The Travis Corner

[Travis]

Just spoke with a guy that got layed off from a milk distribution company.

That's interesting, I had just talked to a few people paid to promote it.

 

[YourUniverse]

@Travis is there a way members can donate to you for your work? Ray of course sells his newsletter, and subscribing is an easy way to say thank-you, do you have any projects like that available? You have been an invaluable resource.

 

[Travis]

@Travis is there a way members can donate to you for your work? Ray of course sells his newsletter, and subscribing is an easy way to say thank-you, do you have any projects like that available? You have been an invaluable resource.

As soon as I finish my first article, I will let you know the website URL that it's going on. Right now the webpage is blank, but I am working on that.

 

[Hairfedup]

I had about ¹⁄₄ oz of olive oil today, mainly just because the shredded garlic in my salads has too much bite without it. This is a massive amount of linoleic acid for me, yet still just a tiny amount compared to what most people consume. Olive oil is mostly oleic acid, generally having only between 5–15% linoleic acid.

Does anyone think hair loss is natural for humans? or does it make more sense that it's accelerated by unnatural eicosanoids? In the tropics during evolution, we would certainly have consumed very little linoleic acid. A high EPA∶arachidonic acid ratio on the cell membrane would correspond to a higher prostaglandin D₃∶D₂ ratio, and also differences in leukotrienes. A lower activity of the 3-series prostaglandins is the general trend, and the EPA-derived leukotrienes are similarly weak. Prostaglandins E & D seem to be involved in thermoregualtion and negative-feedback of 'inflammatory' states, or ṄO and Ȯ₂⁻ production, so adding an invasive fatty acid—proto-biomimetic of natural 3-series prostaglandins—to the natural diet could be expected to lead to consequences. This is especially true since the 2- and 3-series eicosanoid products have differential activity, sometimes extreme, and it is always the former class being more potent. The chemotactic potency between leukotriene B₅—the EPA product—and leukotriene B₄ is 5,000-fold, and Mead acid leukotriene B₃ is about fivefold less potent than B₄. The differential activity of prostaglandins D₃/D₂ are probably not as extreme, but as far as I know this has never been determined. However: studies on the more researched prostaglandin E₃ show that its roughly fourfold less potent as prostaglandin E₂ on cell membrane receptors, and from this you could infer a lower activity of the more natural prostaglandin D₃ on analogous targets (yet D-class prostaglandins have nuclear targets—i.e. PPARγ, p53—unlike E-class prostaglandins).

I think that it would be ludicrous for anyone to believe that hair loss is 'natural'..at least not up until very old age. I've seen some of your other posts regarding the possible lack of MPB in traditional tropical communities where the diet is mostly based on tubers, fish, fruit and coconut...having spent a lot of time in the Tropics, from the Malayan archipelago to the Pacific islands, I can say that baldness is very rare there. Especially, and I think it is important to say so, premature baldness in young men seems non-existent. However in the rapidly globalised world with a shared global culture (thanks to social media, wow what a powerful tool) I am starting to see hairloss in younger men around these parts, but still, much rarer compared to what we see in the UK or the States.

I cannot speak from a chemical perspective as I don't have the appropriate knowledge but I'm definitely learning from you lol. As a professional researcher though, I do think that hairloss is definitely associated to variables outside of the diet. For example, I would love to see a study (one that would never make it past formulation) wherein a very large sample of bald ing men were psychoanalysed and more importantly, have their relationship with their mother-figure examined. I would bet that 1. The mother figure has BPD or NPD ; and 2. A masculinised brain. The balding men would suffer greatly in the inability to emotionally-self regulate and separate the 'mother-God' from whatever belief they hold (Jesus, God etc) and have their inner schema permanently bastardised by the narcissistic mother-figure...no ability to self-soothe and emotionally regulate=extremely high cortisol etc. I'd also hazard a guess that the men who had developed the highest levels of narcissism would suffer the least amount of hairloss.

For me, it is definitely a psycho-physiological phenomenon. I think that narcissism and the inability to feel are what stop rapid hair loss from occurring.

