Millions of people with psoriasis have turned to CBD creams and oils, hoping for relief from the relentless itch, inflammation, and scaling that define this condition. The results, to put it diplomatically, have been mixed. In the laboratory, the case for CBD for psoriasis looks strong: it calms inflammation and slows the runaway growth of skin cells. In people, the handful of controlled trials point in different directions, and a large part of the reason is delivery: CBD is notoriously difficult to get where it needs to go.
That gap between lab and clinic is the subject of a fresh review, published on 23 October 2026 in the peer-reviewed journal Biomedicines. Emanuelly Krefta, Francisney Pinto Nascimento and colleagues from the Laboratory of Cannabis and Psychedelics at the Federal University for Latin American Integration (UNILA) in Foz do Iguaçu, Brazil, and from the Universidad Central del Paraguay pulled together what is known about the skin’s own cannabinoid system in psoriasis, the laboratory evidence for plant cannabinoids, and the clinical studies published so far. Their verdict is sober: the biology is plausible, the human evidence is thin and inconsistent, and cannabinoids should be treated as a promising but investigational approach rather than a ready-made treatment.
Two other studies published this year attack the delivery problem from opposite ends. The first, published in February 2026 in the peer-reviewed journal Pharmaceutics, describes a formulation that wraps CBD inside microscopic oil droplets derived from argan oil, stabilized with a natural polymer called chitosan. The result is a nanoemulsion — think of it as an ultra-fine, skin-smart CBD lotion — that appears to release its active ingredient slowly, steadily, and without damaging the skin cells it is supposed to help. The second, published online on 23 September 2026 in the Journal of Ethnopharmacology, goes in the other direction entirely: instead of engineering a new carrier, researchers at Khon Kaen University took a turmeric-and-cannabis skin remedy documented in a 1953 Thai traditional medicine text, standardized it in the lab, and tested whether it does what the tradition claims.
Key Takeaways on CBD for Psoriasis
The Biomedicines review finds that clinical evidence specific to psoriasis comes down to a few small studies and just two randomized, placebo-controlled trials. In the stronger topical trial, a 2.5% CBD ointment applied twice daily for 12 weeks to plaques in 51 people with mild psoriasis produced a modest but statistically significant improvement over placebo on a local severity score. In the oral trial, 60 mg of CBD a day for 12 weeks did not reduce psoriasis severity, although people fell asleep faster for a while. Across skin diseases, itch is the symptom where cannabinoids show the most consistent benefit. The authors trace the mismatch between laboratory promise and clinical results to five sources of variation — which cannabinoid, which formulation and dose, which route, which outcome and which patients — and call for larger, standardized trials before cannabinoids are used in practice, ideally tested as add-ons to standard treatment rather than replacements.
Researchers in Spain, Morocco and the United States developed four formulations of CBD delivered via argan oil nanoemulsions — with and without a chitosan coating — and tested them extensively for stability, drug release, skin penetration, and safety. The chitosan-stabilized CBD nanoemulsion (called CBD-CS-NE) showed the most promising profile: nanoscale droplet size under 100 nm, sustained drug release over 12 hours, enhanced skin permeation compared to plain CBD in oil, and non-cytotoxic behavior toward human skin cells. A critical safety caveat emerged: chitosan-containing formulations proved toxic to the roundworm C. elegans used in live-organism testing, raising questions that researchers say must be resolved before human trials. The plain CBD nanoemulsion, without chitosan, was safe across all models.
A separate Thai study standardized a combined extract of turmeric rhizome and cannabis leaf, mixed one to one, and measured its content of curcuminoids, ar-turmerone and cannabidiol by validated HPLC. In lab-grown macrophages and keratinocytes, the extract reduced key inflammatory signals — cutting prostaglandin E2 production by more than 90 percent at a concentration of 12.5 micrograms per millilitre — and dampened the overactive behaviour of skin cells stimulated with the same cytokines that drive psoriasis. Delivered in cottonseed oil with a penetration enhancer, the turmeric compounds accumulated in the skin without passing through it over 24 hours.
Neither formulation is a product. Both are proof-of-concept work in cells and pig skin, with no animal disease model and no human data. What they share with the review is a diagnosis: the chemistry of cannabinoids against psoriasis is promising, and the unsolved problems are getting the molecules into the skin, keeping them there, and proving in well-designed trials that this changes anything for patients.
