My Experience of the Ketogenic Diet 2017: The Good, The Bad and The Ugly

My Experience of the Ketogenic Diet 2017: The Good, The Bad and The Ugly

Well hasn’t it been a year. So busy. I’ve spent most of 2018 struggling with gastrointestinal bleeding first due to non cirrhotic portal hypertension (chemotherapy induced) and then radiation enteritis. I have had some difficulty writing as I have felt so unwell and this

June 2017: CT scan showed slight progression of cancer. Diet over the last six months has contained increasing levels of sugar

Can the tumour be beaten down by cutting my sugar intake? The ketogenic diet seemed a possible strategy to achieve this.

The Standard American diet contains up to 60% carbohydrates and is high in meat, dairy, processed and refined food products. Since finishing chemotherapy I have tried to eat organic and vegan to improve my prognosis. The various diets I have tried include the alkaline diet, vegan, raw vegan and the Budwig diet (contains some cottage cheese). Clearly the tumour is starting to be able to outflank these dietary defences so I needed a different approach.

I had read with great fascination the work of Thomas Seyfried and Dominic D’Agostino in developing the ketogenic diet. Most of the science is basic i.e Petri dish and animal based. There are few clinical studies. However Facebook and other websites provided many anecdotes of cancer patients using the ketogenic diet with varying degrees of success.

The idea behind the diet is that cancer cells like to use sugar as their main fuel. If they are deprived of sugar – cancer cells cannot divide and will die off by programmed cell death leading to tumour shrinkage. But deprived of sugar the body needs alternative fuel – and this is provided in the form of fat and also protein.

Fat is metabolised to ketone bodies which can fuel the major organs of the body including heart and brain.

I did understand that the clinical data is rather sparse. However, I had seen enough credible anecdotes to believe that this “diet” might slow down or stop a tumour. Just for reference here are the two opposing arguments:

For the ketogenic diet:

Against the ketogenic diet:

So there you have it.

July 2017

Week 1

Once the disappointing news of the less than satisfactory CT scan had sunk in and the fear had receded I took a closer look at the ketogenic diet but I was not at all keen to eat animal products being a vegan.

So what would I need?

  1. I read all I could about the ketogenic diet.
  2. I downloaded the Cronometer app – a superb device for tracking calories, carbs, fat intake etc
  3. I purchased avocadoes, nuts, non dairy milks and set about developing some meal plans aiming for less than 20g net carbs daily. For reference there are 20g net carbs in just  one apple – so not much room for manoeuvre.

The first few days were quite simple – lots of flaxseed, tofu, avocado and when I measured my         urinary ketones – wow! I was in ketosis! Surely it can’t be this easy I thought!

Week 2

No it is not this easy. I found out what keto flu is. Well I am not sure if it was that – I may have picked up a bug. A visit to the doctors for routine blood test was followed rather quickly by the onset of nausea, vomiting and diarrhoea. This soon resolved and I was out walking again very soon. Ketone levels were rather high after this episode of d+v reaching the 4-5 mM level. The rest of this week passed without too much bother.

Week 3

Fatigue, cramps, nausea and some bloating. These symptoms all seemed to settle quickly but I was having some difficulty staying in nutritional ketosis at the level required. The scientists seemed to be suggesting that the glucose to ketone ratio should be between 1-2. I like the food on this diet – essentially it a strict version of the vegan diet without grains and legumes and restricted. It seems that lots of things can tip one out of ketosis. I purchased Ellen Davis’ book (Fighting Cancer with a ketogenic diet) – pitfalls can be caffeine, too much protein, eating foods with MSG e.g nutritional yeast. It seems fairly straightforward to achieve ketone levels of around 1mM. But getting the level higher seems to require a daily carb intake of 10-15g and fats as 80% of caloric intake. Getting the “macros” right seems essential. One side effect of the Keto genie diet is bad breath due to ketones…. Luckily Jackie is one of those people who can’t smell ketones..”

Week 4

Dealing with keto flu – I try to maintain 3-4 litres intake of fluid a day and take mineral supplements. However the ketone levels aren’t rising too well. So I decide to do some fasting (500 calories per day) on top of the diet. I also add in some exogenous ketones and Medium Chain Triglyceride powder which are easily available on the internet. With added fasting, my blood sugar levels are around 3-4 mM and ketones easily spike over 2-3 mM and at their highest reach 5 mM.  But on completing the fast and refeeding I am afflicted by pain, abdominal swelling and dreadful fatigue. I feel dreadful. These symptoms pass off after a few days.

