Posting for my ‘off-the-grid’ boyfriend. He took fin in his mid twenties. It worked great, and he had no sexual sides. He stopped cause he was afraid of cancer. Now that the 2018 follow up study came out, he’s thinking about going back on. Do you think he has less risk of developing sexual sides cause he didn’t before? If he goes on it and has sides, will they disappear when he goes off? Should he go on it?
I’m a junior in College and my roommates are telling me that I am losing my hair. I never noticed it before but I now realize that I can see through my entire scalp. It looks like my hair is thinning everywhere. I am thinking seriously about getting a hair transplant.
You need to be evaluated by an expert who specializes in hair transplantation, and is honest and doesn’t do it just for the money he gets from you. A good opinion is critical. I met with a man from Reddit last week who thought he was balding and had seen another doctor who offered him a hair transplant. When I examined him with the HAIR CHECK instrument and a trichoscope, it was clear he was not balding (and he did not have DUPA), so what he was seeing was very fine hair with very poor density (which I measured as very low). He was probably born that way and just noticed it recently from comments by friends. If he got a hair transplant with his poor hair and poor density, he would end up deformed for life because he had terrible hair and just would never make a good hair transplant candidate. If he felt strongly about his appearance, a wig might work for him or he should just accept what he has. We could offer him Scalp Micropigmentation which would make his hair appear much thicker. It would make his white scalp less prominent which is a much better option than a wig because it is full freedom to be himself.
First, it’s not a study directly correlating creatine and hair loss. You’re assuming that the findings of the difference in DHT: T ratio and the increased DHT value from creatine consumption means it will lead to hair loss. Also, there’s been several other studies (listed below) showing that creatine doesn’t affect testosterone levels, and with DHT being a metabolite of testosterone, it’s doubtful it would cause an increase in DHT. Another factor to consider is that strength training has been correlated with increasing testosterone
Steroids in creatine? Why? What benefit does a supplement company gain from mislabeling? They have more to lose by incorrectly labeling a product. Oral steroids have been shown to be dangerous on the liver. Also, creatine would be more costly if steroids were placed into the product.
Here are the others studies showing that testosterone does not get affected with creatine consumption:
https://www.ncbi.nlm.nih.gov/pubmed/24633488
https://www.ncbi.nlm.nih.gov/pubmed/21324203
https://www.ncbi.nlm.nih.gov/pubmed/12945829
https://www.ncbi.nlm.nih.gov/pubmed/19741313
https://www.ncbi.nlm.nih.gov/pubmed/17136944
Recently, I got a prescription for oral finasteride from my dermatologist. I’m a bit nervous to take the oral route due to the side effects that appear to be somewhat common and the possibility of the post-finasteride syndrome. I have learned that my pharmacy is able to compound 5% minoxidil with 1mg Finasteride into a topical solution. I was wondering if you had an opinion on this?
Keep in mind that topical only works where you put it. So, if you have hair loss where you don’t see it (like many people do when I perform a HAIR CHECK test), then these areas will still lose hair. Also, Post finasteride syndrome, I believe, doesn’t happen if you stop taking it after you find that even staying on it a month or so does not solve the ED problems.
FUT is cheaper and has better yield. Why does everyone care about the scar when you have hair? If you want the option to shave your head why get a transplant? Ok surgery recovery time is a small factor…
Yes, you have clear hairline corner recession and this is the signature of male pattern balding. If you are over 25 and have tried finasteride without success, then a hair transplant is the way to go
My comments and opinions are really just meant to stand on their own merits or lack thereof. But I can share that I have had close visibility into what research the PFS Foundation has been doing over the past several years. Even once there is an important finding, it can take years before it makes it into the public eye. I wish things moved more quickly, but this is just the reality of research and the media. Just as an example, the legal documents that served as the basis for the Reuters story were (accidentally) filed publicly on the court docket in mid-2016, but it took over 3 years to make it into the mainstream media. The FDA has known about these issues since 2017 from the PFS Foundation’s Citizen Petition, but the FDA has done nothing yet. I hope the media will pick up on this but we will have to see.
The PFS Foundation has accomplished a few things so far:
Their research has established biomarkers in PFS patients. This shows that PFS is a physical condition rather than psychosomatic, as many people have argued for years. The studies looked at small groups of PFS patients and found two very important things. Compared to controls, PFS patients had undetectable (depleted) levels of neurosteroids in their CSF. Additonally, about 50% of PFS patients appear to have their 5AR2 gene silence. It would be great to have these studies done in much larger populations, but it is very hard to recruit PFS patients due to financial and logistical constraints when it is a rare disease. That doesn’t invalidate the findings of these studies of the existence of the disease itself.
Another Northwestern based study was a very high powered epidemiological study that showed about 1% of patients who took 5-AR inhibitors (finasteride and dutasteride) developed persistent erectile dysfunction. This was controlled in many ways using very sophisticated statistical techniques. Even at 1%, this is a low frequency risk but terribly significant if it occurs.
Lastly, a few years ago there was an article published in JAMA Dermatology that critiqued every one of the clinical trials to date that were published on finasteride. The main critique was that they were simply not effectively designed to sensitize for low frequency, persistent side effects. This article seems prescient now because Merck didn’t report the patients who dropped out of their study and there were apparently PFS patients within this group. This does not seem to have been an accident in retrospect in light of the documents that are now available.
