Hyperpigmentation and your skin


Brown patches

Hyperpigmentation occurs when melanocytes produce excessive melanin in one area, or when melanin is not distributed evenly in the epidermis.

Common causes of hyperpigmentation are sun damage, excessive amounts of oestrogen, ageing and pollution.

Skin physiology:

  • Brown uneven patches of skin visible on the surface.
  • Overproduction of melanin and the unregulated distribution of the melanin granules result in the deposits of brown patches on the surface.
  • Hyperpigmentation may also occur post-inflammatory as a result of healing following injury to the skin.
  • Melasma occurs during pregnancy due to the overproduction of oestrogen being unable to be adequately processed by the liver. These brown patches usually disappear after birth when hormones settle down.
  • Pollution and UV radiation combine to create age spots in mature skins.

How do we address this skin condition:

  • Prevention is the key with this condition.
  • Avoid extended exposure to direct sunlight or apply a sunscreen over griffin+row Nourish or Enrich before exposing yourself to the sun.
  • Stay out of the sun completely while your skin is healing, such as following surgery or injury.
  • Use antioxidant rich skincare, such as griffin+row, as this will help neutralise the effects of free radicals in UV radiation and airborne pollution.
  • Cleanse twice a day to remove pollution from your skin, including nanoparticles which settle on your skin, are invisible to the naked eye and wreak havoc on your skin.
  • Once dark spots are present, medical options may include laser treatment or surgery. Most of these treatments are temporary at best and may in fact exacerbate the condition. It is therefore highly recommended that medical advice is obtained from a dermatologist before spending hundreds of dollars on treatments that have no evidence of their long-term effectiveness.


griffin+row Cleanse works well at efficiently removing makeup and airborne pollution from your skin, without upsetting your skin’s natural acid balance.

Hyperpigmentation comes in many shapes, forms and sizes. It can plague skin types because of age, as a consequence of a skin condition and even as a result of sun exposure. Hyperpigmentation can be treated effectively with changes to a person’s lifestyle and skincare routine.

Hyperpigmentation is not inevitable. Following a preventative skincare regimen can help to avoid its contraction. Hyperpigmentation does not have to be permanent. Using appropriate skincare to treat and refresh skin can help reverse its effects. Hyperpigmentation may not be a standalone skin condition. Identifying an individual’s unique triggers and causes will help design an effective anti-hyperpigmentation skincare routine.

What is hyperpigmentation?

A person’s natural skin colouration is determined by unique and specific expression of a pigment called melanin. There are two types of melanin humans express – a red/yellow pigment called pheomelanin and a brown/black pigment called eumelanin. The type of melanin granules produced alongside the size, number and distribution of melanin producing organelles i.e. melanosomes determines an individual’s skin colour1. The number of melanocytes – melanosome producing cells, has no correlation to skin tone. Melanocyte cells produce melanosome organelles which distribute themselves inside of skin cells to produce melanin pigment granules.

Skin colouration is genetically determined however may be temporarily changed on exposure to sunlight with melanin exhibiting mild to moderate photo protective effects2. Initial exposure to sunlight causes a temporarily surface re-distribution of melanin granules3, with long term exposure causing an increase in melanin manufacture.

In cases of hyperpigmentation melanin granules are over produced and unevenly distributed resulting in a patchy, uneven skin tone.

What are the causes of hyperpigmentation?

Hyperpigmentation has many causes. Effective treatment of hyperpigmentation can only be made when the primary cause has been identified and therefore the best treatment plan evolved. Causes of hyperpigmentation range from;

  • Sun exposure
  • Hormones e.g. melasma often nicknamed the ‘mask of pregnancy’
  • Age e.g. age spots/liver spots
  • Acne/spots/wounds – post inflammatory hyperpigmentation
  • Medication e.g. oral contraceptives
Most cases of hyperpigmentation have one of three causes;
  1. Sun exposure
  2. Hormonal changes (age, medication, pregnancy)
  3. Damage (may be caused by acne, eczema, harsh skincare treatments or similar)
Within these three causes there are three specific types of hyperpigmentation4;
  1. Post inflammatory hyperpigmentation
  2. Solar lentigos
  3. Melasma
Post inflammatory hyperpigmentation is caused by external trauma to skin. The most common cause of post inflammatory hyperpigmentation (PIH) is acne, however its occurrence is also common in similar skin traumas such as eczema, mosquito bites, in-grown hairs, surfactant damage and areas of scratching.

