The NMC’s new Guidelines on Ethical Advertising and Public Communication begin from an entirely sensible premise. Medicine is not an ordinary marketplace. Patients may be frightened, vulnerable and unable to judge competing claims. Even a technically truthful advertisement can create unrealistic expectations or encourage treatment that was never really necessary.

So guaranteed cures, fake reviews, manipulated testimonials, dubious “No.1” claims, manufactured urgency and advertising designed to create unnecessary demand deserve strict regulation. The NMC is right about that.

The difficult question is where patient protection ends and legitimate professional visibility begins.

The guidelines certainly do not tell doctors to disappear from the internet. Clause 8.2(iii) expressly permits public-health talks through television, radio and electronic media in the doctor’s own name and designation. Explanation III to clause 3.2 requires doctors posting electronically to disclose their identity, qualifications and registration details. [1]

Explanation I to clause 3.2 says that information shared in the normal course, including information given to the public at large, falls outside the definition of “advertisement” only when it is non-promotional and carries no intent for commercial benefit. Clause 5.1 similarly permits health education provided it does not solicit patients and is not monetised through promotional marketing. Clause 8.1(ii) prohibits self-promotion, indirect solicitation and campaigns giving an impression of commercialisation.

This is where things become unclear.

Suppose a doctor writes a useful article on hair loss and patients find it through Google. That is education. But what if the doctor also links to the clinic, or pays to promote the article? At what point does education become advertising?

The rules should not depend on guessing the doctor’s intention. They should look at clear signs of promotion—discounts, guaranteed results, “limited slots”, paid referrals, fear-based marketing or pushing unnecessary treatment.

The rules should clearly say where education ends and advertising begins.

Commercialisation is a fair concern. Money can influence medical decisions. But earning from medical practice is not the same as exploiting patients. Charging fees and telling people about your services are normal parts of private practice. The problem starts when money leads to unnecessary treatment, exaggerated claims or fear-based selling.

That is what the rules should target

.There is another issue. The guidelines allow clinics and hospitals to share factual information, but they remain much stricter about promoting an individual doctor.

And these new rules still sit on top of the 2002 ethics regulations, which broadly discourage doctors from advertising their skills, qualifications or achievements.

So the real problem may be simple:

We are trying to regulate social media in 2026 using an advertising mindset written in 2002.

And this is where the real-world problem becomes uncomfortable. Qualified doctors do not communicate in a separate internet reserved for registered practitioners. They compete for the same patient’s attention with salons, wellness influencers, non-medics and outright quacks. If legitimate medical communication is tightly constrained while those voices remain far less effectively regulated, we risk giving greater visibility to precisely the people from whom patients may need the most protection- quacks. Surely cannot be the purpose of an ethics code?

Can NMC police the quacks?

The NMC cannot discipline somebody who was never registered with it, but other mechanisms exist. Under sections 19 and 21 of the Consumer Protection Act, the CCPA can investigate false or misleading advertisements and direct their discontinuation or modification, with penalties available in defined circumstances. [6] India Code Health-and-wellness influencer guidance also exists, while ASCI requires relevant qualifications to be disclosed when influencers provide technical health advice in commercial communications—although ASCI is self-regulatory, not a substitute for statutory enforcement. [7,8] Consumer Affairs

So the answer is not that the NMC should regulate everyone. It cannot. The answer is different regulators working together against the same harmful conduct.

They need rules that clearly distinguish education from inducement, commerce from exploitation and visibility from deception.

Patient protection should follow harmful conduct—not merely the registration number.

In an era in which patients increasingly find healthcare through search engines, Instagram and YouTube, professional obscurity should not accidentally become a measure of ethical virtue.

The aim should not merely be to ensure that doctors behave ethically online. It should be to ensure that patients encounter ethical healthcare information online—whoever is providing it.

What Next?

The NMC should revise these guidelines before vague wording becomes restrictive practice. The aim should not be to make doctors less visible. It should be to stop misleading, exploitative and harmful medical promotion—whoever is doing it.

Doctors should be free to educate, communicate their qualifications and services, and remain visible to patients, provided they do so honestly and without inducing unnecessary care.

At the same time, misleading health claims by influencers, salons, non-medics and unqualified practitioners need equally serious attention through the appropriate regulators.

A modern ethics code should protect patients from harmful communication, not protect them from seeing qualified doctors online.

The NMC has started an important conversation. It should now refine the rules—clearly, urgently, and with the realities of modern medical practice in mind.

Disclosure: I run a private dermatology practice and OnlineSkinSpecialist.com, an online dermatology consultation service using AI-assisted communication. The NMC provisions on AI-generated promotional material, patient data used as AI input, and potentially healthcare platforms therefore directly affect my professional interests.

References

1. National Medical Commission. Guidelines on Ethical Advertising and Public Communication by Hospitals/Medical Institutions and Registered Medical Practitioners. Public Notice No. R-13014/01/2024-Ethics, 6 October 2026; especially cls. 3.2–3.4, 4.4, 5.1, 6.2–6.4, 7.2–7.4, 8.1–8.3, 9.1–9.4 and 10–11. 20261006154257-publicnotice-eth…

2. Medical Council of India. Indian Medical Council (Professional Conduct, Etiquette and Ethics) Regulations, 2002, reg. 6.1.1. NMC-hosted regulations

3. National Medical Commission. Registered Medical Practitioners (Professional Conduct) (Amendment) Regulations, 2023, 23 August 2023, regs. 3–6, holding the 2023 regulations in abeyance and making the 2002 regulations effective with immediate effect. National Medical Commission

4. General Medical Council. Using social media as a medical professional, effective 30 January 2024; especially paras 10–12, read with Good medical practice, paras 89–91. GMC UK

5. Australian Health Practitioner Regulation Agency. Guidelines for advertising a regulated health service, especially sections 4.3–4.4 and guidance on testimonials, unnecessary healthcare and images/before-and-after photographs. AHPRA

6. Government of India. Consumer Protection Act, 2019, ss. 19 and 21. India Code

7. Department of Consumer Affairs, Government of India. Additional Influencer Guidelines for Health and Wellness Celebrities, Influencers and Virtual Influencers, 2023. Consumer Affairs

8. Advertising Standards Council of India. Influencer Advertising Guidelines, Addendum II—Health and Financial Influencers, current guidance. Asci Online

• Is sunscreen really the most reliable form of sun protection?

• Are umbrellas, hats and shade enough by themselves?

• What does UPF 50 actually mean? Does it tell us anything about visible-light protection?

• Is every cloth automatically good sun protection? Does colour of clothing matter?

We spend enormous effort discussing sunscreen filters, SPF, UVA Protection Factor, PA++++, Boots stars, photostability, iron oxides and reapplication. There is another way to reduce light exposure that is far less sophisticated.

Put something between the sun and the skin.

Unlike sunscreen, clothing does not need to be spread evenly at 2 mg/cm². It does not leave gaps because the patient missed a spot. It is not wiped away with sweat. It does not need to be reapplied every two hours.

This does not mean every piece of cloth provides excellent protection. But appropriate clothing can provide remarkably effective and consistent photoprotection. This brings us to UPF.

What is UPF?

Clothing protection is usually expressed as Ultraviolet Protection Factor, or UPF.

UPF is essentially a ratio. In the laboratory, researchers compare the biologically effective ultraviolet radiation that would reach the skin without the fabric with the amount transmitted through it. The calculation takes into account that different ultraviolet wavelengths have different biological effects.

So a UPF of 50 means that only about 1/50th of this biologically weighted ultraviolet radiation is transmitted through the fabric under the test conditions. In simpler terms, about 2% gets through and about 98% is blocked.

There is an important difference from sunscreen: once the appropriate garment is covering the skin, protection does not depend on whether the wearer remembered to apply enough product that morning.

Can clothing really outperform sunscreen?

A 2022 laboratory study directly compared four modern sun-protective fabrics with two commercial broad-spectrum sunscreens, SPF 30 and SPF 50. The fabrics blocked approximately 96–98% of UVA and more than 99% of UVB. All four fabrics provided greater UVA and UVB protection than the two sunscreens tested, even when those sunscreens were applied at the full recommended laboratory quantity of 2 mg/cm². In that experiment, the SPF 50 sunscreen blocked only approximately 82% of UVA.1

What the experiment demonstrates very well is the underlying principle: a suitable physical barrier can achieve very low ultraviolet transmission without depending on sunscreen application behaviour.

What matters is not merely whether skin is covered, but what it is covered with.

One of the most useful older studies examined 28 ordinary white fabrics. Nineteen provided less ultraviolet protection than an SPF 15 sunscreen. Polyester generally performed better than cotton, while adding dyes substantially increased protection.

This has an obvious Indian relevance. A thin, loose, white cotton shirt may feel ideal in hot weather, but the fact that it covers the skin does not guarantee high ultraviolet protection.

Purpose-designed UPF clothing removes much of that uncertainty. For someone with severe photosensitivity or prolonged occupational exposure, a certified UPF garment is considerably more predictable than simply recommending “full sleeves”.

What about visible light?

UPF is an ultraviolet rating. It does not certify protection against visible light.

However, an opaque fabric physically reduces visible light as well as ultraviolet radiation. The principle is simple: if very little light passes through the fabric, very little visible light is reaching the covered skin.

This gives clothing an important advantage in conditions such as melasma.

A conventional transparent sunscreen must separately provide protection against UVB, UVA and, where required, visible light. A sufficiently opaque physical barrier can reduce all three simultaneously.

But the word opaque matters. UPF and visible-light transmission are different measurements. A fabric may have good UV protection without being completely opaque to visible light, and a UPF rating by itself tells us nothing about how much visible light passes through.

How do you choose protective clothing without a UPF label?

Certified UPF clothing is not always readily available in India, but there are useful practical clues.

Choose densely woven, reasonably substantial fabrics rather than thin, loose weaves. Darker or strongly dyed fabrics generally provide better ultraviolet protection than very pale fabrics, and stretching should be avoided because it opens spaces between fibres and can reduce protection. Wetting can also reduce protection in some materials.

Perhaps the simplest practical test is to hold the fabric up to bright light. If you can easily see light through it, it is unlikely to be an ideal physical barrier. If very little light passes through, the fabric is more likely to provide good ultraviolet protection and will also reduce visible-light exposure.

This is not a substitute for a measured UPF rating. But when certified UPF clothing is unavailable, dense weave, adequate thickness, darker colour and minimal light transmission provide a sensible practical guide to choosing more protective clothing.

So is clothing better than sunscreen?

For body sites that can conveniently be covered, it is often more dependable.

That is not the same as saying sunscreen is unnecessary. The face, hands and other exposed sites cannot realistically remain covered throughout normal life. In tropical Indian weather, covering every surface with dense fabric would also be impractical and uncomfortable.

The more rational approach is not clothing versus sunscreen.

It is clothing before sunscreen where practical, and sunscreen for the skin that remains exposed.

• An outdoor worker who covers his forearms with appropriate sleeves no longer needs to maintain an adequate sunscreen layer there throughout a day of sweating and wiping.

• A broad-brimmed hat can reduce direct exposure to parts of the face and neck, while sunscreen deals with the residual exposure.

• A person worried about tanning of the arms may obtain more consistent protection from sleeves than from trying to remember repeated sunscreen application.

  ---

What about hats, umbrellas and shade?

They help, but they are not complete barriers. Shade primarily blocks direct sunlight. Ultraviolet and visible radiation can still reach the skin from the open sky and from reflection by buildings, concrete, sand, water and other surfaces. Similarly, an umbrella or hat protects only the regions actually shaded by it.

This is why physical photoprotection works best in layers: reduce unnecessary exposure, use shade, cover what can conveniently be covered, and use sunscreen on what remains exposed.

The great weakness of sunscreen is that their effectiveness depends on human behaviour. SPF and UVA Protection Factor are measured on carefully prepared, uniformly coated test sites. Real patients apply less, miss areas, sweat, wipe their skin and fail to reapply.

Clothing largely removes that variability. Once an adequate garment is on the body, the protection is relatively continuous until the garment is removed or its physical properties change.

That may be particularly important for someone whose aim is cosmetic prevention of tanning. Asking that person to apply a generous layer of sunscreen to both arms and reapply it during a hot Indian day requires substantial effort. Wearing appropriate sleeves may achieve the same practical objective far more reliably.

The best photoprotection is often the one that requires the least repeated human effort.

References

• Berry EG, Bezecny J, Acton M, et al. Slip versus Slop: A Head-to-Head Comparison of UV-Protective Clothing to Sunscreen. Cancers (Basel). 2022;14:542. doi:10.3390/cancers14030542. Columbia Sportswear funded data collection and portions of the analysis; several authors were company employees or consultants contracted by the company.

• Davis S, Capjack L, Kerr N, Fedosejevs R. Clothing as protection from ultraviolet radiation: which fabric is most effective? Int J Dermatol. 1997;36:374–379. doi:10.1046/j.1365-4362.1997.00046.x.

• Boothby-Shoemaker WT, Mohammad TF, Ozog DM, Lim HW. Photoprotection by clothing: a review. Photodermatol Photoimmunol Photomed. 2022;38:478–488. doi:10.1111/phpp.12776.

So perhaps we should ask the obvious question: do we still need human reviewers?

I am not suggesting that journals sack their reviewer databases and hand everything over to ChatGPT. The more useful question is what, exactly, we still need the human reviewer for. If AI can perform much of the visible labour of peer review faster than humans, asking a senior academic to spend an evening checking references and table formatting increasingly looks inefficient.

The machine can do much of the checking. What it cannot reliably do is decide what matters.

Reviewers are already using AI

This is not a hypothetical future. A 2025 Frontiers survey of 1,645 active researchers reported that 53% of peer reviewers were already using AI tools during peer review.

The question is therefore no longer whether reviewers use AI. It is whether they use it as an assistant or allow it to substitute for judgement.

My Personal Experience

I recently had reason to wonder about that distinction. An article I had submitted to a reputed journal remained under review for close to a year despite repeated reminders. Eventually, a decision arrived based on a single reviewer report.

The report was about two pages long, neatly organised with headings, subheadings and bullet points.

To me, there was little doubt that it had been generated, or at least largely drafted, by an LLM. The style was simply too familiar. I could not prove it, so I asked the editor whether AI had been used. I was reassured that the reviewer was very much human—and apparently a very senior one.

That reassurance worried me more.

The problem was not whether the reviewer existed. It was whether the report reflected the reviewer’s own judgement. There were plenty of comments, but little engagement with the central issues. It looked comprehensive, but it did not feel thoughtful.

That is where AI-assisted peer review can go wrong: an impressive-looking review can create the appearance of expert scrutiny without containing much expert judgement.

When AI does not want you to reject…

A reviewer who is very good at finding things to improve but rarely concludes that a paper should be rejected is of limited value. If the default response (this is what AI does) is always “revise and improve”, peer review loses one of its central functions: deciding when a paper is not sufficiently novel, important or methodologically sound to justify publication.

There is evidence that LLM reviewers may have exactly this tendency. Janis Keuper generated 1,000 reviews of 2024 ICLR papers using several LLMs and found that many models recommended acceptance in more than 95% of cases, even without any attempt to manipulate them. These were machine-learning papers, so the finding cannot simply be extrapolated to biomedical publishing, but the degree of leniency is striking.

Russo and colleagues found a related pattern in actual ICLR 2024 reviews. They estimated that at least 15.8% had received AI assistance. Among papers close to the acceptance threshold, receiving an AI-assisted review was associated with a 4.9-percentage-point higher acceptance rate, suggesting that AI assistance may influence the decision itself, rather than merely improve the wording of a review.

Why might this happen? An LLM is very good at finding problems and suggesting how they could be fixed. But deciding that a paper should not be published is a different task. It requires judging whether the central idea is sufficiently novel or important, whether a flaw undermines the whole study, and whether further revision is actually worthwhile.

The same problem may affect authors.

In my own use, I have repeatedly noticed how readily an LLM describes a manuscript as promising before offering an extensive list of improvements. I could find no direct evidence that this systematically gives authors false confidence, so this remains an observation rather than an established finding.

But the trap is obvious: “Here are twenty ways to improve your paper” does not mean “this paper deserves to be published.”

Sometimes the most useful advice is that the central idea is insufficiently novel, the study cannot answer the question being asked, or the paper is simply not worth another month of work.

AI is exceptionally good at helping us improve things. It may be rather less good at telling us when to stop.

The bigger problem: AI can also be manipulated

A 2026 JAMA Network Open experiment inserted invisible white-on-white instructions into manuscripts directing three commercial LLMs to assess them favourably. Under neutral reviewing prompts, acceptance recommendations increased from 0% to nearly 100%.

The manipulation also reduced detection of genuine scientific flaws. Under stringent criteria, overall flaw detection fell from 18.9% to 8.5%, while detection of methodological flaws fell from 56.3% to 25.6%.

So what should the future of peer review look like?

AI should handle the tick-boxing. Does the abstract agree with the Results? Are the numbers internally consistent? Are all figures cited? Do Methods and Results contradict one another? Are outcomes reported consistently? Are references obviously missing? Has the relevant reporting guideline been followed? AI can also flag statistical assumptions that deserve examination, although flagging a possible problem is not the same as validating the statistics.

If such checks can be performed reliably within appropriately governed systems, using expert reviewer time to do them manually makes little sense.

The reviewer should concentrate on the questions for which expertise was sought: Does the science make sense? Is the finding genuinely novel or meaningful? Do the data justify the conclusions? Is the requested additional experiment actually necessary?

The distinction is familiar in dermatopathology. An immunostain may strongly support a diagnosis. But if the morphology and clinical picture do not fit, the stain does not get to make the diagnosis.

AI can provide evidence, identify inconsistencies and raise questions. The reviewer decides what those findings mean and remains responsible for every criticism sent to the author.

Editors remain essential too.

They must decide whether the reviewer understood the paper, whether the criticisms matter, whether revision requests are proportionate and whether another revision is justified at all.

