Black Seed Oil, Eczema, Topical Steroids, Oh My!

Eczema is quite common. According to the National Institute of Allergy and Infectious Diseases, approximately 30% of the U.S. population (including children) deal with this inflammatory disorder each day.[1] We’re given the impression on social media and cinema that perfection is something assumed - when ultimately we are all dealing with our own unique challenges. 

Eczema is one of these challenges. Unfortunately for millions, and possibly for yourself - keeping up with eczema can be expensive and stressful. We won’t dive deep into the prices, but thousands of dollars can be commonplace.[2] It's not irrational to feel a bit helpless. But never forget you’re not alone, and to us - never overlooked. 

Achieving a greater quality of life is a goal worth striving for. A happier life is afterall priceless, but possible side effects can quickly diminish hopeful thinking. 

Side effects such as topical steroid withdrawal can be the most challenging. This condition traditionally occurs after frequent, long-term use of a topical steroid is stopped. Characterized by a red, burning dermatitis - the individuals who are able to discontinue use and wait out the discomfort are nothing short of special.[3] The ideal counterpart to eczema should not include another challenge of its own.

We at SciZenna do not offer medical advice. We are not recommending you to stop your current treatment set out by your physician. We are not claiming that our Black Seed Rub is FDA approved to treat or cure any disease. 

What we are recommending is to keep an open mind, and to scan the horizon for simpler, less expensive, more natural solutions. And of course - arm yourself with a greater understanding of what’s going on physiologically. That’s where we come in.

We started developing our Black Seed Rub to help soothe keto rash - but have been told by a few of our customers that it seems to help calm eczema. This information is strictly qualitative and not backed by a specific clinical trial - its people like you reaching out and telling us that the Black Seed Rub helped their eczema. 

The purpose of this article is to dive deeper into the interactions of black seed oil and eczema. We’ll highlight two research publications that test the effectiveness of black seed oil and Thymoquinone to reduce eczema, compared to two common treatments - Betamethasone (a topical steroid) and tacrolimus (a calcineurin inhibitor). 

Before we dive straight into the research, let's first expand on a few things. First of all, black seed oil is extracted from the black seeds of the Nigella Sativa plant. It’s history is quite old, however the research is just now catching up to the historical antidotes. Our previous post dives further into its history. 

We strive to represent this vast ocean of research by scanning the horizon, and extracting impactful research floating on the surface. One of these gems, published in the Journal of the European Academy of Dermatology and Venereology, compared the effectiveness of black seed oil, Betamethasone and Eucerin on reducing hand eczema as well as improving quality of life of sixty individuals from ages 18-60 years of age in a randomized controlled double blind study.[4]

Individuals with hand eczema originating from atopic dermatitis, occupational dermatitis, or irritant dermatitis were allowed to participate, and were asked to stop all topical medications at least 14 days before the study began. Over the course of four weeks, each patient applied a maximum of one gram of the treatment ointment to their hand eczema twice a day and were tasked with avoiding eczema irritants over the course of the study. The researchers added 0.1% mint to all ointments to mask their identities.[4]

These individuals were assessed on the first, 14th, and 28th day during the four week period. The assessment was performed by physicians and consisted of first measuring the severity of hand eczema using the Hand Eczema Severity Index (HESI), and secondly measuring the patients quality of life using the Dermatology Life Quality Index (DLQI).

The Hand Eczema Severity Index (HESI) is a physician-performed measurement system that involves several components. The goal of the assessment is to generate a qualitative HESI score based on the observed severity of hand eczema. The HESI assessment looks for six signals of eczema: erythema (redness of the skin that results from capillary congestion), infiltration and papulation (the formation of circular areas of elevated, solid skin or papules), vesicles (fluid filled sacs), fissures, and scaling and oedema. The assessment is performed on five areas of the hand - fingers (excluding the fingertips), fingertips, palm, wrist, and the back of the hand.[5]

