Snacking causes cancer?

One of the most interesting bits of research that was recently published isn't even about cancer. The paper, 'Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet', published in the journal Cell Metabolism, looks at the effect of feeding times on a range of metabolic indicators. It shows that by restricting mice to set feeding times and preserving a long fast, the damaging effects of a high-fat and high-carb diet are overcome. Now while cancer isn't mentioned in this research, there are now converging lines of evidence to point to a very strong metabolic component to cancer - and it goes beyond the idea of tumours as being glucose-hungry all the time.

The authors of the paper point out that many people have been encouraged to eat little and often, and that snacking is now endemic in our culture. But the body evolved a set of responses that are cyclic, like the circadian rhythm that controls sleep/wake times. By eating constantly we disrupt this rhythm. Again, there's a link here to cancer in that disrupted circadian rhythms are also implicated in carcinogenesis.

Add to this evidence that selecting fasting improves chemotherapy response (as discussed here: http://www.anticancer.org.uk/2012/02/fasting-and-chemotherapy.html) and you have an argument that says selective fasting, cutting out snacking and taking melatonin to improve circadian rhythms are valid anti-cancer interventions that are not toxic, cheap and can be tried both for cancer-prevention and to improve response to therapy for cancer patients.

Towards An Ideal Anti-cancer Protocol

There was an interesting piece at the Anticancer.Org.Uk website commenting on some new research showing that blocking the mu-opiod receptor pathway (the one exploited by opiate-based medicines such as morphine, fentanyl etc), can slow cancer progression. The source of the article is a journal paper by a group of doctors treating late stage cancer patients with the drug methylnaltrexone (trade name Relistor) for opiate induced constipation. They noticed that patients treated with methylnaltrexone survived for longer than expected. They then followed up in the lab, doing experiments that showed that there is a direct effect of the mu-opiod receptor pathway on disease progression.

While this is plenty interesting, what's also worth pointing out that this is yet another example of an existing drug being shown to have anti-cancer activity. Crafting new drugs from scratch takes years and many millions of dollars, re-using existing drugs is much cheaper as a lot of the trials of toxicity and pharmacology have already been done. The combination of off-label drugs is an area that we are keen to see exapnd. Few of these drugs have direct cancer killing activity, but what they do is act gently to change the environment around the tumours. By attacking the tumour microenvironment you subvert the mechanisms that the tumour puts in place to survive.

A list of some of the most promising off-label drugs with anti-cancer activity include:

• Metformin - targets tumour metabolism, (read up on the reverse warburg effect, for example)
• Statins - targets the mevalonate pathway (starves the tumour of esential building blocks for cell proliferation)
• Aspirin - targets the inflammatory environment
• Beta-blockers - targets the beta-adrenergic pathway
• Naltrexone and methylnatrexone - target the mu-opiod receptor pathway

What we would like to see is a clinical trial that uses combinations of these drugs to target the tumour microenvironment. These drugs have relatively low toxicity, they're cheap and together they attack multiple pathways giving less room for the tumours to evolve resistance. Throw in some omega 3s, some polyphenols and some exercise and you have the ideal anti-cancer protocol.

Li Fraumeni Syndrome

The TP53 gene is one of the major anti-cancer genes in the body. It's the tumour suppressor gene most often knocked out in tumours, which makes those tumours more resistant to treatment. As with many genes, there are a small set of people who are born with the gene knocked out in some way. With TP53, this can lead to a condition called Li Fraumeni Syndrome - which means people born with the damaged TP53 gene are very susceptible to developing cancer.

Often Li Fraumeni sufferers will develop rare sarcomas in childhood, and can develop multiple primary cancers over the years. It's a rare condition, thankfully, but for sufferers things can be grim. There are no cures (gene therapy is still a long way off), and many people are ignorant of the syndrome. A new site has been started to raise the profile of the condition, to provide a forum for sufferers and their families and to publish useful information.

The site is published by the George Pantziarka TP53 Trust, and the URL to visit is http://www.tp53.co.uk