor, their activities should differ due to solubility considerations. Naloxone looks nonpolar enough to penetrate the blood–brain barrier, yet caffeoyl quinide is a bit more polar. The cycloester of caffeoyl quinide appears unstable, and could be rehydrated back into quinic acid in the reverse process of its formation:

caffeoylquinic acid ⟶ coffee roasting caffeoyl quinide + H₂O

Caffeoyl quinide might only work peripherally and could contribute to that gnawing tension that can occur after a few quarts of coffee. Perhaps the displacement of β-casomorphin—or endogenous μ-opiate peptides—by caffeoyl quinide could be responsible for the paradoxical tiredness some observe after drinking it. Caffeoyl quinide has been shown to displace naloxone.
 

Travis

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@Travis so from what I've read in your writing, you recommend plenty of iodine for thyroid production and selenium for t3 conversion. I remember you writing that vegetables have higher amounts of selenium than what's estimated. What vegetables are the best sources of Selenium? I believe you wrote that Broccoli was one if I'm not mistaken, what other ones would be good to consume? Thanks

This stems from the fact that selenium is the only element covalently-bound to proteins also considered a 'mineral' by the USDA. Selenium also exists in a free & soluble form, as selenate ions, and for this reason it has historically been determined by analyzing the water-phase after centrifugation or filtration of homogenized food. Thus: when determining the selenium content of foods having selenomethionine, selenocysteine, and selenohomocysteine, a considerable fraction of selenium can be simply ignored. Accurate selenium concentrations taking this into account can be found for certain foods, but not all of them—certainly not as much as what's included within the USDA database.

Brassica vegetables are considered hyperaccumulators of selenium, yet when grown in low-selenium soil they may not be especially concentrated. Plants have more variable selenium concentrations that seafood because theirs greatly depends on growing location. Yet I think selenium is so important for the creation of selenoenzymes—i.e. iodothyronine deiodinase and glutathione peroxidase—that I have selenized yeast, a yeast grown in high Se²⁻ fluid which it incorporates mostly as selenomethionine in relatively concentrations.

The iodide ion is important for thyroid hormone yet also for myeloperoxidase, a neutrophil enzyme that converts iodide (I⁻) into hypoiodous acid (HIO). This is so effective at defending against certain microbes by killing them directly that iodide can be seen as an immuno-enhancing agent.
 

Travis

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Hey Travis, as per your recommendation I thought I'd let you know I've got my hands on some Cyclosporine. Currently being tested at my local university lab, but I'm confident it will pass quality control. Olive oil is my chosen carrier, with a 5% solution. A part of me was thinking starting low with a 2.5% solution but I'm not sure. As I don't have access to the entire papers where they used such a solution, I'm not sure how long to leave the solution on my scalp. A few hours? All night? In terms of application I was probably thinking every day or maybe 5 on 2 off. Would really appreciate some feedback.
Both of the the case reports—and the small study—had used olive oil. This jives with studies on skin permeability, where oleic acid generally outperforms the rest. Since this is a cyclic peptide of 11 amino acids it's skin penetration is slow. A low permeability is also a notorious property of cyclosporine, and so much so that Stanford chemists try to improve this using covalent modifications to its' structure.

Cyclosporine is indisputable the most effect hair growth agent, and over 90% of people taking it for organ transplants report hypertrichosis. Hair growth is a very consistent 'side-effect' of cyclosporine, and so consistent that its' reliability would appear limited only to the extent it resists absorption. Since the studies that had shown essentially . . . complete reversals of alopecia had used olive oil, I think this should be the go-to solvent—especially since oleic acid's been shown 'most permeable' by others.
 

Travis

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@Travis - What foods are you eating as of late?
I make 'zucchini noodles' with a julienne shredder and like eating salads with chopstix. I cut all my vegetables in long strands, and my salads have visual properties approximating spaghetti. For the next few days it is: zucchini noodles, roma tomatoes, homemade sauerkraut, and white candy onion. I also have broccoli I just eat plain since I don't think it goes well with salads.

I also have seven large Amish cantaloupes, 1¹⁄₂ #coffee, and nearly one pound of ammonia-free tobacco. There is much local food around me right now that doesn't store well so I only keep about a few day's worth. Next few weeks should be better because the watermelons will be done growing and I will eventually drive further for pineapples, kale, and perhaps goat cheese
 
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