For each area of the hand, the physician looks for each signal and scores each signal on a scale of 0-3 - with 0 being no sign and 3 being severe presence of the signal. These scores are then added together to get a total sign score. Then, the total extent of eczema is assessed for each part of the hand and given a score between 0-4. The final step in obtaining the HESI score is to then multiply the total sign score by the total extent of eczema score. This score will be between a range of 0 to 360.[5]

The Dermatology Life Quality Index (DLQI) questionnaire consists of 10 questions ranging from the “how itchy, sore, painful, or stinging has your skin been” to “how embarrassed or self-conscious have you been because of your skin”. The possible answers are “very much”, “a lot”, “a little”, “not at all”, and “not relevant”. The goal of the questionnaire is to not only assess the discomfort one is feeling, but also to better understand how someone’s quality of life is changing with and without treatment. These are questions that are difficult to even ask ourselves.[6] 

Using these two scores, the researchers would be able to monitor the severity of eczema as a function of treatment vs. time, as well as be able to monitor the improvement in quality of life for each patient. This is significant because successful treatments should not only address the ailment, but should also improve the lives of individuals seeking treatment. 

Several interesting things were observed over the course of the study. First of all, all treatment groups (Black Seed Oil, Eucerin, and Betamethasone) experienced a decrease in hand eczema, quantified by their HESI scores, and an improvement in quality of life based on their DLQI scores. However, individuals treated with Nigella Sativa and Betamethasone saw the most dramatic decrease in hand eczema.[4]

By the 14th day of treatment - as reported by their HESI scores, the scores of individuals using Black Seed Oil dropped by 49.3%. Betamethasome users also enjoyed a decrease in score by 52.7%.  Eucerin users only had a 26.6% reduction in score. In non-HESI score terms, this means that the observed severity of hand eczema had dropped by half compared to their starting values - only for the Black Seed Oil and Betamethasone treatment groups.[4]

The fourth week brought the best news. All three scores dropped further. However, Black Seed Oil and Betamethasone had yet again stolen the show. By week four, Black Seed Oil reduced the HESI score from the original 39.89 to 8.78 - that’s a 78.0% reduction in score, and observed eczema. Betamethasone reduced the HESI score for it’s treatment group by 81.4% by the fourth week (42.00 to 7.82). Clearly Black Seed Oil is keeping up with the topical steroid just fine in this study. Over the course of four weeks, Eucerin users only experienced a 38.1% reduction in HESI score.[4]

As for the DLQI scores, they also went down - and Black Seed Oil stole the show. 

As a quick refresher, the higher the DLQI score, the more impairing a skin disease is to a person’s quality of life. Quality of life not only includes physical feelings and symptoms, but improved mental state and self-esteem. The lower the DLQI score, the greater someone is experiencing an improvement in quality of life. The range of scores can range from 0 - 30, with a score of greater than 10 indicating that the skin disease is severely detrimental to their quality of life.[6]

For the entirety of the study, people who used Black Seed Oil reported the most dramatic improvement in quality of life. By week two, Black Seed Oil contributed to a 48% reduction in DLQI scores - initially 8.28, and by week two 4.31. By week four, Black Seed Oil reduced the scores by an additional 58% - plummeting them from 4.31 to 1.81. Over the course of four weeks, the Black Seed Oil group experienced a 78.2% reduction in average DLQI score - correlating to a drastic improvement in quality of life overall.[4]

Betamethasone, the topical steroid, improved DLQI scores from 8.23 to 5 by week two, but then stalled. By week four, Betamethasone users only saw a 15% decrease in DLQI score compared to week two - finishing the study at 4.25 vs. Black Seed Oil’s 1.81 DLQI score.[4]

Unsurprisingly, Eucerin had the least improvement in DLQI score. The mean score started at 8.35, decreased to 8.25 (only a 1.2% reduction) by week two, and then decreased a bit further to 6.54 (an additional 20.7% reduction). At the end of the four week study, Eucerin users had a total decrease of DLQI score of 21.7%, the least improvement in score. Compared to Black Seed Oil’s impressive 78.2% improvement in score and Betamethasone’s 48.9% - Eucerin users did not experience the same degree of life improvement.[4]

Skeptical readers should be asking, why is this happening? Well, in order to dive into this question, we’ll have to look at the active component within Black Seed Oil - our friend, Thymoquinone. 