I would much rather receive one page from an expert who understood my paper than three pages of immaculate commentary discussing everything except what is actually wrong with it.

The Future

AI will not make peer review obsolete. It should make the mechanical part of peer review obsolete.

AI-assisted peer review is already here, whether journals officially admit it or not. Rather than pretend otherwise, journals should legitimise it, regulate it, and build it properly into the review process.

Let AI do the checking.

Let reviewers do the thinking.

Let editors make the decision.

This, my friends, will be the future of peer review…..

References

1. Frontiers Media. Unlocking AI’s untapped potential: responsible innovation in research and publishing. Frontiers Media; 2025. Global survey of 1,645 active researchers. The report found that 53% of peer reviewers surveyed were using AI tools. Frontiers
   Frontiers report

2. Keuper J. Prompt Injection Attacks on LLM Generated Reviews of Scientific Publications. In: Pattern Recognition: 28th International Conference, ICPR 2026. Lecture Notes in Computer Science, vol 16812. Springer, Cham. pp. 122–134. doi: 10.1007/978-3-032-31335-5_9. The study generated 1,000 reviews of ICLR 2024 papers and found acceptance recommendations above 95% for many LLMs even under neutral conditions. Springer
   Springer publication

3. Russo Latona G, Horta Ribeiro M, Davidson TR, Veselovsky V, West R. The AI Review Lottery: Widespread AI-Assisted Peer Reviews Boost Paper Scores and Acceptance Rates. Proc ACM Hum Comput Interact. 2025;9(7). doi: 10.1145/3757667. This is the source for the estimated 15.8% prevalence of AI-assisted ICLR 2024 reviews and the 4.9-percentage-point increase in acceptance among papers near the threshold. Princeton University
   Published article/DOI

4. Choi B, Jun TJ, Sung JW, et al. Invisible Text Injection and Peer Review by AI Models. JAMA Netw Open. 2026;9(1):e2552099. doi: 10.1001/jamanetworkopen.2025.52099. This supports your statements about invisible prompt injection increasing acceptance recommendations from 0% to nearly 100% and reducing detection of genuine flaws. JAMA Network
   JAMA Network Open article

5. Nature Portfolio. Nature Portfolio Journals Guide to Reviewers. Nature Portfolio. Accessed October 2, 2026. The guidance states that reviewers should not upload manuscripts into generative-AI tools and should disclose AI assistance when it supports evaluation of manuscript claims. Nature
   Nature Portfolio reviewer guidance

Modern dermatology usually prefers narrowband ultraviolet B (NB-UVB), delivered through a phototherapy machine. But India has used another effective and remarkably inexpensive form of phototherapy for decades: PUVASOL, using an ultraviolet source available everywhere….the sun.

The following write-up takes a pragmatic view: in a country like India, where most healthcare expenditure is paid out of pocket, affordability and accessibility can determine the real-world effectiveness of a treatment far more than its superiority on paper.

First, what are PUVA and PUVASOL?

PUVA means Psoralen + Ultraviolet A.

Psoralens are medicines that temporarily make the skin more sensitive to UVA, the longer-wavelength component of ultraviolet light. Once the skin is sensitised, UVA can stimulate repigmentation. Because treatment combines a drug with light, PUVA is called photochemotherapy.

In conventional PUVA, UVA comes from a phototherapy machine.

In PUVASOL, it comes from SOLar light: PUVA + SOL.

The principle is the same, but the sun replaces the UVA cabinet.

Psoralen can be taken orally, producing whole-body photosensitisation, or applied directly to individual patches. I therefore tend to use systemic PUVASOL for extensive vitiligo and topical PUVASOL for localised disease.

The drug is inexpensive. The UVA source is free. For a country where repeated hospital attendance is often difficult, that matters.

Why did NB-UVB become preferred?

There are a few good reasons. Psoralen deliberately makes the skin photosensitive. Too much UVA can therefore cause phototoxicity—essentially an exaggerated sunburn—with redness, burning and occasionally blistering. Oral psoralen also requires additional precautions, including eye protection from UVA after taking the drug.

PUVA also acquired a reputation for increasing the risk of skin cancer. That concern is genuine, but its origins need context. The strongest carcinogenicity data come mainly from fair-skinned Western patients with psoriasis who received high cumulative doses of PUVA over many years. Extrapolating those risk estimates directly to darker Indian skin, particularly to patients with vitiligo receiving lower and differently delivered exposure, is not the same.

NB-UVB avoids psoralen altogether. Its ultraviolet dose can be measured accurately, it is generally better tolerated, and the pigment that returns often matches the surrounding skin better. These advantages nevertheless explain why modern guidelines favour NB-UVB.

The question is not whether NB-UVB is technically better. It is how much better—and whether that advantage survives the realities of Indian healthcare.

How much more effective is NB-UVB?

The strongest randomized comparison, by Yones and colleagues, found more than 50% improvement in 64% with NB-UVB versus 36% with oral PUVA. Colour matching was also substantially better with NB-UVB. That is a meaningful difference. But it was one small study of oral PUVA delivered using an artificial UVA cabinet, not Indian PUVASOL.

Other comparisons show much smaller differences.

Bhatnagar and colleagues found average repigmentation of 52.2% with NB-UVB versus 44.7% with systemic PUVA—an absolute difference of only 7.5 percentage points. When the notoriously treatment-resistant hands and feet were excluded, the difference was about 13 percentage points.

Ravishankar and colleagues reported at least 50% repigmentation in 56% with NB-UVB versus 48% with PUVASOL—an eight-percentage-point difference. NB-UVB again performed better for colour matching and adverse effects, but the study contained only 25 patients in each group and was not properly randomized.

Systematic reviews reveal the same problem: very few direct trials and wide confidence intervals around the estimates. The evidence therefore does not show that PUVA and NB-UVB are identical. NB-UVB has clear advantages. But neither does it establish overwhelming clinical supremacy in repigmentation.

A statistically significant difference is not automatically a clinically decisive one. And an 8–13 percentage-point advantage begins to look rather different when the better treatment requires hospital attendance two or three times every week for six months or longer.

Now count the patients who cannot reach the machine

This is where conventional efficacy studies become less useful in India. Consider the patient who stops NB-UVB after six weeks because he cannot lose three mornings of work every week. Or the family travelling 50 kilometres with a child. Or the patient who cannot afford months of private phototherapy.

Do not remove these patients from the denominator. Count them as treatment failures.

That is the logic behind intention-to-treat analysis: outcomes are assessed in everyone for whom a treatment strategy was assigned, not merely in the fortunate group who managed to complete it.

We do not have a properly designed Indian trial comparing NB-UVB and PUVASOL this way. So I cannot claim that PUVASOL has already proved superior on an intention-to-treat basis.

But I strongly suspect that the apparent advantage of NB-UVB would shrink—and in some settings could even reverse—once treatment completion, travel, affordability and adherence are included.

The existing Indian literature gives us clues. In Bhatnagar’s study, repeated hospital attendance proved difficult enough to compromise long-term treatment. In Ravishankar’s study, patients who could attend frequently received NB-UVB, while those who could not received PUVASOL.

Access determined treatment before efficacy had a chance to. The machine may be superior. The patient still has to have access to it.

PUVASOL’s drawbacks

PUVASOL’s major disadvantage is that sunlight cannot be dosed as precisely as a phototherapy machine. UVA intensity varies with season, geography and time of day. Measurements from Chandigarh showed that delivering the same UVA dose could require about 11 minutes in June but more than 50 minutes in January.

So “take this tablet and sit in the sun for ten minutes” is not proper PUVASOL.

PUVASOL should be treated as genuine photochemotherapy. Psoralen dosage should be defined, sunlight exposure should begin conservatively and increase gradually, contraindications should be screened for, and patients should receive clear written instructions. Systemic treatment requires appropriate eye protection; topical treatment requires precise application to the affected patches.

Used carelessly, PUVASOL can burn. Used properly and protocolised by an experienced dermatologist, my experience has been that it is remarkably safe.

What about skin cancer in Indian patients?

This is where Western experience should not simply be imported wholesale. In my own practice, I have never seen a skin cancer attributable to PUVA or PUVASOL. My father, also a dermatologist, has used PUVA-based treatment for approximately four decades and has likewise never encountered one.

That is anecdotal experience, not proof. But it aligns with the available Indian evidence.

The largest Indian safety study included 1,300 phototherapy patients, 929 of whom received PUVA. Some had cumulative UVA exposures above 2,000 J/cm². No cutaneous malignancy was detected. Indian reviews have consequently described the malignancy risk with PUVA in darker Indian skin as very low.

I would not claim that the risk is literally zero. The available Indian follow-up is not long enough to exclude every late cancer, and rare PUVA-associated malignancies have been described outside India.

But in practical terms, the carcinogenic risk of carefully administered PUVA/PUVASOL in darker Indian phototypes appears extremely low and may be negligible, particularly compared with the much larger risk estimates derived from heavily treated, fair-skinned Western psoriasis populations. That distinction is important!

Systemic for extensive disease, topical for localised disease

The argument for reviving PUVASOL is not merely an argument for topical therapy.

For extensive vitiligo, systemic PUVASOL is often the more practical approach. Treating dozens of individual patches topically makes little sense. Oral psoralen followed by carefully timed sunlight provides whole-body photochemotherapy without requiring repeated visits to a UVA unit.

For localised vitiligo, topical PUVASOL is more logical. Psoralen is confined to the white patches, avoiding systemic exposure, although excessive local UVA can still cause phototoxicity.

A case for reviving PUVASOL

The best phototherapy is not the one that produces the highest response rate among patients who manage to complete it. It is the one that produces the best outcome among all the patients we intended to treat.

Until we measure that properly in Indian patients, declaring PUVASOL obsolete may be evidence running ahead of the evidence, especially since the difference in repigmentation between NB-UVB and PUVA has often been modest in small comparative studies, while the difference in accessibility can be enormous.

For adults with extensive vitiligo who cannot realistically attend NB-UVB several times every week, systemic PUVASOL deserves reconsideration. For localised disease where targeted phototherapy is inaccessible, topical PUVASOL deserves the same reconsideration.

This is not an argument for casual home treatment. It is an argument for bringing PUVASOL back as properly selected, protocolised and medically supervised photochemotherapy.

References

1. Yones SS, Palmer RA, Garibaldinos TM, Hawk JLM. Randomized double-blind trial of treatment of vitiligo: efficacy of psoralen–UV-A therapy vs narrowband UV-B therapy. Arch Dermatol. 2007;143:578–584.

2. Bhatnagar A, Kanwar AJ, Parsad D, De D. Comparison of systemic PUVA and NB-UVB in the treatment of vitiligo: an open prospective study. J Eur Acad Dermatol Venereol. 2007;21:638–642.

3. Xiao BH, Wu Y, Sun Y, Chen HD, Gao XH. Treatment of vitiligo with NB-UVB: a systematic review. J Dermatolog Treat. 2015;26:340–346.

4. Ravishankar V, Rathod SP, Saikia S, Chaudhary RG, Solanki RB. A study of comparison of PUVASOL and NBUVB in patients with vitiligo. Pigment Int. 2018;5:96–102.

5. Kaushik A, De D, Handa S, Mittal A. To determine irradiance of ultraviolet A in ambient sunlight and optimum exposure time for PUVASOL in a North Indian location. Indian J Dermatol Venereol Leprol. 2019;85:462–465.

6. Ravindran S, Pai BS, Shetty VM. Risk of cutaneous carcinogenesis with phototherapy in Indian subpopulation: a 10-year analysis and review of literature. Dermatol Ther. 2022;35.

I wrote this nearly 30 years ago, when I was a medical student!

Reading it again now, I can see several arguments I would frame very differently today, and a few conclusions I would no longer state with such certainty. But I have resisted the temptation to rewrite it.

What interested me was how we perceive the world, what we mean by the “self,” and whether our identification with the physical body is as straightforward as it seems.

So here it is exactly as I wrote it then — reasoning, overconfidence, philosophical leaps and all.

Humans take many of nature’s marvels for granted. We believe everything we see and hear, only to realise later that nature has its own mysterious, deceptive ways.

It is not an uncommon experience to wake up from a deep sleep in a perplexed state, wondering who or where we are. Sleep and dreams are among the greatest mysteries of nature, offering valuable clues into the enigma of creation.

Isn’t it amazing that we are blissfully unaware of our surroundings, and thus virtually cease to exist, during sleep?

Imagine being on an island all alone. Is it possible to sleep peacefully at night without doubting Mother Nature, wondering whether she might fool us when we wake up? Fears of not waking up, or of waking up in a completely different place or surroundings, would surely creep into one’s mind.

Indeed, “hypnophobia” is the fear of sleeping that some individuals have, and it is not unreasonable. It is the fear of losing one’s identity.

Sleep is akin to a near-death experience where the “I” no longer exists.

Does the world really exist when we are asleep — when the “I” no longer perceives it?

How can one prove or disprove this?

We blindly believe that everything must continue to exist because of circumstantial evidence — because continuity of events is maintained after one wakes up. However, one cannot be certain of this fact.

The existence of an object or person is only relative to our existence and our perception of it. The “perceived” cannot exist without the “perceiver”, and vice versa. A “subject” cannot exist without the “object”.

Infinite noises surround us in our day-to-day life. Most noises sink into oblivion unless one is “listening”. One can never be sure about the existence of a particular noise unless he or she was listening to it, in spite of being in its vicinity all the while.

Similarly, once the senses are shut, as during sleep, everything around us disappears and virtually ceases to exist.

Conversely, our existence is also relative to the objects surrounding us. Without the world around us, there would not be anyone or anything to recognise our presence.

This statement — that everything exists or does not exist depending on one’s wish or will to perceive it — may sound egoistic and preposterous. It indirectly states that we are the creators of the universe.

However, this may not be far from the truth.

“I am the creator.”

“I” Am the Creator

It is the “I” which recognises and acknowledges the world around.

It is the “I” which has emotions and thoughts.

It is the “I” that sleeps, dreams and wakes up.

The “I” we are talking about here is the ego.

Without the ego, man does not exist. Ego makes man survive. It is this ego we strive to satiate, whatever we do.

However, the ego — and hence man — is selfish, and there are no two sides to it.

We love someone because it makes us happy. Happy that someone is there to love us back. Happy that someone is there to praise or compliment our deeds.

A person who loves purely for the sake of someone else’s happiness would be a rare find indeed.

Therefore, even supposed “true love” is selfish.

Why do we give money to a beggar?

Because his sorrow made us unhappy, and giving him money in turn made us happy.

Similarly, why does one cry on the demise of a dear one?

It is not because we feel sorry that our loved one is no longer able to enjoy this life. It is because previously he or she used to give us happiness by caring for us, loving us, or giving us things.

Outrageous as this may seem, even a person crying is doing so because it is making him or her happy.

Remember how relieved one feels after crying one’s heart out.

Man does everything, only and only to satisfy his ego.

The Theory of “One” Existence

Let us switch off our senses for a moment.

Stimuli of light, sound, touch, pressure and so on would no longer be perceivable. Everything around us would fade away from existence.

Even our own body would vanish, as the senses that perceive it would no longer exist.

Similarly, even the thought process in our brain would cease, since thoughts are provoked by stimuli.

What would remain then is the “I” alone, suspended in an unending space.

Now, do we exist?

Where?

One cannot perceive even one’s own body.

How can such an existence — where neither subject, the world, nor object, ourselves, exists — be proved?

The hypothetical situation imagined here is not too far-fetched. What we are imagining is, in effect, a person who is deaf, mute, blind and deprived of all senses.

Such a state of no-existence of the self can be equated to a state of all-existence: the soul, being no longer bound by the body but by the infinite boundaries of the universe, would exist everywhere.

“If the ‘I’ alone remains after shutting down all the senses, it has to be the truth. It has to be the One.”

Is this what happens after death?

What Is “I”?

Spiritualism has always stated that the world is non-existent or unreal. Having come this far, the statement is not difficult to comprehend.

By extrapolation, it would also mean that our physical body, which is a part of this “world”, is also non-existent.

What exists eternally is the soul — the real “I”.

It alone remains perpetually even after the senses switch off. The body changes relative to the world around it. But the soul is immortal and omnipresent.

Let us analyse this statement and see if it makes any sense.

In colloquial terms, we use the word “I” to describe an individual — ourselves. By that, we mean our body, emotions, intellect and the life-bearing soul beneath.

Absurd as this may sound, why do we believe that this body is ours?

It is because our body obeys our commands only, not someone else’s; gives us stimuli from the outside world; and follows us wherever we go.

However, what about a person paralysed in all four limbs and with no sensations?

His body has none of the above attributes. Then how can he say that it is his body?

In fact, the body outside is now rather like a chain binding him and dragging him down to one place.

But is he really affected at all?

No.

He is simply unable to perform certain functions that other people do.

If one gives him a mechanical limb that perfectly simulates the human body, he becomes a normal person again.

Thus this body is nothing but a gadget for the “I” to play with and express itself. It is a trivial instrument capable only of perceiving limited sensations and obeying limited commands.

Command it to fly — it will not.

Therefore, “I” is not the body.

It is well known that emotions and thought processes can be severely blunted in diseases affecting the brain, such as stroke. However, that does not mean that the person does not exist.

We often comment in such circumstances, “He is a different man.”

Is he really a different man inside?

It is the same soul — the “I” that was there all his life.

Therefore, neither emotions nor intellect can form part of the “I”.

It is a common experience to see a child who is genuinely injured while playing stop crying when offered a chocolate — when distracted.

We often wonder how that is possible despite the obvious injury.

Here is a possible explanation.

On sustaining the injury, the child becomes worried that something is happening, or may happen, to his body. In other words, he identifies himself with his body and starts crying.

Of course, pain plays a major part.

However, as soon as he is distracted by the chocolate, he subconsciously blocks the pain impulse. This is similar to the noise analogy discussed earlier.

In effect, the child ignores his body and stops identifying his “I” with the body. That is why he no longer feels the pain or cries.