After the first four weeks the family holiday is scheduled in Cornwall. I am feeling OK and trying to arrange hyperbaric oxygen at the MS centre. The holiday is fun but I decide to do another fast and the same thing happens when I refeed. I develop a swollen abdomen. This time It is tense and painful. I look in the mirror. My tum sticks out, the veins are distended, my ankles are slightly puffy. I am not jaundiced but when I examine myself I worry that I have developed ascitic fluid. Oh dear – is it malignant or is my liver packing up?

Well one of the effects of the ketogenic diet was to make the lump in my abdomen much much more difficult to feel. So I don’t think it is malignant spread. So what has upset my liver? Is it the off label medications? No. Is it supplement related – too much curcumin? Stop that. But I think back to my physiology – starvation and refeeding can lead to liver injury. My diet has been calorie restricted and low in carbs, so perhaps a fatty liver developed.

Well it all settled down and we returned home to Bristol to prepare for our next challenge: The West Highland Way

I try to do the walk from Glasgow to Fort William on a vegan calorie restricted ketogenic diet while taking Metformin. Not a good idea. Within two days I am having to relax the diet and increase caloric intake. I’m Ok walking on the flat but the power in my legs evaporates on any kind of slope. I start eating eggs and fish. On this regime I manage to complete the 10-15 miles walking every day. Celebrating at the finish with a small feast – including my favourite sticky toffee pudding!!

Oh dear – big big tum again! This time it takes nearly a week to resolve and during this time I have a CT scan….. My oncologist is initially alarmed – a diagnosis of cancer and presenting with ascites is of concern. But I don’t want any more tests at this stage and decide to

persevere with the diet and start hyperbaric oxygen treatment. I am feeling better walking 6-7 miles per day.

But I am trying to to refine my diet to achieve a greater degree of ketosis. I cut my net carb intake to 10-15g daily. I increase my fat intake to 80-85% of caloric intake. I cut caffeine back, avoid nutritional yeast. And presto the ketone levels now rise above 2-3 mM consistently.

However my abdomen starts to swell again – it seems my liver doesn’t like high fat levels / ketones / low carb intake or all of the above.

The graph below shows my blood glucose levels (mM, blue circles) and ketone levels (mM, green circles. The spikes in ketone levels were followed by periods of unwell. Overall my blood sugar didn’t change much overall and even seemed to rise slowly as time passed.


Finally I resolve to increase my carb intake to nearer 50-100g daily. I feel better almost immediately – tummy down, ankles down and the return of energy!

And the food is more diverse and palatable.

So what are the main points:

It is unclear that the Ketogenic diet alone can starve cancer of fuel. Indeed some cancers use the amino acid glutamine as a fuel while others actually feed off fat and ketones… (see Jane McLelland’s new book: How to Starve Cancer – available on amazon and kindle – I strongly recommend this book for those considering off label drugs such as metformin, statins, aspirin and dietary interventions to slow the progression of cancer).

If you are a patient do the keto diet under close supervision.

Don’t push it if your liver reserves are low. I believe the long term effects of the Ketogenic diet on heart, liver, brain etc have not been defined as yet in the clinic. Non alcoholic fatty liver is increasingly prevalent and adding more fat to the diet may cause progression to more serious liver disease. Similarly chemotherapy patients may have damaged livers. A high fat diet may do more harm than good in these individuals. Other patients with reduced liver function also need to be cautious.

The interaction between the ketogenic diet and medications which inhibit metabolic pathways is as yet unclear – so care is needed

Watch for dehydration, mineral loss

Next scan – the cancer has not grown but there are signs of portal hypertension. That is to say the pressure in the blood vessels leading to the level is elevated. This can lead to bleeding if the resulting varicose veins or varicose decide to pop. These changes seem to have preceded the dietary intervention so my belief is that chemotherapy caused most of the liver damage. This has been confirmed by my most recent MRI which showed a picture of platinum based chemotherapy damage.

To summarise:

The good = the cancer seemed to stabilise, I lost weight.

The Bad = difficult diet to follow, Keto flu, needs constant monitoring, difficult for vegans

The Ugly = are there long term complications of this diet? The liver is crucial organ in the struggle to keep the crab at bay. Patients with pre-existing liver disease and chemotherapy induced liver dysfunction should avoid this diet or at the very least receive screening to assess  risk.

