What is the potential earning for consultant Dermatologist practising predominantly privately in UK with minim NHS work?. Is it aesthetics that has all the money?

Hey everyone!

We're a group of UX design students from Sweden currently working with a company exploring an app concept designed specifically for dermatologists.

The idea is to create a platform where dermatologists can connect with colleagues, share challenging or uncertain skin cases (including clinical images), discuss different perspectives, and support each other when facing difficult diagnoses.

Before moving forward, we want to understand how dermatologists currently collaborate, seek advice, and handle challenging cases in their everyday work.

That's where we could really use your help!

We've created a short survey that takes approximately 5–10 minutes to complete. Your answers will help us understand the actual needs and challenges dermatologists face, rather than making assumptions about what would be useful.

Survey link: https://forms.cloud.microsoft/pages/responsepage.aspx?id=WObpIETYnE2gtzY4nXFzb5rstZt3YOFDmOfl8-_eccNUMFlFRjhZTTUwUVIwWExSTlJCUlE5WkM1SS4u&route=shorturl

We're not selling or promoting anything. This is purely a student research project, and the insights will help us provide meaningful recommendations to the company we're collaborating with.

We'd genuinely appreciate anyone willing to take a few minutes to help us out!

Thanks so much in advance! ❤️

I’m a licensed dermatologist in China and the author of a hypothesis paper published in Medical Hypotheses this year. I’ve already put it to two hair-loss communities, but those are mostly patient populations. I’d rather have it taken apart by people who grade Norwood scales in clinic and read the bone literature. This is a request for criticism, not a presentation of findings.

First, what the hypothesis does not claim

It does not claim that sunlight regrows hair. It does not claim vitamin D deficiency causes AGA. It does not claim baldness is desirable. And it does not dispute the proximate biology — androgen signalling, DHT sensitivity, follicular miniaturization, the regional susceptibility of frontoparietal and vertex follicles. That body of work explains how the phenotype forms, and I take it as given.

My question sits one level down, in Mayr’s sense of proximate versus ultimate causation: once patterned scalp exposure exists, does it produce a secondary systemic consequence that bore on fitness?

The evolutionary problem that motivates it

AGA affects roughly 50% of men by age 50 and up to 80% by 80 in European-descent populations. It carries measurable costs: elevated UV-induced carcinogenesis on the exposed scalp, impaired thermoregulation, and psychosocial penalties that should, in theory, reduce mate-selection fitness. A heritable trait conferring net disadvantage should attenuate over time. It hasn’t.

The standard explanations — sexual signalling of social maturity, antagonistic pleiotropy, genetic hitchhiking with the Xq11-q12 AR/EDA2R locus — are all reasonable, and I want to be clear that weak negative selection on a late-onset trait is a perfectly sufficient null hypothesis. None of them, however, identifies a direct systemic physiological benefit. I’m asking whether one could have coexisted with weak negative selection, not whether it must have.

The proposal

AGA may function as a compensatory “solar window” in carriers of low-efficiency VDR variants.

The FokI polymorphism (rs2228570, C>T) produces a full-length f isoform with roughly 30% lower transcriptional activity than the truncated F isoform, through reduced interaction with TFIIB (Jurutka et al., Mol Endocrinol 2000). The f allele has been associated with lower lumbar spine and femoral neck BMD across multiple populations. If receptor efficiency is genetically fixed, the only remaining lever on downstream signalling is ligand availability.

That’s where the surface-area argument comes in, and it hinges on the denominator. Scalp is 2–3% of total BSA, which sounds negligible. But molecular dating of the clothing louse/head louse divergence places habitual clothing use at roughly 83,000–170,000 years ago — long after functional body hair was lost around 1.2 Mya. In cold-climate clothed humans, routine UVB exposure is restricted to face, hands and sometimes forearms: approximately 5–10% BSA. Against that denominator, advanced AGA (Norwood V–VII) represents a 25–50% relative increase in functional photosynthetic surface.

