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IV Curcumin & cancer

Turmeric is a spice extracted from the rhizome of a plant called Curcuma longa, which belongs to the Ginger family. The yellow pigment found in this spice is known as curcumin. This constituent curcumin has numerous benefits to the body. In fact, Maheshwari et al. (2006) in a short review outline the following biological actions:

  • Anti-inflammatory
  • Anti-oxidant activity
  • Enhance wound healing
  • Immunomodulatory
  • Neuroprotection, including prevents ischemia (or loss of blood supply to a tissue area) & reperfusion injury
  • Anti-microbial (anti-viral, anti-fungal, & anti-bacterial)

 

Curcumin also has profound anti-cancer effects in the body. Firstly, the spice acts as an anti-angiogenic (Maheshwari et al. 2006). That is to say, curcumin stops the formation of new blood vessels to supply growing tumours. Furthermore, the anti-metastatic effects of this constituent inhibit the spread of cancer around the body. Likewise, curcumin is anti-mutagenic in that it prevents the mutations leading to cancer (Maheshwari et al. 2006). Lastly, curcumin induces the death of cancer cells by regulating the expression of genetic material. Curcumin increases P53 expression – a gene that controls the normal life cycle of a cell – by inhibiting another transcription factor called NF-kB (Wilken et al. 2011). In addition, the constituent helps induce cell death in cancer cells by upregulating a gene called P21 (Gogado et al. 2011). Another action of curcumin is as an inhibitor of the enzyme, MTOR, which is a kinase that increases growth, proliferation, and motility of cells during cancerous states (Beevers et al. 2013). Ultimately, while a chemo drug will typically target one cancer-causing signal at a time, the benefit of using curcumin is that it works more extensively by stopping 195 of these signals (Pescatore 2016).

As such, many cancers may be prevented and treated with curcumin (Anand et al. 2008), including:

  • Bone cancer
  • Melanoma
  • Thoracic and Head & Neck cancers (lung, oral, & thymus)
  • Gynecologic cancers (cervix, ovary, uterus)
  • Breast cancer
  • Brain tumours
  • Genitourinary cancers (bladder, kidney, prostate)
  • Gastrointestinal cancers (esophagus, intestine, liver, stomach, pancreas, colorectal)
  • Hematological cancers (leukemia, lymphoma, multiple myeloma)

 

Furthermore, curcumin increases the effectiveness of conventional forms of cancer therapy. For example, combining the spice with a chemo drug called cisplatin enhances its inhibition of metastasis and the cell death of migrating cancer cells (Baharuddin et al. 2016). In total, 12 chemo drugs have demonstrated increased effectiveness when used with curcumin (Pescatore 2016). In fact, colon cancers have exhibited an increase in resistance to one such chemo drug, called 5-fluorouracil (5-FU) (Hammond et al. 2016). However, curcumin not only increases the effectiveness of 5-FU in inducing cell death (Zhou et al. 2016), but it also increases the sensitivity of resistant cancer cells to 5-FU (Toden et al. 2015).

In reality, the aforementioned actions are just a few of the mechanisms that curcumin acts on cancer cells. However, Prasad et al. (2014) summarize these mechanisms in the Fig 1:

Fig 1: Molecular target of curcumin. STAT, Signal transducer and activator of transcription; HIF-1, Hypoxia-inducible factors-1; NF-κB, Nuclear factor kappaB; PPAR-γ-Peroxisome proliferator-activated receptors-γ;AP-1, Activatorprotein-1; CBP,CREB1-bindingprotein; ERG, ETS(erythroblast transformation-specific)-related gene; ERE, Estrogenresponse elements; MCP-1, Monocyte chemotactic protein-1; MIP-1, Macrophage inflammatory protein 1; TNF, Tumor necrosis factor; IFN, Interferon; COX-2, Cyclooxygenase-2; TIMP, Tissue inhibitors of metalloproteinases; MMP, Matrixmetalloproteinase; 5-LOX, 5-Lipooxygenase; iNOS, Inducible nitric oxide synthase; ODC, Ornithine decarboxylase; FPTase, Farnesyl-protein transferase; ICAM-1, Intercellular adhesion molecule-1; VCAM-1, Vascular cell adhesion molecule-1; ELAM-1, Endothelial-leukocyte adhesion molecule-1; VEGF, Vascular endothelial growth factor; cIAP, Cellular inhibitor of apoptosis protein; Bcl-2, B-cell lymphoma-2; Bcl-xL B-cell lymphoma-extra large; PCNA, Proliferating cell nuclear antigen; JAK, Janus kinase; JNK, c-Jun amino-Terminal kinase; EGFR, Epidermal growth factor receptor;ERK1/2, Extracellular signal-regulated kinase 1/2; PKA/B/C, Protein kinase A/B/C; PhK, Phosphorylase kinase; FAK, Focal adhesion kinase; AK, Adenylate kinase; IRAK, Interleukin-1 receptor-associated kinase; IKK, IκB kinase; MAPK, Mitogen-activated protein kinase; srcTK,pp60c-src tyrosine kinase; PTK, Protein tyrosine kinase; FGF, Fibroblast growth factors; EGF, Epidermal growth factor; NGF, Nerve growth factor; PDGF, Platelet-derived growth factor; TF, Tissue factor; TGF, Transforming growth factor; FGF, Fibroblast growth factors; CTGF, Connective-tissue growth factor; PARP, Poly (ADP-ribose) polymerase; FADD, Fas-associated protein with death domain; H2R, Histamine H2 receptor; IR, Insulin receptor; LDL-R, Low-density lipoprotein receptor; ITPR, Inositol 1,4,5-triphosphate receptors; ER, Estrogen receptor; CXCR4,C-X-C chemokine receptor type 4; FasR, Fas receptor; AR, Androgen receptor; AHR, Aryl hydrocarbon receptor.