 

[YourUniverse]

Maybe baldness is an adaptation to increase vitamin D, skin exposure to UV... Parathyroid and prolactin are hypothesized to play a role in balding, and both are improved by vitamin D

 

[Amazoniac]

As soon as I finish my first article, I will let you know the website URL that it's going on. Right now the webpage is blank, but I am working on that.

!!
I can only now bet that the theme is going to be brown, dark brown. Raj's is green, which is an imposition for every biologist. But The Writer knows that in nature brown often occurs where nutrients concentrate, soil and liver are examples. Leaves don't count because they have to absorb specific parts of light, kale was supposed to be brown if it wasn't for the rejection of green, the rejection that I guess you did when choosing the theme color. This also happens when people decide to blend various ingredients, the result usually assumes a darker color the more you add them. In addition, Travo is fond of coffee and dates, which starts to leave you with no option. To complete, we also know how simple it is to decide between the irreverence of green and the elegance of brown.

 

[Travis]

!!
I can only now bet that the theme is going to be brown, dark brown. Raj's is green, which is an imposition for every biologist. But The Writer knows that in nature brown often occurs where nutrients concentrate, soil and liver are examples. Leaves don't count because they have to absorb specific parts of light, kale was supposed to be brown if it wasn't for the rejection of green, the rejection that I guess you did when choosing the theme color. This also happens when people decide to blend various ingredients, the result usually assumes a darker color the more you add them. In addition, Travo is fond of coffee and dates, which starts to leave you with no option. To complete, we also know how simple it is to decide between the irreverence of green and the elegance of brown.

I did have a coffee + date phase before, yet I think now they'd be a bit too sweet. Sugar tolerance is somewhat like salt tolerance in interpersonal and temporal variance, and after switching to coffee + figs I don't want anything sweeter. I am fine with just about any whole fruit right now, and I think being on the lower side of blood sugar is much preferred.

It is also melon season nearby in Amish territory so it's easy to get enough calories without figs, dates, or raisens raisins (I always spell that wrong). These fruits have lost much water and can thus be viewed as 'concentrated'—though still raw of course. [Yet it is possible to find dates with most water content still remaining.] I think dried fruits are somewhat unnatural: In the wild: the fruit would get eaten by some bird or whatnot before they'd get to that point, and it would actually be impossible in most places due to air humidity.

 

[YourUniverse]

Travis has a Patreon page where you can donate to him, and he picked a really cool username:

Travis is creating ...molecular explanations for many things. | Patreon

 

[Travis]

I am still writing my first article because it is very involved, so hadn't given much though to the page layout: I had mostly just filled-out required blanks. Someday I hope to have many articles and should that happen, I will reformat them for a website.

 

[Travis]

Yet I did come across some more information on folate receptor autoantibodies, designated as FRα because the specific subtype needs to be stressed. The folate receptors α, β, and γ are all expressed in the human body, yet FRα is the predominate subtype on the blood–brain barrier (choroid plexus). Antibodies against the α-subtype would then naturally be expected to block more brain folate, and also the type expected to be greater risk factor for cerebral folate deficiency.

All three subtypes—FRα, FRβ, and FRγ—are found in the milk of most species, and are cumulatively known as 'folate binding protein.' Folate receptors α and β are adhered to the cell membrane merely by a phosphotidylinositol modification making them easily-exfoliated into the plasma, from which they transfer into the milk of lactating mammals. Folate receptor γ is an exclusively-soluble subtype never attached. Proteins in milk have been known to bind folates as far back as 1969, long before they'd been individually characterized. Initial studies focused primarily on how they effect dietary folate availability, and since their immunological properties were of no concern their variations in protein structure mattered little. Early studies were primarily concerned about the folate-binding capacity of the food analyzed, a method also used to estimate its' concentration of 'folate-binding protein.' Concentration data gathered in this manner is completely unreliable from an immunological standpoint because: (1) the specific subtypes are not differentiated, and (2) a denatured protein could have lost its folate-binding geometry while retaining full immunogenicity. Pasteurization destroys folate binding capacity, yet the protein antigens aren't destroyed.