Overall I still believe it is essential to restrict sugar intake but a gentler approach may be required.

Coping after a Cancer Setback


Coping after a Cancer Setback

My three year chemo-versary is due in August. I will have survived three years since chemo finished without further aid from orthodox oncology. Now, I know that the docs in hospital will say my survival is down to better chemo. However, I have seen no case reports or journal papers documenting such long survival times for metastatic small bowel cancer. I have seen quotes of progression free survival ranging from 6-9 months. In fact median survival for the stage of cancer with which I was diagnosed, treated with chemotherapy is around 15 months.
It is now 42 months since diagnosis. I believe something else is going on. Something miraculous….

So when clinic doesn’t go according to plan what do you do? As each outpatient visit goes by my anxiety levels have climbed – particularly in the month before clinic.
It is June 30th. I have been waiting 3 weeks for the scan results. Jackie and I are on time for the appointment. I like to arrive on time even though I have had to wait in the past as clinics can be delayed by up to an hour or so… So Jackie takes her opportunity to pop to the loo…
But what now? Oh no! My oncologist comes out and calls me straight in… What – no Jackie? I definitely need my hand held. But I also want to know my scan result. I’m feeling well. I walked 46 miles the previous week and am on course for 40 more this time. I have visualised the consultant telling me that I am in full remission. I take the plunge and head to the clinic room.
“The scan isn’t so good this time…” the oncologist delivers the unexpected result as kindly as he can. It is quite a let down to hear that the cancer has progressed.. I try not to fall into despair and luckily, Jackie, my rock, enters the room. I reach for her hand and look up at her with a crestfallen expression. The oncologist explains to us my 3 options: I could have oxaliplatin and capecitabine chemotherapy again. Yuk! I don’t like option 1! Option 2 is a PET scan to see if the cancer is active elsewhere – if not I could have radiotherapy to shrink the newly enlarged lymph nodes. I don’t like option 2 either! Option 3 is to watch and wait – I am reasonably well and want to enjoy the summer – Cornwall and the West Highland Way are on the calendar!

In August 2014 I rebelled against the “watch and wait” approach but now I opt wholeheartedly for option 3. I want the summer and it’s going to be a good one! Scorchio!

But first how to cope with the heartache, fear and anxiety…….
I think to myself – it’s been 7 months since my last scan and all the tumour can do is grow by less than a centimetre- and the primary is still not visible on the scan. I am a little anaemic – that worries me but my liver, lung and bones are clear. I know if I dwell on the small amount of progression that I will descend down into a vortex of angst!
I need a plan. I pray and ask God for healing. I meditate and a picture appears of where I want to be.
If 7 months ago I was OK – perhaps something has slipped. I arrange to see my holistic Doctor Rosy Daniels. We come up with a plan – I will restart some supplements, change the timings around. I will pulse my Low Dose Naltrexone. I will take liposomal vitamin C. Take artemesinin at night, restart high dose curcumin. But most importantly I will work to reduce my sugar intake. I have been eating more fruit and grains in the last few months. So perhaps it is time to try the ketogenic diet.. It’s very “buzz”. Ketogenic – the diet sounds very technical. Also very topical – there is a lot of basic science but not too much data from clinical trials.
The ketogenic diet is an ultra-low carb diet where most of the calories are obtained from fat and to a lesser extent, protein. The idea is to starve the tumour of glucose. Reducing sugar intake is fairly straightforward for meat and dairy eaters. As a vegan, however, the diet is quite restricting as most vegetables and fruit have high sugar levels. The wonderful Facebook provided a solution for me as there are several excellent pages with tasty ketogenic vegan recipes. I am aiming to eat less than 20 g net carbs per day (the amount of sugar in one apple). The ketogenic diet is not for the faint hearted and there are risks so – readers – please consult a healthcare professional before starting on such a rigorous schedule. One of the least pleasant effects is the keto-flu which strikes about a week after starting the diet. Keto-flu is essentially a syndrome of withdrawal from the high-carb diet which is typical of the UK/USA population.
Well I have been following this diet for two weeks. It is quite exciting being the subject of my own science experiment. But, I am in the middle of the keto-flu which occurs when the body is transitioning from using carbs as fuel to using fat and ketone bodies. Extreme fatigue, weak legs, nausea and some abdominal cramps. But I just about managed camping at the weekend and walked 5 miles today. What’s more – the lump which I could feel in my abdomen – is it my imagination but does it feel smaller?? We shall see…… perhaps things can only get better!