Does CBD Help Psoriasis? What the Human Trials Show
For all the attention CBD gets, very few people with psoriasis have taken part in controlled trials of it. The Biomedicines team searched PubMed, Scopus and Web of Science up to July 2026. Because theirs is a narrative review rather than a systematic one, they did not formally score each study’s risk of bias or pool the numbers into a single estimate, so it is best read as an expert map of the field rather than a final verdict.
The most convincing result comes from Thailand. In a dual-centre trial published in the Journal of the European Academy of Dermatology and Venereology, Puaratanaarunkon and colleagues enrolled 51 people with mild plaque psoriasis and assessed 108 paired target plaques, using a split-body design: within each pair, one plaque received a 2.5% CBD ointment and the other an identical-looking placebo, twice a day for 12 weeks, and neither patients nor assessors knew which was which. Comparing two plaques on the same person removes a lot of noise, because the same skin type, diet and stress level apply to both. CBD-treated plaques scored modestly but significantly better on the Local Psoriasis Severity Index (coefficient −0.197; 95% confidence interval −0.370 to −0.024; p = 0.026), and scaling in particular was lower (coefficient −0.094; 95% CI −0.173 to −0.015; p = 0.020). The catch: these were mild cases and single target plaques, not disease across the whole body.
A second Thai study, a single-blind crossover trial by Charoenying and colleagues, gave 20 patients a cream containing both THC (1.35 mg/g) and CBD (1.25 mg/g). Average PASI — the Psoriasis Area and Severity Index, the standard whole-body score dermatologists use to rate redness, thickness and scaling of plaques — fell from 24.32 ± 11.81 at the start to 16.66 ± 12.15 after eight weeks, with a significant drop from week 4 onward. There was no placebo group and the design was only single-blind. A second cream in the same study mixed the cannabinoids with a polyherbal blend, so the reviewers counted only the cannabis-only cream as evidence about cannabinoids.
Swallowing CBD has not worked as well. In a randomized, double-blind, placebo-controlled trial in the Journal of Dermatological Treatment, 28 adults with psoriasis took 30 mg of CBD twice a day (60 mg a day) or placebo for 12 weeks, and 26 finished. In the CBD group, PASI went from 5.5 ± 1.0 to 5.3 ± 0.7 (p = 0.482); in the placebo group, from 3.7 ± 0.5 to 3.8 ± 0.8 (p = 0.912), with no significant difference between the groups at week 12 (p = 0.152). Other severity measures did not improve either. People on CBD fell asleep faster at week 6 (p = 0.030), but that effect was gone by week 12. CBD was well tolerated. We covered this trial in detail in our article on oral CBD oil, itch and psoriasis plaques.
The rest of the human evidence is anecdotal, such as a case report of a 33-year-old man whose psoriasis improved while he used several THC-containing products — a cream, a soap and a hair oil — with no control group and no validated severity score. Looking beyond psoriasis, a 2025 meta-analysis across dermatology found a modest but significant reduction in itch with cannabinoids, without proven benefit on other objective outcomes. That pattern — itch and sleep may move, plaques mostly do not — runs through the whole field.
Why the Results Disagree: Five Things That Vary Between Studies
The review’s most useful contribution may be a checklist. The authors argue that the gap between laboratory promise and clinical uncertainty comes from five overlapping sources of variation that are rarely considered together.
The first is the molecule. THC, CBD, cannabigerol (CBG) and cannabinol (CBN) are not interchangeable; each acts on a different mix of receptors and channels. An early laboratory study found that all four slowed the growth of overactive human skin cells, apparently without going through the classic cannabinoid receptors, but that does not mean they would behave the same way on a patient’s skin. “Cannabinoids help psoriasis” is not a meaningful finding unless you know which one was tested.
The second is formulation and dose. A purified compound, a standardized extract and a non-standardized herbal preparation can behave very differently even when they come from the same plant. In one mouse study of topical CBD, 0.01% and 0.1% creams both eased psoriasis-like lesions, but only the stronger one significantly dampened JAK2–STAT3, a signalling pathway that sits downstream of the IL-23 driver of psoriasis.
The third is the route, which is the real question behind searches for CBD cream versus CBD oil for psoriasis. A cream acts mostly where it is applied and keeps exposure in the rest of the body low, while oil taken by mouth has to be absorbed and pass through the liver, with far more variation along the way. A result from one route says little about the other. The fourth is the outcome: an improvement in itch is not the same as an improvement in plaques, and a change in a laboratory marker is not a clinical benefit. The fifth is the patients. In the oral CBD trial, 96% of participants had mild-to-moderate psoriasis at the start, which leaves little room for PASI to fall. The reviewers stress that this cannot be shown to explain the negative result, but it complicates any comparison.
