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Monobenzone: How Michael Jackson Turned White

This blog post is a companion to a YouTube video, which you can access here.

Like most people who grew up in the late 1980's, I was a fan of Michael Jackson. But there were several Michael Jacksons. I grew up dancing to the music of a beige Michael - not the Michael of 1982, but not entirely white Michael of 1999 either. Our Michael was beige.

As I grew up, I learned that Michael Jackson said he had vitiligo. Vitiligo is an autoimmune disorder that causes one's body to completely destroy the cells that produce melanin, our dark pigment.

Did all of Michael Jackson's Caucasian facial and hair modifications just happen to coincide in someone born with this heritable disease, or did Michael depigment himself?

What Did Michael Say?

First, let’s see what Michael said about his own mysteriously transient skin color.

1. Diagnosed with vitiligo by Arnold Klein in 1986.

2. Told Oprah Winfrey there is no such thing as skin bleaching in 1993.

Could This be True?

Michael’s assertion could be true. He may have had a genetic predisposition towards developing vitiligo. However, there are two noteworthy assertions I’d like to make.

1. Michael Jackson could have created his own vitiligo, either intentionally, or accidentally, via depigmentation drug abuse – this is what this video is mostly about.

2. There is almost no way that Michael Jackson could have believed that there were no skin depigmenting agents in 1993, 7 years after he was allegedly diagnosed with vitiligo.

a. He would have already been offered agents like monobenzone in the 7 years since he was treated, especially as he mentioned being bothered by the uneven skin color.

b. He looked like he already used them.

c. He had monobenzone in his possession when he died, decades later.

The Difference Between Albinism and Vitiligo

In skin, melanin is synthesized by melanocytes within melanosomes which are then diffused into neighboring keratinocytes. The keratinocytes then transport melanin and melanosomes from the basal epidermis to the stratum corneum.

In albinism, melanocytes are unable to produce melanin and consequently result in hypopigmentation. Unlike in vitiligo, in albinism melanocytes are present in skin at normal concentrations.

Devoid of the protection of melanin but still carrying melanocytes, type 2 albinos are at increased risk for squamous cell carcinomas although albinos are still at decreased risk for melanomas[1][2]. Unlike people with vitiligo, they are also more prone to sun damage[3] (called actinic damage).

How Does Vitiligo Develop?

Vitiligo was among the first skin conditions to be described by the medical community, with the earliest reference dating to 1765[4]. In the 1950’s[5][6], academics noted that a portion of those with vitiligo came from families with several vitiligo patients (called “multiplex families”) and some had comorbidities with other autoimmune diseases.

It turns out that most vitiligo cases occur in “simplex” form, where the patient has no family members with the disease[7]. Nonetheless, the disease is about 80% heritable[8]. There are over 50 genetic loci associated with vitiligo, the majority of which (approximately 70%) are associated with common polymorphisms[9].

Interestingly, between 1973 to 2004, age-of-onset of vitiligo among Caucasians was delayed by more than 2x, indicating a variation of exposure to some environmental trigger[10].

The current thinking about the etiology of vitiligo is as follows:

1. Both endogenous and exogenous factors drive an excess generation of reactive oxygen species (ROS) in melanocytes.

a. Exogenous: ultraviolet radiation and monobenzone.

b. Endogenous: the synthesis of melanin (melanogenesis) produces a pro-oxidant state in melanocytes[11].

i. The production of a lot of protein generates misfolded proteins, which activates the UPR-XBP1P1 gene which has been associated with vitiligo[12].

2. A failure in the antioxidant defense system sensitizes the melanocytes to ROS-induced stress[13].

a. For example, dysregulated Nrf2 pathway may inhibit autophagy[14].

b. Simvastatin may protect melanocytes from oxidative stress by activating Nrf2[15].

3. Innate immunity is triggered by pattern recognition receptors (PRRs)[16].

a. Damage-associated molecular patterns (DAMPs) such as heat-shock protein 70 (HSP70i) signal at toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and NOD-like receptors (NLRs).

4. Adaptive immunity develops with antibodies to melanocyte antigens[17].

5. CD8+ T cells[18], which produce TNF-a and IFN-y[19], kill melanocytes.

a. IFN-y appears particularly relevant[20] and inhibiting downstream activities of CXCR3[21] or JAK-STAT[22] may reverse vitiligo.

6. Reduced regulatory T cell (Tregs) activity prevents inhibition of CD8+ T cells[23]. Tregs usually suppressive autoreactive activity.

