Although the literature suggests that there could be a link (as with most medications), a family member of mine uses Propranolol when he goes into meetings, before going into the public or for periods when he gets heavily stressed, and has not experienced hair loss. I think in such situations, this drug will not have a significant risk of hair loss.
I have been asked how this can happen. We are now doing extensive research into wound healing and the appearance of hair after a wound has healed. This man grew hair from the sides of his burn wound (my assessment of the photos) and this new skin brought along with it hair follicles that clearly were different than his balding follicles which had disappeared prior to the burn. In our experimental work, we have created such wounds and found hair growth not-infrequently. This is the theory behind microneedling that is now performed regularly by many men with good results. The wound created by the microneedling go down to the depth of the stem cells (1-1.5mm below the skin) and with persistent wounding, hair is stimulated through the impact on the stem cells reached by the needling. This was shown in the previous post on this blog.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1351888/pdf/bmjcred00266-0059a.pdf
After years of using Finasteride + Minoxodil, my thinning got worse in January. So I added a dermaroller 1.5 mm every 7-10 days. Major progress in 6 months!
Nice improvement. There is no doubt that the use of a dermroller induces wound healing which brings on hair growth to those who recently lost the hair. Add that to the finasteride that held on to your hair, and you are a fortunate man.
I’m 25 years old. I was starting to lose my hair when I was 16. It was very rapid process so when I was 20 my situation is almost NW7. 132 days ago I decided to take this regime ( I don’t want to mention about decision phase)
first 120 day, I started with the big 3 + dermaroller 0.5 mm x1week (dut(0.5) once everyday+ minox %5 twice everyday + nizoral 2-3 times per week with no side effects) biotin(10000) + zinc(50) + d3(5000) + collagen peptides(tablet) + omega3(with fish oil) all of them x1 everyday ogx biotin shampoo
Everything was good for me. It was like a miracle you know. My hair like born again. My head was full of baby hair and they were getting stronger day by day (or its just it seemed to me like that) On day 118, I just noticed to shedding, probably it has began before that then I shaved my head to zero guard. In this 14 days I shed like crazy. It’s like the first day when I was start this, I read something about shedding but I’m still worried about that this will be failure for me. So I bought something and added my regime. It’s been 2 days since I started using. Apple cyder vinegar tablets(750mg) x1 everyday, l-cysteine (500mg) x1 everyday, vitamin A (25000iu) x1 everyday, iron (65mg + 325mg fer.) x1 everyday, Ubiquinol (100mg) x1 everyday, Collagen peptides powder 15g with cold water everyday, dermaroller upper to 1.5 mm x1 week, Castor oil x3 days of week with massage 2 hours waiting, hyaluronic acid after dermaroller
I uploaded every angle and lights position of my head with day numbers. https://imgur.com/gallery/E0KiyIz. So I just need your help. What should I do? Should I continue or It was just a good short dream that end with failure? If I will continue, what would you suggest me to add?
Amazing results in just 80 days. It seems to be working. I would love to see better focused photographs. My recommendation is stick to it.
Started suffering sudden and rapid hair loss, most noticeably on the sides and back of head.. Thought it was telogen effluvium at first but it appears the hairs are miniaturizing rather than just shedding (hairs are coming in thinner and scragglier and not growing as long). Can DUPA be caused by anything other than androgens? If caused by stress or hormonal imbalance or thyroid, if the issue is addressed can the miniaturization be reversed? Or can only shed hairs from TE be grown back to normal?
Most men who say that they have DUPA, don’t have it. As the doctor who first identified DUPA, I don’t believe that anyone knows what causes it. It may be uniquely genetic because it is similar to some women with diffuse alopecia which presents similarly to men with DUPA.