Solar lentigos are caused by exposure to sunlight specifically UVA which may penetrate directly to the depth of melanocyte cells. Recent studies show other environmental factors such as air pollution may play a contributory role5. It is noted that the melanogenic potential of melanocytes is elevated in areas of skin affected by solar lentigos. UVA light is believed to cause the release of pigmentation controlling factors as is evidenced by the ability to tan, however, UVA light can also cause DNA damage therefore adversely affecting or overpowering natural processes in targeted areas of skin6. Solar lentigos are most commonly referred to as age or liver spots.

Melasma is a form of pigmentation expressed as a consequence of a change in hormones and accompanied sensitivity to sunlight. Melasma may be experienced during puberty as a result of contraceptive medication or pregnancy.

What does hyperpigmentation look like?

The size, look and texture of hyperpigmentation is in some part determined by its cause. Areas of hyperpigmentation will appear markedly darker than areas of surrounding skin. In cases of hyperpigmentation these often resolve as roughly edged circular spots up to a centimetre in size. In cases of melasma i.e. hormone induced pigmentation, these patches may expand to cover what is referred to as the butterfly area of skin – T-zone and cheeks.

Post inflammatory hyperpigmentation is determined mostly by the area of trauma. In acne lesions post inflammatory hyperpigmentation resolves as a small area of darkened skin a few millimetres in size. In cases of skin trauma caused by eczema or direct contact, the area of hyperpigmentation often takes on an area similar in size to the initial area of trauma.

Which skin types are most prone to hyperpigmentation?

Darker skin types are known to have an increased risk of hyperpigmentation relative to those with pale/Caucasian skin types. Dark skin type including those of Asian, Mediterranean, African and Latin descent have an increased pigmentation risk.

How can hyperpigmentation be treated?

Hyperpigmentation does not have to be an inevitable consequence of genetics, it also does not have to be accepted. With prevention, hyperpigmentation can be lessened and even avoided. With appropriate skincare, existing areas of hyperpigmentation may be decreased and even resolved.

There are 2 primary methods of pigmentation prevention;

  1. Daily sun protection
Solar lentigos are caused by exposure to sunlight. Other forms of hyperpigmentation such as melasma and post inflammatory hyperpigmentation can be worsened on exposure to sunlight. Therefore daily sun protection of SPF 30 or greater helps to avoid a pigmented, patchy darkening of skin.
  1. Use of antioxidant rich skincare
Most forms of hyperpigmentation are a consequence of damage or trauma. Solar lentigos are caused by harmful UV light. Post inflammatory hyperpigmentation is caused by immune activation – a consequence of conditions such as acne. During immune activation several oxidative compounds are released7. Antioxidants help to combat their effects. Regular use of products such as the griffin+row enrich antioxidant night cream will help combat the incidence and severity of hyperpigmentation. Antioxidants are also able to inhibit the pathways leading to formation of hyperpigmentation e.g. vitamin C. For treatment in areas of existing hyperpigmentation there are predominantly two approaches;
  1. Exfoliation
Exfoliation helps speed up the lightening and brightening of superficial pigmentation marks, for example, those caused by spots. The epidermis is in a constant state of renewal with the average life of each skin cell spanning a one month period8. Therefore the majority of pigmented skin cells will be shed from skin within a four week time period.  Superficial post-inflammatory hyperpigmentation can therefore be effectively treated by exfoliation – a process which speeds skins natural cell turnover rate.

griffin+row Exfoliate is a natural muslin cotton cloth that will exfoliate your skin gently and evenly to remove the top layer of dead cells from your skin, giving your skin a glowing and radiant look, and also aiding the absorption of the antioxidant-rich moisturiser into your skin.