Merck has acted unethically throughout this whole controversy. I can share with you a couple anecdotes with you.
Although I can’t specifically provide names, Merck has interfered with the research publishing process. Somebody from company reached out to at least one journal editor who published an unfavorable study on finasteride. Merck pressured them to withhold support to the journal if the editor did it again.
Personally, I had a physician reach out to Merck about a decade ago to figure out what was going on with my health. The physician spoke with a pharmacovigilance contact, but I don’t remember the name it was so long again. The person said Merck had never received any reports of sexual dysfunction. This was clearly false because of the data that was hidden from the clinical trials. Additionally, at that time Merck had already been forced to warn of such side effects in European countries. And this was shortly before the FDA forced a label change in 2012 to include post-marketing reports, all of which happened before my outreach to Merck.
These are all things I know factually to be true but I can’t provide “proof” until it gets into the public domain. I hope it gets there, but it may never be the case. But if you look at Merck’s response to Vioxx, they did many of the same things I just described for their response to the Propecia scandal.
Be careful about jumping the gun and rushing into a hair transplant until your balding pattern is evident as shown here: https://baldingblog.com/need-master-plan-think-hair-transplants-photos/. This man, had he done hair transplants, would have been very surprised as he got older. Maybe the doctor would have pushed his donor density to make him thick at 22 and use up half of his donor supply. IF that were to happen, sometime between 22 and 35, he would see more balding and possibly chase the balding pattern. His surgeon, wanting to make the most money from him might recommend another larger sized procedure and he might run out of donor hair by the time he got to 35. Sometime between 35 and 62, he might see a freaky looking man in the mirror as a result of a hair transplant that was done with no <aster Plan..
Clearly, I am inferring what I call a Master Plan, critical for all men (young or old) who are going to do a hair transplant. The young are more vulnerable because they want results NOW. So many young men tell me that hair is important for men in their 20s, and that men in their thirties really don’t care, but most of my patients are over 30 because I often put the brakes on the hair transplant process until I can (sometimes with the help of the HAIRCHECK test) predict the balding pattern of my patient and advise accordingly.
I’m 22, Male, and have had a ton of stress over the past four or so years. I’ve been slowly losing hair (noticed a bit of loss about two or three years ago I think) on the right side and now a small bit is gone on the left side. Is it possible that this is stress related but NOT indicative of MPB? I mean is is possible that this isn’t just speeding up MPB that I’d get later on regardless? And if it grows back a bit or stops falling, do I need to worry that it is MPB which will continue? Or can I move on and assume whatever was lost, whether it regrows or not, was just due to stress and that there won’t be any more loss? I really need help please. Thanks so much!
As this is very important to you, you should see a doctor like me who can make the diagnosis and using tools such as the HAIRCHECK test (https://baldingblog.com/haircheck-test-how-it-is-done-video/) and try to predict what your future might look like. Then based upon that assessment, a good doctor will build a Master Plan for you to follow. The key is to keep your hair and with today’s medications and hair transplant technology, it is something that you should want for yourself.
No, the number of harvestable grafts are fixed for your lifetime and depend upon your original donor density which the doctor can measure. That is why we are careful about what we take from the donor area when we do a hair transplant. As the limit for a typical Caucasian is about 7,500 grafts, then as this number is drawn down, it can’t be replaced and eventually there is no donor hair left. This is my concern in Turkey where they will take out 6000 grafts in a single session, leaving almost nothing left for future balding (which is almost a certainty) and they do it all with FUE, but most people can’t handle more than 3,750 FUE grafts before they start looking bald in the back of their head (see: https://baldingblog.com/collection-victim-photos-internet-harvested-depleted-donor-areas/.
Interesting article. I don’t understand the metabolic pathway suggested in the article. I will research this.
2 months ago, I tested my DHT levels and got this value: 747.67 pg/ml.
I have been taking Dutasteride for a month now, but saw no improvement in my hair: the bald spot on my crown continued to grow. I tested my DHT again 2 days ago: 1110.8 pg/ml.
Of course. Increasing the DHT levels has nothing to do with the effectiveness of either finasteride or dutasteride and that is why I never get DHT levels when I prescribe finasteride.
because i always see posts on hear of people saying they loss density on fin cuz of the shed and it didnt get better is this possible because im worried that may happen, Ive seen other ppl say its impossible to lose hair on it.
In my practice, I have never seen finasteride cause hair loss but I have seen genetic hair loss move rapidly evolve while a person is on finasteride.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691938/
Conclusions of article: Minoxidil is a common medication prescribed for treating hair loss-related problems. It provides remarkable benefits to patients with hair disorders. To date, the FDA has approved minoxidil only for AGA. However, minoxidil is used off-label for treating several hair disorders as well as increasing body hair growth. Although topical minoxidil is considered an effective and safe treatment option for various hair disorders, additional evidence-based data are needed for some applications.
Other mention: Salicylate and aspirin can inhibit sulfotransferase. A recent study showed that the follicular enzymatic activity decreased following 14 days of low-dose aspirin use. Thus, prior or concomitant use of aspirin decreases the clinical response to topical minoxidil.
If finasteride doesn’t reverse frontal hair loss, will is slow it down or stop it?
I have seen some patients get good results in the frontal area (not common), more are younger (closer to 20 rather than 30 y/o). Yes it often slows or stops the recession.