optimystic
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Sorry this turned out to be quite a long post, for that reason I have divided it into 3 sections. Read what you may.
1. Background info\My story
Well it's been a year and the half since I last posted on the forum
Last thing I had posted was the infamous thread here: http://www.hairlosstalk.com/interac...le pattern baldness-and-ejaculation-frequency
Probably those that stuck around long enough to recall it are the same people who bad repped me on that thread, even though I wasn't making any definitive statements on that thread (only speculation)
And what on earth is the bad rep all about anyway lol? Who would care about rep on a forum where most of us want to remain completely anonymous, and all of us hope to never have to visit again...
[That said, I've been visiting the forums still because the news and research updates interest me. And sift through enough stuff, you can learn a few things from decent advice given every now and then.]
Now the purpose of this thread: I'm 25 yo now, 1 year graduated from medical school, and I do have an answer for my hair loss at least.
I joined this forum back when I was almost 21, that's in 2009 (You can find my first post about my story somewhere). When I was in my teens, I used to have very rough hair that grows into an afro\rat's nest and is hard to style because it would always assume it's rough dry texture no matter what I put on it. At the age of 19\20\21, my hair started changing. It felt softer, and less bulky. I had a twilight zone where it looked better than it ever did, till I noticed things were going down hill. My hair line was very slightly receding, but the hair on the top of my head was diffusely thinning. Hair on my vertex was declining the fastest, and taller friends could also see my scalp through it. I would have trouble with styling my hair because it's usually puffy all over, but then it started becoming puffy only on the sides whereas the hair on top of my head would collapse. I went to my aunt (a dermatologist) who stroked her hand through my hair a couple of times and compared the top to the sides etc... and she quickly said "you're just like your uncle". She confirmed I was starting male pattern baldness and she started me on minoxidil 2%.
I used minoxidil for almost 2 years (more like a year and the half) without noticing any change, then I stopped it for several months because I felt like it wasn't doing anything (I wasn't getting any worse, but I wasn't getting any better) and a couple of months later I noticed what a ****ty decision that was. My hairline had started receding, and my hair was significantly thinner to the degree that if I'm in a well lit room or if you take a picture at a selfie distance (1-2 arm lengths) or a regular pic with flash on from any angle, you can see my scalp through the hair. At the vertex, there was already an area where I could touch my scalp and feel little to no hair on it.
I started minoxidil again, this time 5%, and saw steady recovery with my hair getting thicker. I also made a decision around then to cut back on p**rn and masturbation. It was a few months later that I made that ambitious and infamous post in 2013.
I tried nofap (abstinence from masturbation) for a while but only made it 2 weeks before caving. I tried again since then maybe 2-3 times and would never make it more than 9 days again. Every time I would relapse so hard the next few days (atleast 3x a day, up to 6-7). I noticed when I relapse I get so driven into compulsion. When I relapse, I feel super happy and relaxed (almost like a high) the first time I do it, but then I want to go again and I feel more and more guilty and get less of a high every subsequent time, until the guilt finally surpasses the high I get and I stop. And then I try again. This went on for months. (I was able to quit the p**rn though)
Now while all this was going on, I was also working out at the gym and trying to lose weight to get my six pack to show. I was never overweight, but I used to be thin as a teenager and had gained weight since college, and I wanted to lose it again (especially the belly fat). If any of you have a six pack or tried to get a six pack, you know how much discipline it takes. It's not enough to just work your abs at the gym, you MUST shed those last few pounds. And shedding those last few pounds takes A LOT of discipline in regulating your eating habits. I got thin again but still had some belly fat preventing my abs from showing, and every time I would try to lose it by practically starving myself for a few days (eating nothing but a salad or two per day and drinking lots of water), I would always relapse and pig out before a week is over. Till I finally listened to my trainer at the gym, and he explained to me I'll never lose the weight if that's how I try to cut down my food. He explained to me the best way to cut back on calories and get used to eating only what I need and nothing more, is to eat more frequent meals that I enjoy that are healthy in moderate portions. So I went online and got familiar with what healthy well rounded meals and snack foods are and I started learning how to stockpile these meals\snacks such that I always have them available at home or at work. Eating those light portions in the morning (very important), then around noon, then around 3pm, then either a dinner (500 calories) or 2 more light meals depending on how long I stayed up or intended to stay up. As a consequence of changing my eating habits, my sleep also improved (I used to be prone to oversleeping, but now 7-8 hours and I will wake up before the alarm). Following that regimen, within 2 months I lost 6 pounds and my 6-pack would finally show.
I was still struggling to figure out how to be in control of my masturbation habits. I realized how similar the relapse masturbation problem was to the relapse eating problem I had when I was aggressively trying to lose weight. Only difference was the masturbation relapse gives much more of a high than food relapse (i.e. eating a whole pizza after 4 days of eating just salads). But it was the same thing. Aiming too high, going aggressively and failing to reach the goal, and then reaching a low that would negate anything I would have gained in my brief period of being aggressive. Same motivation. Same relapse. Same guilt.
I realized what I needed to do was somewhat ration. I tried to make it such that I masturbate once every 2 days, but that failed too because it just made me want to do it more frequently every time I told myself "hey, you are allowed to do it today". I wanted to "allow" myself more. Until I decided I'm not going to try to enforce a limit anymore. I'm going to go by cue. Whenever I get a boner that did not require me to stroke it down there, I will masturbate. This would include morning erections, spontaneous erections, and sex. With that, I have been able to reduce masturbation to an average frequency of 3 times per week. Of course for public boners, I would have to let those go. I would not make up for those until my next boner (which would not always be within the next 2 days, but I wouldn't struggle with it or feel the urge to do it in that time. My point is I wouldn't allow a missed boner as an excuse to initiate one with my thoughts and hands). This was around a year ago, so i've been stable for 1 year.
Since then I'm still on minoxidil 5% (been on it for more than 2 years consecutively now).
The result (the relevant one of course): my hair is as thick as it was when i was a teenager. Density is better than it was when I was 21 and first noticed the problem. My hair is rough again, and the afro grows equally (and quickly) on the top as it does on the sides. The vertex of my head can grow long hear that also stand and complete the afro (so that there isn't a depression in the afro), but if you look through the long hair you will see my scalp at the vertex still.
