JZA70
Banned
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I wonder how john travolta is getting money now days.
Probably turned his focus to drug dealing. I assume him and Jude Law work for the cartels now.
I wonder how john travolta is getting money now days.
super thick hair finally going bald:
View attachment 26607
Thin and greasy hair that has been maintained over time:
View attachment 26608
:
Amazing photos, .....,
These two examples may serve as a paradigm of the third factor, ....., the length of hair. According to my theory people, men or women, who abuse from shaving of the head or carry excessively short hair are those who are more likely to suffer from common baldness, even with thick hair and good hair density ( tonsure clearly explains this factor )
Here John Travolta and Iggy Pop are very illuminating examples. Travolta shave many times his scalp hair and Iggy wear long hair most of the time, and never did shave it
Thank you very much for these photos.
Can you please explain how short hair/shaving have anything to do with male pattern baldness?
Probably turned his focus to drug dealing. I assume him and Jude Law work for the cartels now.
Can you please explain how short hair/shaving have anything to do with male pattern baldness?
I hope you are joking...if not:
You do realize that john travolta cut his hair because he went bald...not the other way round. Plus are you that childish to use just two people on this planet as an example for your un-evolved theory? "very illuminating examples"? omg...it's just one guy with male pattern baldness and another without. Please educate yourself in male pattern baldness and general logic so you can approach these issues with some real conceptual thinking.
I had longish hair and never shaved it before male pattern baldness struck me down (temporarily lol). I've shaved my head many times and have kept it short for over 4 years now and I'm regrowing it at lightning speed!
I respect your opinion, but respect mine.
The hair of the woman and the man does not differ in any respect to their ability to grow. If came an alien at earth, or any human with open mind, they can think that one of the few differences between the hair of men and women is that women have adopted long hair unlike man, and perhaps this detail has something to do with the likelihood of having or not common baldness.
the key that can relate the length of hair and baldness is the sebum and there is much literature.
Moreover, there are cases that women may suffer alopecia if their hair is too short.
http://i.ytimg.com/vi/KYeMLt9GG_8/0.jpg
I'm not the exception to the rule...most success stories are exceptions because they are of people with non-aggressive hair loss and used finasteride or dutasteride. I have extremely aggressive hair loss so if my regime works for me it will work for everyone.
You have every right to have an opinion, but know that shaving or cutting hair short has no effect on male pattern baldness. In fact having short hair makes it easier to regrow hair because you can apply minoxidil more evenly and in smaller amounts. That decreases the inflammation caused by the propylene glycol.
by the way, the main difference between men and women is not the length they usually wear their hair...It's the fact that men have high levels of testosterone (plus the male pattern baldness gene) and women have low levels. It has nothing to do with the length of hair.
I'm not the exception to the rule...most success stories are exceptions because they are of people with non-aggressive hair loss and used finasteride or dutasteride. I have extremely aggressive hair loss so if my regime works for me it will work for everyone.
You have every right to have an opinion, but know that shaving or cutting hair short has no effect on male pattern baldness. In fact having short hair makes it easier to regrow hair because you can apply minoxidil more evenly and in smaller amounts. That decreases the inflammation caused by the propylene glycol.
by the way, the main difference between men and women is not the length they usually wear their hair...It's the fact that men have high levels of testosterone (plus the male pattern baldness gene) and women have low levels. It has nothing to do with the length of hair.
2.3. Inflammation triggers resolution
An intriguing dimension to the physiology of inflammation is the identification of specialised pro-resolving mediators (SPM) encompassing lipoxins such as lipoxin A4 (LXA4) (Serhan et al., 1984) acting upon the resolving receptor FPR2/ALX (Ye et al., 2009) and more recently, the resolvins and maresins (Serhan et al., 2002, 2009). FPR2/ALX is expressed by monocytes and macrophages (Yang et al., 2001) and is central in controlling the duration and magnitude of the inflammatory response, providing endogenous stop signals for inflammation (Serhan et al., 2000b). Resolution pathways are programmed responses activated during inflammation, resulting in a switch in lipid mediators from the dominance of prostaglandins to the lipoxins to promote resolution of inflammation and the return of tissues to their normal homeostatic state (Levy et al., 2001; Serhan et al., 2008, 1984, 2000b). Importantly, resolution has been shown to be an active and highly regulated physiological process (Serhan et al., 2007; Serhan and Chiang, 2008) rather than simple passive cessation of inflammation as previously thought. Key events in resolution of inflammation include phagocytosis of apoptotic cells, modification of inflammatory cell infiltration to the inflamed site and modulation of vascular permeability (Serhan et al., 2007). However, whilst resolution is well studied in experimental murine models of inflammation, there is limited information documenting this process in naturally diseased connective tissues and resolution has only recently been identified in injured equine tendons (Dakin et al., 2012a,b).