In plain terms, comparing today’s psoriasis studies is like comparing recipes that use different ingredients, different ovens and different tasters. Until trials report these five variables in a consistent way, conflicting results are exactly what one should expect.
What Psoriatic Skin Reveals About Its Own Cannabinoid System
Skin has its own version of the endocannabinoid system — the receptors, messenger molecules and enzymes the body uses to regulate inflammation, itch and cell growth. Receptors called CB1 and CB2 sit on keratinocytes, immune cells and nerve fibres, and the body’s own cannabis-like molecules, anandamide and 2-AG, switch them on. The review describes skin as a place where nerves, immune cells and hormones constantly talk to each other, and this system is one of the channels they use.
The strongest recent evidence that the system is disturbed in psoriasis comes from a gene-expression study by Jaime Turk and Mark Kirchhof at the University of Ottawa, which analysed 402 skin samples: 110 from psoriasis plaques, 57 from unaffected skin of psoriasis patients and 235 from healthy donors. In the plaques, the gene for CB2 was more active, as were the genes for several related sensors (TRPV3, TRPA1 and PPARδ), while PPARγ, PPARα and TRPV4 were less active. Unaffected skin from the same patients showed no significant changes in these genes. Separately, a Polish team working with keratinocytes from patients found that the enzymes that break down anandamide and 2-AG were more active, with lower levels of both molecules in the cells.
The Biomedicines authors are careful about what this means. A gene being more or less active shows association, not cause: it cannot say whether the disruption drives psoriasis, results from it, or simply travels alongside it. For two of the sensors, TRPV4 and TRPA1, gene activity and experimental results even point in opposite directions, which is a warning against reading too much into expression data alone.
Animal work on CB2 is more consistent. In mice with imiquimod-induced psoriasis-like inflammation, a standard laboratory model, knocking out the CB2 gene made skin inflammation and itch worse, while switching CB2 on with a selective drug reduced epidermal thickening, inflammatory signals and the influx of immune cells. Mouse skin is not human skin, but together these results suggest that CB2 acts more like a brake than an accelerator in psoriatic inflammation, which is one reason drug developers are interested in it.
Why Getting CBD Through Skin Is Harder Than It Sounds
Psoriasis is one of the most prevalent chronic inflammatory skin conditions on the planet, affecting roughly 125 million people worldwide; the Biomedicines review puts it at 2% to 3% of the world population, with the plaque form accounting for more than 80% of cases. It causes the immune system to go haywire, triggering the rapid overproduction of skin cells: the review notes that skin cells which normally take about 28 days to mature rush through the process in 3 to 5 days. The result: thick, scaly, often painful plaques that can appear anywhere on the body, from elbows and knees to the scalp and lower back. Beyond the physical symptoms, psoriasis carries significant psychological burden, and in severe cases it increases the risk of cardiovascular disease and a form of inflammatory arthritis.
CBD, the non-psychoactive compound found in the Cannabis sativa plant, has attracted sustained scientific interest as a potential tool against psoriasis. Research has shown that it can reduce inflammation, suppress the abnormal proliferation of keratinocytes (the overactive skin cells at the root of psoriasis), ease itching, and support skin hydration — a profile we have covered in depth in our overview of CBD’s science-backed benefits for acne and psoriasis. One frequently cited line of evidence comes from a Polish group that isolated keratinocytes from psoriasis patients and found that CBD accumulates in their cell membranes and helps restore the balance between oxidants and antioxidants that psoriatic skin has lost. On paper, it reads like an ideal therapeutic candidate.
In practice, however, CBD is something of a pharmaceutical nightmare to work with. It does not dissolve in water. It oxidizes and degrades relatively quickly. And when you simply apply it to skin in a lotion or oil, much of it never makes it past the outermost layer. The skin, after all, evolved precisely to keep things out.
This is the challenge the European research team — led by Victoria Díaz-Tomé of the University of Santiago de Compostela, with collaborators from Abdelmalek Essaâdi University in Morocco and the University of Texas Rio Grande Valley — set out to solve.
