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The Author The author of this site is the British writer, John Davidson. Please note that the author is neither a doctor, nor a qualified health practitioner. Every cancer patient should always consult his or her medical practitioner with regard to the use of complementary remedies or treatments, and nothing on this site should be construed in any way as medical or therapeutic advice. It is simply the result of one person's search for solutions. Please read our disclaimer. About This Site Internet searches trawl up vast amounts of information about cancer, from a broad spectrum of viewpoints. The information and internet links on this site are for those seeking to augment the treatment offered by their hospital oncology (cancer) unit. Of course, a great many other internet sites concerning cancer can be found by keying the requisite search words into any of the major search engines. The content of this site was initially prepared, at the request of medical and nursing staff and others, some weeks after I had had an emergency operation for the removal of a colon cancer, and while undergoing chemotherapy in case any cancer cells had gone AWOL. There had been some escape of cancer cells into associated lymph nodes (3 out of 17, including the most distal), but no other tumours had been picked up by a CT scan. When I returned home from hospital in September 2005, with the help of friends, I started doing some research on cancer. I was amazed to discover that despite the billions of pounds/euros/dollars etc. spent on cancer research, and the many advances in understanding the numerous variants of the disease, the standard treatment for my stage of colon cancer is still a drug (fluorouracil, also called 5FU) that has been in use for more than forty years, has uncomfortable side effects, and which only increases the chances of survival after five years by 5 to 10%.

Vitamin K2. Monograph. [No authors listed] Altern Med Rev. 2009 Sep;14(3):284-93. Review. PMID: 19803553

A randomised comparison of increase in serum 25-hydroxyvitamin D concentration after 4 weeks of daily oral intake of 10 microg cholecalciferol from multivitamin tablets or fish oil capsules in healthy young adults. Holvik K, Madar AA, Meyer HE, Lofthus CM, Stene LC. Br J Nutr. 2007 Sep;98(3):620-5. Epub 2007 Apr 24. PMID: 17456248 We conclude that fish oil capsules and multivitamin tablets containing 10 microg cholecalciferol administered over a 4-week period produced a similar mean increase in s-25(OH)D concentration.

Effect of fish oil on heart rate in humans: a meta-analysis of randomized controlled trials. Mozaffarian D, Geelen A, Brouwer IA, Geleijnse JM, Zock PL, Katan MB. Circulation. 2005 Sep 27;112(13):1945-52. Epub 2005 Sep 19. PMID: 16172267 doi: 10.1161/CIRCULATIONAHA.105.556886 Conclusions- In randomized controlled trials in humans, fish oil reduces HR, particularly in those with higher baseline HR or longer treatment duration. These findings provide firm evidence that fish oil consumption directly or indirectly affects cardiac electrophysiology in humans. Potential mechanisms such as effects on the sinus node, ventricular efficiency, or autonomic function deserve further investigation.

Fish intake is associated with a reduced progression of coronary artery atherosclerosis in postmenopausal women with coronary artery disease. Erkkilä AT, Lichtenstein AH, Mozaffarian D, Herrington DM. Am J Clin Nutr. 2004 Sep;80(3):626-32. PMID: 15321802 Conclusions: Consumption of fish is associated with a significantly reduced progression of coronary artery atherosclerosis in women with coronary artery disease.

Serum 25(OH)-vitamin D concentration and risk of esophageal squamous dysplasia. Abnet CC, Chen W, Dawsey SM, Wei WQ, Roth MJ, Liu B, Lu N, Taylor PR, Qiao YL. Cancer Epidemiol Biomarkers Prev. 2007 Sep;16(9):1889-93. PMID: 17855710 doi: 10.1158/1055-9965.EPI-07-0461 Background: Squamous dysplasia is the precursor lesion for esophageal squamous cell carcinoma, and nutritional factors play an important role in the etiology of this cancer. Previous studies using a variety of measures for vitamin D exposure have reached different conclusions about the association between vitamin D and the risk of developing esophageal cancer. Conclusions: Higher serum 25(OH)D concentrations were associated with significantly increased risk of squamous dysplasia. No obvious source of measured or unmeasured confounding explains this finding. In conclusion, we found that a higher serum 25(OH)D concentration was associated with an increased risk of esophageal squamous dysplasia, the precursor lesion for ESCC. This finding concurs with our previous prospective study which found that higher vitamin D status was associated with increased risk of incident ESCC in this same population. These unexpected findings suggest that further studies of the association of vitamin D and digestive tract cancers are needed before the effect of vitamin D in different populations can be elucidated.

