Interesting comment I came across from the admin on a private forum (Perfect Hair Health). It mentions ray peat, Danny Roddy and a little about estrogen.
This is just my opinion, so I'm open to being totally wrong here. I only wanted to recommend that Toni consider doing lab tests to confirm if thyroid is an under-active, and if he's curious, to try Ray Peat's recommendations to see if they help him.
I have read a lot of Ray Peat's work, though I'm certainly not as familiar with it now than I was 6-7 years ago. For context – back in 2011/2012, I experimented with Ray Peat / Danny Roddy's recommendations for hair loss and optimizing thyroid. I tried to minimize my exposure to PUFAs, optimize my calcium:phosphate ratio, and started viewing sugar more so as a supplement. I built a diet around coffee, orange juice, eggs, cottage cheese, coca cola, whole milk, liver, ground beef, Häagen-Dazs ice cream, etc. I exposed myself to lots of sunlight, stopped working out (and replaced my efforts with more walking), and made sure that my macros were roughly aligned with what Ray Peat/Danny Roddy advocated.
I did this for ~6 months. I ended up with continued hair loss and a resurgence of acne all over my face. The acne didn't subsist after switching milk brands, moving from whole milk to 2%, switching to raw cow's milk, or switching to raw goat's milk. So I ended my experiment and moved onto other testing other interventions.
Later on, as I worked to become more scientifically literate, I began to disagree with Danny Roddy's / Ray Peat's recommendations for optimizing thyroid health. This really started to take hold after reading beyond their articles and into their source material (i.e., scholarly references).
The issues I noticed were two-fold:
Quote
Similarly, because estrogen dissolves bone,[1] it would appear that estrogen is not only a candidate for the reason why women are more protected from pattern baldness than men, but possibly as a therapy.
The paper he's referencing is, Effects of estrogen on growth plate senescence and epiphyseal fusion. The study is on rabbits who had their ovaries removed, and who then received estrogen injections once weekly to see how this would impact the fusion of a variety of bone growth plates. The authors concluded that:
Quote
(i) The growth plate undergoes programmed senescence including a decline in growth rate, proliferation rate, and the number and size of chondrocytes. This program may be due to replicative senescence of the growth plate chondrocytes. (ii) Epiphyseal fusion is a rapid process that is triggered when the senescence program reaches a critical point. Specifically, epiphyseal fusion seems to be triggered when the proliferative potential of the growth plate chondrocytes is finally exhausted. (iii) Estrogen accelerates the growth plate senescence program, thereby exhausting the proliferative potential of growth plate chondrocytes sooner, consequently triggering earlier epiphyseal fusion. This model may also apply to humans, providing an explanation for certain clinical observations: the catch-down growth in children following estrogen exposure, the prolonged and age-dependent delay between the onset of estrogen and the onset of fusion, and the acceleration of bone age by estrogen.
If the problem isn't already clear, it's that Danny Roddy is backing up the claim that estrogen dissolves bone by citation a study measuring estrogen's influence on growth plate fusion on ovariectomized rabbits. The study's findings don't support his claim; in fact, they actually argue more of the opposite: that estrogens play a crucial role in helping to fuse growth plates which may explain why some children slow in growth following consistent exogenous estrogen exposure. This is just the first reference of his article.
So, after finding a lot of these types of issues across Ray Peat/Danny Roddy's work, I eventually abandoned their principles and moved onto other things.
Now, this isn't to say that their recommendations WON'T work. They certainly have worked for some people. So, if anyone is curious, I always recommend that they experiment with their recommendations to see if they help them. But for me personally, it didn't work. And digging deeper into their work, I don't find that the sources they cite often support the claims they make about hair, hormones, and health.
If you're curious, here's a thread that echoes a lot of the sentiments above, plus some others that I haven't addressed.
In any case, the last thing I want to do is prevent someone from experimenting with something because of my personal experience / opinion. Based on my conversations with Toni, he didn't fit the profile of others with whom I'd worked who had hypothyroid-related hair shedding in addition to AGA. But I could be totally wrong! My hope is that lab work and/or temperature monitoring will help provide more insights.
As far as my own hair loss, my diagnosis suggested that I had strictly AGA, but my lab tests suggested that I also had subclinical hypothyroidism. So, in this case, it made sense for me to try and tackle both the thyroid and the AGA, which is why I likely saw benefit from a combined approach of massaging + dietary/lifestyle changes that had overlap with Ray Peat/Danny Roddy's ideas.
This is just my opinion, so I'm open to being totally wrong here. I only wanted to recommend that Toni consider doing lab tests to confirm if thyroid is an under-active, and if he's curious, to try Ray Peat's recommendations to see if they help him.
I have read a lot of Ray Peat's work, though I'm certainly not as familiar with it now than I was 6-7 years ago. For context – back in 2011/2012, I experimented with Ray Peat / Danny Roddy's recommendations for hair loss and optimizing thyroid. I tried to minimize my exposure to PUFAs, optimize my calcium:phosphate ratio, and started viewing sugar more so as a supplement. I built a diet around coffee, orange juice, eggs, cottage cheese, coca cola, whole milk, liver, ground beef, Häagen-Dazs ice cream, etc. I exposed myself to lots of sunlight, stopped working out (and replaced my efforts with more walking), and made sure that my macros were roughly aligned with what Ray Peat/Danny Roddy advocated.