But What if You Wanted Vitiligo to Occur?

Michael Jackson failed to mention to us that he was using a medication that could entirely replicate the etiology of vitiligo. And yet, people were using monobenzone to produce near complete depigmentation of their skin since the early 1960’s[24]. Could Michael Jackson, one of the world’s most resourceful men, not have known about depigmenting agents in his interview with Oprah in the 1990’s?

The monobenzyl ether of hydroquinone, monobenzone, produces local and distant depigmentation that is clinically indistinguishable from vitiligo[25]. The effect was first noted in 1939, when academics noted that rubber gloves containing monobenzone induces progressive depigmentation in the leather tannery workers using them[26].

Monobenzone’s Mechanism of Action

Tyrosinase is an enzyme involved in the synthesis of melanin. When monobenzone interacts with tyrosinase, it is converted into a reactive quinone that binds to thiol groups in tyrosinase and other enzymes involved in synthesizing melanin, increasing their immunogenicity. Moreover, monobenzone increases oxidative stress at melanocytes and primes dendritic cells to target them with an immune response[27].

Combining monobenzone with Toll-like Receptor (TLR) agonists (e.g. imiquimod, CpG, or HSP70) vastly enhances the rate and completeness of depigmentation[28].

It Does Matter if You’re Black or White

Whether Michael Jackson developed vitiligo first and then used monobenzone to depigment himself, or whether he developed vitiligo from monobenzone, can’t be known. What we do know is that:

1. Michael Jackson could not have not known about depigmenting agents in 1993. This may indicate that he lied about the subject.

2. Celebrities have been using monobenzone since the 1960’s to depigment themselves. It would be entirely natural for Michael to have learned about the drug in the 1970’s.

3. The depigmentation from monobenzone is indistinguishable to vertigo, even among medical professionals. No doctor could be certain Michael didn’t bring the disease upon himself.

4. Michael Jackson still owned monobenzone product at the time of his death, decades after his depigmentation. This is a clear indicator that he continued to depigment throughout his life, indicating he cared about his skin color.

5. Michael Jackson wasn’t averse to body modifications or biohacking, generally.

Next, we will talk about another side of this discussion: why are people with vitiligo so protected against skin cancer, and can monobenzone make you invulnerable to skin cancers?