Since folate-binding proteins α, β, and γ are small and water-soluble it should be no surprise they'd naturally be found in the whey fraction. High-salt cheese made from raw milk actually has a negligible amount of FRα, as determined via ELISA, perhaps on account of it having been largely removed in the whey and then further reduced through brine-leeching. However: a logical person could rightly expect that homogenization, via liposomal encapsulation, would in fact change the interphase compartmentalization of milk's folate-binding proteins.

'Analyses of other dairy samples for total FBP showed cottage cheese to be a rich source of FBP (540 ± 3 nmol/kg), whereas whey and whey cheeses contained only 30–97 nmol/FBP per kg. Hard cheeses manufactured from whey-separated milk contained less than 25 nmol FBP/kg (n = 36).' ―Jägerstad ⁽²⁾

'In the hard cheeses Herrgård and Grevé, 22 and 25 nmol FBP/kg, respectively, were observed. This is somewhat higher, but in line with, FBP levels in hard cheeses presented previously. Since FBP is a whey protein, it is not surprising to find only a small part of the FBP in cheese. Taking into account that about 10 litres of milk are needed to produce 1 kg of cheese, it can be concluded that less than 2% of the FBP from milk was recovered in hard cheese.' ―Arkbåge ⁽¹⁾​

Autoantibodies having high-affinity to human FRα have also been shown correlated with schizophrenia in those that have them.⁽³⁾ Not surprisingly: folate receptor-α autoantibodies in schizophrenics are also correlated with cerebral folate concentration, presumably a function of: circulating folates, circulating autoantibodies, choroid plexus FRα expression, and even the capacity of immune cells to damage cells tagged with antibodies. Since choroid plexus FRα is also responsible for uptake of tetrahydrobiopterin, it should then be no surprise that this cofactor had also been found reduced in these individuals. Even though tetrahydrobiopterin can be formed in the brain de novo, the synthesis of its' precursor—guanosine triphosphate—depends on a folate cofactor. The GTP ⟶ biopterin conversion occurs via cyclohydrolase, upregulated by TNFα and INFγ.

This study had confirmed the expected reduction in cerebral serotonin and dopamine consequent of lower tetrahydrobiopterin, the cofactor needed for tyrosine and tryptophan hydroxylase. The schizophrenic seems to be characterized by low serotonin and high histamine, two things brought into equilibrium by niacin.

"Fifteen of 18 patients (83.3%) had positive serum FR auto-antibodies compared to only 1 in 30 controls (3.3%). ―Ramaekers​

Niacin is known to spare tryptophan since it's no longer needed for its production: This leads to higher tryptophan concentrations, a higher Fernstrom ratio, and an increase in brain serotonin. Nicotinic acid is also somewhat analogous histamine, structurally, so could be suspected a priori to be an agonist/antagonist; this observation gets credence by the fact they both produce a 'flush' when injected. High doses of nicotinic acid has been confirmed to increase brain serotonin in rats, and it might not be too unreasonable to suggest that it could even antagonize brain histidine uptake.

Since bovine FRα is the protein most homologous to human FRα also commonly-ingested, it would be expected that a milk-free diet would lowered FRα autoantibody titers. This has been observed by Dr. Ramaekers previously, and in this one as well:

'She also started on an animal milk-free diet after starting folinic acid therapy, during which FRα antibodies were downregulated. As soon as she interrupted her milk-free diet, her FRα antibody titer rose again to 0.96 pmol FRα blocked/ml serum.' ―Ramaekers​

Cerebral folate deficiency—induced by folate receptor autoantibodies—have also been shown to impair myelination.⁽⁴⁾ This had been explained by reduced phosphotidylcholine consequent of low methylation, caused by the presumed lowered activity of folate-dependent serine hydroxymethyltransferase and methionine synthase. However: tetrahydrobiopterin is needed for alkylglycerol monooxygenase activity, a phospholipid synthesizing enzyme, and the most common sequelae of tetrahydro- biopterin deficiency is is impaired myelination. This condition is usually explained by the phenylalaninemia associated with low tetrahydrobiopterin, yet is never elaborated-on and such 'explanations' reduce-down to simply restating the association.