I did this for ~6 months. I ended up with continued hair loss and a resurgence of acne all over my face. The acne didn't subsist after switching milk brands, moving from whole milk to 2%, switching to raw cow's milk, or switching to raw goat's milk. So I ended my experiment and moved onto other testing other interventions.
Later on, as I worked to become more scientifically literate, I began to disagree with Danny Roddy's / Ray Peat's recommendations for optimizing thyroid health. This really started to take hold after reading beyond their articles and into their source material (i.e., scholarly references).
The issues I noticed were two-fold:
- Ray Peat / Danny Roddy seemed to group all hair loss disorders together (i.e., hair loss from hypothyroidism, nutrient deficiencies, androgenic alopecia, scarring alopecias, etc.). While there are plenty of cases of overlapping hair loss disorders, each type of hair loss is histologically different, and in general, has a unique set of causes + appropriate treatments. I found that a lot of people were interpreting Danny Roddy / Ray Peat's recommendations for hypothyroid-related hair loss as recommendations for androgenic alopecia-related hair loss. In general, it didn't seem that they were delineating the differences in most of their articles.
- Ray Peat / Danny Roddy seemed to make generalizations of hormones as if they were one-dimensional. For example, something I often read in the Ray Peat forums was that "DHT = pro-hair, estrogen = anti-hair". This is a bit problematic, and not necessarily accurate. For instance, DHT can cause hair loss or hair growth depending on whether the arrival of that DHT induces certain signaling proteins surrounding the mesodermal sheath and dermal papillae of a hair follicle. Moreover, estrogen's role in hair loss/hair growth is both gender-specific and location-specific. High serum estrogen levels in men are often correlated with systemic inflammation, higher insulin levels, and thereby are often associated with early-onset pattern hair loss and/or a hair shedding disorder. But estrogen activity within scalp hair follicles themselves actually helps to regulate the hair growth cycle, which is why topical estrogens sometimes elicit hair-promoting effects in some individuals.
Quote
Similarly, because estrogen dissolves bone,[1] it would appear that estrogen is not only a candidate for the reason why women are more protected from pattern baldness than men, but possibly as a therapy.
The paper he's referencing is, Effects of estrogen on growth plate senescence and epiphyseal fusion. The study is on rabbits who had their ovaries removed, and who then received estrogen injections once weekly to see how this would impact the fusion of a variety of bone growth plates. The authors concluded that:
Quote
(i) The growth plate undergoes programmed senescence including a decline in growth rate, proliferation rate, and the number and size of chondrocytes. This program may be due to replicative senescence of the growth plate chondrocytes. (ii) Epiphyseal fusion is a rapid process that is triggered when the senescence program reaches a critical point. Specifically, epiphyseal fusion seems to be triggered when the proliferative potential of the growth plate chondrocytes is finally exhausted. (iii) Estrogen accelerates the growth plate senescence program, thereby exhausting the proliferative potential of growth plate chondrocytes sooner, consequently triggering earlier epiphyseal fusion. This model may also apply to humans, providing an explanation for certain clinical observations: the catch-down growth in children following estrogen exposure, the prolonged and age-dependent delay between the onset of estrogen and the onset of fusion, and the acceleration of bone age by estrogen.
If the problem isn't already clear, it's that Danny Roddy is backing up the claim that estrogen dissolves bone by citation a study measuring estrogen's influence on growth plate fusion on ovariectomized rabbits. The study's findings don't support his claim; in fact, they actually argue more of the opposite: that estrogens play a crucial role in helping to fuse growth plates which may explain why some children slow in growth following consistent exogenous estrogen exposure. This is just the first reference of his article.
So, after finding a lot of these types of issues across Ray Peat/Danny Roddy's work, I eventually abandoned their principles and moved onto other things.
Now, this isn't to say that their recommendations WON'T work. They certainly have worked for some people. So, if anyone is curious, I always recommend that they experiment with their recommendations to see if they help them. But for me personally, it didn't work. And digging deeper into their work, I don't find that the sources they cite often support the claims they make about hair, hormones, and health.
If you're curious, here's a thread that echoes a lot of the sentiments above, plus some others that I haven't addressed.
In any case, the last thing I want to do is prevent someone from experimenting with something because of my personal experience / opinion. Based on my conversations with Toni, he didn't fit the profile of others with whom I'd worked who had hypothyroid-related hair shedding in addition to AGA. But I could be totally wrong! My hope is that lab work and/or temperature monitoring will help provide more insights.
As far as my own hair loss, my diagnosis suggested that I had strictly AGA, but my lab tests suggested that I also had subclinical hypothyroidism. So, in this case, it made sense for me to try and tackle both the thyroid and the AGA, which is why I likely saw benefit from a combined approach of massaging + dietary/lifestyle changes that had overlap with Ray Peat/Danny Roddy's ideas.