[1] Yakubu, A., & Mabogunje, O. A. (1993). Skin cancer in African albinos. Acta Oncologica, 32(6), 621-622. [2] Kromberg, J. G., Castle, D., Zwane, E. M., & Jenkins, T. (1989). Albinism and skin cancer in Southern Africa. Clinical genetics, 36(1), 43-52. [3] Lookingbill, D. P., Lookingbill, G. L., & Leppard, B. (1995). Actinic damage and skin cancer in albinos in northern Tanzania: findings in 164 patients enrolled in an outreach skin care program. Journal of the American Academy of Dermatology, 32(4), 653-658. [4] Le Cat, C. N. (1765). Traité de la couleur de la peau humaine en général, de celle des nègres en particulier et de la métamorphose d'une de ces couleurs en l'autre, soit de naissance, soit accidentellement... par M. Le Cat... [5] Teindel, H. (1950). Familial vitiligo. Zeitschrift fur Haut-und Geschlechtskrankheiten, 9(11), 457-462. [6] Stuttgen, G. (1950). Die vitiligo in erbbiologischer betrachtung. Z Haut Geschlechtskr, 9, 451-457. [7] Roberts, G. H., Santorico, S. A., & Spritz, R. A. (2020). The genetic architecture of vitiligo. Pigment cell & melanoma research, 33(1), 8-15. [8] Roberts, G. H., Santorico, S. A., & Spritz, R. A. (2020). Deep genotype imputation captures virtually all heritability of autoimmune vitiligo. Human molecular genetics, 29(5), 859-863. [9] Spritz, R. A., & Santorico, S. A. (2021). The genetic basis of vitiligo. Journal of Investigative Dermatology, 141(2), 265-273. [10] Jin, Y., Santorico, S. A., & Spritz, R. A. (2020). Pediatric to adult shift in vitiligo onset suggests altered environmental triggering. The Journal of investigative dermatology, 140(1), 241-243. [11] Denat, L., Kadekaro, A. L., Marrot, L., Leachman, S. A., & Abdel-Malek, Z. A. (2014). Melanocytes as instigators and victims of oxidative stress. Journal of Investigative Dermatology, 134(6), 1512-1518. [12] Birlea, S. A., Jin, Y., Bennett, D. C., Herbstman, D. M., Wallace, M. R., McCormack, W. T., ... & Spritz, R. A. (2011). Comprehensive association analysis of candidate genes for generalized vitiligo supports XBP1, FOXP3, and TSLP. Journal of Investigative Dermatology, 131(2), 371-381. [13] Jimbow, K., Chen, H., Park, J. S., & Thomas, P. D. (2001). Increased sensitivity of melanocytes to oxidative stress and abnormal expression of tyrosinase‐related protein in vitiligo. British Journal of Dermatology, 144(1), 55-65. [14] He, Y., Li, S., Zhang, W., Dai, W., Cui, T., Wang, G., ... & Li, C. (2017). Dysregulated autophagy increased melanocyte sensitivity to H2O2-induced oxidative stress in vitiligo. Sci Rep 7: 42394. [15] Chang, Y., Li, S., Guo, W., Yang, Y., Zhang, W., Zhang, Q., ... & Li, C. (2017). Simvastatin protects human melanocytes from H2O2-induced oxidative stress by activating Nrf2. Journal of Investigative Dermatology, 137(6), 1286-1296. [16] Richmond, J. M., Frisoli, M. L., & Harris, J. E. (2013). Innate immune mechanisms in vitiligo: danger from within. Current opinion in immunology, 25(6), 676-682. [17] Naughton, G. K., Eisinger, M., & Bystryn, J. C. (1983). Detection of antibodies to melanocytes in vitiligo by specific immunoprecipitation. Journal of investigative dermatology, 81(6), 540-542. [18] Van Den Boorn, J. G., Konijnenberg, D., Dellemijn, T. A., Van Der Veen, J. W., Bos, J. D., Melief, C. J., ... & Luiten, R. M. (2009). Autoimmune destruction of skin melanocytes by perilesional T cells from vitiligo patients. Journal of Investigative Dermatology, 129(9), 2220-2232. [19] Boniface, K., Jacquemin, C., Darrigade, A. S., Dessarthe, B., Martins, C., Boukhedouni, N., ... & Seneschal, J. (2018). Vitiligo skin is imprinted with resident memory CD8 T cells expressing CXCR3. Journal of Investigative Dermatology, 138(2), 355-364. [20] Yang, L., Wei, Y., Sun, Y., Shi, W., Yang, J., Zhu, L., & Li, M. (2015). Interferon-gamma inhibits melanogenesis and induces apoptosis in melanocytes: a pivotal role of CD8+ cytotoxic T lymphocytes in vitiligo. Acta dermato-venereologica, 95(6), 664-671. [21] Richmond, J. M., Masterjohn, E., Chu, R., Tedstone, J., Youd, M. E., & Harris, J. E. (2017). CXCR3 depleting antibodies prevent and reverse vitiligo in mice. The Journal of investigative dermatology, 137(4), 982-985. [22] Craiglow, B. G., & King, B. A. (2015). Tofacitinib citrate for the treatment of vitiligo: a pathogenesis-directed therapy. JAMA dermatology, 151(10), 1110-1112. [23] Lin, M., Zhang, B. X., Shen, N., Dong, X. J., Zhang, C., Qi, X. Y., ... & Tu, C. X. (2014). Regulatory T cells from active non-segmental vitiligo exhibit lower suppressive ability on CD8+ CLA+ T cells. European Journal of Dermatology, 24(6), 676-682. [24] Becker, S. W., & Spencer, M. C. (1962). Evaluation of monobenzone. Jama, 180(4), 279-284. [25] Boissy, R. E., & Manga, P. (2004). On the etiology of contact/occupational vitiligo. Pigment Cell Research, 17(3), 208-214. [26] Oliver, E. A., Schwartz, L., & Warren, L. H. (1939). Occupational leukoderma: preliminary report. Journal of the American Medical Association, 113(10), 927-928. [27] van den Boorn, J. G., Melief, C. J., & Luiten, R. M. (2011). Monobenzone‐induced depigmentation: From enzymatic blockade to autoimmunity. Pigment cell & melanoma research, 24(4), 673-679. [28] Webb, K. C., Eby, J. M., Hariharan, V., Hernandez, C., Luiten, R. M., & Le Poole, I. C. (2014). Enhanced bleaching treatment: Opportunities for immune‐assisted melanocyte suicide in vitiligo. Experimental dermatology, 23(8), 529-533.


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