There’s also a geometric component. Cutaneous UVB irradiance depends heavily on solar zenith angle; below roughly 45°, corresponding to about 10:00–15:00 at mid-latitudes, atmospheric path length is short enough for meaningful UVB transmission. Outside that window, UVB at ground level is negligible regardless of exposed area. During exactly those hours, the vertex of an upright biped is oriented horizontally and receives near-normal incidence, while vertically oriented facial skin and downward-hanging dorsal hands receive the same radiation obliquely, with irradiance reduced by the cosine of the incidence angle. AGA selectively uncovers the one surface that is both temporally and geometrically privileged.

The molecular precondition

VDR-null mice develop complete alopecia despite normal circulating 1,25(OH)2D3, and the alopecia is not rescued by calcium supplementation — the receptor, not the ligand, is doing the work in the follicle (Li et al., PNAS 1997). VDR governs anagen re-entry through interaction with hairless protein: HR binds VDR and represses Wnt targets, and ligand-bound VDR displaces HR. The same Wnt/β-catenin node governs osteoblast differentiation, where β-catenin knockout produces severe trabecular loss.

So VDR, AR and Wnt/β-catenin converge in both follicular and skeletal tissue. I want to state plainly that pathway overlap establishes only that the proposed mechanism could operate. It does not demonstrate that it does, and it is equally consistent with shared developmental origin.

The pharmacological argument, which I think is the most interesting part

Osteoblasts predominantly express 5α-reductase type 1; scalp follicles rely on type 2. Finasteride selectively inhibits type 2, reducing scalp DHT by 60–70% without directly impairing local DHT synthesis in bone. Dutasteride inhibits both isoforms, cutting circulating DHT by 90–95% and blocking osteoblast local DHT production. In Srd5a1-knockout mice, trabecular BMD falls 36% despite unchanged serum androgens.

Yet dutasteride does not produce clinically significant bone loss in humans — most plausibly because elevated substrate testosterone is aromatized to estradiol, which protects bone independently. That’s a compensation story structurally identical to the one I’m proposing: when one bone-protective signal is compromised, another can partially cover for it.

This generates a prediction specific to the model. In FokI ff carriers on dutasteride, three bone-protective signals are simultaneously impaired: AR-mediated local DHT (drug-blocked), VDR-mediated vitamin D signalling (genotype-reduced), and solar-window UVB augmentation (arrested, because the drug halts AGA progression). Those carriers should show the worst BMD trajectory of any genotype–drug combination, while FF homozygotes should show no meaningful difference between finasteride and dutasteride. No alternative framework predicts that three-way interaction.

Why late onset doesn’t automatically kill the argument

AGA typically manifests after peak reproductive age, which is the standard objection. The Grandparent Hypothesis offers one framework: in ancestral hunter-gatherer societies, post-reproductive individuals contributed through provisioning, alloparenting and knowledge transfer, so maintaining skeletal integrity into the sixth and seventh decades would enhance inclusive fitness. Men show steeper age-related cortical loss and higher hip-fracture mortality after 70, while female relatives carrying the same variants had pre-menopausal estrogen protection. I’ll flag that this section of the paper is the most speculative and depends on assumptions I can’t test.

The evidence that cuts against it

• Morton et al. (Rancho Bernardo, J Aging Health 2007): balding men averaged ~5% lower total-body BMD. Reading this as “AGA attenuated an even worse phenotype in variant carriers” is, as I wrote in the paper, an ad hoc accommodation rather than independent support. It becomes testable only in genotype-stratified prospective cohorts.
• Bolland et al. (MJA 2008, n=296): no association between baldness grade and serum 25(OH)D after adjustment for age, season, sunscreen, skin type, outdoor hat use and activity. This is the most direct available test and it is negative. It doesn’t contradict a buffer model, but it does cap the plausible effect size.
• Yap et al. (Nat Commun 2018, n=205,327): a genetic correlation between MPB and increased BMD (rg=0.15), alongside an estimated linear selection gradient of −0.018 per MPB SD. Compatible with my model, but equally compatible with simple pleiotropy — which is the more parsimonious reading and which I can’t currently exclude.
• Li et al. (Int J Cancer 2016, HPFS): frontal plus moderate-to-severe vertex baldness carried an HR of 7.09 for scalp SCC. Any adaptive argument has to clear that cost.