As one grows older, we realise that small bruises are really harmless. We therefore ignore such pain stimuli. Adults generally cry only in the face of major or life-threatening injuries.

However, it is only wise men who realise that even larger blows to the physical body do not take away even an ounce of their life, and are hence unaffected by the sorrows of life.

If the body were real — that is, the real “I” — why would the pain disappear?

The real “I”, the soul, is unaffected by what happens to the body.

There was once a great sage in ancient India called Ramana Maharshi, who underwent surgery without anaesthesia.

After all, once we know that the body is an instrument, it is not difficult to switch it on and off at will.

This is what the saying,

“Free yourself from the bondage of this body”

probably implies.

One experiences pain or suffers only as long as one identifies oneself with this body.

Once one realises that one is not this body, nothing in this world is going to affect him.

Not even death.

Because the soul — the “I” — can never die. It is imperishable, unlike the body.

One should, in fact, be happy to die because it is just like wearing a new set of clothes.

People feel so happy to wear a new dress.

But to wear a new body…?

It is just that no one realises that dying is akin to the process of changing clothes.

“When the existence of one entity is but relative to the existence of the other, they do not actually exist.”

The Theory of No-Existence

The statement “I alone exist” is amusing.

In the hypothetical circumstance discussed earlier, where all the senses are switched off, the “I” can only be described as existing. One cannot use any dimensions to describe this existence.

However, “existence” makes sense only when contrasted with a “non-existent” state.

If something exists everywhere and at every time, how can that be called “existence”?

What does “life” mean without “death”?

Therefore, the question begs:

Does anything exist at all?

This Is “The Science of Life” — Vedanta

The truth in the above statements is better understood when one realises how incomplete and deceptive our physical senses are, and how contradictory their interpretations of the world around us can be.

In Part 1, we looked at SPF and why it mainly tells us about protection against sunburn. In Part 2, we moved to UVA protection and examined what PA ratings, UVA Protection Factor and Boots stars actually mean.

But sunlight does not end where these ratings end.

Ultraviolet B (UVB) spans approximately 280–320 nanometres, and ultraviolet A (UVA) about 320–400 nm. Beyond 400 nm lies visible light, roughly 400–700 nm.

SPF does not measure protection against visible light. Neither does the PA rating. Neither do Boots stars.

And for darker skin, melasma and post-inflammatory pigmentation, that missing part of the spectrum may matter more than many people realise.

So what about protection against visible light? Can visible light also cause pigmentation?

Though for many people protection from visible light may not matter greatly, for patients with melasma, post-inflammatory hyperpigmentation and darker skin phototypes, it matters!

In a landmark study, Mahmoud and colleagues exposed 20 volunteers with Fitzpatrick skin types IV–VI to either long-wave UVA, called UVA1, or visible light. Both produced pigmentation, but pigmentation produced by visible light was darker and more persistent. Visible light did not induce pigmentation in the small comparison group with skin type II. ^{The study was supported partly by an unrestricted grant from Johnson & Johnson Consumer Companies; the authors declared no conflict of interest.}

Not every colour of visible light behaves the same way. In another study involving skin types III and IV, blue-violet light at 415 nm produced clear dose-dependent hyperpigmentation, whereas red light at 630 nm did not. Remarkably, pigmentation after a single sufficiently large 415-nm exposure remained measurable for up to three months.

But what about blue light from phones and screens?

If blue-violet light can cause pigmentation, an obvious question follows: should we worry about phones, tablets and computer screens?

Blue-violet light from sunlight can induce pigmentation when the skin receives a sufficiently large dose. But the intensity of visible light emitted by electronic screens is dramatically lower than that of sunlight. Current evidence has not shown that ordinary exposure to phones, computers or televisions causes meaningful pigmentation, worsens melasma or contributes significantly to photoageing.

A 2026 international consensus on hyperpigmentation noted that blue-light intensity from electronic devices is roughly 100–1000 times lower than sunlight, and there is no convincing evidence that normal screen exposure is clinically important.

So when a sunscreen advertises “blue-light protection”, the relevant question is usually whether it protects against solar blue-violet light, not whether it shields you from your phone.

Your WhatsApp screen is not the blue light your melasma needs protection from.

There is another complication. Visible light does not act completely independently of UVA. A study in skin types IV–VI found that visible light containing less than 0.5% UVA1 produced significantly greater pigmentation than pure visible light, suggesting interaction between the two regions of the spectrum.

This matters because the boundary between long-wave UVA1 and visible light sits around 400 nm, precisely where conventional transparent sunscreens may provide increasingly variable protection.

An excellent UV sunscreen is not necessarily an excellent pigmentation sunscreen.

Melasma provides some of the best clinical evidence that protection beyond ultraviolet radiation matters. In a randomized trial of 68 patients with melasma, both groups used sunscreen with SPF 50 or greater and all received 4% hydroquinone. One sunscreen protected mainly against ultraviolet radiation; the other additionally contained iron oxide pigments designed to attenuate visible light.

After eight weeks, the group receiving ultraviolet plus visible-light protection showed 15% greater improvement in the Melasma Area and Severity Index and 28% greater improvement on objective colorimetry than the UV-only group.

What are tinted sunscreens?

Most modern sunscreens are designed to become relatively transparent when applied. That is cosmetically desirable, but transparency means that much of visible light continues through the film.

Iron oxides are pigments. Depending on their type, particle properties, concentration and formulation, they absorb and scatter parts of the visible spectrum. This is why sunscreens designed to provide meaningful visible-light protection are generally tinted.

In one study of Fitzpatrick type IV skin, two iron-oxide-containing tinted formulations reduced visible-light-induced pigmentation substantially better than an untinted mineral SPF 50+ sunscreen containing zinc oxide and titanium dioxide. However, this evidence requires a clear caveat: seven of the eight authors were affiliated with L’Oréal Research and Innovation.

What about mineral sunscreens? The white-cast paradox

Here lies an important irony. Traditional mineral sunscreens could attenuate visible light precisely because they were visibly white on the skin. Larger particles of zinc oxide and titanium dioxide scatter visible wavelengths, producing the familiar white cast.

Modern formulations have worked hard to eliminate that problem. By micronising the particles and making the sunscreen increasingly transparent, manufacturers have made mineral sunscreens far more cosmetically acceptable, especially on darker skin.

But that creates a paradox: the more invisible a mineral sunscreen becomes, the less useful its “mineral” nature may be for visible-light protection. It may still provide excellent UVB and UVA protection, but it no longer follows that it will substantially attenuate visible light.

In other words, the much-disliked white cast was not merely a cosmetic defect; it was evidence that visible light was being scattered. Remove the white cast, and much of that advantage may disappear.

So, when visible-light-induced pigmentation is the concern, the label “mineral sunscreen” is not enough. Iron oxides or other pigments, and preferably testing of the finished formulation against visible-light-induced pigmentation, are far more informative.

But how much visible-light protection does a tinted sunscreen provide?

This is where sunscreen science currently becomes frustrating. SPF has standardized methods. UVA Protection Factor has standardized methods. There is still no universally accepted international standard equivalent to SPF for visible-light protection.

A 2026 international consensus panel specifically concluded that agreed standardized methods for assessing visible-light photoprotection remain lacking. Methods called Visible Light Protection Factor or Pigmentation Protection Factor have been proposed, but different investigators use different light sources, wavelengths, doses and pigmentary endpoints.

A label saying “visible-light protection” or “blue-light protection” cannot presently be interpreted like SPF 50 or UVA-PF 20.

For dermatologists, the sensible question is not simply whether iron oxide appears in the ingredient list, but whether the finished formulation has actually been tested against visible-light-induced pigmentation. Ideally, this should involve in-vivo exposure to solar-simulated visible light, roughly 400–700 nm, with objective colour measurement such as the Individual Typology Angle (ITA°). A reported visible-light protection factor can be useful, but unlike SPF or UVA-PF, there is still no universally standardized visible-light rating. In-vitro visible-light transmission testing can provide supporting evidence, but clinical pigmentation testing of the finished product is stronger.

The Indian problem: the tint itself

Scientifically, tinted iron-oxide sunscreens make excellent sense for melasma and pigmentation-prone darker skin. Cosmetically, they can fail for a much simpler reason: the shade looks wrong.

A tint that blends beautifully on one complexion may look grey, pink, orange, pale or obviously made-up on another. In India, with its enormous range of skin colours and undertones, that matters. Yet there is surprisingly little high-quality evidence on shade acceptability across Indian, particularly South Indian, skin.

And this is not a trivial cosmetic issue. If a patient dislikes the way the sunscreen looks, they will apply less, apply it less often, or stop using it altogether.

The best visible-light protection is useless if the patient will not wear it.

So for melasma and post-inflammatory pigmentation, high UVB and UVA protection remain essential, and iron oxides add meaningful visible-light protection. But the formulation must also be cosmetically acceptable enough to be used properly.

Which leads to the bigger question: If the goal is to stop UVB, UVA and visible light from reaching the skin, are increasingly sophisticated sunscreens really the most reliable answer?

Part 4 asks whether the best sunscreen may, in fact, be something much simpler: A piece of cloth.

References

1. Mahmoud BH, Ruvolo E, Hexsel CL, et al. Impact of long-wavelength UVA and visible light on melanocompetent skin. J Invest Dermatol. 2010;130:2092–2097. doi:10.1038/jid.2010.95. Supported in part by an unrestricted grant from Johnson & Johnson Consumer Companies.

2. Duteil L, Cardot-Leccia N, Queille-Roussel C, et al. Differences in visible light-induced pigmentation according to wavelengths: a clinical and histological study in comparison with UVB exposure. Pigment Cell Melanoma Res. 2014;27:822–826. doi:10.1111/pcmr.12273.

3. Kohli I, Chaowattanapanit S, Mohammad TF, et al. Synergistic effects of long-wavelength ultraviolet A1 and visible light on pigmentation and erythema. Br J Dermatol. 2018;178:1173–1180. doi:10.1111/bjd.15940.

4. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35–42. doi:10.1111/phpp.12086. No conflicts declared; funded by the investigators’ dermatology department.

5. Dumbuya H, Grimes PE, Lynch S, et al. Impact of iron-oxide-containing formulations against visible light-induced skin pigmentation in skin of color individuals. J Drugs Dermatol. 2020;19:712–717. doi:10.36849/JDD.2020.5032. Seven of eight authors were affiliated with L’Oréal Research and Innovation.

6. Passeron T, et al. International modified Delphi consensus statement on visible light photoprotection: effects, measurement, and recommendations. J Invest Dermatol. 2026;146:2094–2104.e2. doi:10.1016/j.jid.2026.03.012.

7. Ceresnie MS, Patel J, Lim HW, Kohli I. The cutaneous effects of blue light from electronic devices: a systematic review with health hazard identification. Photochem Photobiol Sci. 2022. PMID:36245016.

• Role of serum IgE testing in the diagnosis and management of a patient with atopy/ urticaria/ skin rash.

• Role of specific IgE (RAST) tests in the diagnosis and management of a patient with atopy/ urticaria/ skin rash.

• How accurately does skin-prick testing predict true food allergy?

• The patient has high specific IgE levels to pollen and house-dust-mite! What next?

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One of the most common investigations requested in patients with eczema, urticaria and suspected allergy is an total serum IgE, followed increasingly by large panels of allergen-specific IgE tests or skin-prick testing. The logic seems simple: Type I allergy is driven by IgE, so check the IgE. If it is high, test for specific foods or airborne allergens to find out what the patient is allergic to and then avoid or treat the cause.

The problem is that this approach often creates more confusion than clarity. A high total IgE does not prove that the patient’s symptoms are due to allergy, and a positive specific IgE test does not necessarily mean that allergen is actually causing the problem. Let us look into this in a bit more detail….

Sensitisation and clinical allergy are not the same

A person may have IgE antibodies against an allergen, such as pollen, but have no symptoms at all when exposed to it. In that situation, the person is sensitised to pollen, but is not clinically allergic to it. The positive test is simply showing that the immune system recognises pollen; it does not prove that pollen is causing disease.

Clinical allergy means that exposure to that allergen actually produces symptoms, for example repeated sneezing, nasal blockage and watering of the eyes after pollen exposure.

The reverse is also important. A low or even negative blood specific-IgE result does not always exclude a clinically relevant reaction. Blood tests are not perfectly sensitive, and in some conditions the allergic response may occur mainly within the affected tissue rather than being clearly detectable in the blood. In addition, not every reaction that patients call an “allergy” is driven by IgE at all.

The key question is therefore not simply, “Is the test positive?” but “Does exposure to this allergen actually reproduce the patient’s symptoms?”

The Total IgE Trap

A patient with atopic dermatitis gets a total IgE test. The result is 800, 2,000 or even several thousand IU/mL. The next question is almost inevitable:

“Doctor, how do I bring my IgE down?”

The patient may subsequently improve considerably, but the IgE remains high. Another test is done. It is still abnormal. Soon, the patient (and sometimes the doctor too) starts chasing the IgE number rather than the eczema.

Total IgE is frequently elevated in atopic dermatitis, but it is not a reliable measure of disease activity in an individual patient. Population studies may show associations between higher IgE and more severe atopic disease, but the relationship is inconsistent. Severe eczema can occur with normal IgE, while someone with very high IgE may have little active disease.[1,2]

Then Comes the “Allergy Panel”

Once a high IgE is discovered, the next temptation is to test against everything available: milk, egg, wheat, nuts, prawns, dust mite, pollen, fungi, pets and numerous other allergens. Several may come back positive. The patient then receives a long list of foods and environmental exposures to avoid.

But specific IgE, historically called “RAST”, and skin-prick testing primarily detect sensitisation. Highly atopic patients commonly show multiple sensitizations, many of which may have little or no clinical relevance.[3,4]

The Angry Person Analogy

I sometimes explain this using a simple analogy. Imagine somebody who is already extremely irritable. Ten people approach him during the day and he snaps at almost everyone. It would be unreasonable to conclude that all ten people had done something wrong. The common factor may simply be that the person was already angry.

Now imagine somebody who is calm with everyone but repeatedly becomes angry whenever one particular person appears. That particular relationship deserves much closer attention.

This is only an analogy, not a description of immunology. But it illustrates why a highly atopic patient with weak positivity to numerous allergens should make us more cautious, not more convinced that every positive result represents disease.

A laboratory can therefore produce a technically correct positive result while telling us very little about what is actually causing the patient’s symptoms.

When Do I Use Specific IgE?

Almost never as a routine test.

Suppose a patient tells me: “Every time I eat prawns, within 20 minutes I develop urticaria and swelling.” That is a very convincing history of an immediate allergic reaction. If it is clear, reproducible and the patient is already avoiding prawns, what exactly will a prawn-specific IgE test add?

If the test comes back negative, am I going to tell the patient to eat prawns again? Of course not.

At the other extreme, suppose the patient is regularly eating prawns without any symptoms at all. Then finding a positive prawn-specific IgE is also unlikely to help. It may simply show sensitisation, not clinical allergy.

True IgE-mediated, or Type I, food allergy usually produces symptoms within minutes to about 1–2 hours of eating the food. These may include urticaria, angioedema, itching, vomiting, abdominal pain, wheeze, breathlessness or, in severe cases, anaphylaxis. The same principle applies to inhaled allergens: there should be a believable relationship between exposure and symptoms.

So if a patient eats a particular food repeatedly without any such reaction, a positive blood test should not suddenly make us label that food as the cause of unrelated chronic symptoms.

A test should answer an unresolved clinical question. If the history has already established the diagnosis, or clearly argues against it, testing adds little and may actually create unnecessary dietary restrictions, anxiety and confusion.

Skin-Prick Testing Has the Same Problem

A skin-prick test demonstrates that the skin reacts to an allergen extract. That is not identical to eating the food. Foods may be cooked, processed, digested and absorbed. Commercial extracts do not perfectly reproduce every relevant exposure, and cross-reactive proteins can produce positive results without clinically important food allergy.[5]

Therefore, a patient may have a positive prick test yet eat the food without symptoms. Conversely, no sensitisation test is sufficiently perfect to replace the clinical history.

Also read:

A Food Diary Often Tells Me More

In routine dermatology practice, I often find a careful food and symptom diary more useful than an indiscriminate allergy panel.“I think milk worsens my eczema” is weak evidence.

But repeatedly documenting the same reaction following the same food, with an appropriate temporal relationship, deserves attention. This is particularly useful for immediate reactions such as urticaria, angioedema, vomiting or wheezing.

Eczema is more difficult because atopic dermatitis naturally waxes and wanes. Patients can easily attribute a flare to something they ate earlier that day when the association is coincidental. This is one reason broad food panels and unnecessary elimination diets in atopic dermatitis are discouraged.[4]

The diary is not itself a definitive allergy test. Its value is that it helps identify whether there is actually a plausible allergen worth investigating.

When There Is Genuine Doubt, Challenge the Food

When food allergy remains genuinely uncertain, the medically supervised oral food challenge remains the reference diagnostic procedure for IgE-mediated food allergy.[5]

It asks the clinically important question directly: Does eating this food actually produce symptoms?

Specific IgE and skin-prick testing can sometimes help decide which food deserves further evaluation when several possibilities exist. But when the history and laboratory results disagree, repeatedly ordering more allergy tests does not necessarily resolve the problem. A properly supervised food challenge often can. It is, of course, not something to be attempted casually or at home when a significant immediate reaction is possible.

Chronic Urticaria: Stop Hunting for the Mystery Allergen

Chronic spontaneous urticaria (CSU) is probably one of the most over-investigated conditions in this area.Patients naturally assume that recurrent wheals must mean they are allergic to something they are eating, inhaling or touching. Usually, that is not the explanation.

The 2026 international urticaria guideline recognises CSU as a mast-cell-driven disease with important autoimmune mechanisms. IgE-mediated food allergy is extremely rarely its underlying cause, and extensive searches for foods, pollens or dust mites are not part of the routine work-up.[6]

This does not mean IgE biology is irrelevant to CSU. Autoimmune mechanisms involving IgE or its high-affinity receptor may contribute to particular CSU endotypes. But this is very different from saying that an external food, pollen or dust-mite allergen is causing the disease.