My hairline is still receded from the sides, but is noticeably getting better. But at the top of my head, the frontal part the middle part and the vertex of my scalp do not look or feel like they are balding. You can stroke my hair several times before you get one or two hairs on your hand. And you will notice those hairs are not a bunch of thin hairs stuck to each other unlike what I would find in the past.
To sum up my lengthy story, basically I am a minoxidil responder. Even though I was on minoxidil for around a year and the half, then got off it, and restarted it for 2 years again (and I always got good results when I was on it again), I didn't get my best results from it until I made the lifestyle changes I mentioned above.
2. Addressing False Logic
In medicine, the first line of prevention and even treatment of many disorders is lifestyle changes. If you have someone who is prediabetic, or someone who is newly diagnosed with grade I hypertension, you don't start them on drugs until they have failed lifestyle changes. And even when you start the patient on drugs, you EMPHASIZE not only the importance of drug compliance but also compliance with lifestyle modifications.
Like male pattern baldness, both diabetes and hypertension are heritable conditions that run in families. We know the pathogenesis of the sequelae, even though the mechanism for having the disease is unknown (i.e. essential hypertension is most often idiopathic, diabetes is due to inherited insulin resistance, neither of these diseases are due to controllable factors. They are only worsened by controllable factors like being overweight etc..). Similarly, you can never be cured of hypertension or diabetes. They are lifetime diagnoses. You can treat and control them (with lifestyle modifications, or drugs, or both) and prevent their complications though (the major one being coronary artery disease).
Similarly, we know in male pattern baldness you inherent a gene that makes hair follicles in your scalp susceptible to inflammation, with most of that inflammation being caused by DHT. After the introduction of finasteride, and it's success with only 4% rate of side effects, you can also say that hormonal dysregulation is part of the pathogenesis of male pattern baldness (because finasteride works by lowering your DHT levels, not by changing the sensitivity of your scalp to inflammation caused by DHT, therefore that's how we know reducing level of DHT would slow down your hair loss). Finasteride therefore proves that male pattern baldness, like HTN and Diabetes, is CONTROLLABLE.
But the fact remains, like HTN and Diabetes, male pattern baldness is a diagnosis for life. You can prevent or slow down or even reverse the balding, but you will still have a diagnosis of male pattern baldness.
In this day and age, with all that is known about HTN and Diabetes, in first world countries with proper healthcare systems which follow annual guidelines and recommendations, Diabetic and HTN patients can control their own fate to a large extent. Comply with lifestyle changes, comply with meds, and you will not suffer the dreaded complications of those diseases.
It's the same thing with hair loss, except for some reason the lifestyle modifications were deemed obsolete, based on false logic that was never contested enough.
"If masturbation caused hair loss, everybody in the world would be bald by 20." FALSE!
Most 50 year old people can consume as much salt and sugar as they want, and will NOT develop coronary artery disease.
But a 50 year old hypertensive patient, or a 50 year old diabetic patient, will develop coronary artery disease if their BP remains elevated or their glucose remains high.
Another similarity between male pattern baldness, HTN, and Diabetes is that incidence increases with age. You are more likely to develop the disease as you grow older.
Does this mean you won't find an 80 year old with a full head of hair? NO. You can find 80 year olds who are not hypertensive or diabetic as well.
But you can find a 60 year old who had great hair until the age of 55 (NW1) and then male pattern baldness got worse and he became an NW2 or more.
I don't know why this is often overlooked, but the fact that all of us here have different ages and different experiences with different rates of hair loss SHOULD light up a bulb that makes us say "hey, male pattern baldness isn't a 2 faced disease with only 2 outcomes (affected vs. unaffected)". When you see this much variation among those affected, this increases the likelihood of having a role for environmental factors.
Is this post meant to encourage readers and those affected by male pattern baldness to not seek hair loss treatment? NO, NO, AND NO!
If your hairloss has progressed enough for you to notice it, then you ALREADY NEED medical intervention.
Short explanation: If a 60 year old man had undiagnosed hypertension for 10 years, comes to the doctor for the first time and the nurse records an elevated blood pressure discovered on first visit. During medical history, the doctor finds learns the patient sometimes experiences dyspnea (shortness of breath) on exertion. The doctor does a stress test and finds out this patient has already developed Coronary Artery Disease. Does the doctor recommend only lifestyle modifications for newly diagnosed hypertension? NO! The disease has already been going on for a while and the patient now needs to be started on an anti hypertensive. Does the doctor prescribe anti-hypertensive without recommending lifestyle medications? ALSO NO! At this stage medication compliance IS more important than lifestyle modifications in preventing disease progression, but lifestyle modifications DO still play a SIGNIFICANT role. Even though the patient is on a medication to lower his Blood Pressure, the patient can still make things a little better for himself by exercising and restricting salt intake (though restricting salt intake will not lower blood pressure significantly after the patient is already on an anti-hypertensive). More importantly, a completely sedentary lifestyle combined with unchecked\unrestricted salt intake WILL make things significantly worse, DESPITE the anti-hypertensive.
Another false logic when it comes to male pattern baldness and other things in general: "Masturbation is completely normal and has no negative effect on health."
This will be the easiest one for me to demolish. "Birthday cake is completely normal and has no negative effect on health". Also true. Hell, if your blood sugar is low (i.e. you just took insulin, or you are starving) or if you are in a bad mood, birthday cake may be just what you need. But if you are overweight, diabetic, lactose intolerant, eat too much of it in one sitting, or eat it regularly instead of other nutrients, then birthday cake can have several negative effects on your health.
The idea that a process such as masturbation, which is a consciously controlled process that can predispose to addictive behavior because of the large reward it's associated with as well as the minimal effort it requires, can be performed without consequences to your health and does not require moderation, is one of the worst misguidance and falsely reassuring statements in medicine.
Think realistically. Is life THAT awesome? It's like a drug you can give yourself WHENEVER YOU WANT. Like owning a bakery, you can have all the birthday cake you want right? WRONG!
There are consequences, mediated through hormonal changes and feedback mechanisms.