Published in the Journal of Molecular Immunology, researchers specifically looked at the efficacy of Thymoquinone to reduce induced atopic eczema on the ears of mice.7 A word of caution, SciZenna understands fully that research results conducted on animals are not guaranteed to translate to humans. It is however, a stepping stone to more informed conversations involving complex interactions.Unfortunately this study is not an open-access research publication, meaning it’s behind a pay-wall - however, we purchased access to this study so we can provide you with the key takeaways.

In this study, the analysis not only measured the change in observed eczema over time with oral and topical Thymoquinone treatment, but it also measured the serum blood concentrations of various indicators of inflammation, such as Immunoglobulin E (IgE) and Total Leukocyte Count (white blood cell count) (TLC) as well as the the relative mRNA expression of IL-4, IL-5, and IFN-gamma cytokines.

Let’s pause for a moment and define some terms. 

IL-4, IL-5, and IFN-gamma are cytokines produced by leukocytes during an inflammatory response. Cytokines are a wide class of small messenger proteins. These proteins are designated with the task of sending chemical signals from one cell to another. In the case of inflammation, cytokines are produced in order to send a message to neighboring cells that it’s time to have an inflammatory response. The magnitude of an inflammatory response is highly dependent on the concentration of cytokines present. The more cytokines present, the greater the inflammatory response.[8]

Although IL-4, IL-5, and IFN-gamma are all cytokines - they’re produced for different reasons. IFN-gamma is produced during times of infection, and specifically converts T-cells into Th1 helper cells - cells that protect you from bacterial and viral infections.[8]

IL-4, and IL-5 play a slightly different role. When an irritant is present, IL-4 and IL-5 cytokines are produced by irritant-impacted leukocytes. These cytokine messengers then tell white blood cells to start producing Immunoglobulin E (IgE), an antibody.[7]

So as a quick refresher - IL-4, IL-5, and IFN-gamma are cytokine messengers that are produced during specific stimuli. IFN-gamma is produced during an infection, IL-4 and IL-5 are produced during irritation. When IL-4 and IL-5 cytokines are produced, they then tell white blood cells to produce Immunoglobulin E, an antibody. 

As mentioned earlier, Immunoglobulin E (IgE), is one of the key inflammation markers the researchers set out to monitor. This is because IgE is an antibody that when produced, continues the long chain of reactions, including the production of leukotrienes, leading to classic symptoms of inflammation like dry, itchy skin.[7,8]

In a previous post, we dove down the rabbit hole of leukotrienes and discovered that Thymoquinone inhibits the production of these inflammation messengers. Think of IgE as being slightly further upstream of the leukotrienes mentioned in that previous post. 

Back to the study. The mice’s ears were challenged with eczema via a concentrated solution that creates atopic dermatitis lesions when it comes into contact with skin. The solution was applied to the mice on the first and third day, then again on the 14th, 17th, 20th, 23rd, 26th, and 29th day. The mice were divided into six groups: the control group, which did not receive any eczema inducing solution or treatment, the diseased group (this group received the eczema inducing solution and no treatment), the oral tacrolimus group (this group received 30mg/kg of tacrolimus orally), the topical tacrolimus group (this group received 1% topical tacrolimus), the oral Thymoquinone group (this group received 10mg/kg of Thymoquinone orally), and last but not least the topical Thymoquinone group (this group received 5 μmol in 0.2 ml of acetone of Thymoquinone topically).[7]

Although we’d love to give you all the results for each treatment, for each inflammatory marker - we’ll restrain ourselves a bit. For the sake of this post, we’ll focus on topical Thymoquinone and topical tacrolimus. 