The sensible approach is to diagnose and treat the urticaria rather than spend months searching for a mystery allergen.

What About Pollen and Dust Mites?

The same question of actionability applies to airborne allergens. If pollen testing is positive in India, what practical intervention follows?

Pollen is predominantly an ambient environmental exposure. Most patients are not exposed because they keep one offending flowerpot at home. Complete avoidance is usually unrealistic.

Dust-mite testing presents a similar problem. Positive results may lead to expensive covers, mattress changes, extensive cleaning and attempts to modify the home environment.

Yet a 2025 meta-analysis of 17 randomized trials found that dust-mite avoidance measures could reduce environmental dust and Der 1 allergen levels without producing convincing improvement in asthma, allergic rhinitis or quality of life.[7]

There are selected patients with clear respiratory allergy in whom identifying a specific aeroallergen is worthwhile, particularly if allergen immunotherapy is genuinely being considered. But this is a targeted indication. It does not justify routine “airborne allergy panels”.

Is There ever Any Role for Total IgE?

Yes, but in specific situations. In severe allergic asthma, pretreatment total IgE is used together with body weight to determine whether the patient falls within the approved omalizumab dosing range and to calculate the dose. Importantly, this is a dosing convention, not evidence that IgE reflects asthma severity or predicts treatment response. Inface baseline IgE does not predict the likelihood of response once a patient is eligible for omalizumab.[8]

In chronic spontaneous urticaria, omalizumab dosing does not depend on total IgE. Baseline IgE may provide some information about disease endotype and probability of treatment response, but its predictive accuracy for an individual patient remains limited.[6]

These are specialised uses of IgE as a biomarker. They are completely different from trying to “bring the IgE down” to treat eczema.

What I Actually Do

In routine dermatology practice, I hardly ever request total IgE to monitor eczema.

I do not routinely send patients with chronic spontaneous urticaria for specific-IgE panels or skin-prick testing.

If a patient has a clear, reproducible reaction to a particular food and is already avoiding it, I generally do not test simply to confirm what the history has already established.

I consider targeted specific-IgE or skin-prick testing mainly when there is genuine diagnostic uncertainty, especially when several potential allergens are involved.

And when it genuinely matters to establish whether a suspected food causes clinical allergy, the medically supervised oral food challenge remains the reference test.

That is very different from: “Let us test everything and see what comes back positive.”

References

1. Dhar S, De A, Rajgopalan M, et al. Skin Allergy Research Society and Society for Eczema Studies Joint Task Force Guidelines of Care for Management of Atopic Dermatitis for Adults, Children, and Special Populations in India: An Evidence-Based Review and an Expert Consensus. Indian J Dermatol. 2026;71(3):204-230. doi:10.4103/ijd.ijd_421_25.

2. Renert-Yuval Y, Thyssen JP, Bissonnette R, et al. Biomarkers in atopic dermatitis: a review on behalf of the International Eczema Council. J Allergy Clin Immunol. 2021;147(4):1174-1190.e1. doi:10.1016/j.jaci.2021.01.013.

3. Ansotegui IJ, Melioli G, Canonica GW, et al. IgE allergy diagnostics and other relevant tests in allergy: a World Allergy Organization position paper. World Allergy Organ J. 2020;13(2):100080. doi:10.1016/j.waojou.2019.100080.

4. Chu DK, Schneider L, Asiniwasis RN, et al. Atopic dermatitis (eczema) guidelines: 2023 American Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters GRADE- and Institute of Medicine-based recommendations. Ann Allergy Asthma Immunol. 2024;132(3):274-312. doi:10.1016/j.anai.2023.11.009.

5. Santos AF, Riggioni C, Agache I, et al. EAACI guidelines on the diagnosis of IgE-mediated food allergy. Allergy. 2023;78(12):3057-3076. doi:10.1111/all.15902.

6. Zuberbier T, Ansari ZA, Abdul Latiff AH, et al. The International Guideline for the Definition, Classification, Diagnosis and Management of Urticaria. Allergy. 2026;81(8):2582-2632. doi:10.1111/all.70210.

7. Sobczak M, Kowal K, Pawliczak R. Are There Effective Methods to Reduce Exposure to House Dust Mite Allergens? A Meta-Analysis of Randomized Clinical Trials. Int Forum Allergy Rhinol. 2025;15(8):792-802. doi:10.1002/alr.23565.

8. Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention. 2026 update.n.648.

At almost every major medical conference now, one can recognise the AI-assisted slide. Beautifully structured, neatly boxed, grammatically perfect and extraordinarily comprehensive. Pathogenesis, clinical features, investigations, histology and treatment somehow coexist on the same screen. Increasingly, even experienced and otherwise excellent speakers are using Claude, ChatGPT and similar tools to prepare presentations. There is absolutely nothing wrong with that. AI should be encouraged. It can organise our thoughts, identify gaps, simplify complicated concepts and produce excellent illustrations.

The problem begins when we assume that everything AI produces deserves to appear on the slide.

When we prepared presentations manually, adding information required effort and there was a natural tendency to stop. AI has made generating more content almost effortless.

That is not a defect of AI; it is an editing failure by the speaker.

For an ordinary live conference presentation, a slide usually needs only a few important points, perhaps two to five. If the renal manifestations deserve discussion, give them another slide. If the histology matters, show it separately. You are not removing information. You are controlling when the audience receives it.

Same information. Different purpose: one is a reference page; the other is a presentation slide.

Dense slides are only half the problem. The other half has nothing to do with AI and existed long before it: speakers reading the text on their slides aloud. If the audience can see the sentence, they do not need us to read it to them. They can read a textbook themselves. Today, they can also ask an AI model for a perfectly competent summary before the session has even started.

They came to hear what the speaker adds: interpretation, experience, disagreement, emphasis, humour and judgement.

The slide should largely be a cue for what you want to discuss, not a teleprompter containing everything you intend to say.

AI-generated illustrations need the same restraint. A beautiful diagram can quickly become useless when every structure, pathway and arrow is labelled. If an image contains several important ideas, divide it across several slides and reveal them sequentially. Minimal labelling usually works better because the explanation should come from the speaker.

This is a beautiful slide. But how much can the audience take in?

The same pathway, presented two ways. AI can generate a beautiful, information-rich diagram, but for a live talk, minimal labelling and a simple sequential pathway make the message easier to follow.

When generating text slides, Instead of asking, “Make a slide on cryoglobulinaemic vasculitis,” try asking, “What are the four things I want a dermatologist to remember six months after this talk?” Or paste a crowded slide back into the AI and ask it what can safely be removed and explained verbally. The technology is very good at producing information. The increasingly important human skill is deciding what not to show.

AI can generate the material. Selection remains the speaker’s job.

“The audience has not come to see what you asked Claude. They have come to hear what you think about the answer.”

• What does PA++++ actually tell us?

• How different are PA+++ and PA++++?

• Can two PA++++ sunscreens provide very different levels of UVA protection?

• Is a five-star Boots rating the same as high UVA protection?

• Why is the actual UVA Protection Factor rarely printed on sunscreen labels?

• Can we calculate how long somebody can remain outdoors without tanning?

• Does one short exposure matter if it causes no visible tanning?

• What matters more for everyday pigmentation: one large exposure or small repeated exposures over many days?

• Is sunlight before 9 AM or after 4 PM really safe from tanning?

If sunburn is the concern, SPF is extremely useful. I have already discussed this recently in Part 1 of this series……

But if tanning, melasma or pigmentation is the concern, another part of sunlight becomes increasingly important: UVA, or ultraviolet A radiation.

UVA occupies wavelengths from approximately 320 to 400 nanometres and penetrates more deeply into the skin than UVB. It contributes importantly to immediate pigment darkening, persistent pigmentation, photoageing and several photodermatoses.

For someone concerned about pigmentation, the most useful numerical measure would therefore be the UVA Protection Factor, or UVA-PF.

What is UVA-PF?

UVA-PF is conceptually similar to SPF. Instead of asking how much radiation is required to produce sunburn, UVA-PF compares the UVA dose required to produce a defined pigment-darkening response on sunscreen-protected skin with that required on unprotected skin.

A UVA-PF of 20 means that approximately 20 times the UVA dose is required to produce that laboratory pigmentation endpoint. A UVA-PF of 40 represents twice that measured protection factor. Unfortunately, the actual numerical UVA-PF is rarely displayed prominently on sunscreen labels. Instead, we usually see the PA system.

This immediately explains an important point about PA+++ versus PA++++. The minimum UVA-PF required for PA++++ is twice the minimum required for PA+++: 16 versus 8. But that does not mean that every PA++++ sunscreen provides twice the UVA protection of every PA+++ sunscreen.

Consider two products:

• UVA-PF 15 = PA+++

• UVA-PF 16 = PA++++

They fall into different PA categories despite having very similar measured UVA protection. Now consider another sunscreen with a UVA-PF of 40. It is also simply labelled PA++++. So PA++++ tells us that a sunscreen has crossed a minimum UVA-protection threshold. It does not tell us how far beyond that threshold the product has gone.

That is the fundamental limitation of the PA system: the plus signs tell us which category the sunscreen has reached, not its actual UVA Protection Factor.

Not all PA++++ sunscreens are equal

A 2026 study illustrates this particularly well. Researchers measured UVA-PF in 38 commercial SPF 50 or SPF 50+ sunscreens using the same standardised in-vivo method. UVA-PF values ranged from 3.6 to 46.6, with an average of 21.4. Five products exceeded a UVA-PF of 30. Yet only a minority displayed a numerical UVA value on their packaging.

This means that products carrying apparently similar high-SPF labels can differ substantially in their measured UVA protection.

And what are Boots stars?

The Boots star system does not measure UVA-PF. Instead, it is essentially a spectral balance rating. It compares the average absorbance of a sunscreen across the UVA range with that across the UVB range, before and after irradiation.

A high star rating therefore means that the sunscreen’s UVA protection is reasonably well balanced relative to its UVB protection. But it does not tell us the absolute strength of that UVA protection.

A five-star sunscreen does not mean:

• UVA-PF 50

• 99% UVA protection

• that it provides more UVA protection than another five-star sunscreen

• that it necessarily provides better UVA protection than a lower-star product

If your main concern is melasma, tanning, pigmentation or photoageing, the question you really want answered is: How much UVA protection am I actually getting?

For that, numerical UVA-PF is the most informative measure, followed by the PA system, which at least places UVA-PF into defined categories. The Boots star rating does not answer that question.

So the practical message is simple: If strong UVA protection is your priority, do not choose a sunscreen based on Boots stars. Follow the UVA-PF, or at least the PA rating, instead.

Why “How long before I tan?” is the wrong question

This is where pigmentation differs markedly from sunburn. Sunburn is an acute endpoint. After sufficient UVB exposure, erythema develops. SPF testing can therefore compare the radiation dose required to produce that defined endpoint on protected and unprotected skin.

Pigmentation is more complicated. Studies can measure a minimal melanogenic dose, meaning the smallest single UVA exposure capable of producing a detectable pigmentary response. In Asian skin phototypes III and IV, average values in one study were approximately 4.1 and 4.9 J/cm², respectively.

To put that into perspective, measurements from Coimbatore in July found UVA irradiance of about 6.4 mW/cm² at noon. At that intensity, a UVA dose of 4.1–4.9 J/cm² would accumulate in only about 11–13 minutes.

This does not mean that everyone will visibly tan after 11–13 minutes. It simply shows how quickly a UVA dose comparable to experimentally measured melanogenic doses can accumulate in Indian midday sunlight.

But that does not mean someone will necessarily look visibly tanned after a single 10- or 20-minute exposure. There are two important reasons.

First, experimental investigators can detect small pigmentary changes that may not yet be obvious to someone looking in the mirror.

Second, and more importantly, repeated exposure changes the biology.

Small exposures add up

One particularly useful study repeatedly exposed volunteers to fractions of their individual single-exposure tanning threshold. Some received only 20%, 40%, 60% or 80% of the UVA dose that would ordinarily be required to produce pigmentation after a single exposure. These apparently “subthreshold” doses still produced pigmentation when repeated.

After six exposures, the UVA dose required per exposure to produce pigmentation was roughly half the single-exposure threshold. After twelve exposures, it was roughly one-third. Pigmentation accumulated progressively and approached its maximum over approximately 15–19 days.

This is much closer to everyday life than a single laboratory exposure. Someone may spend a modest amount of time outdoors each morning and notice no obvious change on any individual day. After ten or fifteen days, however, the cumulative effect may become visible.

No visible tan after today’s exposure does not mean today’s exposure contributed nothing to next week’s tan.

This is why converting UVA-PF into statements such as “you can remain in the sun 16 times longer without tanning” is scientifically misleading.

UVA-PF describes protection against a defined laboratory pigmentation endpoint under controlled conditions. Everyday pigmentation reflects repeated UVA exposure, UVB-driven delayed melanogenesis, visible light, individual skin biology and the cumulative effects of multiple exposures.

What about early morning and evening?

Another common belief is that sunlight before 9 AM and after 4 PM is harmless. These periods certainly contain less total ultraviolet radiation than midday, particularly less UVB. But UVA does not fall as dramatically as UVB when the sun is lower in the sky.

Measurements from Coimbatore showed that meaningful UVA exposure remained during the morning and afternoon, while sunlight became proportionately more UVA-rich as UVB declined.

So early-morning and late-afternoon sunlight means lower exposure, not zero pigmentation exposure.

Again, cumulative exposure matters. Twenty minutes on one morning may produce no visible change. Twenty minutes every morning for several weeks is a very different biological situation.

The more useful question

For pigmentation, asking: “How long can I stay in the sun before I tan?” may therefore be the wrong way to think about sunscreen protection.

A more useful question is: How much cumulative UVA exposure am I receiving over days and weeks, and how much of it is my sunscreen actually reducing?

That is the question the next parts of this series will build on…..

References

1. Japan Cosmetic Industry Association. Standards for Sun Protection Factor, UVA Protection Grade and Water Resistance. PA+: UVA-PF 2 to <4; PA++: 4 to <8; PA+++: 8 to <16; PA++++: ≥16.

2. Young AR, Tricaud C, Bernerd F, et al. In Vivo Measurement of UVA Protection Factor Across 38 Different SPF 50 and SPF 50+ Sunscreens Reveals High Heterogeneity and Limitations in the Level of Protection. Photodermatol Photoimmunol Photomed. 2026;42:e70092. doi:10.1111/phpp.70092.

3. Ravnbak MH, Philipsen PA, Wiegell SR, Wulf HC. Skin pigmentation kinetics after exposure to ultraviolet A. Acta Derm Venereol. 2009;89:357-363. doi:10.2340/00015555-0635.

4. Wong LC, Jamil A, Md Nor N. The effect of pre-phototest sun exposure on minimal erythema dose and minimal melanogenic dose among skin phototypes III, IV and V. Photodermatol Photoimmunol Photomed. 2018;34:400-404. doi:10.1111/phpp.12410.

5. Balasaraswathy P, Kumar U, Srinivas CR, Nair S. UVA and UVB in sunlight: optimal utilization of UV rays in sunlight for phototherapy. Indian J Dermatol Venereol Leprol. 2002;68:198-201.

Most people choose sunscreen by one number: SPF, or Sun Protection Factor. It is commonly explained by saying that SPF 30 blocks about 97% of ultraviolet B radiation, SPF 50 about 98%, and SPF 100 about 99%. Those figures make SPF 30, 50 and 100 sound almost identical.

But that explanation is incomplete.

What does SPF actually measure?

SPF is not fundamentally a measurement of the percentage of ultraviolet B photons blocked. It is a biological protection factor based on sunburn.

In standardized testing, sunscreen is applied at 2 mg/cm². Researchers then determine the ultraviolet dose required to produce minimal visible redness, or erythema, on protected skin and compare it with the dose required on unprotected skin. ISO 24444 standard specifically defines SPF as protection against erythema (redness) induced by solar ultraviolet radiation. The US Food and Drug Administration similarly defines SPF according to the amount of solar ultraviolet energy required to produce sunburn on protected versus unprotected skin.

So, conceptually:

SPF = UV dose required to produce erythema with sunscreen ÷ UV dose required without sunscreen.

An SPF 30 sunscreen therefore requires approximately 30 times the erythemally effective ultraviolet dose to reach the same sunburn endpoint under laboratory conditions. SPF 50 means approximately 50 times the dose; SPF 100, approximately 100 times.

Because sunburn is driven predominantly by ultraviolet B radiation, SPF primarily reflects UVB protection, although the test is not literally a measurement of the percentage of all UVB wavelengths being blocked.

So where do 97%, 98% and 99% come from?

They are essentially a mathematical translation of the protection factor.

If SPF 30 means that approximately one-thirtieth of the erythemally effective dose remains, then:

Another way to understand SPF is to look at how much sunburn-causing ultraviolet radiation still gets through.

In simple terms, SPF 30 lets through about 3.3% of the sunburn-causing UV, SPF 50 about 2%, and SPF 100 about 1%. That is why SPF 50 and SPF 100 may look similar when described as “98% versus 99% protection,” but SPF 100 actually allows only half as much residual sunburn-causing UV through as SPF 50.

This is the origin of the familiar statement that SPF 30 “blocks 97%” and SPF 50 “blocks 98%”. The American Academy of Dermatology itself uses this simplified language for public education.

But scientifically, it is better to say “approximately 96.7% attenuation of erythemally effective UV under the assumptions of the SPF model” rather than “97% of UVB photons are blocked”.

The distinction matters.

Why SPF 50 and SPF 100 are not almost identical

If we describe protection as percentages, SPF 50 and SPF 100 look very similar:

98% versus 99%.

But look instead at what gets through:

SPF 50 leaves approximately 2% of the erythemally effective dose.

SPF 100 leaves approximately 1%.

The residual dose has therefore been halved.