Whilst the inflammatory component of tendinopathy has received much attention, the processes concerned with resolution of tendon inflammation have been neglected from a therapeutic perspective. Improved understanding of inflammation is crucial to the development of novel anti-inflammatory agents that preserve the beneficial, yet remove the detrimental components of the cascade. Although the field of resolving inflammation is relatively new, understanding of pro-resolution processes is rapidly evolving using murine models of experimentally induced inflammation (Navarro-Xavier et al., 2010; Rajakariar et al., 2008). Inhibiting inflammation has been shown to ‘switch off’ the activation of key inflammation-resolving mechanisms (Gilroy et al., 1999). Harnessing the potential of pro-resolving mediators represents a new approach to managing inflammatory diseases in the future. Pro-resolving pathways have not been widely studied in injured tendons, although we have demonstrated increased expression of the pro-resolving receptor FPR2/ALX (Dakin et al., 2012b) and the switch from pro-inflammatory prostaglandins to the production of pro-resolving lipids such as LXA4 during the early stage of tendon injury (Dakin et al., 2012a). However, it is hypothesised that this resolving response is somehow dysregulated or of insufficient duration or magnitude, as tendon inflammation is not adequately ‘switched off’ (Dakin et al., 2012b). This favours the development of chronic inflammation and the formation of a fibrogenic repair scar (Fig. 1). In support of this concept, expression of the pro-resolving receptor FPR2/ALX (a critical component in mediating pro-resolving mechanisms) has been shown to reduce with time after tendon injury and with ageing (Dakin et al., 2012a). This is likely to have implications for sustaining chronic tendon injury if acute inflammation is insufficiently resolved, and in the development of re-injury with age because the ability to resolve tendon inflammation diminishes with ageing.
You realize that it's incredibly lame just to post abstracts, right? An abstract study should be followed by an opinion and maybe a summery.
Background: Accurate and selective assessment of testosterone requires use of a sensitive LC-MS/MS method, especially at low levels as those seen in young children. Methods: The present longitudinal study of 20 healthy children from the Copenhagen Puberty Study followed every 6 months for 5 years evaluates the longitudinal increase in serum testosterone before, during and after pubertal onset quantified by a newly developed LC-MS/MS method in comparison with immunoassay. Testosterone concentrations in serum samples (n = 177) were determined by LC-MS/MS (detection limit 0.1 nmol/l) and by immunoassay (detection limit 0.23 nmol/l). Results: Serum concentrations of testosterone increased gradually with age by both methods. However, serum testosterone was quantifiable in 9/10 girls prior to pubic hair development measured with LC-MS/MS, and in 2/10 girls measured with immunoassay. In boys, testosterone was quantifiable in 10/10 boys 1 year prior to pubic hair development measured with LC-MS/MS, and only in 1/10 boys measured with immunoassay. Serum testosterone levels were quantifiable 1.5 years (range 0.5-2.5) earlier using LC-MS/MS. Conclusion: Assessment of longitudinal circulating levels of serum testosterone using a selective LC-MS/MS method proved to be more sensitive in predicting early peripubertal changes in healthy children compared to levels determined by immunoassay. © 2014 S. Karger AG, Basel.
Sexual Dimorphisms in the Associations of BMI and Body Fat with Indices of Pubertal Development in Girls and Boys.
Crocker MK1, Stern EA, Sedaka NM, Shomaker LB, Brady SM, Ali AH, Shawker TH, Hubbard VS, Yanovski JA.
Author information
Abstract
CONTEXT:
The effect of obesity and concomitant insulin resistance on pubertal development is incompletely elucidated.
OBJECTIVE:
To determine how measures of adiposity and insulin resistance are associated with pubertal maturation in boys and girls.
SETTING AND DESIGN:
Breast and pubic hair Tanner stage and testicular volume by orchidometry were determined by physical examination in 1066 children. Ovarian volume was estimated by trans-abdominal ultrasound. Fat mass, skeletal age, and fasting serum for insulin and glucose, total T, estradiol, estrone, dehydroepiandrosterone-sulfate, and androstenedione were measured at the National Institutes of Health Clinical Research Center. Convenience sample; 52% obese, 59% female.
RESULTS:
Logistic regression identified a significant interaction between sex and obesity for prediction of pubertal development (P ≤ .01). There was a negative association between boys' testicular volume and body mass index (BMI)/fat mass but a positive association between girls' breast stage and BMI/fat mass. Ovarian volume in girls was positively associated with insulin resistance but not with BMI/fat mass. There was a positive association between obesity and measures of estrogen exposure (breast development and skeletal age) in both sexes. Positive correlations were seen for girls between BMI and pubic hair development and between insulin resistance and T production, whereas adiposity was negatively associated with pubic hair in boys.
CONCLUSIONS:
Significant sexual dimorphisms in the manifestations of pubertal development are seen in obese girls and boys. Two known effects of obesity, increased peripheral conversion of low-potency androgens to estrogens by adipose tissue-aromatase and increased insulin resistance, may be in large part responsible for these differences.
Only under the assumption that there is any "flip the switch condition" to begin with. I assume that there is no flip switched at all in the scalp, i.e. the follicles are prone to androgens for miniaturization right from the start. However, androgen levels only become sufficiently high for that effect once puberty starts (cf. Wikipedia on androgen levels).
If that assumption is correct, then there is likely no difference between the onset of Androgenetic Alopecia where the very first hair follicles (right at the lowest point of "healthy" temples) are hit as compared to follicles of a NW3 being initially hit and miniaturizing once the Androgenetic Alopecia/male pattern baldness has progressed this far.