Many people also claim that you masturbate BECAUSE of your hormones, but your hormones ARE NOT AFFECTED by masturbation.
But that's like saying to obese people "they are fat because they have a big appetite, they don't have a big appetite because they are fat". Truth is it's both. Your body has several regulatory feedback mechanisms. When you get used to eating a lot of food in one sitting your stomach will get distended every time and eventually tolerate more food, predisposing you to get obese because you develop a bigger appetite. And conversely, when you lose weight your peritoneal cavity decreases in size (and so does your upper waist size from loss of fat from subcutaneous tissue), and your appetite becomes smaller.
Don't try to convince yourself masturbation and hormones are not subject to feedback control. I grew up in the era of modems and dial up connections. Before faster internet, when all we could do is download a few p**rn pictures, I would masturbate once or twice a week. When faster internet became available and I started watching p**rn videos which were much more stimulating, my habits started increasing and I could do it once or twice a day, but I couldn't do it more than twice a day with the initial transition. With time, as I got more and more used to watching p**rn videos, I could work it up to 4, 5, 6 times a day. This wasn't a preset disposition of mine due to my hormones. My hormones were conditioned through feedback. Therefore there IS regulation.
It is so self-evident that masturbation DOES have an influence on your hormone levels. Are you kidding me? Anyone who tries to abstain for a long enough period of time will notice mood changes, irritability, personality changes, anxiety, altered levels of arousal, etc... This is all due to hormonal influences. Many people who've accomplished the feat of abstaining for a very long period of time claim altered levels of confidence, voice deepening, increased muscle strength, better posture and resting muscle tone, better concentration. Those are also all due to hormonal influences.
3. Debunking the study that debunked "the myth"
And last but not least this study: http://www.ncbi.nlm.nih.gov/pubmed/14674898
The one study that came to the conclusion that the relationship between male pattern baldness and masturbation is a myth, a conclusion that has been echoed by physicians and hair loss sufferers for more than a decade.
Straight from wikipedia: "The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1390 subjects) and found no correlation...."
Firstly here I would like to invoke status on my criticism of this paper, in that I am actually qualified to evaluate such research. I graduated med school nearly a year ago, and since then I have been doing clinical research (not in the field of dermatology). I've been involved in all aspects of clinical research, from proposal and designing the study, to data collection and analysis, to reporting and writing the paper, and finally to the process of getting the paper published. I am familiar with the different study designs and have read, presented, discussed, criticized and appraised many papers in journal clubs (three times per week).
I have accessed the full text of this study, and read it twice. The study above is far from being a complicated study for me to read and understand, in fact it's quite easy to read and understand what has been done even with just rudimentary understanding of statistics and epidemiology.
Some of the criticism I make you guys can follow based on the abstract alone. Some other things you need to see the paper for yourself to verify what I am saying (you wouldn't be able to tell from the abstract alone).
First of all this is a retrospective study, which means it's a study where the outcome has already occurred, which gives it a much weaker level of evidence than a prospective study (prospective cohort or clinical trial), where ideally you would follow up a group of young men with different ejaculatory frequencies for a set amount of time, and then evaluate the severity of their hair loss, and then you could draw some conclusions as to whether or not ejaculatory frequency was a risk factor for the development of male pattern baldness. (side note: I will use the term Androgenetic Alopecia as used by the paper. As I'm sure most of you know, Androgenetic Alopecia stands for Androgenetic Alopecia, and is synonymous with male pattern baldness)
As mentioned in the abstract, subjects included were men aged 40-69. They were divided into groups based on where they had hair loss (no Androgenetic Alopecia, frontal Androgenetic Alopecia, vertex Androgenetic Alopecia, full Androgenetic Alopecia = vertex + frontal).
Pro: an unbias observer (and not the participating individual) made this assessment, and probably (although it's not mentioned, and one should mention this in the paper) was blinded or not informed of his category prior to interviewing him (otherwise there could have been increased bias).
Con: They did not divide the groups into more levels of severity of Androgenetic Alopecia. The Norwood scale was created for a reason, and NW1 frontal Androgenetic Alopecia is not the same as NW2A frontal Androgenetic Alopecia.
Major Con: They did not look into the history of Androgenetic Alopecia in those affected. Individuals could have developed their Androgenetic Alopecia at any age. Don't you think it's relevant whether an individual starts balding at age 20, 30, 40, 50, or 60? Well based on their demographic, the only thing they could say was that vertex Androgenetic Alopecia and full Androgenetic Alopecia was more common at older ages, proving definitively that there are different degrees of Androgenetic Alopecia (just in case anyone had doubts about that). Interestingly, the incidence of frontal Androgenetic Alopecia was not more common at older ages. Neither of these however look into the age at which an individual started developing Androgenetic Alopecia, nor the severity of Androgenetic Alopecia.
Clarification: The study did use the Norwood scale, however only by adopting only 4 images from it: one corresponding to no Androgenetic Alopecia, one corresponding to frontal Androgenetic Alopecia, one corresponding to vertex Androgenetic Alopecia, and one corresponding to both. Why they would limit themselves like that and eliminate the power of the scale is beyond me.
The norwood scale is incorporated into US Medical License Equivalent exam and required that all physicians be familiar with it, and in USMLE Step 3 physicians should be able to quickly and accurately assess a patient's Norwood status given the scale in front of them as a resource (we are not required to memorize it, just know that it exists and how it's used). It is fairly easy to use (I'll try to explain in another post
).
It is odd that this study decided to condense the Norwood scale instead of utilize it for it's true potential. If you're not going to use it for research, what the hell is the scale developed for? Just to be able to tell the patient exactly how bad his hair looks?
Now for the BIGGEST cons, based on the paper (not the abstract alone).
Firstly, they did not include the interview with the exact questions asked and the exact type of response.
They have in their table examining risk factors, "Ejaculations, average in the most active years age 20–49 years (times per week)", and their response categories include <=2.3 (as reference), 2.4-3.4, 3.4-4.7, 4.8-7.0, >7.0
They did not explain how they got their responses. Did they give the participants options of different values? Did they accept ranges and average them out? Did they ask participants to give them exact numbers to their best estimate?
Did they ask participants to estimate their frequency over different decades of their life, and then average those out? Where did the response numbers come from?
