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Tragically, 1.4 million die from lung cancer each year, with 1.6 million newly diagnosed. Could this humble leaf extract beat a drug that can cost over 100,000 dollars to improve lung cancer survival only a few months?
A promising new study published in the journal Food & Function titled, "Morinda citrifolia edible leaf extract enhanced immune response against lung cancer," has found that an alcohol-based leaf extract of the noni tree (Morinda Citrifolia) was more effective than a commonly used chemotherapy drug in treating lung cancer in an animal model.
In the new study, a team of Malaysian researchers tested the relative effectiveness of the drug erlotinib (trade name Tarceva), a so-called epidemal growth factor receptor inhibitor (EGFR inhibitor), to a noni leaf extract, in lung tumor-induced albino house mice (BALB/c), and found that 21 days of treatment with a 300 mg kg-1 body weight of leaf extract was more effective suppressing lung tumour growth than a 50 mg kg-1 body weight erlotinib treatment.
Remarkably, the noni leaf extract was observed to positively modulate a wide range of biological pathways, without discernable adverse effects:
Increasing blood lymphocyte counts
Increasing spleen tissue B cells
Increasing T cells
Increasing natural killer cells
Reduced epidemal growth factor receptor (EGFR)
Suppressed cyclooxgenase 2 (COX2) inflammatory markers
Enhanced the tumor suppressor gene (phosphatase and tensin homolog, PTEN)
Inhibited the tumour growth cellular genes transformed mouse 3T3 cell double minute 2 (MDM2) and V-raf-leukemia viral oncogene 1 (RAF1)
Inhibited the mechanistic target of rapamycin (MTOR)) mRNA expression in the tumors.
The study provided background on present-day lung cancer statistics, and dismal conventional treatment outcomes:
Lung cancer is the leading cause of cancer-related deaths worldwide, with 1.6 million new cases and 1.4 million deaths per year. Non-small-cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases, with a 5-year survival rate of only 16%. Chemotherapy is relatively ineffective for patients with advanced NSCLC and the response rate is only 20% to 35% with a median survival of 10 to 12 months. In a phase III study, the use of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) drugs, such as erlotinib, significantly improved the overall survival rate relative to supportive care for refractory stage IIIB/IV NSCLC. However, erlotinib use is limited because of several serious side effects3 and the emergence of cancer mutations which confer drug resistance. The common erlotinib side effects are weakness, diarrhoea, rashes, shortness of breath, coughing, loss of appetite, fatigue (feeling tired), and nausea. Erlotinib may cause more serious side effects such as lung problems (shortness of breath, coughing, and fever); interstitial lung disease and liver and kidney problems; blistering and skin peeling; gastrointestinal perforation; bleeding and clotting problems which may lead to heart attacks, strokes, dry eyes, unusual eyelash growth, or swelling of the corneas; harm to unborn babies and even death."
Not mentioned in the study, but highly relevant to the topic at hand, is the extraordinarily high cost of chemotherapy drugs like erlotinib, despite the relatively small gains they produce.
A 2010 Medscape article reported that erlotinib, which has been the standard of care for advanced non-small cell lung cancer (NSCLC) in the U.S. in Canada ever since the NCIC Clinical Trials Group BR.21 trial showed a 2 month improvement in overall survival when added to supportive care in patients who had failed all of their previous chemotherapy options. The article also calculated how much these seemingly minor gains cost in dollar-per-survival year terms:
The investigators determined that the specific cost of erlotinib treatment was $94,638 (in 2007 Canadian dollars) per life-year gained (95% confidence interval [CI], $59,359 to $429,148)."
Clearly, if the results of this latest animal study are found to extend to human lung cancer, as well, noni leaf extract could provide an ideal alternative, and could be produced at a much lower cost (A quick internet search yielded a price of about $50 for 12 ounces).