The Cheese Trap

Cheese Trap

Cheese: The ultimate processed food. Highly calorific and full of salt. Cheese as we all know is extremely more-ish. Neal Barnard is an eminent physician – a Fellow of the American College of Cardiologists. He describes the addictive properties of cheese in detail, attributing this to morphine like molecules – casomorphins – released during digestion of the milk protein casein. The cheese cravers get hooked not realising  the dangers ahead. Cheese is packed full of worrisome hormones and growth factors. It is implicated in the development of heart disease and the hormone dependent cancers e.g. breast and prostate. Other cancer types may also also be promoted by constituents of cheese. Migraines, asthma, joint diseases, type 2 diabetes, acne – Neal Barnard states that cheese is a major culprit in many medical conditions.

In the second half of the book Dr. Barnard relates the unpleasantness of the cheese manufacturing process and what the animals go through.  The dirty tricks used by the cheese industry to keep people hooked are pretty eye popping – “triggering the cravings” e.g the Wendy’s triple cheese combo – two types of cheese, 3 bacon rashers, then the burger, topped off with cheese coated fries.

But all is not lost and what I really like about this book is how Dr Barnard provides solutions to the problem i.e how to eliminate cheese and adopt a healthy diet. I love the recipes and today tried his pizza and tomato sauce which in combination with some Violife vegan mozzarella went down very well in our house!!

In conclusion this is a well written book, easily readable over a few days with the added benefit of delicious recipes which can help to break the dangerous cheese habit.


To Fast or not to Fast….


At my Oncology follow-up appointments, I generally ask if there is anything new on the horizon. Last time I asked about fasting – the reason – well I had just finished a fantastic book about fasting for health:

How to do fasting in intricate detail – but it can be tough so so always consult an expert… (and I am not one of those having received next to no training on nutrition at medical school!!)

My oncologist considered that fasting was interesting in theory but he was concerned about the effects of fasting on frail patients undergoing intensive chemotherapy and also the lack of clinical trial data.

Fasting seems to be very “buzz” and my interest was piqued last year when I espied a paper from Newcastle University describing the use of ultra low calorie diets to reverse type 2 diabetes. And the initial studies do suggest that a 2 month lifestyle change to an ultra low calorie diet can infact reverse type 2 diabetes if caught in the early stages… This is MASSIVE!

Looking into this subject further revealed a researcher named Valter Longo who is the current Edna M Jones Professor of Gerontology at USC Davis.

This intrepid researcher boasts a huge list of publications investigating fasting, longevity, cancer etc. The research started as basic science in rodents but is now moving forward into the clinical trial arena. Indeed some of the research is now hitting the press and social media:

Of note Longo does admit that fasting is tough and perhaps for that reason he has devised a fasting-mimicking diet plan to achieve the same ends with a more patient-friendly method. This method involves a 5 days per month of dietary restriction to 700-1100 calories.

Fasting, at least in rodents seems to work by reducing blood glucose levels and levels of the important growth factor IGF-1 (Insulin like growth factor). This effect may be beneficial in a number of chronic diseases like cancer and cardiovascular disease, not to mention type 2 diabetes. Early studies in humans are promising but Longo cautions that patients should not try this at home without medical supervision.

Summarising – fasting seems to have profound benefits for weight loss in obesity and type 2 diabetes and that is just for starters. Benefits in cancer and heart disease in human need further study.

Mice lose weight and live longer

Sugar and insulin levels fall in both rodents and humans. Immune function is improved.

IGF-1 levels fall

Mice seem to develop less tumours when fasted

Fasting around chemo seems to be safe in small clinical studies

Fasting may sensitise tumours to chemotherapy (i.e the response is greater)

Side effects of chemotherapy may be reduced by intermittent or periodic fasting

Fasting in combination with other integrative approaches such as herbal medicine is under investigation

Will I try fasting if I am offered second-line chemo in the future? Well I don’t want to lose weight – I have lost 20kg over the last 3 years – mainly dietary. My weight is stable but I’m not sure. The theory sounds great but I need to see more success stories and clinical trials using this approach.

If interested, below are summarised some of Valter Longo’s major papers:

Di Biase et al 2017

PLoS Biol. 2017 Mar; 15(3): e2001951.