The Elegance of Nanoemulsions: Making CBD Invisible to the Skin’s Defenses
A nanoemulsion is essentially a very, very fine emulsion — oil-in-water droplets so small (we are talking tens to hundreds of nanometers in diameter; for reference, a human hair is roughly 80,000 nm wide) that they behave quite differently from conventional lotions or creams. Their tiny size vastly increases surface area, which helps them interact with biological membranes. They can encapsulate hydrophobic (water-hating) molecules like CBD and escort them into the skin far more efficiently than conventional formulations.
For the oil phase of their nanoemulsion, the researchers chose argan oil — the same Moroccan-origin oil prized in cosmetics for its skin-healing, emollient properties. Argan oil is rich in unsaturated fatty acids, tocopherols, and squalene, all of which have documented skin-compatible and mildly anti-inflammatory properties of their own. It is not just a carrier; it actively complements the therapeutic goal. For readers wondering about argan oil for psoriasis on its own, though, this study does not answer that question: plain argan oil was not tested as a psoriasis treatment, only as the base of the formulation.
The researchers prepared four formulations: a plain argan oil nanoemulsion (NE), a chitosan-stabilized nanoemulsion (CS-NE), and CBD-loaded versions of each (CBD-NE and CBD-CS-NE). They added a small amount of Tocobiol — an antioxidant blend of tocopherol, beta-sitosterol, and squalene — to protect the CBD from oxidative degradation.
Chitosan: The Unlikely Hero From Shrimp Shells
Here is where the story gets interesting. Chitosan is a natural biopolymer derived from chitin — the stuff that makes up shrimp shells and insect exoskeletons. When processed and dissolved in dilute acetic acid, it forms a sticky, mildly viscous solution with a positive electrical charge.
That positive charge turns out to be critically useful. Human skin carries a net negative surface charge. Positively charged particles are attracted to it — they stick around longer, penetrate more efficiently, and resist being washed away. When the researchers coated their argan oil nanodroplets with chitosan, the droplets acquired exactly this positive charge (measured zeta potential of around +47 mV), transforming them into what scientists call bioadhesive particles.
The chitosan coating also thickened the formulation — giving it a gel-like consistency that spreads well, stays put on skin rather than running off, and feels more like a conventional topical product. Chitosan itself has antibacterial and wound-healing properties that may benefit psoriatic skin directly.
Most importantly for therapeutic purposes, the chitosan layer around each nanodroplet acted like a slow-release valve. Rather than dumping all the CBD at once, the CBD-CS-NE formulation released its active ingredient steadily over a sustained 12-hour window — a behavior the researchers confirmed matched the Higuchi mathematical model of diffusion-controlled drug release.
The Numbers: How Well Did the Nanoemulsion Actually Work?
The physicochemical results were, by the standards of pharmaceutical formulation science, genuinely strong.
The CBD-CS-NE formulation produced droplets averaging 94 nm in diameter — well within the nanoscale range considered optimal for skin penetration. Polydispersity index (PDI) values were low, indicating a uniform population of droplets rather than a chaotic mix of sizes. Viscosity was in the right range for topical application: thick enough to stay on skin, but exhibiting “shear-thinning” behavior — meaning it flows more easily when rubbed in, and thickens again when left alone. That is exactly what you want in a cream or lotion.
In three months of stability testing at room temperature, all formulations remained physically intact — no phase separation, no dramatic changes in droplet size during the first weeks. The chitosan formulations showed more changes in droplet size distribution over the full 91 days, a known limitation of chitosan-based systems that the authors flag as needing further optimization.
Skin permeation testing, conducted using real porcine ear skin mounted in laboratory diffusion cells, showed that CBD-CS-NE delivered approximately 62 micrograms of CBD per square centimeter of skin over 24 hours — about 10% more than plain CBD in argan oil alone, and 4% more than the non-chitosan nanoemulsion. These are modest but meaningful improvements, and the authors note that chitosan’s bioadhesive effect on the skin surface likely prolonged drug residence time rather than fundamentally accelerating penetration rate.
Cytotoxicity testing on HaCaT cells — a standard human keratinocyte line used as a skin safety model — placed CBD-CS-NE in the “non-cytotoxic” range under ISO standards, with cell viability above 80%. This was actually the best safety profile among all formulations tested, with the researchers suggesting a possible synergistic interaction between CBD and chitosan that improved overall biocompatibility compared to chitosan alone. These are cell-level findings, though, and the human trials described above are a reminder that good behaviour in a dish does not guarantee a clinical effect.
The Problem That Cannot Be Glossed Over
Scientific honesty is not always commercially convenient, and this paper is admirably direct about a serious complication.