It's already pretty hard to answer how many times on average per week an individual has done it over the past 30 years, subject to a lot of recall bias. It adds even more bias when the answer expected doesn't follow a certain format.
Challenge: You are telling me some participants at the age of 69 (the upper age limit in their study) when asked how many times did you masturbate per year, over a 30 year period that ended 20 years ago (so you are talking about an average where the start date was 50 years ago!), some people answered "hmm, i would say about 4.2"? Cool.
The other thing is, even if those were accurate answers, why did they run their analysis based on those subgroups and cutoffs? Where did those response categories with these ranges come from? Why do they expect to see a difference with the given ranges? Why not bigger ranges to improve power (i.e. 0-3 vs. 3-6 etc...)? Or why didn't they just do a logistic regression taking ejaculatory frequency as a continuous variable to see if any difference exists, and then see if there is a trend?
Why was their reference interval 0 to 2.3, twice as big as most of the other intervals? This is your reference interval and if it overshoots the exposure all the given odds ratios will be incorrect. Many people do in fact ejaculate once a week or less, so maybe they are at decreased risk for hair loss and all other groups are at increased risk compared to <1? And why weren't the other intervals equal anyway? Did they choose the intervals based on percentiles of responses? I.e. the 20% with least frequency ejaculated <2.3 times per week, the next 20% between 2.4-3.4, etc... and finally 20% of participants ejaculated more than 7 times a week? Is that how they decided on the categories? How was the analysis conducted? This makes a difference in interpretation of the results.
They didn't even specify whether ejaculation frequency meant due to masturbation only or masturbation and sexual activity (but who cares...most people think it's the same thing right? because it looks the same, and that's how we get valid conclusions in clinical research, by making assumptions. Let alone assuming the participants weren't wondering what was meant by ejaculation. If some of them answer without counting sex as ejaculation while others don't this could skew EVERYTHING).
Also in the table legend for their analysis of risk factors they have this lovely disclaimer:
Ejaculatory frequency was used only for about two-thirds of the study and was then discontinued because of work overload for both interviewer and interviewee.
Lovely. So that means the result everyone is pointing to and referencing, including wikipedia, is based on 917 individuals, not 1390, for evaluating ejaculation as a risk factor.
MAJOR MISCONCEPTION:
Finally, even if this study was perfect in execution, and all the above mentioned issues were taken care of, their finding STILL would not prove a lack of correlation between ejaculation frequency and male pattern baldness BASED ON THE CURRENT PROPOSED MECHANISM that almost everyone on this forum accepts.
If you scroll back to the beginning of this Rosetta Stone post of mine, as I mentioned, it's currently believed that male pattern baldness is likely due to a process that involves both increased susceptibility of the hair follicle to DHT and increased DHT. If we were to say that some (or most? or all non-bald?) individuals have scalps that are resistant to the damage caused by DHT, than these individuals would not lose hair no matter what their level of DHT is, correct?
Since the baseline disputed hypothesis of whether or not masturbation is related to male pattern baldness largely assumes that masturbation will worsen hair loss by affecting DHT levels NOT by altering the susceptibility of the scalp to DHT, then BY DEFINITION if you are going to compare ejaculation frequency between NO Androgenetic Alopecia and ANY Androgenetic Alopecia (regardless of severity) you SHOULD NOT find a correlation between ejaculation frequency and whether or not you have male pattern baldness. On the other hand, YOU WOULD expect to find a correlation when comparing LESS SEVERE Androgenetic Alopecia vs. MORE SEVERE Androgenetic Alopecia according to ejaculation frequency.
The study I mentioned above ONLY COMPARED FRONTAL Androgenetic Alopecia, VERTEX Androgenetic Alopecia, and FULL Androgenetic Alopecia to NO Androgenetic Alopecia. They did NOT compare different types of Androgenetic Alopecia to each other (i.e. Frontal vs. Vertex vs. Full, which they could have done, assuming these three types of Androgenetic Alopecia represent different degrees of severity which is also unclear in this study.)
Impact of the article:
And somehow, from this retrospective study, which limited itself in patient demographic by focusing only on those aged 40 to 69, and did not take into account the severity of the hairloss, and did not take into account the age of onset of the hairloss, and tried to draw conclusions by asking their patients to recite their average ejaculatory frequency over a 30 year period, and followed that with an incomplete method of statistical analysis comparing subgroups based on unjustified cutoffs (and a very odd cutoff for the reference group, <2.3 times per week, WHY?!?)...
Somehow, this lead physicians and patients with hairloss to say many of the statements mentioned above....
This shameful excuse of clinical research is also the reason many of you will neg rep me. And I'm fine with it. And if you don't want to try lifestyle modifications, I'm fine with it.
And if you want to take everything I said with a grain of salt, I actually recommend that. You should approach everything with an open mind, but also question everything and be very mindful of anything you read.
If you still believe the conclusions of that article are valid, that's also fine with me, just as long as you realize how poor the quality of the evidence used to generate the conclusions is.
CORRECT INTERPRETATION:
You should also understand exactly what the conclusion means and it's correct interpretation. SPECIFICALLY, the conclusion made is that WHEN COMPARING MIDDLE AGED MEN (40-69) AFFECTED BY ANY TYPE OF ANDROGENETIC ALOPECIA, TO THOSE THAT HAVE NOT DEVELOPED ANDROGENIC ALOPECIA AT ALL, NO CORRELATION WAS FOUND BETWEEN FREQUENCY OF EJACULATION AND HAVING Androgenetic Alopecia.
This makes perfect sense. In fact, in 40+ year old individuals who have not yet developed Androgenetic Alopecia (and therefore are unlikely to ever develop it, because if you have a full head of hair by 40 you can almost safely say you are keeping that hair), you would expect that all the risk factors that would normally make Androgenetic Alopecia worse (i.e. things that would exacerbate inflammation) would have no consequence on these individuals because their hair follicles are resistant to any inflammation. (I know I am repeating myself here but this is a very important point to get across).