At the 14 day mark, the diseased untreated group had a Total Leukocyte Count of 7.875 - approximately double that of the control group. Clearly the untreated group was experiencing an inflammatory event with that level of white blood cells present. Oral and topical tacrolimus reduced the white blood cell count to 5.375 and 4.625 - lower than the diseased group of 7.875. However, Thymoquinone had the best performance. Oral TQ was able to reduce the white blood cell count to 5.50, and topical TQ reduced it to 4.25 - almost the same white blood cell count as the control group that didn’t have eczema.[7]

So what about the other inflammatory markers? Well, things get more interesting. First some great news - topical Thymoquinone reduced the relative mRNA expression of IL-4 and IL-5 cytokine dramatically. The word “relative” is used because the researchers measured the mRNA expression of the control group and placed that value at 1. Keep in mind this group didn’t receive the eczema inducing solution or treatment.  For perspective, the untreated group had a relative mRNA expression of 1.890, which coincides with being almost twice as high as the control group. Topical TQ reduced relative mRNA expression of IL-4 to 0.8614. Yes, you read that correctly - topical TQ dropped the inflammatory expression of IL-4 to below that of the control. As for IL-5, topical TQ still performed beautifully, reducing expression to 1.390 compared to the untreated group of 1.982. Topical tacrolimus also reduced IL-4 and IL-5 considerably, reducing IL-4 expression to 0.8614 and IL-5 expression to 1.135.[7]

As for IgE blood concentration, the news keeps getting better. Remember, increased levels of IgE will most likely result in increased production of leukotrienes and other inflammation inducing cytokine messengers. The more cytokine messengers present, the greater the magnitude of inflammation symptoms someone will experience. Let’s get back to the results.[7]

The untreated group had an IgE concentration of 2177 ng/ml, more than triple that of the healthy control group whose IgE concentration was only 591.4 ng/ml. The oral treatments performed well in reducing IgE concentration - oral TQ reduced the IgE concentration to 812.1 ng/ml and the oral tacrolimus reduced the IgE concentration to 655.71 ng/ml, fairly close to the control of 591.4 ng/ml.[7]

However, and somewhat surprisingly, the topical treatments using TQ and tacrolimus tell a slightly different story. For topical tacrolimus, the IgE concentration for this group of mice was 863.6 ng/ml - similar to the oral TQ results of 812.1 ng/ml. But the real eyebrow raiser is topical TQ’s performance. Topical TQ was able to reduce IgE concentration to 693.6 ng/m.[7] Why is this significant?

Well, Topical TQ was able to reduce IgE concentration to 693.6 ng/ml - similar to oral tacrolimus of 655.71 ng/ml and not far off from the control of 812.1 ng/ml. Let’s put these values into percentages compared to the untreated group. The control group, which didn’t have eczema or recieve treatment, had a 72.8% lower IgE concentration compared than the untreated group, oral tacrolimus had a 69.9% lower IgE concentration than the untreated group, and topical Thymoquinone had a 68.1% lower IgE concentration than the untreated group.[7] 

The significance is that Thymoquinone can perform the desired functions (in this research study, reducing eczema most likely through the reduction of various inflammation mediators) without needing to be taken orally - no pills. 

The final results we’ll analyze are the ear clinical scores. These scores were generated by evaluating the severity of eczema symptoms observed. Two independent researchers individually rated the ears of every mice on a scale of 0-3, 0 signifying no visible symptoms, 1 signifying mild symptoms, 2 signifying moderate symptoms, and 3 signifying severe observed symptoms. Then, an overall group score was generated by taking the average score of each mice in a specific group. 

At the two week mark, the ear clinical scores for all groups excluding the control were quite high, signifying significant eczema symptoms were present for all groups excluding the control. Not a great start, however by day 29, the story dramatically changed.