When the researchers tested their chitosan-containing formulations on the roundworm Caenorhabditis elegans — a tiny nematode widely used in toxicology research precisely because it gives a whole-organism perspective that cell culture cannot — the results were alarming. Both the chitosan nanoemulsion (CS-NE) and the chitosan-CBD combination (CBD-CS-NE) caused near-complete worm mortality at all tested concentrations.
The plain nanoemulsion without chitosan? Perfectly safe, with survival rates above 90% at all concentrations.
The researchers propose two explanations. Chitosan’s positive charge may aggressively disrupt the worm’s protective outer cuticle and intestinal barrier — structures that simply do not exist in a flat layer of cells grown on plastic. Alternatively, chitosan particles ingested by the worm may interfere with neurological or metabolic processes in ways that are lethal at a systems level but invisible in a cell viability assay. There is also a confounding factor the authors candidly acknowledge: chitosan requires acetic acid to dissolve, giving the formulation a mildly acidic pH of around 4.8. The worm exposure medium has limited buffering capacity, so low pH itself may have contributed to toxicity — an important variable that future studies must disentangle.
None of this necessarily means chitosan is dangerous for humans. The skin is not a roundworm. Topical application to intact skin is a very different biological scenario from whole-organism ingestion. But it does mean that additional safety work — in more complex models, and with properly pH-controlled controls — is required before anyone should consider moving this toward human trials.
The Curcuma Cannabis Psoriasis Extract Study: A 1953 Thai Formula Gets a Modern Test
While the European team was building a delivery vehicle from scratch, a group in Thailand started from the opposite end — with a remedy that already existed. Traditional Thai medicine has long combined turmeric rhizome (Curcuma longa) with cannabis leaf (Cannabis sativa) in cottonseed oil as a rub for inflamed skin. The combination is recorded in a 1953 Thai medical text, and it fits the broader logic of Thai herbal practice, which favours multi-plant mixtures on the assumption that the ingredients reinforce each other.
The study, led by Sarunya Tuntiyasawasdikul at Khon Kaen University’s Center for Research and Development of Herbal Health Products, with colleagues from Ubon Ratchathani Rajabhat University, asked a simple question: if you standardize this mixture so that every batch contains the same amounts of the active compounds, does it actually do something measurable against the biology of psoriasis, and do the compounds reach the skin? The work was funded by Thailand’s National Science, Research and Innovation Fund through Khon Kaen University, and the authors declare no competing interests. It appeared online as a journal pre-proof — peer-reviewed and accepted, but not yet in its final typeset form.
The researchers ground turmeric rhizomes from Si Sa Ket province and cannabis leaves from Sakon Nakhon province, combined them in equal weights, and extracted the mix with 95 percent ethanol. The result was a dark yellow, viscous extract they call CLCS. Using a validated chromatography method, they measured five marker compounds in it: three curcuminoids — curcumin at 22.12 mg per gram, demethoxycurcumin at 12.89 mg/g and bisdemethoxycurcumin at 18.79 mg/g — plus ar-turmerone, an aromatic compound from turmeric oil, at 75.35 mg/g, and cannabidiol at 35.47 mg/g. That last number is worth pausing on. Cannabis leaf is a far weaker source of CBD than flower, but the extraction concentrated it to roughly 3.5 percent of the finished extract by weight.
Two details matter for interpreting this. First, the study used leaves, not flower — a choice that keeps THC content low and aligns with how the traditional preparation was made. Second, the authors compared the combined extract against turmeric alone and cannabis alone, which is the only way to test whether combining them adds anything. The abstract reports that the combination was evaluated against the single extracts; the detailed side-by-side figures sit in the full paper behind a paywall, so we cannot report them here. It is also worth saying plainly that this is not a recipe: a lab-standardized ethanol extract with validated chemical content is a different thing from mixing kitchen turmeric with cannabis at home.
What the Turmeric–Cannabis Extract Did in Cells
The team used two laboratory models that mirror the two halves of psoriasis. The first is the immune half: RAW264.7 macrophages, mouse immune cells that, when provoked with a bacterial toxin, pump out inflammatory signals. The second is the skin half: HaCaT keratinocytes, the same human skin-cell line the argan oil team used, but here stimulated with TNF-α and IL-17A — two cytokines that sit at the very centre of psoriasis and are the targets of several blockbuster biologic drugs.