Docosahexaenoic acid inhibits superoxide dismutase 1 gene transcription in human cancer cells: the involvement of peroxisome proliferator-activated receptor alpha and hypoxia-inducible factor-2alpha signaling. Tuller ER, Beavers CT, Lou JR, Ihnat MA, Benbrook DM, Ding WQ. Mol Pharmacol. 2009 Sep;76(3):588-95. Epub 2009 Jun 15. PMID: 19528198

Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Nevin KG, Rajamohan T. Clin Biochem. 2004 Sep;37(9):830-5. PMID: 15329324 doi:10.1016/j.clinbiochem.2004.04.010 Conclusion: The results demonstrated the potential beneficiary effect of virgin coconut oil in lowering lipid levels in serum and tissues and LDL oxidation by physiological oxidants. This property of VCO may be attributed to the biologically active polyphenol components present in the oil

"ScienceDaily (Sep. 10, 2009) - Monolaurin, an extract from coconut oil could be used as a microbial agent in foods, according to a study in the Journal of Food Science, published by the Institute of Food Technologists."

A new study in animals demonstrates that a diet rich in coconut oil protects against 'insulin resistance' (an impaired ability of cells to respond to insulin) in muscle and fat. The diet also avoids the accumulation of body fat caused by other high fat diets of similar calorie content. Together these findings are important because obesity and insulin resistance are major factors leading to the development of Type 2 diabetes. "

Blood pressure and atherogenic lipoprotein profiles of fish-diet and vegetarian villagers in Tanzania: the Lugalawa study. Pauletto P, Puato M, Caroli MG, Casiglia E, Munhambo AE, Cazzolato G, Bittolo Bon G, Angeli MT, Galli C, Pessina AC. Lancet. 1996 Sep 21;348(9030):784-8. PMID: 8813985 Interpretation In these villagers, consumption of freshwater fish (300-600 g daily) was associated with raised plasma concentrations of n-3 polyunsaturated fatty acids, lower blood pressure, and lower plasma lipid concentrations. In conclusion, our findings confirm that the favourable risk factor profile originally described for Eskimos living on a diet rich in n-3 polyunsaturated fatty acids is real, and not overestimated.

Berberine lowers blood glucose in type 2 diabetes mellitus patients through increasing insulin receptor expression. Zhang H, Wei J, Xue R, Wu JD, Zhao W, Wang ZZ, Wang SK, Zhou ZX, Song DQ, Wang YM, Pan HN, Kong WJ, Jiang JD. Metabolism. 2009 Sep 3 doi:10.1016/j.metabol.2009.07.029 Liver function was improved greatly in these patients by showing reduction of liver enzymes. Our results confirmed the activity of BBR on InsR in humans and its relationship with the glucose-lowering effect. Together with our previous report, we strongly suggest BBR as an ideal medicine for T2DM with a mechanism different from metformin and rosiglitazone.

Vitamin D effective ultraviolet wavelengths due to scattering in shade. Turnbull DJ, Parisi AV, Kimlin MG. J Steroid Biochem Mol Biol. 2005 Sep;96(5):431-6. Epub 2005 Jul 6. PMID: 16005208

Decreased bioavailability of vitamin D in obesity. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Am J Clin Nutr. 2000 Sep;72(3):690-3. Erratum in: Am J Clin Nutr. 2003 May;77(5):1342. PMID: 10966885 Conclusions: Obesity-associated vitamin D insufficiency is likely due to the decreased bioavailability of vitamin D3 from cutaneous and dietary sources because of its deposition in body fat compartments.

Obesity and Vitamin D One third of Americans are obese. While much of that epidemic is surely due to playing Nintendo instead of baseball, or the consumption of soft drinks instead of water, does that explain it all? Is it a coincidence that the twin epidemics of obesity and vitamin D deficiency are occurring together?

"One of the problems - if it could be called a problem - in writing this blog and moderating the comments is most readers are pretty intelligent. Occasionally I have the angry vegetarian wander in, take me to task for my errant ways, and, after a comeback or two on my part, drift away to never be heard from again. Thanks to the confirmation bias, this blog pretty much selects against the non-meat eater. So, I tend to forget how many people there are out there who are pretty much clueless about basic nutrition, and how many people there are who bobble through life spouting cliches they've heard along the way as great nutritional truths. Based on the comments I get on this blog, it seems to me that most people are pretty nutritionally sophisticated and reasonable."

"Meat eating made us human. The anthropological evidence strongly supports the idea that the addition of increasingly larger amounts of meat in the diet of our predecessors was essential in the evolution of the large human brain. Our large brains came at the metabolic expense of our guts, which shrank as our brains grew. In April 1995 an article appeared in the journal Current Anthropology that was an intellectual tour de force and, in my view, an example of a perfect theoretical paper. "The Expensive-Tissue Hypothesis" (ETH) by Leslie Aiello and Peter Wheeler demonstrated by a brilliant thought experiment that our species didn't evolve to eat meat but evolved because it ate meat. It was our gradual drift toward the much higher quality diet provided by food from animal sources that allowed us to develop the large brains we have. It was hunting and meat eating that reduced our GI tracts and freed up our brains to grow. As I wrote at the start of this post, the evidence indicates that we didn't evolve to eat meat - we evolved because we ate meat."