The difference between SPF 50 and SPF 100 is not merely “one percentage point”. SPF 100 represents twice the protection factor and approximately half the residual erythemally effective exposure.

Under constant laboratory irradiance, SPF 100 would require approximately twice the ultraviolet dose to reach the same erythema endpoint as SPF 50.

This should not be interpreted literally as “SPF 100 lets you stay in the sun twice as long”. The Food and Drug Administration specifically cautions against converting SPF directly into clock time because solar intensity varies enormously with latitude, season, cloud cover and time of day. Sunscreen is also rubbed, sweated and wiped away.

Does this difference matter in real life?

Apparently, yes, at least for sunburn.

In a randomized split-face natural-sunlight study of 199 adults exposed outdoors for an average of 6.1 hours, 55.3% were judged more sunburned on the SPF 50+ side compared with only 5% on the SPF 100+ side.

A later five-day beach study found a similar difference: 56% had greater sunburn on the SPF 50+ side compared with 7% on the SPF 100+ side.

Both studies were supported by Johnson & Johnson Consumer Inc., and company employees were among the investigators. That potential conflict should be acknowledged. More importantly, these studies measured erythema or sunburn. They did not demonstrate that SPF 100 is twice as good as SPF 50 for preventing tanning, melasma, photoageing or skin cancer.

That distinction is crucial.

Then why is SPF 30 usually considered enough?

Because SPF 30 already provides substantial protection against sunburn when it is applied properly. It remains a reasonable minimum recommendation for routine photoprotection.

But “SPF 30 is adequate for most situations” is quite different from saying “SPF 30, 50 and 100 are practically identical”.

Higher SPF also provides some margin for the fact that people rarely reproduce laboratory conditions. Sunscreens are tested at approximately 2 mg/cm², while real-world application is usually considerably lower and often uneven. The American Academy of Dermatology specifically notes that higher SPF can help compensate partly for underapplication. It does not, however, last longer simply because the SPF number is higher; outdoor reapplication is still required.

But what if the concern is tanning rather than sunburn?

This is where SPF becomes much less satisfactory as the only number used to choose sunscreen.

SPF is based on an erythema endpoint and therefore predominantly reflects protection against UVB. UVB remains important in Indian skin because it contributes to DNA damage, delayed melanogenesis and several photodermatoses. Sunburn is also not absent in Indian skin, although it is less readily produced and may be less conspicuous in more deeply pigmented phototypes.

But many Indian patients are not buying sunscreen primarily to avoid sunburn. They are buying it because they do not want to become darker.

For that purpose, ultraviolet A radiation, or UVA, becomes particularly important.

An SPF 100 sunscreen may protect very well against sunburn but still offer less UVA protection than some SPF 50+ sunscreens.

SPF is a sunburn protection factor. It should not be mistaken for an anti-tanning protection factor.

That takes us to Part 2, and to the number I would much rather know when treating pigmentation: the actual UVA Protection Factor.

References

1. International Organization for Standardization. ISO 24444:2019. Cosmetics — Sun protection test methods — In vivo determination of the sun protection factor (SPF).

2. US Food and Drug Administration. Sun Protection Factor (SPF). SPF is defined according to the amount of solar ultraviolet energy required to produce sunburn on protected versus unprotected skin.

3. Williams JD, Maitra P, Atillasoy E, et al. SPF 100+ sunscreen is more protective against sunburn than SPF 50+ in actual use: results of a randomized, double-blind, split-face, natural sunlight exposure clinical trial. J Am Acad Dermatol. 2018;78:902-910.e2. doi:10.1016/j.jaad.2017.12.062. Supported by Johnson & Johnson Consumer Inc.

4. Kohli I, Nicholson CL, Williams JD, et al. Greater efficacy of SPF 100+ sunscreen compared with SPF 50+ in sunburn prevention during 5 consecutive days of sunlight exposure: a randomized, double-blind clinical trial. J Am Acad Dermatol. 2020;82:869-877. doi:10.1016/j.jaad.2019.09.018. Supported by Johnson & Johnson Consumer Inc.

5. Petersen B, Wulf HC. Application of sunscreen: theory and reality. Photodermatol Photoimmunol Photomed. 2014;30:96-101. doi:10.1111/phpp.12099.

Sometimes, a change in the skin is the first visible sign that something is wrong inside.

A lump in the skin that revealed an internal cancer

Early in my career, I treated an 86-year-old woman who had several painless lumps over her neck and upper back.

The lumps looked like a skin problem. But she had also been losing weight and having repeated episodes of diarrhoea.

A biopsy showed that the lumps were actually deposits of an internal cancer that had spread to the skin.

This was a rare case, but it taught me an important lesson:

The skin may sometimes speak before the internal disease becomes obvious.

Fortunately, most skin problems are not signs of cancer or serious internal disease. But certain patterns should make us look beyond the skin.

Diabetes often shows itself through ordinary skin problems

The skin signs of diabetes are usually not the dramatic conditions shown in medical textbooks.

More often, patients come with very common problems such as:

• repeated fungal infections

• itching or infection around the genitals

• recurrent boils

• repeated cellulitis

• wounds that are slow to heal

• severe itching without a clear rash

• foot ulcers or gangrene

A man with repeated redness and itching around the foreskin, or a woman with repeated fungal infection in the groin or genital area, may have undiagnosed or poorly controlled diabetes.

These problems do not automatically mean diabetes. But when they keep returning, checking blood sugar is often sensible.

Some patients say, “My wounds heal well, so I cannot have diabetes.”

That is not a reliable test. Many people with diabetes continue to heal normally, especially in the early stages.

A dark neck may be more than pigmentation

Some people develop dark, thick, velvety skin around the neck, armpits or groin.

This is often linked to the body becoming less responsive to insulin. It is especially common in people who are overweight.

The important clue is not simply the colour. The skin also feels thicker and velvety.

It does not mean that the person definitely has diabetes. But it is a reason to look at weight, waist size, blood pressure, family history and blood sugar.

In children, this should not lead to a large battery of hormone tests. Most overweight children need sensible assessment, healthier eating, more physical activity and blood sugar testing at the appropriate age or when other risk factors are present.

Acne and facial hair do not always mean a hormone problem

Acne is common. A few facial hairs are also common.

Neither automatically means that a woman has a hormonal disorder.

Investigation becomes more useful when there is:

• obvious coarse facial or body hair

• repeatedly irregular periods

• significant scalp hair thinning

• very rapid worsening

• deepening of the voice or other masculine changes

The speed of change is important.

Facial hair that has slowly increased over many years is different from coarse hair appearing suddenly over a few months, together with voice change, muscle development or rapid scalp hair loss.

Sudden changes need prompt investigation. They should not simply be labelled as menopause or polycystic ovarian syndrome.

Sudden yellow bumps may warn of very high blood fats

A sudden outbreak of many small yellowish bumps over the buttocks, elbows or limbs can occasionally indicate extremely high levels of triglycerides—one type of fat in the blood.

This may happen in people with poorly controlled diabetes.

Very high triglycerides can inflame the pancreas and cause severe abdominal pain. In such cases, the skin may provide an early warning of a potentially serious problem.

Hair loss and dry skin may occur with thyroid disease

Hair loss and dry skin are common complaints in people with thyroid disease.

However, they are also extremely common in people without thyroid disease. Stress, ageing, nutritional problems, medicines and genetic hair loss can produce the same symptoms.

Hair loss alone is therefore not proof of a thyroid problem.

Testing is more useful when hair or skin changes occur along with symptoms such as unexplained weight change, unusual tiredness, constipation, palpitations, menstrual changes or intolerance to heat or cold.

Unusual skin darkening can occasionally signal an adrenal problem

A rare condition called Addison’s disease can cause unusual darkening of the skin.

The darkening may be especially visible over the knuckles, gums, scars and skin folds. The person may also have severe tiredness, weight loss, dizziness, vomiting or salt craving.

However, several other conditions—including vitamin B12 deficiency—can produce similar pigmentation.

Pigmentation alone is not enough to make the diagnosis.

Sometimes the treatment causes the internal problem

Steroid creams are widely misused for fungal infections, itching, acne, fairness and even diaper rash.

Some so-called combination, fairness or herbal creams also contain strong steroids without making this clear.

When powerful steroid creams are used over large areas or for long periods, they can enter the bloodstream. This may cause weight gain, a rounded face, acne, stretch marks, high blood pressure, raised blood sugar, muscle weakness and poor growth in children.

Long-term steroid use can also reduce the body’s own production of natural steroid hormones. Suddenly stopping heavy steroid use may therefore be dangerous.

Patients should tell their doctor about every form of steroid they use—not only tablets, but also creams, injections, inhalers and nasal sprays.

Rare skin signs can occasionally protect an entire family

Some rare inherited diseases affect both the skin and hormone-producing organs.

Small lumps on the lips or tongue, unusual facial bumps, multiple fatty lumps or firm skin-coloured nodules may occasionally be clues to inherited conditions linked to thyroid, parathyroid, pituitary or pancreatic tumours.

These conditions are uncommon, and people should not try to diagnose them from internet photographs.

But when the pattern is recognised by a doctor, it may lead to early testing—not only for the patient, but sometimes for close relatives as well.

When should a skin problem raise concern?

A skin problem deserves a closer look when it:

• appears suddenly or spreads rapidly

• keeps returning despite proper treatment

• occurs with unexplained weight loss or severe tiredness

• is associated with repeated infections

• comes with menstrual or rapid hormonal changes

• appears together with unusual thirst or frequent urination

• occurs with abdominal pain or other general symptoms

• is also present in several family members

This does not mean that every rash needs blood tests or scans.

Most skin diseases remain diseases of the skin.

The skill lies in recognising when the skin problem does not fit the usual pattern.

The skin is a clue—not a diagnosis

The skin can reflect changes in blood sugar, hormones, nutrition, circulation, immunity and internal organs.

Sometimes it provides the first warning that something is wrong.

But a skin sign is not a diagnosis by itself. It must be interpreted along with the person’s symptoms, medical history and carefully chosen tests.

The skin may be the mirror of internal health—but the reflection still needs to be interpreted correctly.

A patient recently came to see me with persistent facial pain, tenderness and swelling, two months after having Endolift elsewhere. The symptoms were maximal over the cheekbone region — the same area where she had received dermal filler roughly two years earlier.

That association is interesting. It does not establish causation. The possibilities remain open: a delayed inflammatory reaction involving the old filler, thermal alteration of pre-existing filler, infection, or a direct complication of Endolift. I have not yet concluded which.

But it made me look closely at Endolift. How good is the evidence that it actually tightens skin? What do we know about applying thermal energy where filler may already exist? And perhaps most practically: is it actually better than fractional CO₂ laser, which we already know remodels collagen?

What exactly is Endolift?

Endolift uses a 1470-nm diode laser delivered through a very fine optical fibre inserted beneath the skin. The aim is to heat deep dermal and superficial subcutaneous tissue, producing collagen remodelling and, depending on treatment depth and energy, some effect on superficial fat.

Calling it a “non-surgical facelift” is generous. There is no dissection or repositioning of tissue, and a laser fibre is physically being passed under the skin. Minimally invasive laser treatment is less glamorous but more accurate.

Does it work?

Probably — but the evidence is much thinner than the advertising.

A 2022 study involving 96 patients reported improvement in lower-face laxity after Endolift, with follow-up extending to 18 months. However, there was no untreated or sham-Endolift group, and the outcome depended largely on clinical ptosis grading rather than objective three-dimensional measurement.[1]

A 2024 systematic review of 23 studies was broadly favourable, while acknowledging that most of the evidence was lower-level observational research.[2] A more critical systematic review in 2025 found only seven eligible studies and reported high risk of bias, inconsistent treatment parameters and inadequate safety data. The authors concluded that confidently establishing efficacy and safety remains difficult.[3]

There is genuine biological evidence. A 2025 human histological study found increased dermal thickness and collagen deposition after subdermal 1470-nm laser treatment at moderate energy settings. At the highest energy tested, however, collagen fragmentation and poorer elastin organisation appeared.[4]

In laser medicine, apparently, more cooking does not necessarily improve the dish.

But fractional CO₂ already stimulates collagen

This is the comparison I find more interesting.

“Stimulates collagen” is often presented as though it were some special property of Endolift. It isn’t.

Fractional CO₂ has considerably more established evidence for dermal remodelling. In a prospective study, Naouri and colleagues objectively measured skin mechanical properties using a Cutometer before and after fractional CO₂ resurfacing. Elasticity improved by 5.9%, with significant improvements in several other biomechanical parameters.[5]

Even more persuasive is a split-face human histology study. Sixteen women received fractional CO₂ treatment to one periorbital side before blepharoplasty, while the opposite side served as an untreated control. Histology showed significantly greater type I and type III collagen on the treated side.[6]

So if the argument for Endolift is simply:

“It heats tissue, stimulates collagen and tightens skin,”

fractional CO₂ can reasonably reply:

“Welcome to the club.”

Is Endolift actually better than fractional CO₂?

Here the answer is remarkably simple.

We do not know.

I could find no head-to-head randomized trial showing that Endolift produces greater tightening than fractional CO₂, no comparative histological study showing greater collagen production, and no convincing evidence that its results last longer.

Endolift does have a plausible anatomical advantage. Because the fibre is passed beneath the skin, it can deliver energy to superficial fat and fibrous septa that fractional CO₂ cannot directly reach. That may prove useful for some patients with lower-face heaviness or jowling.

But that is a theoretical advantage based on treatment depth, not demonstrated clinical superiority.

For wrinkles, photodamage, texture and dermal collagen remodelling, fractional CO₂ has the more mature and objectively measured evidence base.

And what if there is already filler there?

This is where my patient’s presentation becomes particularly relevant.

Hyaluronic-acid filler is not thermally inert. A 2024 review found that energy-based treatments can alter HA filler degradation, depending on the device, depth, energy, filler characteristics and treatment timing.[7]

Delayed inflammatory reactions to HA filler are also recognised. Published incidence estimates vary substantially — roughly 0.3% to 4.25% has been reported — and reactions may present with swelling, tenderness or nodules months after injection. Immune stimulation and local trauma are among the proposed triggers.[8,9]

Most importantly, I could find no published study specifically examining Endolift performed through or adjacent to pre-existing HA filler.

That does not prove that Endolift caused my patient’s symptoms.

It means we do not know.

And “we don’t know” should never quietly turn into “there is no risk”.

What about the FDA?

The laser platform used for Endolift has US FDA 510(k) clearance as a Class II surgical laser, including for soft-tissue applications and laser-assisted lipolysis.

That does not mean the FDA has clinically proven Endolift to be a “non-surgical facelift”. The FDA’s 2026 clearance documentation specifically states that clinical performance data were not required to establish substantial equivalence.

“FDA-cleared laser platform” is accurate.

“FDA-approved non-surgical facelift” has clearly spent some time with the marketing department.

Am I missing out by not offering Endolift?

At present, I don’t think the evidence says that I am.

I already use fractional CO₂ laser when dermal remodelling, wrinkles and skin tightening are appropriate treatment goals. It has objective biomechanical evidence, controlled human histological evidence and a much longer clinical track record.

That does not make Endolift useless. Its deeper treatment plane may eventually prove advantageous in selected patients, particularly where superficial fat and subcutaneous structures contribute to laxity.

But the burden of proof should be on a newer procedure to demonstrate that it offers something meaningfully better than treatments we already have.

At present, Endolift has not done that.

The bottom line

Endolift is an interesting technology with a credible biological effect and preliminary evidence of tightening. It should not be dismissed.

But there is currently no hard evidence that it tightens skin better than fractional CO₂ laser, while fractional CO₂ has the stronger evidence base for objective dermal collagen remodelling.

Endolift may eventually establish a useful niche because it works at a deeper anatomical level. Until comparative trials demonstrate that advantage clinically, buying another expensive machine simply because it “stimulates collagen” is difficult to justify scientifically.

My CO₂ laser already knows that trick.

References

1. Longo L, Dell’Avanzato R, Longo D. ENDOLIFT® and multi-wavelength laser photobiomodulation: a randomized controlled trial study on 96 subjects, treating skin laxity of the lower third of the face. Laser Therapy. 2022;29:115–120. doi:10.4081/ltj.2022.298.

2. Nilforoushzadeh MA, Heidari A, Ghane Y, et al. The Endo-lift Laser (Intralesional 1470 nm Diode Laser) for Dermatological Aesthetic Conditions: A Systematic Review. Aesthetic Plast Surg. 2024;48:5097–5114. doi:10.1007/s00266-024-04082-2.

3. Modena DAO, Yamamoto APM, da Silva TBF. Endolift® is a non-surgical treatment for skin tissue conditions. Is there evidence for its application? Lasers Med Sci. 2025;40:22. doi:10.1007/s10103-025-04288-z.

4. Bollero D, Orlando G, Dell’Avanzato R, et al. In vivo pilot study of the effects of a subdermal 1470 nm diode laser on human skin. Laser Therapy. 2025;32(1). doi:10.4081/ltj.2025.422.

5. Naouri M, Atlan M, Perrodeau E, et al. Skin tightening induced by fractional CO₂ laser treatment: quantified assessment of variations in mechanical properties of the skin. J Cosmet Dermatol. 2012;11:201–206. doi:10.1111/j.1473-2165.2012.00627.x.

6. Sartori JF, Osaki TH, Osaki MH, et al. “Split-Face” Evaluation of Collagen Changes Induced by Periorbital Fractional CO₂ Laser Resurfacing. Aesthet Surg J. 2022;42:239–248. doi:10.1093/asj/sjab357.

7. Yi KH. Thermal degradation of hyaluronic acid dermal fillers. Plast Aesthet Res. 2024;11:56. doi:10.20517/2347-9264.2024.119.

8. Michon A. Hyaluronic acid soft tissue filler delayed inflammatory reaction following COVID-19 vaccination — A case report. J Cosmet Dermatol. 2021;20:2684–2690. doi:10.1111/jocd.14312.

