Hair Thinning

dreamcatcher

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I did a search on the Internet on an eyebrow serum which contains isopropyl cloprostenate (a synthetic prostaglandin analog). The product claims that this is the main ingredient which causes the eyebrows to grow.
The product does work but only until one uses it.
I've also read an article that natural prostaglandin production declines as we age, especially when a woman enters menopause.
My question is how does one increase prostaglandin production naturally? I guess we talk about prostaglandin E2. Thanks.
 

Blossom

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I did a search on the Internet on an eyebrow serum which contains isopropyl cloprostenate (a synthetic prostaglandin analog). The product claims that this is the main ingredient which causes the eyebrows to grow.
The product does work but only until one uses it.
I've also read an article that natural prostaglandin production declines as we age, especially when a woman enters menopause.
My question is how does one increase prostaglandin production naturally? I guess we talk about prostaglandin E2. Thanks.
I asked Travis what he thought of a similar product (Latisse) and he thought it was probably safe. I’m fairly certain pufa’s increase prostaglandins. I’ll try to find his response.
 

Blossom

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That's a good question. I know the first studies showing prostaglandin‐induced 'hair growth was one with prostaglandin F₂α—or was is lantaprost?—on eyelashes. Sure, it lengthens eyelashes, but how can anyone justify putting a prostaglandin analogue in their eye?

I also would like to know why they do this.
Here he doesn’t sound too keen on the idea. I’ll try to find the other post I was thinking of.
 

Blossom

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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).
 
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D

dreamcatcher

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It's very interesting, thank you very much for sharing it @Blossom
I have to read through this a few times!
Apart from science, once I stopped using PUFA oils in 2008, I lost most of my eyebrows (70%). It is still the biggest puzzle :disappointed:
 

Birdie

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It's very interesting, thank you very much for sharing it @Blossom
I have to read through this a few times!
Apart from science, once I stopped using PUFA oils in 2008, I lost most of my eyebrows (70%). It is still the biggest puzzle :disappointed:
That is odd this happened. I had the opposite effect starting to follow Ray's ideas. My hair and eyebrows got thicker. And my hair stopped turning white and turned back to it's original color.

I wonder how you figured out it was reducing pufas that thinned yours. Do you do other things Ray advised? I mean, when I started this, I didn't just reduce pufas.
Not sure how to explain what I mean, but it would be unusual if you just reduced pufas and changed nothing else.

And that would be the only way I can think of to know that reducing pufas led to your eyebrow hair loss. Do you know what I mean.

It's just that my hair color returning is something I attribute to all the Peat ideas I started: gelatin, milky coffee, liver, orange juice, butter, coconut oil, the raw carrot. I was already taking NDT but did adjust my dose. I adjusted different supplements as I learned more about them. I'm sure I'm not remembering everything that I changed beginning in 2011.

Everyone is different in responses but it would help to know more about what dietary and other life changes you made besides reduced pufa, if there were any other changes.

Then, I think of all the people who claim the omega 3s help their skin and hair conditions. And Ray, as well as others, has commented on why this could be so. Unfortunately, I can't remember the reasoning for short term improvement, but he said there are safer ways, in the long run for better health, to help these conditions.
 

Birdie

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I just remembered that at one point, a couple of years ago, my eyebrows started to thin due to rosacea and seborrheic dermatitis. And I had to treat those two problems before they grew back. I did use castor oil on them, but I think it was the entire approach to those two conditions that worked in my case.
 

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