 

       In terms of treating cancer, the absorption and distribution of Curcumin is maximized through IV administration (Anand et al. 2008, Chen et al. 2009, Li et al. 2005, and Wilken et al. 2011). While IV curcumin is known to have adverse effects such as nausea, vomiting, and hand foot itching, these reactions can be avoided through better dilution of the extract (Anderson 2017). The IV is administered at a speed which is tolerated by the individual patient. The easiest way to screen whether IV curcumin is suitable for you is for your practitioner to first administer an oral dose. However, lab studies also exist, including a CBC and chemistry panel (Anderson 2017). Nonetheless, caution should be taken with any patients on anticoagulants or with known gallbladder disease. Likewise, patients with liver and kidney impairment must be closely monitored by a health practitioner (Anderson 2017). Ultimately, IV curcumin is powerful tool offered by Naturopathic Physicians for combating cancer.

 

References

Anand, P., Sundaram, C., Jhurani, S., et al. (2008) Curcumin and cancer: an "old-age" disease with an "age-old" solution. Cancer Lett. 267(1):133–64.

Anderson, P. (2017) Curcumin Monograph for Intravenous Use. Retrieved from: http://www.academia.edu/20316553/Curcumin_IV_Use_Monograph

Baharuddin, P., Satar, N., Shaik, K. et al. (2016) Curcumin improves the efficacy of cisplatin by targeting cancer stem-like cells through p21 and cyclin D1-mediated tumour cell inhibition in non-small cell lung cancer cell lines. Oncol Rep. 35(1):13–25.

Beevers, C. S., Zhou, H., and Huang, S. (2013) Hitting the Golden TORget: Curcumin’s Effects on mTOR Signaling. Anticancer Agents Med Chem. 13(7):988–94.

Chen, C. Johnson, T. D., Jeon, H., et.al. (2009) An in vitro study of liposomal curcumin: Stability, toxicity and biological activity in human lymphocytes and Epstein-Barr virus-transformed human B-cells. Int J Pharm. 366(1):133–9.

Gogada, R., Amadori, M., Zhang, H. et al. (2011) Curcumin induces Apaf-1-dependent, p21-mediated caspase activation and apoptosis. Cell Cycle. 10(23):4128–37.

Hammond, W. A., Swaika, A., and Mody, K. (2016) Pharmacologic resistance in colorectal cancer: a review. Ther Adv Med Oncol. 8(1):57–84.

Li, L., Braiteh, F. S., and Kurzrock, R. (2005) Liposome-encapsulated curcumin: in vitro and in vivo effects on proliferation, apoptosis, signaling, and angiogenesis. Cancer. 104(6):1322-31.

Maheshwari, R. K., Singh, A. K., Gaddipati, J. et al. (2006) Multiple biological activities of curcumin: A short review. Life Sci. 78(18):2081–7.

Pescatore, F. (2016) 303 Natural Healing Miracles Big Pharma Doesn’t Want You to Have. Baltimore, MD: OmniVista Health Media, L.L.C.

Prasad, S., Gupta, S., Tyagi, A., et al. (2014) Curcumin, a component of golden spice: From bedside to bench and back. Biotechnol Adv32(6): 1053-6.

Toden, S., Okugawa, Y., Jascur, T., et al. (2015) Curcumin mediates chemosensitization to 5-fluorouracil through miRNA-induced suppression of epithelial-to-mesenchymal transition in chemoresistant colorectal cancer. Carcinogenesis. 36(3):355-67.

Wilken, R., Veena, M. S., Wang, M. B., et al. (2011) Curcumin: A review of anti-cancer properties and therapeutic activity in head and neck squamous cell carcinoma. Mol Cancer10:12.

Zhou, X., Wang, W., Li, P., et al. (2016). Curcumin Enhances the Effects of 5-Fluorouracil and Oxaliplatin in Inducing Gastric Cancer Cell Apoptosis Both In Vitro and In Vivo. Oncol Res. 23(1-2):29-34.