9. Bhojani-Lynch T. Late-Onset Inflammatory Response to Hyaluronic Acid Dermal Fillers. Plast Reconstr Surg Glob Open. 2017;5:e1532. doi:10.1097/GOX.0000000000001532.

Some consultations stay with you long after the prescription is forgotten.

Several years ago, a child was brought to me with a persistent skin problem. On examination, I found multiple warts around the anus — perianal condylomata acuminata, or genital warts.

The diagnosis itself was easy.

The important question was not:

What are these lesions?

It was:

Why does this child have them?

That question changed everything.

Genital warts in a child are different

Genital warts are caused by human papillomavirus (HPV).

In adults, HPV is usually sexually transmitted. In children, the situation is more complicated. HPV may occasionally be acquired during birth, transferred from warts elsewhere on the child’s body, or transmitted by other non-sexual routes.

So genital warts in a child do not prove sexual abuse.

But neither can they simply be treated as “just warts.”

International guidance regards anogenital warts in a child as a finding that should raise the possibility of sexual abuse and prompt appropriate assessment. Age matters too: warts appearing for the first time in an older child are more concerning for sexual transmission, although there is no magic age at which the diagnosis suddenly becomes certain.

In this child, the age, location and circumstances concerned me enough to tell the parents that sexual contact had to be considered.

They spoke to their child.

The child disclosed abuse by an adult in a position of trust.

The matter was reported and entered the criminal justice system.

Much later, I was called to court to explain what I had seen and why those findings had raised concern.

What if I had simply treated the warts?

That is the question I still remember.

Imagine the consultation ending like this:

Perianal warts. Diagnosis made. Treatment prescribed. Next patient.

Dermatologically, that diagnosis would have been perfectly correct.

Clinically, it could have been a serious failure.

If the significance of those lesions had been overlooked, recognition of the abuse might have been delayed and the child potentially exposed to further harm.

That is an important distinction in medicine.

Sometimes naming the disease is only half the diagnosis.

Why can experienced doctors miss something this important?

The child had received medical attention before reaching me.

Knowing what happened afterwards, it is tempting to wonder how such an important clue could have been missed.

But that is hindsight bias.

The lesions may have been less obvious earlier. The clinical picture may have evolved. The child may have said nothing. The parents may have had absolutely no reason to suspect abuse.

And even experienced clinicians can miss a diagnosis when the possibility itself has not entered their mental frame.

There is another bias worth recognising.

Most of us carry an unconscious picture of where child sexual abuse happens.

A troubled household perhaps. An obviously vulnerable child. An unsafe environment.

But abuse does not respect those boundaries.

A child may come from an educated, caring family. Attend a respected school. Appear well looked after. Have attentive parents.

None of that protects a child from abuse.

And it should not lower a doctor’s index of suspicion when the clinical findings suggest otherwise.

The lesson is therefore not that somebody else missed something that I recognised.

The lesson is that any of us can miss it if we never consider it.

Suspicion is not proof — but it requires action

This distinction is crucial.

A doctor should never conclude that a child has been sexually abused merely because anogenital warts are present. Such an accusation, made without proper assessment, could itself cause enormous harm.

But uncertainty cannot become an excuse to do nothing.

The doctor’s role is not to interrogate the child or conduct a criminal investigation.

It is to recognise the possibility, document the findings objectively, avoid suggestive questioning, arrange appropriate safeguarding assessment and fulfil the legal reporting requirements.

In India, Section 19 of the Protection of Children from Sexual Offences Act (POCSO) creates a duty to report suspected sexual offences against children.

And sometimes the responsibility does not end when the child leaves the consulting room.

When I was later summoned to court, I went and explained the medical findings and why they had concerned me.

That was simply part of the responsibility that followed from recognising the warning sign.

Sometimes the skin speaks first

Children being sexually abused do not always disclose it spontaneously.

They may be frightened.

Threatened.

Confused.

Or simply too young to understand what is happening to them.

Sometimes the first clue is therefore not a disclosure.

It may be pain.

Discharge.

An injury.

A sexually transmitted infection.

Or, as in this case, a few warts around the anus.

That is why safeguarding is not solely the responsibility of paediatricians, forensic doctors or the police.

Sometimes the first clue appears in a dermatology clinic.

I have treated thousands of warts during my career.

I remember very few of them.

I remember this child.

Not because recognising the wart was difficult.

Because recognising what the wart might mean mattered far more.

And that consultation left me with a question that applies well beyond dermatology:

Once you know what something is, don’t stop thinking.

Sometimes the more important question is:

Why is it here?

Aesthetic clinics advertise it. Influencers film it. Machines gurgle satisfyingly while little reservoirs fill with what appears to be the debris of one’s past sins.

And afterwards, quite often, the skin looks good.

Cleaner. Smoother. Plumper. Brighter.

A glow, as they say.

I have no quarrel with glow.

The question is whether HydraFacial is a scientifically established treatment for skin disease—or primarily a cosmetic procedure that makes skin look better for a while.

These are not the same thing.

Why the white coat matters

A facial in a beauty salon is judged simply: did you enjoy it, and did your skin look better?

But place the same machine inside a dermatologist’s clinic and it acquires something extra: medical credibility.

Patients may reasonably assume that if a procedure is offered for acne, pigmentation, rosacea or ageing, it must have convincing clinical evidence behind it.

That assumption deserves scrutiny.

There is a fundamental difference between:

“My skin looked better afterwards.”

and

“This treatment has been shown to meaningfully improve my disease.”

HydraFacial fits the first statement rather comfortably.

The second is where things become interesting.

What exactly does it do?

HydraFacial is a proprietary form of hydradermabrasion, combining cleansing, exfoliation, suction and application of solutions containing acids, humectants and antioxidants.

Many of those ingredients are biologically active. Salicylic acid works. Glycolic acid works. Hyaluronic acid hydrates.

But that does not answer the more important question:

Does delivering them through a HydraFacial produce better or longer-lasting results than using appropriate topical products?

Evidence for an ingredient is not automatically evidence for the machine delivering it.

Otherwise, putting paracetamol in a gold-plated dispenser would constitute pharmaceutical innovation.

What does the evidence show?

The literature is surprisingly small.

The 2008 study

Twenty women were randomised to receive either six hydradermabrasion treatments with an antioxidant serum or manual application of the serum.

The hydradermabrasion group showed improvements in fine lines and pigmentation, with histological changes including increased epidermal and papillary dermal thickness and fibroblast density.

Interesting? Yes.

Definitive? No.

There were only about ten patients per group, and the comparator was weak. Manual serum application does not tell us whether hydradermabrasion is superior to good skincare, microdermabrasion, a superficial peel or another reasonable cosmetic intervention.

Nearly two decades later, robust independent replication remains lacking.

Science has an annoying habit.

It likes repetition.

Preferably by people who did not manufacture the machine.

The acne study

A 2022 study treated twenty adults with mild-to-moderate acne using six HydraFacial Clarifying treatments.

Acne improved.

But there was no untreated control group and no comparison with established acne treatment.

Worse, the protocol also included blue LED therapy.

So which component deserves the applause?

The suction?

The acids?

The LED?

Existing acne treatment?

The combination?

Nobody knows.

One of the authors was also an employee of the HydraFacial company. That does not invalidate the study.

It simply makes independent replication more important.

The 2024 imaging study

Eight volunteers were examined using line-field confocal optical coherence tomography (LC-OCT) after hydradermabrasion.

The study showed measurable changes in the stratum corneum and superficial dermis.

So yes, hydradermabrasion clearly does something.

But by two weeks, much of the superficial dermal change had returned towards baseline, and there was no visible improvement in collagen quantity or quality.

That is worth remembering when the procedure is promoted as “rejuvenation”.

The glow arrives loudly.
Collagen remains rather more reserved.

What is still missing?

We still lack good comparative evidence answering basic questions:

• Is HydraFacial better than appropriate skincare?

• Does it improve acne beyond standard treatment?

• Does it meaningfully improve melasma or rosacea?

• Does repeated treatment produce durable improvement in photoageing?

• How long does the visible benefit last?

• Do expensive boosters genuinely improve outcomes?

These are not academic details.

They are exactly what patients are paying to know.

“But my skin looked better”

I believe you.

That is not sarcasm.

Cleansing, exfoliating and hydrating the stratum corneum can genuinely make skin appear smoother and brighter. Fine lines may look softer. Light reflects differently from a smooth hydrated surface.

But aesthetic medicine often performs a little linguistic magic:

Looking better is not automatically the same as becoming biologically younger.

A wet road looks darker after rain.

The asphalt has not undergone rejuvenation.

Glow is not disease modification

Acne is not simply dirty pores waiting to be vacuumed.

Melasma is not pigment sitting on the surface waiting for a nozzle.

Rosacea is not dry skin needing hydration.

And ageing is certainly not merely a shortage of serum.

A temporary cosmetic improvement can coexist perfectly well with persistence of the underlying disease.

Both things can be true.

So is HydraFacial useless?

No.

That would be equally unscientific.

The evidence suggests that it is biologically active, generally well tolerated and capable of producing short-term cosmetic improvement.

The problem is not evidence of failure.

It is insufficient evidence of durable therapeutic success.

HydraFacial may therefore be a perfectly reasonable cosmetic procedure for someone who understands what they are buying:

cleaner-feeling skin, exfoliation, hydration and perhaps a pleasant glow.

Nothing wrong with that.

People buy haircuts and massages without demanding randomised controlled trials.

Cosmetic pleasure does not require medical justification.

The problem begins when pleasure is repackaged as therapy.

Should dermatologists offer it?

Maybe?—provided it is described honestly.

Patients should understand that the evidence for durable therapeutic benefit is limited, that most demonstrated effects are short-term, and that HydraFacial should not replace established treatment for genuine skin disease.

The ethical problem is not the machine.

Machines are innocent.

The problem begins when the authority of a medical setting blurs the boundary between a cosmetic service and an evidence-based treatment.

A white coat should clarify that distinction.

Not camouflage it.

The bottom line

HydraFacial does something.

It cleans, exfoliates, hydrates and can temporarily improve the appearance of skin.

Small studies also suggest measurable biological effects.

But the evidence remains limited, the studies are tiny, durable outcomes are poorly demonstrated and convincing comparative trials are largely absent.

So HydraFacial does not need to be ineffective to be oversold.

That is the point.

The suction is real.
The serum is real.
The glow may be real.
The transformation remains considerably less certain.

And patients deserve to know the difference.

References

1. Freedman BM. Hydradermabrasion: an innovative modality for nonablative facial rejuvenation. Journal of Cosmetic Dermatology. 2008;7(4):275–280.

2. Storgard R, Mauricio-Lee J, Mauricio T, Zaiac M, Karnik J. Efficacy and tolerability of HydraFacial clarifying treatment series in the treatment of active acne vulgaris. Journal of Clinical and Aesthetic Dermatology. 2022;15(12):42–46.

3. Razi S, Truong TM, Khan S, Sanabria B, Rao B. Hydradermabrasion through the lens of line-field confocal optical coherence tomography. Skin Research and Technology. 2024;30(4):e13684.

What does our caste actually tell us about who we are today?

The folowing is an interesting case study- The Aruvela Niyogis, commonly called the “6000 Niyogis,” are a sub-group of Telugu Brahmins (I apparently belong to this tribe). The obvious legend is irresistible: six thousand Brahmins were supposedly recruited by a king for administration or warfare, becoming Brahmins who performed the functions of Kshatriyas.

It is a good story. History appears to be slightly different.

Aruvela literally means six thousand. In medieval Andhra inscriptions, a region south of the Krishna was known as Ṣaṭsahasra—the Six-Thousand country, with the Amaravati–Dharanikota region associated with it. Historical scholarship therefore suggests that Aruvela probably began as a geographical identity, much like several other Telugu communities named after the nadu or territory from which they came.

The second half of the name is even more revealing.

Niyogi derives from niyoga—an appointment or employment. Historian Phillip Wagoner describes Niyogis as laukika, or secular Brahmins, who supported themselves by accepting political and administrative appointments. Their emergence can be traced at least tentatively to the Kakatiya period of the twelfth and thirteenth centuries. Some became village accountants; others became ministers, bureaucrats and court officials. By the Vijayanagara period, Brahmins of this tradition could also become provincial governors, fort commanders and commanders of armies.

Think about what that means.

The ancestors of a community classified as Brahmin were spending generations doing jobs that classical varna theory would often associate with Kshatriyas—governing territories, collecting revenue and sometimes commanding soldiers.

They did not cease to be Brahmins. But their profession had already escaped the neat four-box diagram of Brahmin, Kshatriya, Vaishya and Shudra.

And perhaps therein lies something worth remembering about caste.

Many Indian caste and sub-caste identities undoubtedly became associated with particular occupations. Washermen washed clothes. Smiths worked metal. Trading communities traded. Priestly families performed rituals. Administrative communities administered. Over generations, occupations became family identities, identities became hereditary, and hereditary identities acquired social rank and rules of marriage. Historians consequently caution against imagining caste as a single, unchanged system frozen from antiquity; caste identities have repeatedly been created, altered and renegotiated over time.

But the occupation often disappeared long before the caste name did.

A Niyogi today may be a doctor, engineer, businessman, artist or software developer. A person born into a traditional agricultural caste need never have entered a field. The descendant of a trading community may be a civil servant. The descendant of a priest may never have learnt a Vedic mantra.

We inherited the labels. We did not necessarily inherit the jobs.

That thought seems relevant to the present reservation debate. Protesters at the recent Reservation Hatao Andolan at Jantar Mantar have argued that economic disadvantage rather than caste should increasingly determine state assistance. Those defending caste-based reservation counter that caste is not merely an obsolete occupational label: discrimination, unequal representation and accumulated social disadvantage can persist even when occupations change. Both propositions deserve to be confronted rather than caricatured.

The history of the 6000 Niyogis does not settle that debate.

But it does pose an uncomfortable question.

If caste once partly described what our ancestors did, how much should it determine what their descendants are entitled to—or denied—centuries later?

Perhaps a modern India should increasingly be interested not simply in the caste into which someone was born, but in the disadvantage, discrimination and opportunity that person actually experiences.

After all, history gave us our surnames and our caste labels.

It need not dictate our occupations.

And perhaps, one day, it need not dictate our opportunities either.

But there is a rather basic question hiding underneath all that biology: does the thread itself actually add anything?

Or are we inserting a foreign material into the scalp and then giving it credit for a wound-healing response that might have occurred simply because we punctured the skin?

The biology is plausible. That is not the same as proof.

There is some biological basis for the idea. Shin and colleagues found increased anagen activity and changes in hair-growth-related markers after thread-embedding therapy in mice.¹ Interesting, certainly—but it was an acupuncture-derived thread-embedding technique in mice, not necessarily the PDO scalp-threading procedure now offered in aesthetic clinics. Different technique, different tissue biology and, most importantly, different species.

Animal studies are excellent for asking whether something might work. They are rather less good at deciding what humans should pay for.

Mice have been cured of enough human diseases to deserve their own Nobel Prize.

The first human evidence: encouraging, but five men

Bharti and colleagues treated five men with androgenetic alopecia using PDO monofilament threads every two weeks for five sessions. Hair count reportedly increased from 48.5 to 93.7 hairs/cm² at 12 weeks.² That is an impressive numerical change.

Unfortunately, there was no control group. So we cannot separate the effect of the thread from the trauma of insertion, natural fluctuation, measurement variability or other influences. It was a useful proof-of-concept report, but not proof that the thread itself was responsible.

Five patients can justify a larger trial. They probably should not justify a treatment package.

The best controlled evidence is more interesting

Metwalli and colleagues conducted the most important controlled study: 30 women with female-pattern hair loss received either three monthly sessions of monofilament threads or intradermal saline injections.³ At six months, the thread-treated group showed significant improvements in hair count and Hair Mass Index, while the saline group did not.

This is genuine evidence in favour of threading and should not be dismissed. It suggests that PDO threads may produce an effect beyond ordinary saline injections.

But notice what the study actually proves. It shows that threading performed better than saline injections in women with female-pattern hair loss. It does not establish efficacy in men, nor does it establish that threading is better than an active hair-restoration procedure.

The comparator that actually matters: PRP

If a patient is considering a procedural treatment involving multiple scalp punctures, the clinically relevant question is not whether threading beats salt water. It is whether it offers an advantage over treatments we already use—particularly platelet-rich plasma (PRP).

PRP is imperfect. Protocols vary, preparation methods are poorly standardised and not every trial has been positive. But its evidence base is substantially broader. A 2023 meta-analysis included nine randomised trials involving 238 patients and found a significant improvement in hair density versus placebo at three and six months, although benefits for hair count and diameter were less consistent.⁴ So PRP should not be presented as miraculous either, but it has considerably more clinical evidence behind it than threading.

More importantly, we now have a direct comparison. Hassan and colleagues studied 30 patients with androgenetic alopecia—15 men and 15 women—using a split-scalp design, with PRP on one side and monofilament threads on the other.⁵ PRP produced significantly greater improvements in both hair density and hair diameter.

This is only one relatively small study, and its methodological limitations mean it should not be treated as the final word. But the direction of the evidence is awkward for threading. The only direct comparison we currently have favours PRP.

That raises the obvious clinical question: if PRP has a broader evidence base, avoids implantation of foreign material and may produce better results, what exactly is the advantage of putting a thread into the scalp?

At present, nobody has demonstrated one convincingly.

Perhaps it is the wounding, not the thread

This is the most interesting part of the entire story. Controlled injury itself can stimulate hair growth. Microneedling and fractional lasers activate wound-healing pathways and growth signals around follicles. Vathananai and Jimenez specifically discussed wound-induced hair growth in relation to several procedures, including scalp threading.⁶

Thread insertion inevitably produces injury. A needle or cannula passes through the scalp, inflammation occurs and wound healing follows. The PDO thread then remains behind and eventually dissolves.

If hair subsequently grows, how much came from the puncture and how much from the polymer?

We do not know.