  • Skin lightening actives

For treatment of deep reaching hyperpigmentation or ongoing treatment of hyperpigmentation caused by hormone imbalance, skin lightening actives may be appropriate. Skin lightening actives interact with the biological steps required to manufacture melanin. Many skin lightening actives treat hyperpigmentation by inhibition of an enzyme named tyrosinase9. The tyrosinase enzyme is rate limiting, meaning if it is indisposed, melanin creation will not occur. Other controversial skin lightening actives cause cytotoxicity of melanocytes rendering then inactive.

Which skin lightening actives are used to treat disorders of hyperpigmentation?

Skin lightening treatments vary from shelf available to over the counter to prescription. They range in concentration from those designed for mild hyperpigmentation to products designed for deeper reaching melasma. Their safety profile and side effects go from minimal to causing alternate disorders of pigmentation.

For example;

  • Hydroquinone
Skin lightening treatments containing hydroquinone act via two pathways – they firstly inhibit the tyrosinase enzyme, they secondly cause melanocyte toxicity10. In the past this dual action has advanced the popularity of hydroquinone. Not only does the treatment cause reversal of hyperpigmentation it also prevents reoccurrence after treatment has ended due to the permanent toxicity to melanocyte cells. Over the years, hydroquinone treatments have been linked to ochronosis – the darkening of skin, increased cancer risk and mercury poisoning11. Hydroquinone is not considered to have a high safety profile.
  • Niacinamide ( also paired with N-acetyl glucosamine)
Niacinamide, also known as vitamin B3 is an antioxidant commonly used in skincare products. In addition to antioxidant activity, it’s also a well-documented anti-inflammatory with known activity against acne and rosacea12. Studies show after four weeks use at 5% concentration, participants showed a significant decrease in hyperpigmentation. Analysis shows niacinamide is an active inhibiter of melanosome transfer13. Melanosome are the organelles which express melanin granules within skin cells and therefore their inhibition reduces pigment disorders. Niacinamide is widely accepted as safe for use with its effects on hyperpigmentation being non-cytotoxic.
  • Vitamin C
Vitamin C, also known for its antioxidant activity alongside its positive effects on collagen production is often used as a lightning and brightening agent. Vitamin C is an active anti-pigmentation agent because of its antioxidant activity14. Vitamin C suppresses melanin synthesis by reducing the effects of the tyrosinase enzyme. Tyrosinase works by oxidising L-tyrosine to L-DOPA. Vitamin C as an antioxidant inhibits this conversion hindering melanin synthesis15. Vitamin C is considered safe for use and is active in mild cases of hyperpigmentation.
  • Kojic acid
Kojic acid is naturally found in fungi and commercially made as a by-product of rice fermentation. Its activity against hyperpigmentation proceeds through inhibition of the tyrosinase enzyme. Kojic acid has been associated with contact allergy and should be avoided by sensitive skin types16.

In addition to these four well known skin lightening and brightening actives, many skincare preparations also use ingredients such as;

  • Azelic acid
  • Retinoids – (vitamin A) safety concerns regarding sun sensitivity
  • Resorcinol
  • Ellagic acid – naturally found in fruits and vegetables/ found in skincare within pomegranate extracts
  • Arbutin
  • Liquorice extract

An effective anti-pigmentation skincare routine should feature both methods of prevention – daily use of sun protection and an antioxidant rich moisturiser alongside a preferred method of hyperpigmentation treatment.

