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Originally Posted by garlicandginger
There are theories that suggest baldness is a defense mechanisms for other diseases: http://www.ncbi.nlm.nih.gov/pubmed/17910907
Androgenic alopecia may have evolved to protect men from prostate cancer by increasing skin exposure to ultraviolet radiation.
So there can be a link between vitamin D synthesis and DHT or other markers/hormones etc
Pair that with the fact that vitamin D synthesis needs cholesterol/fat to metabolize in skin, and there's an explanation for greasy scalp and hair loss. And consider that people are advised to wash hair frequently in case of hair loss which might worsen the symptoms since it strips the fats needed to make vitamin D.
The scalp is very vascularised which might explain the horseshoe pattern. http://www.erexam.org/wp-content/upl...asculature.png
Pair that with the fact that western society rarely gets any Sun, and vit D synthesis happens under UVB only (which is a narror timeframe, usually noon and in warm months when Sun is perpendicular to Earth - basically, the more inclined the angle it enters the atmosphere, the less UVB gets through), and that glass filters out UVB (so if you sit indoors behind a glass and Sun shines on you at noon, there will be 0 vitamin D synthesis).
I've read 90% of hair loss sufferers have a vitamin D deficiency. Getting 30 mins of sun is a part of my treatment method. Something I did notice with 30 min sun baths, when I applied minox before my sun time, my peach fuzz seemed darker. I've recently started using Emu oil before my sun time and I believe I'm seeing the beginning of some magic taking place. I can't say for sure its the combo of emu oil and sun which would be in line with what you wrote because I am now 7 months past my 3 month derma rolling treatment and it's basically the time supposed to start seeing results. Also have been using minox for 10 months. Whatever it is, this past month I've had an increase in hair at my temples. More and more terminal hairs popping out, darker and longer hairs that aren't terminal but way darker and stronger than peach fuzz.
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I should be an NW10 then.
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This is such bro science BS it's not even funny. EVERYBODY after the age of 12 or 13 masturbates. Unless someone is going into the priesthood, literally everyone does it with regularity.
When you get older, you start having sex. That must be just as bad for hair then right? I mean it's setting off the same chain of biological responses. But no, for some reason everyone thinks it's just JO'ing that leads to hair loss. Show me a normal functioning person who doesn't do this and ill show you a liar. This thread shouldn't be anywhere near the cutting edge section, it's like something the Native Americans would have believed.
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Originally Posted by Trouse5858
This is such bro science BS it's not even funny. EVERYBODY after the age of 12 or 13 masturbates. Unless someone is going into the priesthood, literally everyone does it with regularity.
When you get older, you start having sex. That must be just as bad for hair then right? I mean it's setting off the same chain of biological responses. But no, for some reason everyone thinks it's just JO'ing that leads to hair loss. Show me a normal functioning person who doesn't do this and ill show you a liar. This thread shouldn't be anywhere near the cutting edge section, it's like something the Native Americans would have believed.
OP says those who are genetically prone to getting hair loss. Not everyone who masturbates.
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Originally Posted by PatientlyWaiting
OP says those who are genetically prone to getting hair loss. Not everyone who masturbates.
Of course he has to say that otherwise he would be factually wrong. At least now there is no major evidence proving him wrong, but nothing proving him right either.
IMO it can increase hair loss because it probably does increase T levels for a short time before and maybe after. That being said is it enough to make any difference? Probably not, and its not worth going over a theory with no evidence when so many other better explanations exist
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Benign prostatic hyperplasia, metabolic syndrome and androgenic alopecia: Is there a
Benign prostatic hyperplasia, metabolic syndrome and androgenic alopecia: Is there a possible relationship?
Abstract
Objective
To evaluate the incidence of benign prostatic hyperplasia (BPH) and metabolic syndrome in patients with androgenetic alopecia (AGA) in comparison with those with no AGA, as several previous studies have reported inconsistent results of an association between metabolic syndrome and BPH with AGA.