The decisive experiment would therefore not be threads versus saline. It would be thread insertion versus identical needle or cannula passes without deploying the thread. Only then could we isolate the additional effect of leaving PDO behind.

Before debating which thread is best, it might be worth proving that we need the thread at all.

And which thread are we even talking about?

“PDO threading” is not one standardised procedure. Smooth monofilament, screw and barbed threads differ in structure, surface area and the tissue reaction they provoke. Studies have also used different numbers of threads, treatment intervals and insertion techniques.

It is therefore difficult to take a result obtained with one thread and casually apply it to every other PDO device being inserted into scalps.

This problem is hardly unique to aesthetic medicine, but aesthetic medicine does seem particularly talented at turning a heterogeneous collection of procedures into a single marketable noun.

What about safety?

Published scalp-threading studies have mainly reported short-term effects such as pain, redness, swelling and headache. That is reassuring, but the studies are small and long-term evidence is sparse.

Related facial thread-lifting literature reports inflammatory nodules, extrusion, dimpling and foreign-body reactions.⁷ Whether repeated scalp threading carries similar risks is uncertain. More relevantly for hair-loss patients, we do not know whether repeated treatments could produce subclinical fibrosis or alter tissue planes for a future hair transplant.

That does not mean these complications necessarily occur. It means we do not yet know that they do not.

“No long-term problems have been reported” and “long-term safety has been established” are two very different sentences.

So what would I tell a patient?

Scalp threading is not nonsense. There is a plausible mechanism, an encouraging uncontrolled report and a small sham-controlled study suggesting that it can improve hair parameters in women. That is enough to make it scientifically interesting.

It is not enough to make it an established treatment for androgenetic alopecia.

The central unanswered question remains whether the PDO thread provides a clinically worthwhile effect beyond the injury required to insert it. And when threading has been compared directly with PRP, albeit in only one small study, PRP performed better.

So if a patient asked me today to choose between the two purely on current evidence, I would favour PRP as the better-supported procedural option, while making clear that PRP itself has limitations and should not displace established medical treatment where appropriate. Threading could reasonably be offered as an experimental or inadequately established option—but patients should be told exactly that.

Scalp threading may ultimately prove useful. What it has not yet demonstrated is a clear reason why implanting a foreign material is preferable to simpler and better-studied approaches.

Until that question is answered, PDO scalp threading remains an interesting procedure with a plausible story, some encouraging data—and a specific advantage that is still looking for evidence.

References

1. Shin HJ, Lee DJ, Kwon K, Lee JY, Ha KT, Lee CH, et al. The success of thread-embedding therapy in generating hair re-growth in mice points to its possibly having a similar effect in humans. J Pharmacopuncture. 2015;18(4):20-25. doi:10.3831/KPI.2015.18.033.

2. Bharti J, Sonthalia S, Patil P, Dhurat R. Scalp threading with polydioxanone monofilament threads: a novel, effective and safe modality for hair restoration. J Eur Acad Dermatol Venereol. 2017;31(11):e492-e493. doi:10.1111/jdv.14336.

3. Metwalli M, Khattab FM, Mandour S. Monofilament threads in treatment of female hair loss. J Dermatolog Treat. 2021;32(5):521-525. doi:10.1080/09546634.2019.1682499.

4. Zhang XX, Ji YX, Zhou MC, Zhou XZ, Xie YJ, Zeng X, et al. Platelet-rich plasma for androgenetic alopecia: a systematic review and meta-analysis of randomized controlled trials. J Cutan Med Surg. 2023;27(5):504-508. doi:10.1177/12034754231191461.

5. Hassan MS, El-Taweel AEI, Gohary YM. Comparison between monofilament threads and platelet rich plasma in treatment of androgenetic alopecia. Egypt J Med Res. 2025;6(3):142-156. doi:10.21608/ejmr.2025.328433.1716.

6. Vathananai W, Jimenez F. What do we know about hair growth induced by wounding and its therapeutic applications? Dermatol Surg. 2023;49(11):995-1000. doi:10.1097/DSS.0000000000003901.

7. Niu Z, Zhang K, Yao W, Li Y, Jiang W, Zhang Q, et al. A meta-analysis and systematic review of the incidences of complications following facial thread-lifting. Aesthetic Plast Surg. 2021;45(5):2148-2158. doi:10.1007/s00266-021-02256-w.

But increasingly, I find myself wondering whether our definition of quackery has become too dependent on who is giving the treatment rather than what treatment is actually being given.

One of my uncles was a very well-known MBBS doctor with a roaring general practice. His clinic would run until midnight, and patients loved him. He was popularly known as the “Soodi Mandu Doctor” — the injection doctor — because an extraordinary number of patients who walked through his door received an injection. Sometimes it was B-complex. Sometimes, I am told, it was essentially saline. And they got better.

Of course they did. A large proportion of everyday ailments get better anyway. Viral fevers settle, body aches resolve, minor gastrointestinal illnesses pass and respiratory infections run their course. The injection acquires the credit, the patient associates recovery with treatment, and the doctor develops a reputation for producing dramatic results.

Was that quackery? Perhaps. But he was a qualified MBBS doctor, so nobody would ordinarily have called him a quack. If precisely the same therapeutic ritual had been performed by someone without a recognised medical qualification, however, we would probably have had no hesitation in using that word.

That is the contradiction that interests me. The practitioner may be legitimate, while the treatment itself may still be irrational, unnecessary or essentially placebo.

I encountered a more institutional version of the same problem as a house surgeon in 2001. At one government primary health centre, patients presenting with a wide variety of complaints were being given whatever injectable medicines happened to be available — typically things such as B-complex or paracetamol, often with little meaningful relationship to the underlying illness. I was sufficiently disturbed that I complained about it to the then Chief Minister, N. Chandrababu Naidu. I have written about that episode previously.

What was happening there was not unlicensed medicine. It was medicine being practised within the legitimate healthcare system, by legitimate healthcare personnel, using treatments that in many instances were little more than therapeutic theatre.

The white coat and the government building did not magically improve the evidence base.

The same issue persists in subtler forms today. In resource-constrained government hospitals, the appropriate treatment may simply not be available. A patient with vitiligo may attend a dermatology outpatient department and eventually leave with nothing more than a vitamin C capsule because that is what the pharmacy stocks. I have written about this too:

Nobody involved may be deliberately deceiving the patient, and the dermatologist may know perfectly well that the treatment is inadequate. But from the patient’s perspective, they have travelled to a hospital, waited, seen a qualified specialist, and received a medicine that may contribute essentially nothing towards treating the disease for which they sought help.

Now extrapolate this to modern cosmetology. Consider the fashionable IV “glow drip”. Vitamins, antioxidants and assorted compounds are infused intravenously with promises or implications of brighter skin, rejuvenation, detoxification or wellness. If an inadequately qualified cosmetologist (even if he/ she is a MBBS doctor) administers the drip, many dermatologists will immediately call it quackery. If exactly the same drip, with exactly the same evidence base and exactly the same claims, is administered by a dermatologist, does it suddenly become legitimate medicine?

The evidence has not changed. The pharmacology has not changed. The risk-benefit equation has not changed. Only the qualification of the person holding the cannula has changed.

This is where I think the anti-quackery debate becomes muddled. There are really two separate issues. One is practising medicine without the legally required qualification or outside one’s permitted scope of practice. That is fundamentally a regulatory issue, and it is entirely legitimate to enforce it. The second issue is providing ineffective, irrational, unsafe or misleading treatments. That is a question of medical quality and patient welfare. The two overlap, but they are not the same thing.

Qualification matters enormously because proper training should improve diagnosis, appraise evidence, risk assessment, recognition of complications and understanding of when not to treat. But a degree certifies training; it does not confer lifelong immunity from bad medicine.

This is also why I remain uneasy with much of the rhetoric around anti-quackery campaigns, which I discussed in my earlier post on quackery. Too often, the debate is framed less around whether a treatment is rational, evidence-based and safe, and more around who is entitled to deliver it. Who may inject, who may use a laser, who may prescribe a drug, who may perform an aesthetic procedure. Those are legitimate questions of regulation and scope of practice.

If patient welfare is genuinely the principle at stake, then the scrutiny has to turn inward as well.

Irrational prescriptions, unnecessary injections, IV “wellness” or “glow” drips with dubious claims, unsupported aesthetic procedures, expensive interventions marketed far beyond their evidence, and placebo treatments dressed up as active therapy do not become respectable medicine simply because they are delivered in a clinic by a qualified doctor. A medical degree may qualify someone to diagnose, prescribe or perform a procedure; it does not confer scientific legitimacy on whatever they choose to offer.

Quackery should not become respectable merely because it is practised by someone qualified to perform it.

One of these is:

“Never use topical tretinoin during pregnancy.”

For oral isotretinoin, the prohibition is unquestionably justified. Systemic isotretinoin is a potent human teratogen capable of producing a characteristic retinoid embryopathy.

But topical tretinoin is not oral isotretinoin.

The route is different. The systemic exposure is dramatically different. And, crucially, decades of human pregnancy data have failed to demonstrate the teratogenic signal that we continue to warn patients about.

That is why my own practice differs from the conventional recommendation.

I do prescribe topical tretinoin during pregnancy when I think there is a reasonable dermatological indication, particularly when it is being used conventionally in a small quantity over a limited area such as the face.

I do not do this because tretinoin has been proved to carry absolutely zero fetal risk. Almost no drug can meet that standard in pregnancy.

I do it because the available evidence does not establish that conventional topical tretinoin exposure is teratogenic, while its systemic exposure is extremely small.

That distinction matters.

Oral and topical exposure are not pharmacologically equivalent

The anxiety around topical tretinoin is understandable.

Retinoids influence embryonic development. Oral retinoids can be profoundly teratogenic. So when congenital abnormalities were reported after maternal topical tretinoin exposure, concern was inevitable.

But teratogenicity depends not merely on the identity of a molecule, but on the dose reaching the embryo.

A tablet deliberately designed to create systemic drug concentrations and a pea-sized amount of cream applied to facial skin are not equivalent exposures simply because both involve a retinoid.

The relevant question is therefore not:

Can retinoic acid cause fetal abnormalities?

Clearly, sufficiently high systemic exposure can.

The relevant question is:

Does ordinary topical tretinoin use produce sufficient systemic exposure to cause them?

So far, the evidence suggests that it does not.

How much actually reaches the bloodstream?

Not zero—but very little.

In the classic pharmacokinetic study by Latriano and colleagues, approximately 2% of applied topical tretinoin was absorbed after short-term use. In long-term users, absorption averaged approximately 1.1%.

Even more importantly, regular topical application did not significantly alter circulating tretinoin concentrations from endogenous pretreatment levels.

That point is often lost.

Retinoic acid already exists naturally in human plasma as part of normal vitamin-A metabolism. Detecting some percutaneous absorption does not itself establish biologically meaningful fetal exposure.

For conventional facial application, the important pharmacological observation is that treatment has not been shown to appreciably raise circulating retinoic-acid concentrations.

That makes extrapolation from oral isotretinoin biologically questionable from the outset.

The case reports mattered—but they were never proof

Several early reports described congenital abnormalities after maternal topical tretinoin exposure, some resembling parts of the retinoid embryopathy phenotype.

They were important.

They generated a safety signal that deserved investigation.

But case reports establish temporal association, not causality. Congenital malformations occur spontaneously in every population, so some will inevitably occur in pregnancies exposed to commonly used medications.

The correct response was therefore to ask whether larger controlled studies demonstrated either:

• an overall excess of congenital abnormalities; or

• a reproducible pattern resembling retinoid embryopathy.

They have not.

What happened when pregnancy outcomes were actually studied?

The prospective multicentre study by Panchaud and colleagues followed 235 pregnancies exposed to topical retinoids and compared them with 444 controls.

Major birth defects occurred in 3.4% of exposed pregnancies versus 2.0% of controls, but the difference was not statistically significant, with an OR of 1.8 and a very wide 95% CI of 0.6–5.4.

More importantly, none of the affected infants showed the characteristic pattern of retinoid embryopathy.

The authors were nevertheless cautious. They concluded that topical retinoids still could not be recommended during pregnancy because the risk-benefit ratio remained uncertain.

That deserves acknowledgement.

But their recommendation and their data are two different things.

The data said:

We did not demonstrate teratogenicity.

Their clinical interpretation was:

Given the remaining uncertainty and limited therapeutic necessity, we still would not advise using them.

That is a perfectly reasonable position.

It is not the only possible interpretation of the evidence.

The subsequent evidence became more reassuring, not less

The 2015 systematic review and meta-analysis included 654 pregnancies exposed to topical retinoids, 532 involving tretinoin.

The estimated odds ratio for major congenital malformations was 1.22 (95% CI 0.65–2.29). It also found no significant increase in miscarriage, stillbirth, low birth weight or prematurity.

Its main limitation was precision: it could exclude a very large teratogenic effect, but not a smaller one.

A later US claims-database study included 1,430 pregnancies exposed specifically to topical tretinoin. Birth defects occurred in 4.5% of exposed pregnancies compared with 4.2% of unexposed pregnancies, giving an adjusted OR of 1.16 (95% CI 0.85–1.58). The recent Nordic investigators cite these findings as consistent with their own.

Again, no convincing signal emerged.

And then came the largest study so far.

More than 2,000 first-trimester exposures

The recent Nordic cohort included pregnancies across Denmark, Iceland, Norway and Sweden.

Among 2,172 infants exposed to topical retinoids during the first trimester, major congenital malformations occurred in 3.3%.

Among more than 3.6 million unexposed infants, the rate was 3.0%.

The adjusted risk ratio was:

1.10 (95% CI 0.87–1.38).

No significant excess was demonstrated. Nor was there an increased group-level pattern of malformations characteristic of fetal retinoid syndrome.

Analyses separating tretinoin and adapalene produced results broadly similar to the combined analysis, although—as expected—the smaller numbers produced much less precise estimates.

So after several decades of looking for a teratogenic signal, the largest study yet again failed to find one.

That is difficult simply to dismiss as “lack of evidence”.

At some stage, repeatedly failing to detect an expected effect is itself evidence that any effect, if present, is probably small.

But could there still be a small risk?

Absolutely.

The Nordic confidence interval is important.

The point estimate was 1.10, but the upper 95% confidence limit was 1.38.

Using the approximately 3% background risk, the investigators calculated an adjusted risk difference of 0.30%, with a 95% confidence interval extending up to 1.14 additional percentage points.

In other words, their data are compatible with anything from essentially no effect to, at the upper statistical boundary, roughly one additional major malformation per 100 exposed pregnancies.

That is not trivial.

But neither is it evidence that such an increase actually exists.

It is the residual statistical uncertainty around an estimate that did not demonstrate increased risk.

This is where pregnancy counselling becomes a question of how we interpret uncertainty.

“We cannot exclude harm” is not the same as “this causes harm”

Regulators and investigators generally take the more conservative position.

That is understandable.

Acne and pigmentation are rarely life-threatening. Alternative treatments such as azelaic acid exist. Why accept even a theoretical fetal risk for a treatment that can usually be deferred?

Indeed, the Nordic authors themselves conclude that topical retinoids should still be avoided in pregnancy despite their reassuring results, largely because their study cannot establish absolute safety and pregnancies ending before 22 weeks were incompletely represented.

I understand that reasoning.

I simply reach a somewhat different clinical conclusion.

If a patient has mild acne that can be managed equally well with azelaic acid, I have no philosophical commitment to prescribing tretinoin merely to prove a point.

But neither do I regard pregnancy itself as an automatic contraindication to conventional, limited-area topical tretinoin when I believe the treatment offers sufficient benefit.

Because my starting question is slightly different:

What evidence shows that this level of topical exposure actually causes fetal harm?

At present, I do not think that evidence exists.

I am not talking about every topical retinoid

This distinction is important.

I would not extrapolate this argument indiscriminately to tazarotene.

Tazarotene has a stronger animal developmental-toxicity signal, pregnancy exposure data remain extremely sparse, and current prescribing information specifically contraindicates its use during pregnancy. Systemic exposure can also increase substantially when larger body surface areas are treated.

The Nordic study contained only 10 tazarotene-exposed pregnancies, far too few to provide meaningful human reassurance.

My argument applies principally to the drugs for which we actually have accumulating human evidence—particularly tretinoin, with supportive data for adapalene—used conventionally over limited skin surface area.

“Topical retinoid” should not become another careless class label any more than “retinoid” should.

Nor am I merely talking about accidental exposure

There is another distinction worth making explicit.

Most papers understandably frame their results as reassurance for the woman who accidentally used tretinoin before discovering that she was pregnant.

That is the easiest clinical conclusion.

I go somewhat further.

I am prepared to initiate or continue limited facial topical tretinoin during pregnancy when I think the indication justifies it.

That position goes beyond what the authors of these studies recommend.

I do not pretend otherwise.

But the disagreement is primarily about the risk-benefit threshold, not about what the studies found.

Their position is:

There is residual uncertainty, the indications are usually non-essential, therefore avoid treatment.

Mine is:

Systemic exposure is extremely low, repeated human studies have failed to demonstrate teratogenicity, and a theoretical risk that has progressively diminished with accumulating evidence should not automatically be treated as a contraindication.

Both approaches acknowledge uncertainty.

They simply place the threshold differently.

The problem with the word “unsafe”

This is why I think the language surrounding topical tretinoin needs updating.

There are three very different statements:

1. Topical tretinoin has been demonstrated to cause congenital malformations.

There is no convincing human evidence for this.

2. Topical tretinoin has been demonstrated to have absolutely zero fetal risk.

We cannot say this either.

3. Available pharmacokinetic and epidemiological evidence suggests that ordinary topical exposure carries little, if any, measurable teratogenic risk, although a small increase cannot be conclusively excluded.

That is the statement that best fits the evidence.

Yet textbooks, patient information and clinical conversations frequently compress all of this into:

“Tretinoin is unsafe in pregnancy.”

And once that statement is repeated often enough, a precaution begins to sound like an established pharmacological fact.

It isn’t.

