Turmeric May Help Reduce the Risk of Skin Cancer

UV radiation from the sun can damage skin, even for people with darker skin tones.

Skin Cancer and Wrinkles

Did you know that many of the factors that increase the risk of skin cancer are also linked to aging skin? Toxins, cigarette smoking, and especially UV radiation all cause skin damage that leads to wrinkles and uneven skin tone. The good news is that turmeric compounds could help keep your skin looking its best and healthy too! (vi.483-485)

Sunburnt Woman at risk for Skin Cancer

With skin cancer rates on the rise, experts suggest that natural compounds can help protecting your skin inside and out. Studies show that using turmeric and its compounds (both nutritionally and topically) may be able to prevent or even treat skin cancer. In fact, cooking turmeric with coconut or olive oil transforms its curcumin compounds into even more powerful anticancer fighters. (vi.443-447)

Causes and Risk Factors for Skin Cancer

Skin cancer causes and risk factors include:

All of these factors increase the likelihood of DNA damage in skin cells that can lead to cancer. (vi.443)

How Can Turmeric Help?

Turmeric's curcumin compounds were tested in one small clinical study involving patients with precancerous lesions with a high risk of progressing to full-blown cancer. In the 6 patients with Bowen's disease of the skin, none progressed to malignancy during the 3 month study. Two of the patients actually showed improvement at the cellular level. (vi.8)

The antioxidant and anti-inflammatory properties of turmeric and many of its compounds help protect against free radicals, inflammation, and DNA damage that can cause or promote skin cancer. Combinations of compounds (as they are in turmeric and other foods) may also have a cumulative effect against cancer cells. In fact, studies suggest they may even work better together in suppressing cancer cell growth(vi.153443-448)

Table VI.50: Turmeric's Phytochemical and Nutrient Effects in Skin Cancer
Turmeric Compound Effects in Preclinical Studies

1,8-cineole (vi.71-72)

(also known as eucalyptol)

Alpha-linolenic acid (vi.71)

(a polyunsaturated fatty acid)

Alpha-pinene (vi.71-72)

Alpha-terpineol (vi.7174)

Ar-turmerone (vi.74)

Beta elemene (vi.415)

Borneol (vi.74)

When combined with curcumin, borneol increased curcumin's effectiveness in the following: (vi.448)

Caffeic acid (vi.74)

Camphor (vi.74)

Curcumin (vi.74)

Both topical and oral doses of curcumin have been tested in lab and animal studies against skin cancer, especially melanoma. They suggest that curcumin can help prevent and treat skin cancer. Curcumin also works well with different chemotherapy drugs. Interestingly, in lab studies low doses of curcumin combined with exposure to visible light and UVA radiation significantly blocks melanoma growth. (vi.452)

Curcumin blocks expression of growth cycle proteins such as Ki-67 and cyclin D1, including in melanoma and squamous cell carcinoma. Research indicates that substances that suppress Ki-67 can stop cancer cells from growing and is a strong indicator of survival in melanoma. In an animal model of this aggressive type of skin cancer, curcumin suppressed levels of Ki-67 by itself, although the effect was much greater when animals were exposed to UVA radiation. This may be especially important in thick, nodular melanomas, since recent analysis of cancer patient cases confirms that high Ki-67 levels themselves are associated with a poorer prognosis in this type of melanoma — more so than even mitotic count. (vi.107-108122275453-454)

In another animal study, curcumin significantly inhibited growth of squamous cell carcinoma skin tumors. The strength of its antitumor effect was dose-dependent. Other animal studies show that oral curcumin doses significantly reduce the size of chemoresistant and highly metastatic melanoma tumors. (vi.122275455)

Multiple lab and animal studies also show the following anti-skin cancer dose and time-dependent effects of curcumin:

Note: M14 melanoma cells are resistant to curcumin treatment due to overexpression of a gene involved in lipid removal from cells. (vi.475)

Eugenol (vi.74)

Farnesene and Farnesol (vi.110163200)

Ferulic acid (vi.138)

  • Levels of free radicals with antioxidant activity. (vi.55)
  • Tyrosinase activity in melanoma cells. (vi.55)

Fisetin (vi.79)

Geraniol (vi.112)

Limonene (vi.74)

Quercetin (vi.79)

Resveratrol (vi.83)

ρ-cymene (vi.71-72)

Vanillic acid (vi.5574)

Vitamin C (vi.71)

Vitamin E (vi.71)

Whole turmeric extract

Xanthorrhizol (vi.132)

  • Metastasis to lung from melanoma. (vi.123)
  • Based on studies in other types of cancer, may synergistically boost curcumin's anticancer effects. (vi.183)

Figure VI.32: How Turmeric's Curcumin Compounds Stop Skin Cancer Cells

Figure VI.32: How Turmeric Compounds Stop Skin Cancer Cells (vi.16567580-8184108122275415450454456-474476)

Caution: Curcumin and Cytokine Therapy

Lab studies suggest that curcumin could inhibit the effectiveness of cytokine therapy for melanoma. (vi.472)

Enzymes that enhance, stimulate, or suppress other proteins. (vi.118)
Specifically, caspase-3 activity. (vi.450)
IBMX-induced microphthalmia-associated transcription factor (MITF). (vi.75)
Alpha-melanocyte stimulating hormone (α-MSH). (vi.75)
Specifically, TRP-1 and TRP-2. (vi.75)
Such as VEGF. (vi.415)
Such as p21, p23, p27, p38, p53. (vi.454458462)
Specifically, Chk2. (vi.454)
Caspase-3, caspase-7, caspase-8, caspase-9, and caspase-12 enzymes. (vi.459-460462)
Such as Foxo3a. (vi.466)
Such as mmu-miR-205-5p in melanoma tumors. (vi.467)
Specifically, Bax and Bim-1 proteins. (vi.462466)
Specifically, MST1 and JNK. (vi.466)
Specifically, melanoma surface antigen Muc18. (vi.459)
Specifically, c-myc oncogene in the human melanoma A375 cell line and PRL-3 oncogene in the highly metastatic B16BL6 melanoma tumors. (vi.469-470)
Such as X-linked inhibitor of apoptosis protein (XIAP), Bcl-2, and Mcl-1 protein. (vi.457460472)
Specifically, IκB, IκBα kinases (IKK), as well as MTOR, PDE1, PDE4, pS6, and Src kinases. (vi.81122470)
Such as the main inflammatory transcription factor NF-κB and cell cycle proteins that help cancer cells divide and multiply. (vi.5681)
Such as NFκB and STAT3. (vi.457)
For example, COX-2. (vi.444454)
Specifically, E2F1. (vi.78)
Specifically, β-catenin, Brn-2, and microphthalmia-associated transcription factor (MITF). (vi.80476)
Specifically, c-myc oncogene in the 451Lu human melanoma cells. (vi.476)
Cyclin-dependent kinases (CDK2, CDK4, and CDK6). (vi.476)
Such as c-myc, c-jun, and c-fos. (vi.84)
Specifically, cyclins D1 and D2. (vi.80)
Specifically, p21. (vi.80)
Such as TGF-β1. (vi.84)
Specifically, MAPK and CDKs 2, 4, and 6. (vi.8084)
Such as IFN-α, IFN-γ, IL-2, and IL-12. (vi.472)

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