Noni leaf, unlike conventional chemotherapy drugs, is an exceedingly complex biological material, containing hundreds of different naturally occurring, and 'intelligently interwoven' phytochemicals. The sheer complexity and density of gene- and physiology-regulating information in a natural substance like noni leaf vis-à-vis synthetically produced, mono-chemical chemotherapy drugs, is astounding. The article listed an immense, though still non-exhaustive array of biomolecules identified within noni leaf which could, together, account for the remarkable therapeutic effects the study observed:
Scopoletin, Δ5 sterol β-sitosterol, Δ5,7 sterol campesta-5,7,22-trien-3β-ol, (+)-catechin, α-ionone, β-carotene, β-ionone, β-sitosterol, 1,2-dihydro-1,1,6-trimethyl- naphthalene, 1,5,15-trimethylmorindol, 2,6,10,14,18,22-tetra- cosahexaene, 2-methyl- 3,5,6-trihydroxyanthraquinone,2-methyl-3,5,6-trihydroxyanthraquinone-6-O-β-D- xylopyranosyl- (1–6)-β-D-glucopyranoside, 3-hydroxymorindone, 3-hydroxymorindone 6-O-β-D-xylopyranosyl-(1–6)-β-D-glucopyranoside, 3-O- acetylpomolic acid, 4-(3′(R)-hydroxybutyl )-3,5,5-trimethyl-cyclo- hex-2-en-1-one, 5,6-dihydroxylucidin, 5,6-dihydorxylucidin 3-O- β-D-xylopyranosyl-(1–6)-β-D-glucopyranoside, 5,15-dimethyl- morindol, 5,15-DMM, 5-methylfurfural, 5-benzofuran car- boxylic acid-6-formyl methyl ester, 6,10,14-trimethyl-2- pentadecanone, 13-epi-phaeophorbide a methyl ester, 13- hydroxy-9,11,15-octadecatrienoic acid, 132(R)-hydroxypheo- phorbide a methyl ester, 13(S)-hydroxypheophorbide a methyl ester, 151(R)-hydroxypurpurin-7 lactone dimethyl ester, 15(S)- hydroxypurpurin-7 lactone dimethyl ester, alanine, arginine, aspartic acid, asperuloside, asperulosidic acid, aucubin, barbi- nervic acid, benzaldehyde, benzeneacetaldehyde, campesta-5,7,22-trien-3β-ol, campesterol, citrifolinin A, citrifolinin A-1, citrifolinin Ba, citrifolinin Bb, citrifolinoside A, citrifolinoside B, citrifoside, clethric acid, cycloartenol, cysteine, cystine, de-acetyl asperuloside, deacetylasperulosidic acid (DAA), E-phytol, epicatechin, geranyl acetone, glutamic acid, glycine, hedera- genin, histidine, isoleucine, kaempferol, kaempferol-3-O-α-L- rhamnopyranosyl-(1–6)-β-D-glucopyranoside kaempferol 3-O- β-D-glucopyranosyl-(1→2)-α-lrhamnopyranosyl-(1→6)-β-D-galac- topyranoside, ketosteroid stigmasta-4-en-3-one, leucine, lino- leic acid, lucidin, lucidin 3-O-β-dxylopyranosyl-(1–6)- β-D-glucopyranoside, methionine, methyl oleate, methyl pheo- phorbide a, methyl pheophorbide b, methyl plamitate, nicoti- floroside, oleanolic acid, oxalic acid, palmitic acid, peucedanocoumarin III, phenylalanine, pheophorbide a, phytic acid, phytol, proline, pteryxin, quercetin, quercetin-3-O- α-L-rhamnopyranosyl-(1→6)- β-D-glucopyranoside, quercetin 3-O-β-D-glucopyranoside, quercetin 3-O-β-D-glucopyranosyl- (1→2)-α-lrhamnopyranosyl-(1→6)-β-D-galactopyranoside, roseo- side II, rotungenic acid, rutin, scopoletin, serine, stigmasta- 4–22-dien-3-one, stigmasta-4-en-3-one, stigmasterol, tannic acid, threonine, triterpene cycloartenol, tryptophan, tyrosine, ursolic acid, and valine.
The study concluded:
The evidence demonstrated that the epicatechin and scopoletin rich M. citrifolia leaf extract may be used as a functional food and complementary therapy to suppress lung cancer by stimulating the immune responses and modulating multiple cancer cell gene signaling pathways against cancer cell proliferation and towards apoptosis, without producing detectable undesirable effects. The extract suppressed key inflammatory markers and inhibited various molecular and cellular markers involved in proliferation and angiogenesis, suggesting a mode of action targeting, as proposed in Fig. 6. The epicatechin and scopoletin rich M. citrifolia leaves may be used as a complementary/adjunct therapy or functional food to help fight lung cancer or adenocarcinoma".
Incidentally, this was not the first study to investigate the potential anti-lung cancer properties of a noni tree component. There are several others, including:
In 2012, the Indian Journal of Molecular Medicine published a study which found that noni fruit juice down-regulated an inflammatory process within human lung cancer cells, indicating it might play a therapeutic role in inflammation-associated lung pathologies, including but not limited to lung cancer.
In 2001, the Annals of the New York Academy of Sciences published a study that found noni fruit juice was capable of preventing carcinogenic DMBA-DNA adduct formation in the lungs of mice, indicating its likely cancer preventive properties.
In 1999, the journal Phytotherapeutic Research published a study which found that the fruit juice of noni had antitumor activity in a mouse model of Lewis lung cancer.
It should be emphasized that the noni tree is certainly not the only natural substance that has been studied to provide natural chemopreventive and chemotherapeutic activity against lung cancer. Indeed, we have indexed 129 additional natural substances, many of which are foods, that have demonstrable anti-lung cancer activity. Curcumin, since it is able to target the cancer stem cells at the heart of lung cancer malignancy, may be the most promising of them all.
For additional research on the health benefits of noni, view our research database on the topic: Noni health benefits research.
Lastly, consider that lung cancer is one of the most commonly overdiagnosed and overtreated cancers in existence today, as identified in an important 2013 JAMA report commissioned by the National Cancer Institute. So, please always get a second opinion and do your own research so you can make as much of an informed choice as possible.