The side effect and complications of oral minoxidil are not so much of a problem if the dose is kept low. Too many doctors prescribe higher doses and patients get blood pressure problems, even some cardiac complications. See article here: https://www.jaad.org/article/S0190-9622(19)30685-1/fulltext
Development of Liposomal Systems of Finasteride for Topical Applications: Design, Characterization, and in Vitro Evaluation
Affiliations
- PMID: 18161632
- DOI: 10.1080/10837450701481181
Abstract
Finasteride (FNS) is a “drug of choice” for benign prostate hypertrophy and prostate cancer. The drug has also been reported to be useful orally in the treatment of some difficult-to-treat androgen-dependent skin disorders, such as seborrhea, acne, hirsutism, and androgenetic alopecia. However, the ideal route for its administration (i.e., topical) remains unexplored. This has logically suggested the search for strategic formulation approaches to make the drug effective on topical applications, hitherto unexplored. The present study targets the encasement of drug molecules in the interiors of vesicular compartments (liposomes) made up of hydrogenated phospholipids, as an attempt toward the development of a trans-epidermal therapeutic system of FNS. Multilamellar drug-loaded liposomes were prepared by thin-film hydration with sonication method and optimized with respect to drug payload, entrapment efficiency, and size by formulating different vesicular compositions under different process conditions. The vesicular systems consisting of saturated phospholipid (100 mg), cholesterol (50 mg), and FNS (5 mg) showed highest drug payload (2.9 mg/100 mg of total lipids), and drug entrapment efficiency (88.6%). Mean (+/-SD) vesicle size of the prepared liposomes was found to be 3.66+/-1.6 microm. Significantly higher skin permeation of FNS through excised abdominal mice skin of FNS was achieved from the liposomal formulations vis-à-vis corresponding solution and conventional gels. Liposomal FNS formulations also showed more than fivefold higher deposition of drug in skin than the corresponding plain drug solution and conventional gel. Stability studies indicated that the liposomal formulations were quite stable in the refrigerated conditions for 2 months with negligible drug leakage or vesicle size alteration during the storage period. Results of the current studies with FNS-loaded vesicular systems project the high plausibility of a topical liposomal formulation for effective localized delivery of Finasteride.
The picture is worth 1000 words so that there is little I can say other than compliment this man for staying the line. Whatever you do, just don’t stop the finasteride as you will lose it and go back at least to where you were when you started.
This is a compilation of information gleamed from a Reddit poster who put together a series of articles which may point to risks brought on by finasteride in pregnancy. I will quote the entire post and all of the references for you to draw your own conclusions. I have commented on two of the references. Many of the articles are controversial. We have known for some time, that finasteride can impact the fetus on sexual identification. Many hermaphrodites come from women who have ingested finasteride or any similar compound during the first trimester of pregnancy, so items #1-6 have to my knowledge been previously identified. But to develop such abnormalities women were required to have significant exposure to finasteride with some of it being absorbed in their body during pregnancy. In my own practice, I have seen hundreds of men father normal children while they were on finasteride, so there is no 1:1 relationship when a man is taking finasteride and abnormal children and have not seen any patient come to me complaining of an abnormal child while they conceived a baby while on the drug. Of course, that is just my experience and does not guarantee the safety of this drug. I leave that up to the FDA. The rest I will leave for you to judge after reading the material below.
Risks of Finasteride Exposure in Pregnancy
Finasteride, Propecia and Duasteride labels warn that pregnant women must not be exposed to the drug. This includes by taking it, touching a tablet, or by being exposed to semen from a man who is taking it.1
This is because if the active ingredient in Finasteride is absorbed by a woman who is pregnant with a male baby, it can cause the male baby to be born with abnormalities of the sex organs. Finasteride blocks DHT, which is necessary for male baby organs to form and grow. Prenatal Finasteride exposure has also been shown to affect cognitive function in both male and female babies.
What are the specific problems? According to the research they include:
Higher rates of miscarriage
A small penis
Hypospadias
A small underdeveloped scrotum
A prominent midline raphe (scrotum doesn’t join normally)
Ectopic testicles (which don’t reach the scrotum)
Cognitive problems in both males AND females
Memory problems in both males AND females
Three sources detailing these effects are provided below.
Source 1: S. Prahalada (1997) Effects of Finasteride, a Type 2 5-Alpha Reductase Inhibitor, on Fetal Development in the Rhesus Monkey2
In this study pregnant female monkeys were orally given 2mg/kg/day. Every single one of their male babies had genital birth defects.
“The male external genital anomalies were characterised by hypospadias which were confined to the glans penis (5/6; 83.3%), preputial adhesion to the glans (6/6; 100%), a small underdeveloped scrotum (6/6; 100%), a small penis (5/6; 100%) and a prominent midline raphe (6/6; 100%).”
“An apparent incidence in the fetal loss rate was observed in the 2mg/kg/day (23.1%) and the 800ng/kg/day (20%) finasteride treated groups when compared to concurrent controls…”
Source 2: Christopher Bowman, et al (2003). Effects of in Utero Exposure to Finasteride on Androgen-Dependent Reproductive Development in the Male Rat3
In this study Finasteride is shown to impact testicular descent: “Prenatal finasteride exposure significantly impaired testicular descent. Approximately 3, 23, and 73% of the adult males displayed ectopic testes in the 1.0, 10, and 100 mg/kg/day dose groups, respectively… The data from the current study suggest that the conversion of T to DHT in the developing gubernaculum is necessary for normal testicular descent.”