By day 29, the ear clinical scores for the treatment groups had significantly decreased. The untreated group suffering from eczema had an ear clinical score of 14.00, compared to the control group of approximately 1. As for the treatment groups, the clinical scores had dropped significantly. Oral and topical tacrolimus reduced the clinical ear scores to 3.00 and 3.50 respectively - demonstrating tacrolimus effectiveness. Oral and topical Thymoquinone also reduced the clinical ear scores significantly as well. By day 29, oral TQ reduced the clinical ear score to 2.90 and topical TQ reduced the clinical ear score to 4.40. Compared to the untreated eczema group of 14.00 - that’s a dramatic decrease.[7]

The researchers concluded that based on the similarity in scores between tacrolimus and Thymoquinone - it’s simply not possible to determine which treatment was more effective.7 Sometimes research doesn’t present a clear winner, however the result bears similar weight. Thymoquinone is clearly just getting started.

We’ve covered quite a bit here. Let’s take a moment and digest a few things. In general, published research is indicating that black seed oil can be quite effective in reducing not only the symptoms and appearance of eczema, but also reducing various inflammation markers due to its active compound Thymoquinone. This is fantastic - and clearly more research will be published that builds off of this work. We’ll have to wait for a clinical trial to be performed before more bold assertions can be made - but it’s a great start. 

We at SciZenna would like to emphasize a more important aspect stemming from these publications. That aspect is quality of life. 

At the end of the day, it doesn’t matter if your cytokine levels drop, or your IgE concentration is reduced - what matters is does your overall life improve because of the treatment method you’ve chosen? If that treatment method reduces your eczema but comes with the trade-off of possible addiction or even opens up the door to another more severe problem - is that truly a viable treatment method? These are questions you’ll have to ask yourself and your healthcare practitioner. 

We’d like to reiterate again - we are not offering medical advice, we are not suggesting you quit your prescribed treatment, we are not saying that our Black Seed Rub is FDA approved to treat or cure any disease - what we are saying is that the research surrounding black seed oil is quite interesting and needs to be explored further. 

That’s the sole goal of this article, and something we believe companies should be doing more often - we simply want to inform you on what we are seeing, and ideally help explain the scientific landscape surrounding these complex biological interactions. Feel free to share this article, and we’ll be sure to update you if things change. The better educated we all are, including yourself, the better we can all make decisions on where to go from here. 

Because ultimately, we are all in this together. 


  1. Eczema (Atopic Dermatitis). (2017, April 17). Retrieved April 27, 2020, from https://www.niaid.nih.gov/diseases-conditions/eczema-atopic-dermatitis.
  2. Block J. Improving Value for Patients with Eczema. Value Health. 2018;21(4):380–385. doi:10.1016/j.jval.2018.01.014
  3. Schmitt J, Apfelbacher CJ, Flohr C. Eczema. BMJ Clin Evid. 2011;2011:1716. Published 2011 May 17.
  4. Yousefi M, Barikbin B, Kamalinejad M, et al. Comparison of therapeutic effect of topical Nigella with Betamethasone and Eucerin in hand eczema. J Eur Acad Dermatol Venereol. 2013;27(12):1498–1504. doi:10.1111/jdv.12033
  5. Oosterhaven JAF, Schuttelaar MLA. Responsiveness and interpretability of the Hand Eczema Severity Index. Br J Dermatol. 2020;182(4):932–939. doi:10.1111/bjd.18295
  6. Finlay AY, Khan GK. Dermatology Life Quality Index (DLQI)--a simple practical measure for routine clinical use. Clin Exp Dermatol. 1994;19(3):210–216. doi:10.1111/j.1365-2230.1994.tb01167.x
  7. Aslam H, Shahzad M, Shabbir A, Irshad S. Immunomodulatory effect of thymoquinone on atopic dermatitis. Mol Immunol. 2018;101:276–283. doi:10.1016/j.molimm.2018.07.013
  8. Zhang JM, An J. Cytokines, inflammation, and pain. Int Anesthesiol Clin. 2007;45(2):27–37. doi:10.1097/AIA.0b013e318034194e