[1] Arkbåge, K. Vitamin B12, folate and folate-binding proteins in dairy products. Vol. 430. 2003.
[2] Jägerstad, M. '"Folate-binding protein in milk: a review of biochemistry, physiology, and analytical methods." Critical reviews in food science and nutrition (2012)
[3] Ramaekers, V. T. "Folinic acid treatment for schizophrenia associated with folate receptor autoantibodies." Molecular genetics and metabolism (2014)
[4] Steinfeld, R. "Folate receptor alpha defect causes cerebral folate transport deficiency: a treatable neurodegenerative disorder associated with disturbed myelin metabolism." The American Journal of Human Genetics (2009)​

 

[Amazoniac]

You know, guru, I have always preferred clean and simple website layouts. If you're undecided and haven't defined yours yet, here are some that can inspire you:
un, deux (favorite here), trois, quatre..
greenpeace.org:
..cinq, six.

I'm not sending you a private message because there are various members here who have blogs and might be inspired as vvcll.

 

[Mito]

Since folate-binding proteins α, β, and γ are small and water-soluble it should be no surprise they'd naturally be found in the whey fraction. High-salt cheese made from raw milk actually has a negligible amount of FRα, as determined via ELISA, perhaps on account of it having been largely removed in the whey and then further reduced through brine-leeching. However: a logical person could rightly expect that homogenization, via liposomal encapsulation, would in fact change the interphase compartmentalization of milk's folate-binding proteins.

'Analyses of other dairy samples for total FBP showed cottage cheese to be a rich source of FBP (540 ± 3 nmol/kg), whereas whey and whey cheeses contained only 30–97 nmol/FBP per kg. Hard cheeses manufactured from whey-separated milk contained less than 25 nmol FBP/kg (n = 36).' ―Jägerstad ⁽²⁾

'In the hard cheeses Herrgård and Grevé, 22 and 25 nmol FBP/kg, respectively, were observed. This is somewhat higher, but in line with, FBP levels in hard cheeses presented previously. Since FBP is a whey protein, it is not surprising to find only a small part of the FBP in cheese. Taking into account that about 10 litres of milk are needed to produce 1 kg of cheese, it can be concluded that less than 2% of the FBP from milk was recovered in hard cheese.' ―Arkbåge ⁽¹⁾​

Since folate binding proteins are found in the whey portion it’s seems cottage cheese should have low amounts, but apparently that is not the case?

 

[Travis]

Since folate binding proteins are found in the whey portion it’s seems cottage cheese should have low amounts, but apparently that is not the case?

As reported, the folate receptor concentration in Keso® cottage cheese is over twice that of Swedish milk. The author of the study did not explicitly state whether this had been made from homogenized milk, and if it had the concentration reported could reflect liposome-encapsulated protein. However, cottage cheese is neither pressed nor brined and some whey does remain; upon the straining procedure the folate receptor could associate with the crosslinked casein 'curds,' actually concentrating the soluble folate receptor.

Without knowing which of these products had been homogenized, if any, definitive statements concerning U.S. brands extrapolated from above date may not be accurate.

'The cottage cheese, 40 g fat/kg (Keso®), was supplied by Arla (Skövde, Sweden) and was manufactured from milk heat treated at 72–74 °C for 15–20 s, inoculated with 50–70 ml/l of a mixed mesophilic starter culture of Lc. lactis subsp. lactis, Lc. lactis subsp. cremoris and Ln. mesenteroides subsp. cremoris, and cultured at 30–35 °C for 4·5–5 h.' ―Wigertz​

Equating the folate receptor concentration with the foods' immunogenicity could be speculative. The author hadn't reported whether monoclonal or polyclonal antibodies had been used during the ELISA procedure to quantify folate binding protein, so there is no way of knowing from their article whether all three subtypes—i.e. α, β, or γ—had been cumulatively determined or just one. A monoclonal ELISA antibody would have affinity for just one subtype because it had originated from only one B-cell. Polyclonal antibodies, on the other hand, would be a mix of many types binding to several areas of all three subtypes—that is, of all three subtypes had been used to raise them.