FINAL REMARK:
Alas, I end my exhaustively long post with a quote that's become one of my favorites:
“Study without thought is vain: thought without study is dangerous.” —Confucius
1. Background info\My story
Well it's been a year and the half since I last posted on the forum
Last thing I had posted was the infamous thread here: http://www.hairlosstalk.com/interac...le pattern baldness-and-ejaculation-frequency
Probably those that stuck around long enough to recall it are the same people who bad repped me on that thread, even though I wasn't making any definitive statements on that thread (only speculation)
And what on earth is the bad rep all about anyway lol? Who would care about rep on a forum where most of us want to remain completely anonymous, and all of us hope to never have to visit again...
[That said, I've been visiting the forums still because the news and research updates interest me. And sift through enough stuff, you can learn a few things from decent advice given every now and then.]
Now the purpose of this thread: I'm 25 yo now, 1 year graduated from medical school, and I do have an answer for my hair loss at least.
I joined this forum back when I was almost 21, that's in 2009 (You can find my first post about my story somewhere). When I was in my teens, I used to have very rough hair that grows into an afro\rat's nest and is hard to style because it would always assume it's rough dry texture no matter what I put on it. At the age of 19\20\21, my hair started changing. It felt softer, and less bulky. I had a twilight zone where it looked better than it ever did, till I noticed things were going down hill. My hair line was very slightly receding, but the hair on the top of my head was diffusely thinning. Hair on my vertex was declining the fastest, and taller friends could also see my scalp through it. I would have trouble with styling my hair because it's usually puffy all over, but then it started becoming puffy only on the sides whereas the hair on top of my head would collapse. I went to my aunt (a dermatologist) who stroked her hand through my hair a couple of times and compared the top to the sides etc... and she quickly said "you're just like your uncle". She confirmed I was starting male pattern baldness and she started me on minoxidil 2%.
I used minoxidil for almost 2 years (more like a year and the half) without noticing any change, then I stopped it for several months because I felt like it wasn't doing anything (I wasn't getting any worse, but I wasn't getting any better) and a couple of months later I noticed what a ****ty decision that was. My hairline had started receding, and my hair was significantly thinner to the degree that if I'm in a well lit room or if you take a picture at a selfie distance (1-2 arm lengths) or a regular pic with flash on from any angle, you can see my scalp through the hair. At the vertex, there was already an area where I could touch my scalp and feel little to no hair on it.
I started minoxidil again, this time 5%, and saw steady recovery with my hair getting thicker. I also made a decision around then to cut back on p**rn and masturbation. It was a few months later that I made that ambitious and infamous post in 2013.
I tried nofap (abstinence from masturbation) for a while but only made it 2 weeks before caving. I tried again since then maybe 2-3 times and would never make it more than 9 days again. Every time I would relapse so hard the next few days (atleast 3x a day, up to 6-7). I noticed when I relapse I get so driven into compulsion. When I relapse, I feel super happy and relaxed (almost like a high) the first time I do it, but then I want to go again and I feel more and more guilty and get less of a high every subsequent time, until the guilt finally surpasses the high I get and I stop. And then I try again. This went on for months. (I was able to quit the p**rn though)
Now while all this was going on, I was also working out at the gym and trying to lose weight to get my six pack to show. I was never overweight, but I used to be thin as a teenager and had gained weight since college, and I wanted to lose it again (especially the belly fat). If any of you have a six pack or tried to get a six pack, you know how much discipline it takes. It's not enough to just work your abs at the gym, you MUST shed those last few pounds. And shedding those last few pounds takes A LOT of discipline in regulating your eating habits. I got thin again but still had some belly fat preventing my abs from showing, and every time I would try to lose it by practically starving myself for a few days (eating nothing but a salad or two per day and drinking lots of water), I would always relapse and pig out before a week is over. Till I finally listened to my trainer at the gym, and he explained to me I'll never lose the weight if that's how I try to cut down my food. He explained to me the best way to cut back on calories and get used to eating only what I need and nothing more, is to eat more frequent meals that I enjoy that are healthy in moderate portions. So I went online and got familiar with what healthy well rounded meals and snack foods are and I started learning how to stockpile these meals\snacks such that I always have them available at home or at work. Eating those light portions in the morning (very important), then around noon, then around 3pm, then either a dinner (500 calories) or 2 more light meals depending on how long I stayed up or intended to stay up. As a consequence of changing my eating habits, my sleep also improved (I used to be prone to oversleeping, but now 7-8 hours and I will wake up before the alarm). Following that regimen, within 2 months I lost 6 pounds and my 6-pack would finally show.
I was still struggling to figure out how to be in control of my masturbation habits. I realized how similar the relapse masturbation problem was to the relapse eating problem I had when I was aggressively trying to lose weight. Only difference was the masturbation relapse gives much more of a high than food relapse (i.e. eating a whole pizza after 4 days of eating just salads). But it was the same thing. Aiming too high, going aggressively and failing to reach the goal, and then reaching a low that would negate anything I would have gained in my brief period of being aggressive. Same motivation. Same relapse. Same guilt.
I realized what I needed to do was somewhat ration. I tried to make it such that I masturbate once every 2 days, but that failed too because it just made me want to do it more frequently every time I told myself "hey, you are allowed to do it today". I wanted to "allow" myself more. Until I decided I'm not going to try to enforce a limit anymore. I'm going to go by cue. Whenever I get a boner that did not require me to stroke it down there, I will masturbate. This would include morning erections, spontaneous erections, and sex. With that, I have been able to reduce masturbation to an average frequency of 3 times per week. Of course for public boners, I would have to let those go. I would not make up for those until my next boner (which would not always be within the next 2 days, but I wouldn't struggle with it or feel the urge to do it in that time. My point is I wouldn't allow a missed boner as an excuse to initiate one with my thoughts and hands). This was around a year ago, so i've been stable for 1 year.
Since then I'm still on minoxidil 5% (been on it for more than 2 years consecutively now).
The result (the relevant one of course): my hair is as thick as it was when i was a teenager. Density is better than it was when I was 21 and first noticed the problem. My hair is rough again, and the afro grows equally (and quickly) on the top as it does on the sides. The vertex of my head can grow long hear that also stand and complete the afro (so that there isn't a depression in the afro), but if you look through the long hair you will see my scalp at the vertex still.