  1. Brenner, M. and Hearing, V. J. (2008), The Protective Role of Melanin Against UV Damage in Human Skin†. Photochemistry and Photobiology, 84: 539–549. doi:10.1111/j.1751-1097.2007.00226.x
  2. Gilchrest, B. A., M. S. Eller, A. C. Geller and M. Yaar (1999) The pathogenesis of melanoma induced by ultraviolet radiation. N. Engl. J. Med. 340, 1341–1348.
  3. Routaboul, C., A. Denis and A. Vinche (1999) Immediate pigment darkening: Description, kinetic and biological function. Eur. J. Dermatol. 9, 95–99.
  4. Latest insights into skin hyperpigmentation. Ortonne JP, Bissett DL. J Investig Dermatol Symp Proc. 2008 Apr;13(1):10-4. doi: 10.1038/jidsymp.2008.7.
  5. Nakamura, M., Morita, A., Seité, S., Haarmann-Stemmann, T., Grether-Beck, S. and Krutmann, J. (2015), Environment-induced lentigines: formation of solar lentigines beyond ultraviolet radiation. Exp Dermatol, 24: 407–411. doi:10.1111/exd.12690
  6. Comprehensive analysis of melanogenesis and proliferation potential of melanocyte lineage in solar lentigines. Yamada T, Hasegawa S, Inoue Y, Date Y, Arima M, Yagami A, Iwata Y, Abe M, Takahashi M, Yamamoto N, Mizutani H, Nakata S, Matsunaga K, Akamatsu H. J Dermatol Sci. 2014 Mar;73(3):251-7. doi: 10.1016/j.jdermsci.2013.11.005. Epub 2013 Nov 14.
  7. Wagener FADTG, Carels CE, Lundvig DMS. Targeting the Redox Balance in Inflammatory Skin Conditions. International Journal of Molecular Sciences. 2013;14(5):9126-9167. doi:10.3390/ijms14059126.
  8. Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Epidermis and Its Renewal by Stem Cells.
  9. Disorders of hyperpigmentation. Pandya AG, Guevara IL. Dermatol Clin. 2000 Jan;18(1):91-8, ix.
  10. Draelos, Z. D. (2007), Skin lightening preparations and the hydroquinone controversy. Dermatologic Therapy, 20: 308–313. doi:10.1111/j.1529-8019.2007.00144.x
  11. Research, Center for Drug Evaluation and. “About the Center for Drug Evaluation and Research – Hydroquinone Studies Under The National Toxicology Program (NTP)”. www.fda.gov.
  12. Gehring, W. (2004), Nicotinic acid/niacinamide and the skin. Journal of Cosmetic Dermatology, 3: 88–93. doi:10.1111/j.1473-2130.2004.00115.x
  13. Hakozaki, T., Minwalla, L., Zhuang, J., Chhoa, M., Matsubara, A., Miyamoto, K., Greatens, A., Hillebrand, G.G., Bissett, D.L. and Boissy, R.E. (2002), The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer. British Journal of Dermatology, 147: 20–31. doi:10.1046/j.1365-2133.2002.04834.x
  14. Postinflammatory hyperpigmentation: etiologic and therapeutic considerations. Callender VD, St Surin-Lord S, Davis EC, Maclin M. Am J Clin Dermatol. 2011 Apr 1;12(2):87-99. doi: 10.2165/11536930-000000000-00000
  15. Positive regulation of melanin pigmentation by two key substrates of the melanogenic pathway, L-tyrosine and L-dopa. Słominski A, Moellmann G, Kuklinska E, Bomirski A, Pawelek J. J Cell Sci. 1988 Mar;89 ( Pt 3):287-96.
  16. Final report of the safety assessment of Kojic acid as used in cosmetics. Burnett CL, Bergfeld WF, Belsito DV, Hill RA, Klaassen CD, Liebler DC, Marks JG Jr, Shank RC, Slaga TJ, Snyder PW, Andersen FA. Int J Toxicol. 2010 Nov-Dec;29(6 Suppl):244S-73. doi: 10.1177/1091581810385956.

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