Monoclonal antibodies would also be unsuitable in this case because it is possible for them to bind only to non-denatured proteins. Globular proteins generally have one long peptide backbone yet can gain a spherical shape through internal crosslink bonds. The folate receptor has eight internal disulfides and should the monoclonal antibody, assumed this had been used, have an epitope lying far apart in open-chain form it may not bind the denatured protein—and hence, not detected via ELISA. Upon reducing conditions: disulfide bonds are reduced to thiols and globular proteins can 'spring open,' losing tertiary geometry and becoming long and straight peptides. Straight peptide forms can still have immunogenic potential, yet at the same time be interpreted as 'not present' depending on the specific method(s) used for their quantification.

A random monoclonal antibody raised towards bovine FRα binds it by definition, yet same antibody may or may not also bind folate receptor α's straight chain form.

 

[Waremu]

Hello Travis. I’m guessing raw milk doesn’t have this problem as much because it isn’t homogenized, or is this not correct? (So far, from what I have read, it seems this is what I have gathered, or are these folate receptors not just the result of homogenized milk but milk itself whether raw or not?) Thank you.

 

[Travis]

Hello Travis. I’m guessing raw milk doesn’t have this problem as much because it isn’t homogenized, or is this not correct? (So far, from what I have read, it seems this is what I have gathered, or are these folate receptors not just the result of homogenized milk but milk itself whether raw or not?) Thank you.

All three subtypes—α, β, and γ—naturally exist in milk and collectively take the name 'folate binding protein,' the name given to them in the late '60s before their true function had been known. In the bodies of mammals, folate receptors of α and β subtype are found on cell membranes where they are responsible for cellular folate uptake. Unlike most membrane receptors, folate receptors are not firmly anchored to the cell membrane. Thus, some are exfoliated into the plasma and make their way into the milk of various mammals. Folate receptor α is found on the choroid plexus and is responsible for brain folate uptake; autoantibodies that bind FRα inhibit that process. Such antibodies are found in people having cerebral folate deficiency and autism, and have even been associated with birth defects. Folate receptor autoantibodies had been discovered in the pursuit of determining why moms with normal blood folate levels had children with neural tube defects, which is a classic folate-associated disorder. Folate receptor autoantibodies also block placental folate uptake.

Antibodies are formed against like proteins, and not one is more similar to human FRα than the bovine analogue—or at least, none commonly ingested. Homogenization breaks-down milk's relatively-large 12 micron liposomes into ones only 2 microns in diameter, and smaller, and in the process of liposome reformation milk proteins can become encapsulated. This had actually been demonstrated using a different milk protein, called bovine xanthine oxidase, during research pertaining to cardiovascular disease. The folate receptor has a tenfold smaller mass than xanthine oxidase, and for this reason it could be expected to be similarly-encapsulated. A milk-free diet has been shown to reduce FRα autoantibody titers.

The associations are strong between FRα autoantibodies and autism, where roughly 50% of those effected have been shown positive for the blocking type. Antibodies that bind, yet do not block, exist as well; studies indicate that the two types are found in roughly equally prevalence. Concentrations of FRα autoantibodies of the binding type are harder to measure so are rarely reported, yet they can also induce brain folate deficiency by eliciting immunogenic attack. Circulating neutrophils and natural killer cells would be expected to attack the choroid plexus should it be tagged with antibodies as immune cells have affinity for their 'opposite end'—i.e. the 'Fc region.' Autoimmunity against the choroid plexus has been demonstrated in the case of schizophrenia, vide infra, a condition found highly-associated with FRα autoantibodies 35 years later (Ramaekers, 2014).

Rudin, Donald. "Covert transport dysfunction in the choroid plexus as a possible cause of schizophrenia." Schizophrenia bulletin (1979)​

It is my contention that the process of homogenization encapsulates bovine FRα into small micelles that can be persorbed whole, a phenomenon that gives homogenized milk and its' derivatives enhanced immunogenic potential. I think this is quite logical and follows directly from published evidence. Raw cow's milk is presumed safer for this reason—and the cheese made from it—yet the milk from goats and sheep entirely lack FRα immunocrossreactivity and are never homogenized.

Nothing correlates better with FRα autoantibodies than CSF folate levels, and low brain folate is a serious concern for anyone.

 

[YourUniverse]

Are there any molecules that can block/bind/chelate the folate receptors in milk, like medium roast coffee for beta-casomorphin?