Published online 2017 Mar 30. doi:  10.1371/journal.pbio.2001951

Fasting reduces glucose levels and protects mice against chemotoxicity, yet drugs that promote hyperglycemia are widely used in cancer treatment. Here, we show that dexamethasone (Dexa) and rapamycin (Rapa), commonly administered to cancer patients, elevate glucose and sensitize cardiomyocytes and mice to the cancer drug doxorubicin (DXR). Such toxicity can be reversed by reducing circulating glucose levels by fasting or insulin. Furthermore, glucose injections alone reversed the fasting-dependent protection against DXR in mice, indicating that elevated glucose mediates, at least in part, the sensitizing effects of rapamycin and dexamethasone. In yeast, glucose activates protein kinase A (PKA) to accelerate aging by inhibiting transcription factors Msn2/4. Here, we show that fasting or glucose restriction (GR) regulate PKA and AMP-activated protein kinase (AMPK) to protect against DXR in part by activating the mammalian Msn2/4 ortholog early growth response protein 1 (EGR1). Increased expression of the EGR1-regulated cardioprotective peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in heart tissue may also contribute to DXR resistance. Our findings suggest the existence of a glucose–PKA pathway that inactivates conserved zinc finger stress-resistance transcription factors to sensitize cells to toxins conserved from yeast to mammals. Our findings also describe a toxic role for drugs widely used in cancer treatment that promote hyperglycemia and identify dietary interventions that reverse these effects.

Impact of intermittent fasting on health and disease processes

Mark P. Mattsona, b, , , Valter D. Longoc, Michelle Harvied

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Mattson et al. 2016

Ageing Research Reviews


Humans in modern societies typically consume food at least three times daily, while laboratory animals are fed ad libitum. Overconsumption of food with such eating patterns often leads to metabolic morbidities (insulin resistance, excessive accumulation of visceral fat, etc.), particularly when associated with a sedentary lifestyle. Because animals, including humans, evolved in environments where food was relatively scarce, they developed numerous adaptations that enabled them to function at a high level, both physically and cognitively, when in a food-deprived/fasted state. Intermittent fasting (IF) encompasses eating patterns in which individuals go extended time periods (e.g., 16–48 h) with little or no energy intake, with intervening periods of normal food intake, on a recurring basis. We use the term periodic fasting (PF) to refer to IF with periods of fasting or fasting mimicking diets lasting from 2 to as many as 21 or more days. In laboratory rats and mice IF and PF have profound beneficial effects on many different indices of health and, importantly, can counteract disease processes and improve functional outcome in experimental models of a wide range of age-related disorders including diabetes, cardiovascular disease, cancers and neurological disorders such as Alzheimer’s disease Parkinson’s disease and stroke. Studies of IF (e.g., 60% energy restriction on 2 days per week or every other day), PF (e.g., a 5 day diet providing 750–1100 kcal) and time-restricted feeding (TRF; limiting the daily period of food intake to 8 h or less) in normal and overweight human subjects have demonstrated efficacy for weight loss and improvements in multiple health indicators including insulin resistance and reductions in risk factors for cardiovascular disease. The cellular and molecular mechanisms by which IF improves health and counteracts disease processes involve activation of adaptive cellular stress response signaling pathways that enhance mitochondrial health, DNA repair and autophagy. PF also promotes stem cell-based regeneration as well as long-lasting metabolic effects. Randomized controlled clinical trials of IF versus PF and isoenergetic continuous energy restriction in human subjects will be required to establish the efficacy of IF in improving general health, and preventing and managing major diseases of aging.

BMC Cancer. 2016; 16: 360.

Published online 2016 Jun 10. doi:  10.1186/s12885-016-2370-6

PMCID: PMC4901417

Safety and feasibility of fasting in combination with platinum-based chemotherapy

Tanya B. Dorff, Susan Groshen, Agustin Garcia, Manali Shah, Denice Tsao-Wei, Huyen Pham, Chia-Wei Cheng, Sebastian Brandhorst, Pinchas Cohen, Min Wei, Valter Longo,pastedGraphic.png and David I. QuinnpastedGraphic.png

Author information ► Article notes ► Copyright and License information ►




Short-term starvation prior to chemotherapy administration protects mice against toxicity. We undertook dose-escalation of fasting prior to platinum-based chemotherapy to determine safety and feasibility in cancer patients.