Medicine should update probabilities, not merely preserve warnings

The purpose of accumulating evidence is not simply to keep repeating that absolute safety has never been proved.

It is to update what we believe the probability of harm actually is.

We began with a plausible theoretical concern because systemic retinoids are powerful teratogens.

We then demonstrated that systemic exposure after topical tretinoin is minimal.

We accumulated prospective pregnancy data.

We performed a meta-analysis.

We accumulated more than a thousand tretinoin-exposed pregnancies in a large US database.

And now we have more than 2,000 first-trimester topical-retinoid exposures in a Nordic population study, again without a substantial malformation signal.

None of this proves that risk is zero.

But the evidence has certainly not been moving towards teratogenicity.

It has been moving away from it.

For me, that is clinically meaningful.

I therefore do not regard a small amount of topical tretinoin applied to limited facial skin as equivalent to systemic retinoid exposure, and I do not believe current evidence justifies describing it as a proven teratogen in pregnancy.

Others may quite reasonably decide that the residual uncertainty is sufficient reason never to prescribe it.

That is a legitimate clinical choice.

But it should be described accurately:

a precautionary choice in the face of residual uncertainty—not a conclusion that topical tretinoin has been shown to harm the human fetus.

Those are very different things.

And after three decades of reassuring human data, perhaps it is time we stopped pretending otherwise.

The field of dermatology has fostered a spirited and determined crusade against quackery. Much of it is entirely justified. Patients are harmed by people treating diseases they do not understand, prescribing inappropriate drugs, injecting fillers without knowing vascular anatomy, and operating lasers on lesions they cannot diagnose. Such practices certainly should be condemned.

But there is an uncomfortable question hiding inside the crusade: Are we always fighting quackery—or are we sometimes also fighting competition? The two may overlap. They are not the same thing.

A Boundary We Helped Blur

The terminology itself is revealing. Cosmetics traditionally improve appearance at the surface: makeup, creams, grooming and facials. Modern aesthetic dermatology does rather more: Lasers remodel collagen. Energy-based devices destroy vessels and pigment. Chemical peels deliberately injure skin. Botulinum toxin alters muscle activity. Fillers alter tissue volume and facial contours. These are interventions on living tissue.

Nearly two decades ago, Verma and Draelos made exactly this distinction in the Indian Journal of Dermatology, Venereology and Leprology. They argued that dermatologists calling themselves cosmetologists were misusing the term and, rather unflatteringly, downgrading their own professional identity. Their preferred term was cosmetic dermatologist.

Twenty years later, the nomenclature has become considerably more imaginative. We now have cosmetologists, cosmetic dermatologists, aesthetic dermatologists, aesthetic physicians, aesthetic practitioners, skin therapists and laser technicians, often offering remarkably similar services on remarkably similar social-media pages.

And dermatologists have not exactly helped. Many dermatology clinics now advertise Hydrafacials, skin polishing, “glow” treatments, LED masks and assorted combinations of cleansing, suction, exfoliation and serums. There is nothing inherently wrong with offering them. But we cannot blur the boundary commercially and then be astonished that patients cannot see the boundary professionally.

Apparently, a facial becomes more medical simply by travelling from the salon into the dermatology clinic.

The boundary problem is compounded by Influencer-Dermatologists doing paid promotions (covertly or overtly) for cosmetics, including moisturisers and sunscreens. Is that what they have spent years studying for?

So What Exactly Is Quackery?

If quack simply means “someone who is not a dermatologist treating skin”, the definition rapidly becomes absurd. A general practitioner treating acne becomes a quack. A paediatrician treating childhood eczema becomes a quack. A physician managing uncomplicated psoriasis becomes a quack. Medicine has never worked that way.

A more useful definition of quackery would focus on competence, misrepresentation, inappropriate treatment, inadequate supervision, lack of transparency and practising beyond one’s limits.

Perhaps the more useful distinction is not cosmetic versus medical, but surface care versus intervention in living tissue. Applying makeup is cosmetic. Performing a facial is cosmetology. Injecting filler beside a major blood vessel is something else. Such interventions require appropriate diagnosis, anatomy, patient selection and the ability to recognise and manage complications. That is considerably more persuasive than: “Skin belongs to dermatologists.” Skin, inconveniently, has never signed an exclusivity agreement with us.

Someone falsely presenting themselves as a dermatologist is a problem. Someone injecting fillers without understanding vascular anatomy is a problem. Someone operating a laser without being able to recognise the disease being treated is a problem. Someone unable to manage the complication they create is a problem. Credentials are important evidence of specialised training. They are not a claim of ownership over human tissue.

The original anti-quackery argument in dermatology was powerful precisely because the patient harm was obvious. Patients with tinea, acne and other common disorders were repeatedly given inappropriate steroid-containing combination creams. We saw tinea incognito, steroid-damaged skin, worsening acne and delayed diagnosis. That was clearly patient protection.

The logic becomes less straightforward when the same language of quackery is applied to aesthetic practice primarily on the basis of who is doing it, rather than their competence, supervision, transparency and the actual risk of the intervention.

The Awkward Delegation Problem

Consider a familiar scenario. A patient attends a dermatology clinic for a laser procedure. The dermatologist assesses the patient and prescribes the treatment, but a technician or therapist performs much—or sometimes all—of the procedure. Hair transplantation makes the contradiction even clearer. Patient selection, donor assessment, hairline design and complication management are presented as requiring specialist expertise. Yet in some centres, technicians perform much of the extraction, graft handling and implantation—sometimes accounting for most of the actual operative time.

The profession may simultaneously warn patients against lasers or hair transplantation performed by non-medical personnel. There is an obvious tension here. Delegation itself is not the problem. Properly trained personnel can perform defined technical tasks under genuine medical supervision. But if we argue that these procedures require specialist judgment, then specialist involvement must be meaningful at the points where that judgment matters.

Otherwise, something rather magical happens…..The technician performing the procedure outside our clinic is a quack. The same technician performing it inside our clinic is part of the dermatology team.

There may, of course, be a legitimate distinction: proper diagnosis, physician-directed planning, defined protocols, genuine supervision and immediate complication management. If so, those are the distinctions we should defend.

But if technicians are trained within specialist clinics to perform most of a procedure and later reproduce those same skills independently, we should perhaps acknowledge another irony: our own clinics may sometimes become the training grounds for the technician-led practice we subsequently condemn as quackery.

The logical problem is difficult to escape. If these procedural steps inherently require specialist expertise, routinely delegating them is hard to defend. If they can safely be delegated after appropriate training and supervision, then the argument against similar practice elsewhere cannot rest simply on professional title.

And the patient should know who is actually performing the procedure. “You will be treated by our trained technician under my supervision” is transparent. Allowing a patient to assume that the dermatologist will perform the laser—or most of the hair transplant—when that is not what happens is rather less so. A profession demanding competence, supervision and transparency from others should probably apply the same standards to itself.

Patient Safety or Professional Territory?

Three things often get bundled together in the anti-quackery debate: patient safety, professional standards and professional territory. The first two are unquestionably legitimate. The third is understandable too. Dermatologists train for years, and aesthetic practice has become an important part of the specialty. But professional self-interest does not invalidate a patient-safety argument. It simply means we should acknowledge that patient safety and professional interest can sometimes point in the same direction. That makes consistency especially important.

I was struck by this recently at an endocrinology meeting where general practitioners and doctors from other specialties were openly encouraged to learn. Nobody seemed particularly worried that someone might hear a thyroid lecture on Saturday and open an endocrine centre on Monday.

Dermatology sometimes appears more anxious about non-dermatologists simply learning dermatology. Yet much of common dermatology can obviously be learnt by non-specialists. That does not make dermatologists redundant. Specialist expertise becomes more valuable precisely when diagnosis is difficult, disease is severe, treatment is complex, or the consequences of error are greater. Medicine is not a collection of sovereign states separated by barbed-wire fencing.

I Have Tried Publishing This Before

I should disclose that versions of this argument have already had a small tour of Indian dermatology journals. None accepted them. Perhaps the manuscripts simply were not good enough. That remains entirely possible.

But I suspect the argument also creates discomfort because questioning whether anti-quackery advocacy sometimes overlaps with professional protectionism can sound suspiciously like being anti-dermatology. It isn’t.

Criticism of one’s own profession is not hostility towards it. A specialty confident in the strength of its expertise should be able to examine the places where its public arguments and its private practices do not quite match. We are, after all, enthusiastic advocates of critical appraisal, usually of other people’s papers.

The Best Defence of Dermatology

Perhaps we have been using the wrong argument.

“Only dermatologists should do this because dermatologists own skin” is unlikely to remain persuasive indefinitely

.

A much stronger position is:

Procedures carrying meaningful risk should be performed within a system that ensures appropriate knowledge, training, supervision, transparency and the ability to manage complications.

That argument is harder to dismiss because it is about competence rather than territory. It also places obligations on us. If we delegate procedures, patients should know. If we insist specialist judgment is essential, specialist involvement should be genuine. If we criticise inadequate supervision outside dermatology clinics, we should not practise it inside them. And if specialist training really produces better care, that difference should be visible.

Diagnose better. Choose treatments better. Recognise when not to treat. Understand complications. Manage them properly. Remain evidence-based while the surrounding market sells glow, detoxification and the occasional miracle serum.

Perhaps the real irony of the anti-quackery crusade is this: The more energy we spend telling patients whom not to visit, the less attention we may pay to demonstrating why they should visit us.

Reference

Verma SB, Draelos ZD. Cosmetic dermatology versus cosmetology: A misnomer in need of urgent correction. Indian J Dermatol Venereol Leprol. 2008;74:92–93. doi:10.4103/0378-6323.39687.

But dermoscopy of inflammatory dermatoses—grandly rechristened “inflammoscopy”—deserves more scepticism than it usually receives.

Consider the familiar sequence. A dermatologist takes a history, examines the morphology and distribution, and clinically diagnoses psoriasis. The dermatoscope is then applied. Dotted vessels and white scale appear, and these are presented as confirmation.

There is nothing inherently wrong with that. Every diagnostic test is interpreted within a clinical context. But the important question is not whether dermoscopic findings correlate with psoriasis.

It is whether adding dermoscopy to a competent clinical examination improves diagnosis or management enough to justify the enormous vocabulary that has grown around it.

That remains inadequately demonstrated.

Welcome to the Dermoscopic Safari

Inflammoscopy has produced a spectacular lexicon: dermoscopic Auspitz sign, red globular ring, rail-like scaling, leaf-venation, starry-sky Wickham striae, white starburst, vascular polygons, strawberry patterns, white clouds and orange-yellow structureless areas.

One almost expects the next paper to describe the crescent moon over a misty lake sign.

These names are memorable and make excellent conference slides. But metaphors do not create specificity.

“Leaf venation” is still white lines. A “white starburst” represents radial hyperkeratosis and fibrosis. A “strawberry pattern” reflects erythema, follicular plugging and scale.

Much of the inflammoscopic vocabulary therefore describes variations on a relatively small number of biological phenomena: vascular dilatation, scale, crust, follicular plugging, pigment, fibrosis and superficial inflammation. All of these recur across multiple diseases.

Dotted vessels may favour psoriasis; yellow serocrust may favour dermatitis; white network-like structures may favour lichen planus. But none of these observations becomes a diagnosis simply because it has acquired an attractive name.

The major inflammoscopy review itself acknowledges that terminology is variable and metaphorical, that inflammatory disorders often show poorly specific findings, and that dermoscopy should be interpreted after a clinical differential has been established.[1]

That is entirely reasonable.

What remains uncertain is how much the dermatoscope adds once that clinical work has already been done.

Pattern Discrimination Is Not Added Clinical Value

The study by Lallas and colleagues is often cited as strong evidence for inflammoscopy.[2]

It was prospective and methodologically respectable. Dermoscopic readers were blinded to clinical information and histopathological diagnosis, and the combination of regularly distributed dotted vessels, a light-red background and white scale predicted psoriasis with a reported sensitivity of 84.9% and specificity of 88%.

That demonstrates that dermoscopic images contain diagnostically useful information.

But it does not demonstrate that dermoscopy improves the dermatologist’s diagnosis.

The study did not ask clinicians to examine the same patients, record a diagnosis or level of certainty, then add dermoscopy and determine how often the diagnosis became more accurate. Instead, readers were deliberately deprived of the clinical information they would normally have.

They were essentially asked whether dermoscopic features could discriminate among four predefined diagnoses: psoriasis, dermatitis, lichen planus and pityriasis rosea.

That is a valid question. It is simply not the same question as whether dermoscopy adds useful information beyond clinical examination.

A subsequent editorial nevertheless cited this study while stating that dermoscopy had proved significantly superior to clinical examination alone.[3] That comparison was not actually performed.

The claim outran the study design.

And any diagnostic test looks more impressive when it is told that only four diseases are allowed into the room.

This does not mean inflammoscopy has no role in diagnostically uncertain cases. Within an already restricted differential, regular dotted vessels with diffuse white scale may increase the probability of psoriasis, while patchy vessels and yellow serocrust may push the clinician towards dermatitis.

That is plausible probability modification.

But to establish genuine clinical value, we need studies comparing clinical examination alone with clinical examination plus dermoscopy and asking whether the additional information corrects important diagnostic errors, changes treatment appropriately, reduces investigations safely or improves outcomes.

Much of the existing literature instead establishes associations between dermoscopic appearances and diagnoses that are already known or subsequently confirmed.

Association is not the same as added clinical utility.

Dermatology Does Not Need More Low-Value Trivia

Dermatology already asks trainees to learn an enormous taxonomy of diseases, variants, synonyms and historical labels while acquiring the skills that actually matter: morphology, distribution, disease evolution, differential diagnosis and clinicopathological correlation.

Inflammoscopy has added another dictionary.

The learner must now remember which diseases supposedly produce strawberries, starbursts, rosettes, polygons, clouds, rail tracks, leaves and starry skies.

For what return?

A systematic review of inflammoscopy in skin of colour identified 85 papers covering 76 dermatoses. Seventy-four were case reports or case series, and only one reached level-III evidence.[4]

That is an extraordinary volume of terminology resting on a remarkably shallow evidence base.

A sign deserves space in the postgraduate brain when it reproducibly improves diagnosis, changes management or prevents harm.

Otherwise, it becomes curricular pollution.

Why the Dictionary Keeps Expanding

This does not require assuming that authors invent signs merely to obtain publications. Their motives cannot be known.

The academic incentive is structural.

A newly noticed arrangement of vessels, scale and colour can become a case report, correspondence, conference presentation or named sign. External validation is much harder.

A negative study showing that a proposed sign contributes little beyond clinical examination is also less eye-catching than another metaphor accompanied by three attractive photographs.

The predictable result is a literature rich in first descriptions and relatively poor in independent testing.

The system makes it easier to name signs than to prove that they matter.

Did the Dermatoscope Avoid the Biopsy—or Did the Biopsy Validate the Dermatoscope?

Claims that inflammoscopy can reduce “unnecessary biopsies” deserve particular scrutiny.

Pakornphadungsit and colleagues studied 102 patients with inflammatory and infectious dermatoses. Dermoscopic images were interpreted by a blinded dermatologist, and every participant underwent biopsy to establish the diagnosis.[5]

The study did not record whether clinicians intended to biopsy before dermoscopy, whether dermoscopy changed that decision, how many biopsies were actually avoided, whether diagnoses were missed or delayed, or what happened to patients subsequently.

Nevertheless, the authors suggested that dermoscopy might minimise unnecessary invasive investigations.

It might. But that was a hypothesis generated by the study, not an outcome demonstrated by it.

When everyone in a diagnostic study undergoes biopsy, the study can tell us whether dermoscopic findings correlate with histopathological diagnoses.

It cannot tell us whether omitting the biopsy would have been safe.

The biopsy did the validating.

Dermoscopy received the applause.

So Where Does That Leave Inflammoscopy?

Inflammoscopy is not invalid because it is interpreted after clinical examination. That is how diagnostic medicine works.

Its problem is that a relatively limited collection of overlapping surface reactions has accumulated an elaborate vocabulary without equivalent evidence that learning this vocabulary materially improves clinical care.

Some patterns probably do modify probability within a restricted differential. That is useful.

But pattern association is not incremental benefit. Greater diagnostic confidence is not necessarily greater diagnostic accuracy. And a biopsy not performed is not automatically a biopsy safely avoided.

When the diagnosis is clinically obvious, inflammoscopy may add little beyond terminology. When the diagnosis is genuinely uncertain and the answer will change treatment, prognosis or surveillance, the dermatoscope does not make dermatopathology redundant.

Inflammoscopy certainly magnifies vessels, scale and pigment.

The unresolved question is whether we have also magnified its clinical importance.

References

1. Errichetti E. Dermoscopy of inflammatory dermatoses (inflammoscopy): an up-to-date overview. Dermatol Pract Concept. 2019;9:169–180. doi:10.5826/dpc.0903a01.

2. Lallas A, Kyrgidis A, Tzellos TG, et al. Accuracy of dermoscopic criteria for the diagnosis of psoriasis, dermatitis, lichen planus and pityriasis rosea. Br J Dermatol. 2012;166:1198–1205. doi:10.1111/j.1365-2133.2012.10868.x.

3. Lallas A, Argenziano G. Dermatoscope—the dermatologist’s stethoscope. Indian J Dermatol Venereol Leprol. 2014;80:493–494. doi:10.4103/0378-6323.144141.

4. Sławińska M, Żółkiewicz J, Behera B, et al. Dermoscopy of inflammatory dermatoses in skin of color: a systematic review by the International Dermoscopy Society “Imaging in Skin of Color” Task Force. Dermatol Pract Concept. 2023;13:e2023297S. doi:10.5826/dpc.1304S1a297S.

5. Pakornphadungsit K, Suchonwanit P, Thadanipon K, et al. Dermoscopic features and their diagnostic values among common inflammatory and infectious dermatoses: a cross-sectional study. Clin Cosmet Investig Dermatol. 2023;16:211–220. doi:10.2147/CCID.S397212.