 

[Pomegranateman]

Hello @Travis I was wondering if I could get your opinion on some health complications of mine. You just seem very knowledgable so I thought why not see if you might know something that I don't. Do you know what would cause rapid hair growth all over the arms/hands, legs/feet. But also I'm losing hair all over my head, eyebrows, eyelashes, armpit, pubic area. And I've been forming brown spots (age pigment) all over, mainly arms and legs. Any thoughts? Thanks

 

[Travis]

Are there any molecules that can block/bind/chelate the folate receptors in milk, like medium roast coffee for beta-casomorphin?

Yes. An affinity chromatography column packed with folate-bound agarose will bind the folate receptor as it passes through, yielding FRα-free milk. The biggest challenge would of course be immobilizing the folate onto the agarose using a covalent link, perhaps through its (poly)glutamyl tail. Doctor Salter saves us time and effort by and informing us of one manner in which can be done (Salter, 1972):

'Following the procedure of Cuatrecasas [5] for preparing ω-aminoalkyl derivatives of agarose, 25 ml of Sepharose 6B were activated with 5 g cyanogen bromide at pH 11, washed with 1 ml cold water and added to 50 ml cold 12% (w/v) solution of 1,6-diaminohexane that had been adjusted to pH 10 with concentrated HCl. The mixture was stirred overnight in the cold, filtered, and the residue washed with 1 ml water. Folic acid was coupled to the ω-aminohexyl agarose by means of a carbodiimide condensation. The substituted agarose gel (20 ml) was suspended in an equal volume of water, folic acid (10 mg) dissolved in 0.05 M NaHCO₃ (10 ml) was added and the pH of the mixture adjusted to 6 with N HCl. Then, with the mixture kept in the dark at room temp and continuously stirred, 100 mg 1 -ethyl-3-(3-dimethylaminopropyl)carbodiimide (Cycle Chemicals, Los Angeles, California, USA) was added in portions of about 10 mg at 10 min intervals. The reaction mixture was kept at pH 6 by adding 0.1 N HCl as necessary. After addition of the carbodiimide stirring was continued for 1 hr. The gel, which had become pale yellow, was then filtered off and washed with 1 10.05 M NaHCO₃. The folate content of the washings, estimated from absorbance at 283 nm, indicated that about 0.3 mg folic acid/ml gel had been bound.' ―Salter​

Folic acid–agarose is an especially attractive substrate because folic acid is the cheapest commercial folate; agarose is a ubiquitous polysaccharide and is certainly not expensive either. However, this material may not remove FRα from homogenized milk should it be trapped in liposomes. And also, denatured FRα from pasteurized milk may not bind folate at all yet could retain immunogenicity. While a glass column packed with this material should remove all non-encapsulated FRα still having folate affinity, after a few passes, I think it could only reliably remove all folate receptors from raw milk.

 

[Travis]

Hello @Travis I was wondering if I could get your opinion on some health complications of mine. You just seem very knowledgable so I thought why not see if you might know something that I don't. Do you know what would cause rapid hair growth all over the arms/hands, legs/feet. But also I'm losing hair all over my head, eyebrows, eyelashes, armpit, pubic area. And I've been forming brown spots (age pigment) all over, mainly arms and legs. Any thoughts? Thanks

The lipofuscin has a very well-defined mechanism, and Brunk & Terman know all about it. This material is essentially proteins that've been crosslinked by remnants of peroxided lipids. After a hydrogen is abstracted from the lipid chain, oxygen can add to it thereby cleaving the fatty chain in two. Lipid peroxidation forms two shorter lipids each having one oxygen derived from the initial O₂ addition, yet these oxygen atoms are in the form of reactive aldehyde groups. These groups reliably add to primary amino groups such as found on lysyl side-chains of peptides, crosslinking them together in a proteinaceous lipid mass. Since this process is catalyzed by free iron, it's no surprise that this element also forms a significant component of lipofuscin.

Lipofuscin can be formed in vitro and is a function of: (1) free iron, (2) oxygen, and (3) polyunsaturated fatty acids. 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.The best way to minimize age spots appears to be minimizing both polyunsaturated fatty acids and dietary iron, together, and consuming selenium should help because glutathione peroxidase—a selenoenzyme—lowers cytosolic H₂O₂ concentration thereby attenuating peroxidation. Phytic acid chelates free iron, and vitamin E mitigates peroxidation by safely-storing free radical electrons at lipid membranes. Mixed tocopherols should also help prevent age spots.