My hairline is still receded from the sides, but is noticeably getting better. But at the top of my head, the frontal part the middle part and the vertex of my scalp do not look or feel like they are balding. You can stroke my hair several times before you get one or two hairs on your hand. And you will notice those hairs are not a bunch of thin hairs stuck to each other unlike what I would find in the past.
To sum up my lengthy story, basically I am a minoxidil responder. Even though I was on minoxidil for around a year and the half, then got off it, and restarted it for 2 years again (and I always got good results when I was on it again), I didn't get my best results from it until I made the lifestyle changes I mentioned above.
2. Addressing False Logic
In medicine, the first line of prevention and even treatment of many disorders is lifestyle changes. If you have someone who is prediabetic, or someone who is newly diagnosed with grade I hypertension, you don't start them on drugs until they have failed lifestyle changes. And even when you start the patient on drugs, you EMPHASIZE not only the importance of drug compliance but also compliance with lifestyle modifications.
Like male pattern baldness, both diabetes and hypertension are heritable conditions that run in families. We know the pathogenesis of the sequelae, even though the mechanism for having the disease is unknown (i.e. essential hypertension is most often idiopathic, diabetes is due to inherited insulin resistance, neither of these diseases are due to controllable factors. They are only worsened by controllable factors like being overweight etc..). Similarly, you can never be cured of hypertension or diabetes. They are lifetime diagnoses. You can treat and control them (with lifestyle modifications, or drugs, or both) and prevent their complications though (the major one being coronary artery disease).
Similarly, we know in male pattern baldness you inherent a gene that makes hair follicles in your scalp susceptible to inflammation, with most of that inflammation being caused by DHT. After the introduction of finasteride, and it's success with only 4% rate of side effects, you can also say that hormonal dysregulation is part of the pathogenesis of male pattern baldness (because finasteride works by lowering your DHT levels, not by changing the sensitivity of your scalp to inflammation caused by DHT, therefore that's how we know reducing level of DHT would slow down your hair loss). Finasteride therefore proves that male pattern baldness, like HTN and Diabetes, is CONTROLLABLE.
But the fact remains, like HTN and Diabetes, male pattern baldness is a diagnosis for life. You can prevent or slow down or even reverse the balding, but you will still have a diagnosis of male pattern baldness.
In this day and age, with all that is known about HTN and Diabetes, in first world countries with proper healthcare systems which follow annual guidelines and recommendations, Diabetic and HTN patients can control their own fate to a large extent. Comply with lifestyle changes, comply with meds, and you will not suffer the dreaded complications of those diseases.
It's the same thing with hair loss, except for some reason the lifestyle modifications were deemed obsolete, based on false logic that was never contested enough.
"If masturbation caused hair loss, everybody in the world would be bald by 20." FALSE!
Most 50 year old people can consume as much salt and sugar as they want, and will NOT develop coronary artery disease.
But a 50 year old hypertensive patient, or a 50 year old diabetic patient, will develop coronary artery disease if their BP remains elevated or their glucose remains high.
Another similarity between male pattern baldness, HTN, and Diabetes is that incidence increases with age. You are more likely to develop the disease as you grow older.
Does this mean you won't find an 80 year old with a full head of hair? NO. You can find 80 year olds who are not hypertensive or diabetic as well.
But you can find a 60 year old who had great hair until the age of 55 (NW1) and then male pattern baldness got worse and he became an NW2 or more.
I don't know why this is often overlooked, but the fact that all of us here have different ages and different experiences with different rates of hair loss SHOULD light up a bulb that makes us say "hey, male pattern baldness isn't a 2 faced disease with only 2 outcomes (affected vs. unaffected)". When you see this much variation among those affected, this increases the likelihood of having a role for environmental factors.
Is this post meant to encourage readers and those affected by male pattern baldness to not seek hair loss treatment? NO, NO, AND NO!
If your hairloss has progressed enough for you to notice it, then you ALREADY NEED medical intervention.
Short explanation: If a 60 year old man had undiagnosed hypertension for 10 years, comes to the doctor for the first time and the nurse records an elevated blood pressure discovered on first visit. During medical history, the doctor finds learns the patient sometimes experiences dyspnea (shortness of breath) on exertion. The doctor does a stress test and finds out this patient has already developed Coronary Artery Disease. Does the doctor recommend only lifestyle modifications for newly diagnosed hypertension? NO! The disease has already been going on for a while and the patient now needs to be started on an anti hypertensive. Does the doctor prescribe anti-hypertensive without recommending lifestyle medications? ALSO NO! At this stage medication compliance IS more important than lifestyle modifications in preventing disease progression, but lifestyle modifications DO still play a SIGNIFICANT role. Even though the patient is on a medication to lower his Blood Pressure, the patient can still make things a little better for himself by exercising and restricting salt intake (though restricting salt intake will not lower blood pressure significantly after the patient is already on an anti-hypertensive). More importantly, a completely sedentary lifestyle combined with unchecked\unrestricted salt intake WILL make things significantly worse, DESPITE the anti-hypertensive.
Another false logic when it comes to male pattern baldness and other things in general: "Masturbation is completely normal and has no negative effect on health."
This will be the easiest one for me to demolish. "Birthday cake is completely normal and has no negative effect on health". Also true. Hell, if your blood sugar is low (i.e. you just took insulin, or you are starving) or if you are in a bad mood, birthday cake may be just what you need. But if you are overweight, diabetic, lactose intolerant, eat too much of it in one sitting, or eat it regularly instead of other nutrients, then birthday cake can have several negative effects on your health.
The idea that a process such as masturbation, which is a consciously controlled process that can predispose to addictive behavior because of the large reward it's associated with as well as the minimal effort it requires, can be performed without consequences to your health and does not require moderation, is one of the worst misguidance and falsely reassuring statements in medicine.
Think realistically. Is life THAT awesome? It's like a drug you can give yourself WHENEVER YOU WANT. Like owning a bakery, you can have all the birthday cake you want right? WRONG!
There are consequences, mediated through hormonal changes and feedback mechanisms.
Many people also claim that you masturbate BECAUSE of your hormones, but your hormones ARE NOT AFFECTED by masturbation.