Patients, subjects and methods
This cross-sectional study included 400 participants, divided into 300 patients diagnosed with AGA, with different grades according to Norwood–Hamilton classification, and 100 control subjects with no AGA. Criteria for diagnosis of metabolic syndrome according to Adult Treatment Panel-III criteria (waist circumference, blood pressure, fasting blood sugar, high-density lipoprotein and triglycerides), as well as criteria for diagnosis of BPH (prostatic volume, urine flow, and prostate-specific antigen) were assessed in all patients and compared with the control subjects.
Results
There were significant differences between the AGA and no-AGA groups for the following variables: waist circumference, body mass index, fibrinogen level, fasting blood sugar, cholesterol, C-reactive protein, erythrocyte sedimentation rate, and glycosylated haemoglobin. There was a significant difference in number of patients with AGA manifesting criteria of metabolic syndrome (51% vs 28%), as well as BPH diagnostic criteria (36% vs 6.8%) compared with the control subjects. Both BPH and metabolic syndrome were shown to be significant independent variables associated with AGA.
Conclusions
Dermatologists, urologists, and primary care physicians should monitor patients with early onset AGA for the development of urinary symptoms, to permit an earlier diagnosis of BPH; and for metabolic syndrome symptoms, to permit early diagnosis of cardiovascular risk factors.
http://www.sciencedirect.com/science...90598X1600005X
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Correlation of Carotid Intima Media Thickness and Aortic Stiffness
Index With Androgenetic Alopecia
Aim: Androgenetic alopecia (AGA) is a common health problem which is well associated with
hair loss in both male and female subjects by the effect of androgens under the presence of
genetic predisposition. Recent studies showed that there is an increased risk for coronary artery
disease in AGA patients. The aortic stiffness index (ASI) and the carotid intima media
thickness (CIMT) are accepted as a strong marker for the presence of atherosclerosis. The aim
of this study is to determine the possible correlation of CIMT and ASI with presence of AGA.
Materials and methods: A total of 159 male asymptomatic AGA patients between 18-55 years
old without any history of chronic disease enrolled to the study. Patients were classified in the
means of their AGA stage as group I (stage 1-2) (n=49), group II (stage 3-5) (n=71) and group III
(stage 6) (n=39) according to the Hamilton scale. Echocardiography was used to determine the
elastic properties of aorta assessed by ASI and aortic distensibility (AD) parameters. CIMT was
measured by color Doppler ultrasonography. ASI, AD and mean CIMT were calculated. The
data including the patient’s metabolic profile and anthropometric measurements were recorded.
Results: There was no significant difference between the groups in the means of age, height,
body mass index, and left ventricle ejection fraction. The values of mean ASI, CIMT and systolic
blood pressures were significantly higher in group III than group I and group II statistically
(p<0.001 for all three parameters). On the other hand, AD was significantly higher in group I
compared with group II and III statistically (p<0.001).
Conclusions: ASI and AD are parameters reflecting the aortic elastic properties. In case of an
aortic elasticity deterioration, ASI value increases while AD value decrease. This study concluded
that the patients at higher stages of AGA had higher CIMT and more deteriorated aortic
elasticity which are indicators of atherosclerosis. Thus, we assumed that patients with advanced
AGA stages may have subclinical atherosclerosis more commonly compared to the
patients with beginning stages of AGA.
http://dergiler.ankara.edu.tr/dergil...2055/21333.pdf
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Bumping this for new users!
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I still think no one really knows. What about men that are susceptible to MPB that are athletes that do not suffer insulin resistance and have normal SHBG yet suffer early onset of MPB? I can assure you plenty of men fitting those circumstances exist and kind of contradicts this theory. If this statement were pure fact everyone with MPB would basically be pre-diabetic then, and thats simply not true.
So maybe its evidence towards environment has influence, but its a question of how much? shbg isnt even a constant it could high one month and lower the next from different variables like excercise/drinking alcohol which supposedly raise it
Study A - It's been observed that men with early onset of baldness suffers from insulin resistance (pre-diabetics) and have low level of SHBG
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