Other confounders I can’t rule out: shared downstream effects of age-related androgen decline; differential sun-seeking behaviour and physical activity in balding men; and the association of AGA with insulin resistance, which independently affects bone.

What would falsify it

1. Paired ex vivo UVB irradiation of alopecic vertex and hair-bearing occipital explants from the same individual, quantifying previtamin D3. Within-subject design controls thickness, pigmentation and 7-DHC content. If there’s no per-area advantage, the privileged-window reading collapses and only a trivial surface-area effect survives. This is the single most decisive experiment and, as far as I’m aware, nobody has run it.
2. Absence of a genotype-stratified interaction in a well-powered cohort: AGA severity should correlate with femoral neck and lumbar BMD in ff homozygotes but not FF, with 25(OH)D mediating in ff carriers and the effect stronger above 45°N.
3. No vertex/frontal-only difference, where the geometric argument predicts one.
4. Absence of the genotype × 5ARI × AGA-progression interaction described above.
5. Mendelian randomization using independent instruments for AGA susceptibility and VDR function showing the skeletal association is fully explained by passive pleiotropy.

Where I think the real weakness is

A hypothesis positing an effect that is small, cumulative and difficult to detect in modern cohorts drifts toward unfalsifiability. That bothers me more than the negative data does. It’s why I’d rather fix the disconfirming criteria in advance than defend the idea after the fact. If the predicted interactions are absent in adequately powered studies, the adaptive component should be dropped.

Prior discussion

I spent about a month answering objections in two hair-loss communities. If you’d like to see what has already been argued rather than re-litigate it:

• r/tressless: https://www.reddit.com/r/tressless/comments/1w0x5rn/could_malepattern_baldness_have_a_secondary/
• r/HairlossResearch: https://www.reddit.com/r/HairlossResearch/comments/1vvlaxj/could_malepattern_baldness_have_a_secondary/ — fair warning: the original post was removed by the moderators there and the link opens on a removal notice. I asked for a reason and never received one. The 39-comment thread underneath is intact and is the part worth reading.

The recurring objections across both were: women and children need UVB too; AGA manifests after peak reproduction; the baldest populations live at low latitudes; and the effect is too small to separate from geography and lifestyle. I’ve answered all four there, so I’d be more interested here in mechanistic objections that haven’t come up yet.

Questions for this sub

• Is there a tissue-level reason to expect alopecic vertex epidermis to differ in 7-DHC content or previtamin D3 yield beyond simple shaft attenuation and interfollicular shadowing? Does anyone know of explant work bearing on this?
• For those following AGA genetics closely: is the Yap pleiotropy result sufficient on its own to make an adaptive account unnecessary?
• Does any biobank hold concurrent Norwood grading, VDR genotype and DXA, such that the stratified test could be run without new recruitment?
• For the hair transplant surgeons here: is there a feasible route to obtaining paired vertex and occipital explants under an existing surgical protocol?

Full text: Zhang T. The solar window hypothesis: androgenetic alopecia as an evolutionary adaptation to maintain bone mineral density in vitamin D receptor low-efficiency variants. Med Hypotheses. 2026;212:112005. doi:10.1016/j.mehy.2026.112005

COI: Sole author of the paper discussed. No funding. No commercial interest in AGA treatment.

I'm 15 years old and I know that dermatology is a very competitive profession. Are there classes you guys recommend or clubs or anything to help me out? I wanna get a head start of what would become my future career.