But that's like saying to obese people "they are fat because they have a big appetite, they don't have a big appetite because they are fat". Truth is it's both. Your body has several regulatory feedback mechanisms. When you get used to eating a lot of food in one sitting your stomach will get distended every time and eventually tolerate more food, predisposing you to get obese because you develop a bigger appetite. And conversely, when you lose weight your peritoneal cavity decreases in size (and so does your upper waist size from loss of fat from subcutaneous tissue), and your appetite becomes smaller.
Don't try to convince yourself masturbation and hormones are not subject to feedback control. I grew up in the era of modems and dial up connections. Before faster internet, when all we could do is download a few p**rn pictures, I would masturbate once or twice a week. When faster internet became available and I started watching p**rn videos which were much more stimulating, my habits started increasing and I could do it once or twice a day, but I couldn't do it more than twice a day with the initial transition. With time, as I got more and more used to watching p**rn videos, I could work it up to 4, 5, 6 times a day. This wasn't a preset disposition of mine due to my hormones. My hormones were conditioned through feedback. Therefore there IS regulation.
It is so self-evident that masturbation DOES have an influence on your hormone levels. Are you kidding me? Anyone who tries to abstain for a long enough period of time will notice mood changes, irritability, personality changes, anxiety, altered levels of arousal, etc... This is all due to hormonal influences. Many people who've accomplished the feat of abstaining for a very long period of time claim altered levels of confidence, voice deepening, increased muscle strength, better posture and resting muscle tone, better concentration. Those are also all due to hormonal influences.
3. Debunking the study that debunked "the myth"
And last but not least this study: http://www.ncbi.nlm.nih.gov/pubmed/14674898
The one study that came to the conclusion that the relationship between male pattern baldness and masturbation is a myth, a conclusion that has been echoed by physicians and hair loss sufferers for more than a decade.
Straight from wikipedia: "The only published study to test correlation between ejaculation frequency and baldness was probably large enough to detect an association (1390 subjects) and found no correlation...."
Firstly here I would like to invoke status on my criticism of this paper, in that I am actually qualified to evaluate such research. I graduated med school nearly a year ago, and since then I have been doing clinical research (not in the field of dermatology). I've been involved in all aspects of clinical research, from proposal and designing the study, to data collection and analysis, to reporting and writing the paper, and finally to the process of getting the paper published. I am familiar with the different study designs and have read, presented, discussed, criticized and appraised many papers in journal clubs (three times per week).
I have accessed the full text of this study, and read it twice. The study above is far from being a complicated study for me to read and understand, in fact it's quite easy to read and understand what has been done even with just rudimentary understanding of statistics and epidemiology.
Some of the criticism I make you guys can follow based on the abstract alone. Some other things you need to see the paper for yourself to verify what I am saying (you wouldn't be able to tell from the abstract alone).
First of all this is a retrospective study, which means it's a study where the outcome has already occurred, which gives it a much weaker level of evidence than a prospective study (prospective cohort or clinical trial), where ideally you would follow up a group of young men with different ejaculatory frequencies for a set amount of time, and then evaluate the severity of their hair loss, and then you could draw some conclusions as to whether or not ejaculatory frequency was a risk factor for the development of male pattern baldness. (side note: I will use the term Androgenetic Alopecia as used by the paper. As I'm sure most of you know, Androgenetic Alopecia stands for Androgenetic Alopecia, and is synonymous with male pattern baldness)
As mentioned in the abstract, subjects included were men aged 40-69. They were divided into groups based on where they had hair loss (no Androgenetic Alopecia, frontal Androgenetic Alopecia, vertex Androgenetic Alopecia, full Androgenetic Alopecia = vertex + frontal).
Pro: an unbias observer (and not the participating individual) made this assessment, and probably (although it's not mentioned, and one should mention this in the paper) was blinded or not informed of his category prior to interviewing him (otherwise there could have been increased bias).
Con: They did not divide the groups into more levels of severity of Androgenetic Alopecia. The Norwood scale was created for a reason, and NW1 frontal Androgenetic Alopecia is not the same as NW2A frontal Androgenetic Alopecia.
Major Con: They did not look into the history of Androgenetic Alopecia in those affected. Individuals could have developed their Androgenetic Alopecia at any age. Don't you think it's relevant whether an individual starts balding at age 20, 30, 40, 50, or 60? Well based on their demographic, the only thing they could say was that vertex Androgenetic Alopecia and full Androgenetic Alopecia was more common at older ages, proving definitively that there are different degrees of Androgenetic Alopecia (just in case anyone had doubts about that). Interestingly, the incidence of frontal Androgenetic Alopecia was not more common at older ages. Neither of these however look into the age at which an individual started developing Androgenetic Alopecia, nor the severity of Androgenetic Alopecia.
Clarification: The study did use the Norwood scale, however only by adopting only 4 images from it: one corresponding to no Androgenetic Alopecia, one corresponding to frontal Androgenetic Alopecia, one corresponding to vertex Androgenetic Alopecia, and one corresponding to both. Why they would limit themselves like that and eliminate the power of the scale is beyond me.
The norwood scale is incorporated into US Medical License Equivalent exam and required that all physicians be familiar with it, and in USMLE Step 3 physicians should be able to quickly and accurately assess a patient's Norwood status given the scale in front of them as a resource (we are not required to memorize it, just know that it exists and how it's used). It is fairly easy to use (I'll try to explain in another post
).It is odd that this study decided to condense the Norwood scale instead of utilize it for it's true potential. If you're not going to use it for research, what the hell is the scale developed for? Just to be able to tell the patient exactly how bad his hair looks?
Now for the BIGGEST cons, based on the paper (not the abstract alone).
Firstly, they did not include the interview with the exact questions asked and the exact type of response.
They have in their table examining risk factors, "Ejaculations, average in the most active years age 20–49 years (times per week)", and their response categories include <=2.3 (as reference), 2.4-3.4, 3.4-4.7, 4.8-7.0, >7.0
They did not explain how they got their responses. Did they give the participants options of different values? Did they accept ranges and average them out? Did they ask participants to give them exact numbers to their best estimate?
Did they ask participants to estimate their frequency over different decades of their life, and then average those out? Where did the response numbers come from?