The first thing to establish was that the extract does not simply kill cells. Its IC50 — the concentration at which half the cells stop growing — was 41.22 micrograms per millilitre in keratinocytes and 22.91 micrograms per millilitre in macrophages. The researchers then worked well below those levels. At 12.5 micrograms per millilitre, the extract cut nitric oxide production in macrophages by 48.97 percent and prostaglandin E2 production by 91.15 percent. Nitric oxide and prostaglandin E2 are two of the workhorse inflammatory messengers of the immune system; the enzymes that make them, iNOS and COX-2, are the same enzymes that ibuprofen and similar drugs target. The extract also turned down the genes for IL-1β, IL-6, TNF-α, iNOS and COX-2 in the macrophages.
In the keratinocytes, the extract slowed the runaway proliferation that TNF-α and IL-17A trigger — the cellular equivalent of the thickened plaque — and broadly dialled down psoriasis-associated inflammatory genes. The abstract does not itemize which genes moved by how much, but the highlights describe the modulation as broad rather than confined to one pathway.
A word on what an IC50 of 41 micrograms per millilitre means in plain terms: it is a moderate figure. The extract is not so gentle that it does nothing, nor so aggressive that it damages skin cells at working doses. It leaves a workable window between “reduces inflammation” and “harms the cell,” which is precisely what a topical formulation needs.
Cottonseed Oil as a Carrier: Keeping the Compounds in the Skin
Here the Thai study offers its most practically interesting result, and it contrasts neatly with the nanoemulsion approach. The argan oil team measured how much CBD passed through pig skin into the fluid beneath — permeation. The Thai team measured both permeation and deposition, meaning how much of each compound stayed inside the skin layers rather than passing through.
They stayed with the traditional vehicle, cottonseed oil, but tested versions with a penetration enhancer added: diethylene glycol monoethyl ether, a widely used pharmaceutical solvent that loosens the outer skin barrier. Cottonseed oil containing 20 percent of this enhancer produced the highest deposition of all three curcuminoids in the skin. Crucially, none of the marker compounds were detected in the receptor fluid beneath the skin over 24 hours.
For a psoriasis treatment, that is arguably the ideal profile. You want the active molecules to accumulate in the epidermis where the disease lives, not to cross into the bloodstream where they could cause side effects and where they do nothing for the plaque. The argan oil nanoemulsion was optimized to get more CBD through; the Thai formulation appears to be optimized to keep it in. Both matter, and which is preferable depends on whether a drug is meant to act locally or systemically. Note that the abstract reports deposition data specifically for the curcuminoids; how much of the cannabidiol was retained is not stated in the publicly available summary.
Two Studies, One Diagnosis
Read together, the papers tell a consistent story about topical cannabinoids and psoriasis. The mechanism is plausible and reproducible: in two independent laboratories using the same human keratinocyte line, cannabinoid-containing preparations reduced inflammatory signalling and cell overgrowth. And in both cases, the researchers spent as much effort on the vehicle — nanodroplets and chitosan in one case, cottonseed oil and a solvent in the other — as on the active ingredient, because the vehicle is where topical products succeed or fail. The Biomedicines review arrives at the same place from the clinical side: formulation and route are two of the five variables that differ most between trials, and two of the main reasons their results are hard to compare.
The Thai study also puts a different kind of evidence on the table. Much of the literature on cannabis and skin comes from isolated CBD. This is a whole-plant, two-plant extract with a mixture of curcuminoids, a turmeric essential oil compound and cannabidiol acting together, standardized so that the mixture is reproducible. That is closer to how such remedies are actually used, and it opens the door to a question this study raises but cannot settle: does turmeric add something CBD alone does not, or vice versa? Similar delivery challenges are being tackled for other inflammatory skin conditions too — research into CBD and CBG combinations for eczema is following a comparable trajectory, suggesting the entire class of topical cannabinoid therapeutics is approaching a formulation inflection point. If you are unclear on the differences between CBD, CBG, CBN and hemp seed oil, our science-based guide to cannabidiol lays them out.
What Neither Study Can Tell Us Yet
It is worth being blunt about the limits, because the marketing around CBD skincare rarely is.
Both studies were carried out in cell cultures and on excised pig ear skin. Neither used a living animal with psoriasis-like disease, let alone a human patient. Cell lines are simplified stand-ins: HaCaT keratinocytes are immortalized cells that behave differently from the skin of a person with psoriasis, and RAW264.7 macrophages are mouse cells. Pig skin is a good proxy for human skin in permeation studies, but a plaque of psoriasis is not intact healthy skin — it is thicker, more inflamed and structurally disrupted, and no one has yet tested either formulation on that.