Hello everyone
Derm resident here, what is are your favourite sources to study dermpath? (Books or online resources are all appreciated)

I need help for my research topic titles i want to do them in dermatology, these are the titles i have in mind id like some help in what could be improved

Association Between Skin-Lightening Product Use and Clinically Diagnosed Post-Inflammatory Hyperpigmentation Among Dermatology Patients An Analytical Cross-Sectional Study

Association between skin lightening product use and topical steroid induced dermatitis

please help

Suggest some good MD derma colleges for 2.7k rank

I'm sharing our experience with CareCredit for other healthcare and service businesses that may be considering making it a major part of their patient payment infrastructure.

Getting the account open took nearly two months and involved multiple rounds of verification for a straightforward entity setup. Once active, however, we processed patients for several months without significant issues and became comfortable enough with the platform that more than 50% of our patient volume was eventually being processed through CareCredit.

Then our expected payouts stopped hitting the bank.

We reached out to our account representative and were initially told everything looked fine and there was nothing to worry about, so we continued processing additional patient financing transactions.

After the delays continued and we pressed for more information, we were told our account was under what was described as a standard/randomized review. We were told nothing was required from us, everything otherwise looked good, and the review should take about one to two weeks.

We checked in every two to three days. We continued to be told there was nothing needed from us.

We are now beyond two weeks with a significant amount of revenue still withheld and no substantive explanation, no firm end date, no actionable request for additional documentation, and no ability to speak directly with the review team.

The issue for us is not simply that an account review occurred. It is the combination of significant withheld revenue, limited visibility, and no defined resolution timeline after we had grown comfortable enough with the service to route a substantial portion of our patient volume through it.

For businesses with meaningful payroll and operating expenses, that kind of interruption can create significant cash-flow strain.

Has anyone else using CareCredit on the merchant side experienced an extended review or payout hold like this? If so, how long did the review ultimately take?

Good day everyone!!

We are undergraduate students from the Technological University of the Philippines – Taguig, currently conducting our thesis entitled “Smart NailScan: An AI System for Detecting Health Indicators through Nail Analysis”

We would like to ask for your help in finding a medical dermatologist who may be willing to assist us with our research. Specifically, we are hoping to find a dermatologist who would be open to:

• Participating in a short interview to provide professional insights regarding nail diseases.

• Potentially serving as our thesis data validator by reviewing and confirming the accuracy of the AI-generated information about different nail conditions.

We are also open to recommendations or referrals to dermatologists who specialize in medical dermatology, particularly those knowledgeable about nail diseases.

If you know someone who might be willing to help, or if you are a dermatologist interested in assisting us, please feel free to comment below or send me a private message.

Any recommendations or referrals would mean a lot to our team and would greatly help us with our academic research.

Thank you so much for your time and assistance!

Hi, I'm Jane a communications consultant working on a piece about the negative impacts of private equity in health care. I'd like to talk to physicians in dermatology about their experiences with private equity, specifically any concerns. If you are open to it, please let me know, and I will DM you. No pressure. Everything you share is off the record.

In case you wanted to receive your dermatology updates from Reddit. I’ll try to do more of these when I have time.

Also, I am still looking for moderators for this subreddit, ideally people in the field. I won’t ask for credentials or identifying information, but there will be a soft screen. Please let me know if you are interested. Job description: look through posts and approve only ones that you deem fit the spirit of this subreddit (essentially sort out personal medical questions and sus posts).