Interferon-γ is likely responsible for causing the patchy hair loss seen in some infections, yet prostaglandins can certainly influence the process as well. Considering the lipofuscin also present, a person would be forced to suspect the involvement of prostaglandins—hormonal lipids also formed from omega−6 fatty acids. On this forum here, there is some debate about omega−3 fatty acids yet everyone unanimously avoids omega−6. There's a considerable amount of published research highlighting the problematic nature of that lipid class.

Interferon-γ appears to cause global hair loss, yet prostaglandins as a class appear to have diphasic effects. Prostaglandin F₂α and its congeners have an unusual ability to promote eyelash growth, while prostaglandin D₂—and its' dehydration product prostaglandin J₂—are highly correlated with hair loss on the scalp. These are all 2-series prostaglandins, the ones most-studied due their their enhanced potency. All of the 1- and 2-series prostaglandins are derived from omega−6 fatty acids, while those off the 3-series originate from the omega−3 class. Every prostaglandin has three subtypes denoted by a subscript ordinal, and all three subtypes have differential activity. Because prostaglandin E₁ has only ¹⁄₄ the potency of prostaglandin E₂, it follows that the dietary ω−3/ω−6 ratio—as well as the total amounts ingested—can affect the lipid hormones. information concerning the differential potency of D-class and F-class prostaglandins is hard to find.

 

[Pomegranateman]

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!

The lipofuscin has a very well-defined mechanism, and Brunk & Terman know all about it. This material is essentially proteins that've been crosslinked by remnants of peroxided lipids. After a hydrogen is abstracted from the lipid chain, oxygen can add to it thereby cleaving the fatty chain in two. Lipid peroxidation forms two shorter lipids each having one oxygen derived from the initial O₂ addition, yet these oxygen atoms are in the form of reactive aldehyde groups. These groups reliably add to primary amino groups such as found on lysyl side-chains of peptides, crosslinking them together in a proteinaceous lipid mass. Since this process is catalyzed by free iron, it's no surprise that this element also forms a significant component of lipofuscin.

Lipofuscin can be formed in vitro and is a function of: (1) free iron, (2) oxygen, and (3) polyunsaturated fatty acids. 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.The best way to minimize age spots appears to be minimizing both polyunsaturated fatty acids and dietary iron, together, and consuming selenium should help because glutathione peroxidase—a selenoenzyme—lowers cytosolic H₂O₂ concentration thereby attenuating peroxidation. Phytic acid chelates free iron, and vitamin E mitigates peroxidation by safely-storing free radical electrons at lipid membranes. Mixed tocopherols should also help prevent age spots.

Interferon-γ is likely responsible for causing the patchy hair loss seen in some infections, yet prostaglandins can certainly influence the process as well. Considering the lipofuscin also present, a person would be forced to suspect the involvement of prostaglandins—hormonal lipids also formed from omega−6 fatty acids. On this forum here, there is some debate about omega−3 fatty acids yet everyone unanimously avoids omega−6. There's a considerable amount of published research highlighting the problematic nature of that lipid class.

Interferon-γ appears to cause global hair loss, yet prostaglandins as a class appear to have diphasic effects. Prostaglandin F₂α and its congeners have an unusual ability to promote eyelash growth, while prostaglandin D₂—and its' dehydration product prostaglandin J₂—are highly correlated with hair loss on the scalp. These are all 2-series prostaglandins, the ones most-studied due their their enhanced potency. All of the 1- and 2-series prostaglandins are derived from omega−6 fatty acids, while those off the 3-series originate from the omega−3 class. Every prostaglandin has three subtypes denoted by a subscript ordinal, and all three subtypes have differential activity. Because prostaglandin E₁ has only ¹⁄₄ the potency of prostaglandin E₂, it follows that the dietary ω−3/ω−6 ratio—as well as the total amounts ingested—can affect the lipid hormones. information concerning the differential potency of D-class and F-class prostaglandins is hard to find.