The Thai paper is a journal pre-proof, meaning the final published version may still carry small corrections. Its comparison with the single extracts, which is the scientific heart of a “synergy” claim, is not quantified in the abstract. And the extract’s THC content is not reported in the publicly available summary — leaf material is low in THC, but “low” is not “zero,” which matters for any product that might follow.
There is also the regulatory reality in the study’s home country. Thailand, which decriminalized cannabis in 2022, reclassified cannabis flower as a controlled herb in June 2025, restricting sales to prescription holders. A standardized leaf extract for skin use would sit at the intersection of the traditional medicine framework and the country’s still-unfinished Cannabis and Hemp Act, and there is no indication in the paper that a product is being developed.
Beyond the Skin: Psoriatic Arthritis, Mood and Sleep
Psoriasis is increasingly understood as a whole-body disease. The review lists psoriatic arthritis, metabolic syndrome, cardiovascular disease, anxiety and depression among its frequent companions, and it notes that psychological stress can feed the disease through nerve endings in the skin that release an inflammatory messenger called substance P. In mouse work summarized in the review, activating CB1 receptors on those sensory nerves reduced both inflammation and scratching.
That raises a question many people ask in search engines: can cannabis relieve psoriasis and psoriatic arthritis at the same time? The honest answer is that nobody has tested it properly. The authors write that the possibility of cannabinoids taken by mouth acting on both the skin and these related problems remains largely unexplored in psoriasis-specific trials, and they want future studies to measure sleep, mood, quality of life and inflammatory markers alongside plaque scores. For joint pain, the evidence in a related disease is similarly thin: a recent review of cannabinoids for rheumatoid arthritis pain found just one randomized trial in more than three decades of literature.
What US Dermatologists Think About Cannabis for Psoriasis
The uncertainty is not confined to journals. In a survey of the National Psoriasis Foundation’s Medical Advisory Board, run in December 2021 with 24 of 33 members responding, 83.3% of dermatologists said they were unsure whether psoriasis is an indication for medical cannabis, and 79.2% of respondents said they did not know enough to explain its risks and benefits. Only 16.7% had received any education on medical cannabis, although all respondents wanted to learn more. At the same time, 54.2% reported that at least 10 patients had asked them about medical cannabis in the previous year, while only 21.7% had previously recommended it. Among the dermatologists, 55.5% considered medical cannabis safe for their patients, and none considered it unsafe.
The review reads these numbers as a mismatch: patients are asking faster than evidence and training are arriving. For a person with psoriasis, the practical consequence is that a dermatologist may not have a confident answer about CBD — which is, in itself, an accurate reflection of the data.
The Trials Still Under Way
Two ongoing studies may fill some of the gaps. The CanPatch trial, a randomized, double-blind study planned at a university hospital in Thailand, is testing a skin patch containing 1.0 mg of CBD in a medium-chain triglyceride oil against a placebo patch in 60 people with mild-to-moderate plaque psoriasis, with patches applied to comparable plaques on each patient. Its main outcome is the local severity score used in the 2.5% ointment trial, and it will also look at itch, safety and the skin, gut and oral microbiome.
The second, CBDermis (NCT07839455), comes from the review authors’ own group in Brazil. It is, to their knowledge, the first clinical trial designed to compare topical and oral cannabis directly in psoriasis vulgaris. Its 37 participants receive either a cream or an oil to swallow, both full-spectrum formulations containing CBD, THC and CBG at 20 mg/mL each in a 1:1:1 ratio, as single treatments for the first 60 days, and then both together for the following 120 days, with severity, safety and quality of life tracked over 180 days. Neither study has published efficacy results yet.
Readers should know the context. The corresponding author, Francisney Pinto Nascimento, discloses that he is a partner in a cannabis research organization focused on clinical trials, and the group is running one of the trials it describes. The authors also state that they used ChatGPT to help with grammar and to generate and refine one of the paper’s figures, which they say they reviewed and verified. The first author was supported by a scholarship from Fundação Araucária, the research foundation of the Brazilian state of Paraná.
Where Does This Leave the CBD Skincare Space?
The honest answer is: closer to a real answer, but not there yet.