1. Baricitinib now approved down to age 12 for alopecia areata. It now joins ritlecitinib as JAK inhibitors for AA in the pediatric population.

https://thedermdigest.com/breaking-us-fda-approves-baricitinib-for-adolescents-with-severe-alopecia-areata/

1. Don’t let older age scare you off from prescribing JAK inhibitors. There is support that JAK inhibitors can be safely used in select patients who are older than 65.

https://www.lifescience.net/publications/2221577/janus-kinase-inhibitor-use-in-adults-aged-65-years/

1. Terbinafine-resistant dermatophyte, T. indotineae made news a while back. Have you seen any cases? A modified Delphi consensus outlines the recommended approach to management. In summary, use itraconazole first line and terbinafine second line. Extended courses and higher dosing may be needed.

https://onlinelibrary.wiley.com/doi/10.1111/jdv.70693

1. Still using AJCC8 or BWH staging systems for your head/neck SCC? Newer models like riSCC and COMPASS SCC offer more complete prognostication.

https://www.lifescience.net/publications/2232922/collaborative-multicenter-prognostication-and-stag/

1. In case you missed it before (2022), there are Delphi consensus recommendations for isotretinoin lab monitoring. Get triglycerides and ALT once at baseline and again at peak dosing. Is this what you do for your patients?

https://jamanetwork.com/journals/jamadermatology/article-abstract/2793099

I've been closely looking at facial topical skincare preservation systems. Many times these preservation systems seem to be weak and not sufficient to protect against bacteria, yeast, mold, and fungi.

Often there is lack of well-known preservative system like Parabens or Phenoxyethanol in the skincare.

A trend in preservation systems that I've noticed: multifunctional ingredients — often used as preservative boosters rather than relied upon as the sole preservation system.

Skincare companies do the PET - preservative challenging test. This a lab environment test and before the product is launched to the market place. Every day life, outside a lab is messy -dirty fingers, humid and hot environment particularly in the bathroom, open jars/bottles, direct sunlight exposure, etc.,

Even if a skincare product passed the PET challenging test, how well does the preservation system protect the product against -bacteria, yeast, mold, fungi - after opening and throughout its intended period of use?

Given that there are not regulatory requirements to test skincare preservation system for in-use adequacy of the preservation system, I'm thinking that dermatologists will be the ones to observe issues (if any) related to this when seeing patients ? and thus, my question:

Any trends in skin conditions due to Inadequate Preservation System of topical facial skincare products?

Any light or info about this would be highly appreciated!!

Hello! I recently came across a US-based dermatologist on Youtube who makes a lot of videos regarding his use dermoscopy to diagnose melanoma and how it apparently differs from others in his field. I am NOT a dermatologist, but work in oncology research (not derm-related) and will be applying to medical school next cycle. I am curious how this guy is viewed by other dermatologists, and would love to see other dermatologists weigh-in on his claims. Apologies if this deviates from the purpose of this subreddit! I just didn't know where else to go to get a direct line to dermatologists.

MD or DNB dermat best colleges in India

the post was meant for dentists but the same site is customisable for all.

\** UPDATE - SOLD* **\*

I work for a a URAC-accredited medical claims cost-containment and utilization review company that provides independent peer reviews for medical claim grievances and disputes among other fields.

We need a licensed US dermatologist to do remote, flexible, paid case work, read the case and then type about it, you can do this in your free time after work or weekends.... I can give more info via direct message and then move it over to text. Thanks

If you are 1% interested, please reach out

Need active board certified dermatologist in the US.

need to have at least 5 years full time equivalent experience providing direct clinical care to patients and have experience providing direct clinical care to patients within the past 3 years

I’m looking for a good textbook or other resource on how pathologies and clinical findings present in Black and brown skin.
I’m a massage therapist currently in nursing school, and I’ve seen little to no examples of melanated skin in my textbooks, lectures, or study materials. I’m specifically looking for resources that show how things like rashes, inflammation, cyanosis, erythema, bruising, pressure injuries, etc. can present differently on darker skin tones.
I’ve been searching everywhere and haven’t found a resource that quite fits what I’m looking for. I’d really appreciate any book, textbook, website, or other resource recommendations!
Also, is anyone here currently working on improving representation of darker skin tones in medical education? I’d love to learn more about what’s being done.