As some of you might remember, some time ago there were was a study which managed to model the pattern of hair loss through a von Mises mechanical stress model. See this thread here.
The model is surprisingly accurate but no one ever quite figured out why the mechanical stress, which seems to be connected to the skull bones, works this way in a progressive fashion. Some people on these forums proposed the skull expansion theory which was met with a lot of criticism. I am still not sure if skull expansion would be correct in the way it was proposed back then, but by now I also don't think it was completely wrong either.
As a reminder, before I get into the new link I found recently, I want to point out that Androgenetic Alopecia is associated with insulin resistance and with metabolic syndrome as shown by many studies.
So it turns out that insulin, IGF-1 and insulin resistance have certain metabolic effects on bone growth. I'll provide quotes from the following articles:
- Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues
- Insulin and bone: Recent developments
Most important quote that summarizes the findings:
In type 2 diabetes or pre-diabetic states, bone area and volume can be increased between 2 and 8%:
What is also interesting is that IGF-1 receptors are locally downregulated. IGF-1 is necessary for hair growth:
This might also explain the roles of vitamin D and K because they help in calcium absorption and resorption:
Some people also noted on various hair loss forums (see this thread here and this one there) before that glucocorticoids play a role in Androgenetic Alopecia or are at least statistically strongly correlated. Surprise:
NAFLD and insulin resistance are in a feedback loop where one contributes to the other. This explains metabolic syndrome (where insulin resistance and "fat problems" like abnormal cholesterol and atherosclerosis/plaques appear together) and, most importantly, why abnormal lipid profiles are correlated with Androgenetic Alopecia, probably as a contributing factor.
To summarize all of the above:
- Insulin is an anabolic agent for bone growth
- Bone volume and density in individuals with elevated insulin levels like type 2 diabetes or pre-diabetes can increase between 2 and up to 8%
- Fat metabolism and glucocorticoids contribute to these problems through various means (not all of which I covered in this post; see my post history for more information related to cholesterol, trans fats, saturated fats and oxidized fats)
- there is local IGF-1 insufficiency as a consequence of the above; IGF-1 however is necessary for healthy hair growth
Ultimately, this insulin- or insulin-resistance-mediated bone growth can be a potential explanation why von-Mises mechanical stress models predict Androgenetic Alopecia hair loss patterns. It also gives a bit of credence to the skull expansion theory and would explain why it isn't completely wrong. Likely, this expansion is not visible in most cases, but happens nonetheless as explained by the articles I cited.
The model is surprisingly accurate but no one ever quite figured out why the mechanical stress, which seems to be connected to the skull bones, works this way in a progressive fashion. Some people on these forums proposed the skull expansion theory which was met with a lot of criticism. I am still not sure if skull expansion would be correct in the way it was proposed back then, but by now I also don't think it was completely wrong either.
As a reminder, before I get into the new link I found recently, I want to point out that Androgenetic Alopecia is associated with insulin resistance and with metabolic syndrome as shown by many studies.
So it turns out that insulin, IGF-1 and insulin resistance have certain metabolic effects on bone growth. I'll provide quotes from the following articles:
- Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues
- Insulin and bone: Recent developments
Most important quote that summarizes the findings:
[W]e present evidence that insulin, acting as an anabolic agent in bone, can preserve and increase bone density and bone strength, presumably through direct and/or indirect effects on bone formation. [...] Type 2 diabetes, a state of hyperinsulinemia and insulin resistance, is typically associated with increased bone density, yet seemingly decreased bone strength contributing again to an increased risk of fracture. Recognizing that these two clinical entities are typically characterized by differences in insulin secretion, insulin sensitivity, and/or exogenous insulin administration, we present a review of clinical, in vivo and in vitro evidence examining whether insulin, as both a drug and hormone, qualifies as an anabolic agent for bone.
In type 2 diabetes or pre-diabetic states, bone area and volume can be increased between 2 and 8%:
they demonstrated that T2DM “was associated cross-sectionally with 2−8% higher regional and whole body BMD, both areal and volumetric measures, even with adjustment for body composition variables of lean mass, fat mass, and abdominal visceral fat and other confounding factors.”
What is also interesting is that IGF-1 receptors are locally downregulated. IGF-1 is necessary for hair growth:
IRS molecules also mediate IGF receptor signaling, so some cross talk through IRS may take place via insulin and IGF signaling in osteoblasts; however, knowing that levels of IGF-I, IGF-I receptors, and IRs are all reduced in the skeletal growth centers of diabetic animals (75), it could be speculated that impaired insulin signaling in bone-forming cells results in a secondary and local IGF-I deficiency.
This might also explain the roles of vitamin D and K because they help in calcium absorption and resorption:
... the net effect of insulin on bone, as suggested by in vivo models, is one of proformation and possibly of decreased resorption, both attributes of an anabolic agent for bone.
Some people also noted on various hair loss forums (see this thread here and this one there) before that glucocorticoids play a role in Androgenetic Alopecia or are at least statistically strongly correlated. Surprise:
In addition, we know that insulin resistance is also caused by factors that cause bone resorption, such as the interleukin-6-mediated chronic low grade inflammation that contributes to non-alcoholic fatty liver disease (NAFLD)[9] and excessive glucocorticoid production, another significant contributor to NAFLD[10].
NAFLD and insulin resistance are in a feedback loop where one contributes to the other. This explains metabolic syndrome (where insulin resistance and "fat problems" like abnormal cholesterol and atherosclerosis/plaques appear together) and, most importantly, why abnormal lipid profiles are correlated with Androgenetic Alopecia, probably as a contributing factor.
To summarize all of the above:
- Insulin is an anabolic agent for bone growth
- Bone volume and density in individuals with elevated insulin levels like type 2 diabetes or pre-diabetes can increase between 2 and up to 8%
- Fat metabolism and glucocorticoids contribute to these problems through various means (not all of which I covered in this post; see my post history for more information related to cholesterol, trans fats, saturated fats and oxidized fats)
- there is local IGF-1 insufficiency as a consequence of the above; IGF-1 however is necessary for healthy hair growth
Ultimately, this insulin- or insulin-resistance-mediated bone growth can be a potential explanation why von-Mises mechanical stress models predict Androgenetic Alopecia hair loss patterns. It also gives a bit of credence to the skull expansion theory and would explain why it isn't completely wrong. Likely, this expansion is not visible in most cases, but happens nonetheless as explained by the articles I cited.
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