What the argan oil study contributes is a clear and well-characterized formulation platform. The researchers have established what the nanoemulsion looks like, how it behaves physically and chemically over time, how it releases CBD, and how it interacts with skin cells. They have also identified the precise problem to solve next: either reformulate the chitosan component to eliminate toxicity concerns — perhaps through purification steps that remove residual acetic acid, or by using lower molecular weight chitosan variants — or explore alternative bioadhesive polymers that achieve the same coating effect without the safety signal.
What the Thai study contributes is a reproducible, chemically defined version of a traditional remedy, with evidence that it acts on the right biological targets and stays where it is put. The logical next step for that work is a psoriasis animal model, and then a controlled comparison against either a placebo vehicle or a standard topical treatment.
What the Biomedicines review contributes is the frame around both: a reminder that a promising molecule and a clever carrier still have to be tested in adequately sized trials, with standardized products, clearly defined doses and longer follow-up. Its authors suggest that the most realistic role for cannabinoids, if they earn one, may be as an add-on to established treatment — for example, for itch that persists despite it — rather than as a replacement for the creams, tablets and biologic drugs that already work for many patients.
Meanwhile, for the millions of people already using CBD skin products, the picture is both reassuring and sobering. The anti-inflammatory and anti-proliferative mechanisms are real in the laboratory. The delivery problem is real. And the commercially available products on shelves today — most of which are essentially CBD stirred into conventional cream bases — are probably delivering a fraction of what a properly engineered formulation could achieve.
That gap is precisely why research like this matters.
FAQ
Possibly with some symptoms, but it is not a proven treatment. Laboratory and animal studies consistently show that CBD can calm the inflammation and skin-cell overgrowth behind psoriasis. In people, the evidence is limited to a handful of small studies. A 2.5% CBD ointment modestly improved mild plaques compared with placebo in a 51-patient trial, while 60 mg of CBD taken by mouth every day did not reduce psoriasis severity in a 28-patient trial. Across skin conditions, itch is the symptom where cannabinoids show the most consistent benefit. A review published in October 2026 concludes that cannabinoids remain an investigational approach, worth testing as an add-on to standard treatment rather than a replacement for it.
Topical CBD has the best of the limited human data, but “good” would be overstating it. The only placebo-controlled topical trial found a modest improvement in local severity and scaling on mild plaques over 12 weeks. Shop-bought creams differ widely in how much CBD they contain, what else is in them and how well they get CBD into the skin, which is exactly why researchers are developing carriers such as argan oil nanoemulsions and cottonseed oil vehicles with penetration enhancers. Neither of those experimental formulations is available as a product, and no CBD cream has been approved as a psoriasis treatment.
In laboratory dishes, THC slowed the growth of overactive human skin cells, as did CBD, CBG and CBN. In people, the data are very thin: one small single-blind study of 20 patients found that a cream containing both THC and CBD lowered average PASI over eight weeks, and a single case report described improvement with several THC-containing products. Neither had a placebo group, so neither can show that THC itself was responsible. THC is also the intoxicating component of cannabis and is tightly regulated, which matters for any product that contains it.
Hemp-derived CBD became legal at the federal level with the 2018 Farm Bill, which defined hemp as cannabis with no more than 0.3% delta-9 THC by dry weight. That definition is about to tighten. A federal spending law signed in November 2025 switches the test to total THC, including THCA, and caps finished hemp-derived cannabinoid products at 0.4 mg of total THC per container. The change was due on 12 November 2026, but a continuing resolution signed on 2 September 2026 pushed most of it back to 11 December 2026, and Congress could delay it again. Full-spectrum CBD products that carry traces of THC may no longer qualify as hemp once the cap applies. Separately, the FDA has approved only one CBD medicine, Epidiolex, for rare seizure disorders, and has not approved any CBD product for psoriasis. A CBD cream sold as a cosmetic may not legally claim to treat, cure or prevent a disease, and state rules on THC limits and labelling differ.
Disclaimer
This article is for informational and educational purposes only. It summarizes findings from peer-reviewed scientific studies and a review of the literature and does not constitute medical or legal advice. CBD products and turmeric–cannabis preparations are not approved by the FDA or EMA as treatments for psoriasis or any other skin condition. CBD taken by mouth can interact with prescription medicines and may affect liver function. Individuals with psoriasis or other medical conditions should consult a qualified healthcare provider before using any CBD product and should not stop or change prescribed treatment without medical advice. Much of the research described is preclinical; results in cell cultures, laboratory skin models and animals do not guarantee equivalent outcomes in humans, and the clinical trials to date are small. The legal status of cannabis-derived products varies by country and, in the United States, by state, and federal hemp rules are changing.