It's already pretty hard to answer how many times on average per week an individual has done it over the past 30 years, subject to a lot of recall bias. It adds even more bias when the answer expected doesn't follow a certain format.
Challenge: You are telling me some participants at the age of 69 (the upper age limit in their study) when asked how many times did you masturbate per year, over a 30 year period that ended 20 years ago (so you are talking about an average where the start date was 50 years ago!), some people answered "hmm, i would say about 4.2"? Cool.
The other thing is, even if those were accurate answers, why did they run their analysis based on those subgroups and cutoffs? Where did those response categories with these ranges come from? Why do they expect to see a difference with the given ranges? Why not bigger ranges to improve power (i.e. 0-3 vs. 3-6 etc...)? Or why didn't they just do a logistic regression taking ejaculatory frequency as a continuous variable to see if any difference exists, and then see if there is a trend?
Why was their reference interval 0 to 2.3, twice as big as most of the other intervals? This is your reference interval and if it overshoots the exposure all the given odds ratios will be incorrect. Many people do in fact ejaculate once a week or less, so maybe they are at decreased risk for hair loss and all other groups are at increased risk compared to <1? And why weren't the other intervals equal anyway? Did they choose the intervals based on percentiles of responses? I.e. the 20% with least frequency ejaculated <2.3 times per week, the next 20% between 2.4-3.4, etc... and finally 20% of participants ejaculated more than 7 times a week? Is that how they decided on the categories? How was the analysis conducted? This makes a difference in interpretation of the results.
They didn't even specify whether ejaculation frequency meant due to masturbation only or masturbation and sexual activity (but who cares...most people think it's the same thing right? because it looks the same, and that's how we get valid conclusions in clinical research, by making assumptions. Let alone assuming the participants weren't wondering what was meant by ejaculation. If some of them answer without counting sex as ejaculation while others don't this could skew EVERYTHING).
Also in the table legend for their analysis of risk factors they have this lovely disclaimer:
Ejaculatory frequency was used only for about two-thirds of the study and was then discontinued because of work overload for both interviewer and interviewee.
Lovely. So that means the result everyone is pointing to and referencing, including wikipedia, is based on 917 individuals, not 1390, for evaluating ejaculation as a risk factor.
MAJOR MISCONCEPTION:
Finally, even if this study was perfect in execution, and all the above mentioned issues were taken care of, their finding STILL would not prove a lack of correlation between ejaculation frequency and male pattern baldness BASED ON THE CURRENT PROPOSED MECHANISM that almost everyone on this forum accepts.
If you scroll back to the beginning of this Rosetta Stone post of mine, as I mentioned, it's currently believed that male pattern baldness is likely due to a process that involves both increased susceptibility of the hair follicle to DHT and increased DHT. If we were to say that some (or most? or all non-bald?) individuals have scalps that are resistant to the damage caused by DHT, than these individuals would not lose hair no matter what their level of DHT is, correct?
Since the baseline disputed hypothesis of whether or not masturbation is related to male pattern baldness largely assumes that masturbation will worsen hair loss by affecting DHT levels NOT by altering the susceptibility of the scalp to DHT, then BY DEFINITION if you are going to compare ejaculation frequency between NO Androgenetic Alopecia and ANY Androgenetic Alopecia (regardless of severity) you SHOULD NOT find a correlation between ejaculation frequency and whether or not you have male pattern baldness. On the other hand, YOU WOULD expect to find a correlation when comparing LESS SEVERE Androgenetic Alopecia vs. MORE SEVERE Androgenetic Alopecia according to ejaculation frequency.
The study I mentioned above ONLY COMPARED FRONTAL Androgenetic Alopecia, VERTEX Androgenetic Alopecia, and FULL Androgenetic Alopecia to NO Androgenetic Alopecia. They did NOT compare different types of Androgenetic Alopecia to each other (i.e. Frontal vs. Vertex vs. Full, which they could have done, assuming these three types of Androgenetic Alopecia represent different degrees of severity which is also unclear in this study.)
Impact of the article:
And somehow, from this retrospective study, which limited itself in patient demographic by focusing only on those aged 40 to 69, and did not take into account the severity of the hairloss, and did not take into account the age of onset of the hairloss, and tried to draw conclusions by asking their patients to recite their average ejaculatory frequency over a 30 year period, and followed that with an incomplete method of statistical analysis comparing subgroups based on unjustified cutoffs (and a very odd cutoff for the reference group, <2.3 times per week, WHY?!?)...
Somehow, this lead physicians and patients with hairloss to say many of the statements mentioned above....
This shameful excuse of clinical research is also the reason many of you will neg rep me. And I'm fine with it. And if you don't want to try lifestyle modifications, I'm fine with it.
And if you want to take everything I said with a grain of salt, I actually recommend that. You should approach everything with an open mind, but also question everything and be very mindful of anything you read.
If you still believe the conclusions of that article are valid, that's also fine with me, just as long as you realize how poor the quality of the evidence used to generate the conclusions is.
CORRECT INTERPRETATION:
You should also understand exactly what the conclusion means and it's correct interpretation. SPECIFICALLY, the conclusion made is that WHEN COMPARING MIDDLE AGED MEN (40-69) AFFECTED BY ANY TYPE OF ANDROGENETIC ALOPECIA, TO THOSE THAT HAVE NOT DEVELOPED ANDROGENIC ALOPECIA AT ALL, NO CORRELATION WAS FOUND BETWEEN FREQUENCY OF EJACULATION AND HAVING Androgenetic Alopecia.
This makes perfect sense. In fact, in 40+ year old individuals who have not yet developed Androgenetic Alopecia (and therefore are unlikely to ever develop it, because if you have a full head of hair by 40 you can almost safely say you are keeping that hair), you would expect that all the risk factors that would normally make Androgenetic Alopecia worse (i.e. things that would exacerbate inflammation) would have no consequence on these individuals because their hair follicles are resistant to any inflammation. (I know I am repeating myself here but this is a very important point to get across).
FINAL REMARK:
Alas, I end my exhaustively long post with a quote that's become one of my favorites:
“Study without thought is vain: thought without study is dangerous.” —Confucius