Even in the smallest dose of 0.01 mg/kg/day in the last stages of gestation there were genital issues affecting anogenital distance (AGD) of the males after the rats were born. “Late gestational exposure to finasteride significantly decreased AGD of male offspring in a dose-responsive manner… the AGD of male offspring displayed significant decreases of 8, 16, 23, 25, and 33% in the 0.01, 0.1, 1.0, 10, and 100 mg/kg/day dose groups, respectively.”
“The dose-response curves for finasteride-induced malformations fell into two groups. External structural changes such as decreased AGD and increased nipple retention had similar dose-response curves. These external changes were almost linear over the entire dose range (0.01 to 100 mg/kg/day) and approached 100% incidence by the highest dose.”
The authors note that “The lack of a no observed effect level (NOEL) in the current study was consistent” with the study by Clark (1990) which showed effects at doses down to 0.003 mg/kg/day. (DR RASSMAN’S COMMENT: THIS STUDY WAS DONE IN MONKEYS ADMINISTERED FINASTERIDE IN VARIOUS DOSES DURING PREGNANCY. THIS IS NOT THE SAME AS THE MALE MONKEY BEING ON FINASTERIDE WHEN THE FEMALE MONKEY BECAME PREGNANT)
Source 3: Jason Paris et al (2012) Inhibition of 5?-reductase activity in late pregnancy decreases gestational length and fecundity and impairs object memory and central progestogen milieu of juvenile rat offspring4
“Finasteride significantly reduced the length of gestation and the number of pups per litter…”
“Prenatal finasteride treatment significantly reduced object recognition, decreased hippocampal 3?,5?-THP content… inhibiting the formation of 5?-reduced steroids during late gestation in rats reduces gestational length, the number of viable pups per litter, and impairs cognitive and neuroendocrine function in the juvenile offspring.” (THIS STUDY WAS DONE IN RATS, AGAIN IN PREGNANCY AND DOES NOT CORRESPOND TO A MALE RAT TAKING FINASTERIDE WHEN THE FEMALE RAT BECAME PREGNANT)
While some of these research exposures were a lot higher than would be expected from semen exposure, don’t risk exposing a baby to any amount of this extremely dangerous US FDA pregnancy category X drug.5 Studies have demonstrated fetal abnormalities and there is positive evidence of human fetal risk.
Links:
2.https://www.docme.su/doc/1721148/effects-of-finasteride–a-type-2-5-alpha-reductase-inhibi…
3.https://academic.oup.com/toxsci/article/74/2/393/1716348
4.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196810/#__ffn_sectitle
Back in the 80’s & early 90’s this was an acceptable hairstyle to rock for men with hair loss. The shaved head has only been a more recent trend among balding dudes. At some point will the horseshoe be considered a more stylish option than shaving your head? I’m curious because I’m sick of balding dudes all having to rock the same haircut.
Balding with a shaved head works for many men. Some men get Scalp Micropigmentation (https://scalpmicropigmentation.com/ and look at the men on the front page. Also drill down on the bold men in the gallery). Either way, it is more what is in your head than what is on top of it.
I know this is going to sound weird, but my hairloss really started only 1 or 2 weeks after I began obsessively taking pictures of my temples, crown, etc and becoming anxious over it. Back then I seriously panicked thinking I had MPB as a teen, leading me to this sub. In retrospect, it looked perfectly fine. It then suddenly became much thinner, and since then my hairline, primarily the temples, has been steadily receding and my hair turned thinner, like a self-fulfilling prophecy.
MPB is certainly genetic, but what factors (like stress) could trigger it to start occurring earlier?
Some men practice denial, and one day they look and there it is! Are you really balding? See a good doctor and find out.
I have performed hair transplants on many men who will not take drugs of any type. The nice thing about a hair transplant, is that other than its progressive nature, there is no maintenance required for the transplanted hair to grow for your lifetime in 95% of men who get it.
Always look up the doctor and see his credentials (here are mine: https://newhair.com/doctors/rassman/ ). Ask to see his patients and meet them one-on-one because what you see is what you are going to get. It is not very complicated but too many doctors are ‘sold’ by salesmen who know how to convert you to get your money.
I weighed around 85-86kg before this, and now, two weeks and two days later from the initial depression episode starting, ended two days ago, I weigh around 80-81kg apparently according to the scales. I am concerned, thats alot of weight to lose in such a short time.
It is different with different people, but 15 pounds per months could trigger hair loss with the genes for balding on board. When the genes kick in, it rarely reverses.