3 cohorts fasted before chemotherapy for 24, 48 and 72 h (divided as 48 pre-chemo and 24 post-chemo) and recorded all calories consumed. Feasibility was defined as ≥ 3/6 subjects in each cohort consuming ≤ 200 kcal per 24 h during the fast period without excess toxicity. Oxidative stress was evaluated in leukocytes using the COMET assay. Insulin, glucose, ketones, insulin-like growth factor-1 (IGF-1) and IGF binding proteins (IGFBPs) were measured as biomarkers of the fasting state.


The median age of our 20 subjects was 61, and 85 % were women. Feasibility criteria were met. Fasting-related toxicities were limited to ≤ grade 2, most commonly fatigue, headache, and dizziness. The COMET assay indicated reduced DNA damage in leukocytes from subjects who fasted for ≥48 h (p = 0.08). There was a non-significant trend toward less grade 3 or 4 neutropenia in the 48 and 72 h cohorts compared to 24 h cohort (p = 0.17). IGF-1 levels decreased by 30, 33 and 8 % in the 24, 48 and 72 h fasting cohorts respectively after the first fasting period.


Fasting for 72 h around chemotherapy administration is safe and feasible for cancer patients. Biomarkers such as IGF-1 may facilitate assessment of differences in chemotherapy toxicity in subgroups achieving the physiologic fasting state. An onging randomized trial is studying the effect of 72 h of fasting.

Version 1. F1000Res. 2016; 5: F1000 Faculty Rev-117.

Published online 2016 Jan 29. doi:  10.12688/f1000research.7136.1

PMCID: PMC4755412

Dietary restriction with and without caloric restriction for healthy aging

Changhan Leea,1 and Valter Longob,1,2

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This article has been cited by other articles in PMC.

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Caloric restriction is the most effective and reproducible dietary intervention known to regulate aging and increase the healthy lifespan in various model organisms, ranging from the unicellular yeast to worms, flies, rodents, and primates. However, caloric restriction, which in most cases entails a 20–40% reduction of food consumption relative to normal intake, is a severe intervention that results in both beneficial and detrimental effects. Specific types of chronic, intermittent, or periodic dietary restrictions without chronic caloric restriction have instead the potential to provide a significant healthspan increase while minimizing adverse effects. Improved periodic or targeted dietary restriction regimens that uncouple the challenge of food deprivation from the beneficial effects will allow a safe intervention feasible for a major portion of the population. Here we focus on healthspan interventions that are not chronic or do not require calorie restriction.

Keywords: Caloric restriction, mechanisms of aging, Dietary restriction, aging, healthspan

Semin Cancer Biol. Author manuscript; available in PMC 2016 Dec 1.

Published in final edited form as:

Semin Cancer Biol. 2015 Dec; 35(Suppl): S276–S304.

doi:  10.1016/j.semcancer.2015.09.007

PMCID: PMC4819002


A Broad-Spectrum Integrative Design for Cancer Prevention and Therapy

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Targeted therapies and the consequent adoption of “personalized” oncology have achieved notable successes in some cancers; however, significant problems remain with this approach. Many targeted therapies are highly toxic, costs are extremely high, and most patients experience relapse after a few disease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistant immortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are not reliant upon the same mechanisms as those which have been targeted). To address these limitations, an international task force of 180 scientists was assembled to explore the concept of a low-toxicity “broad-spectrum” therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspects of relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a wide range of high-priority targets (74 in total) that could be modified to improve patient outcomes. For these targets, corresponding low-toxicity therapeutic approaches were then suggested; many of which were phytochemicals. Proposed actions on each target and all of the approaches were further reviewed for known effects on other hallmark areas and the tumor microenvironment. Potential contrary or procarcinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixed evidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of the relationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. This novel approach has potential to help us address disease relapse, which is a substantial and longstanding problem, so a proposed agenda for future research is offered.

Fontana et al. 2012

Growth Factors, Nutrient Signalling, and Cardiovascular Ageing

Growth factors regulated by specific macronutrients have been shown to promote aging and accelerate mortality in the majority of the organisms studied. In particular, the enzymes activated by growth hormone, insulin, and insulin-like growth factor-1 in mammals and their orthologs in simple model organisms represent perhaps the best-understood proteins involved in the aging process. Dietary restriction, which reduces the level of insulin-like growth factor-1 and of other growth factors, has been associated with protection from diabetes, cancer, and cardiovascular diseases, and deficiencies in growth hormone signaling and insulin-like growth factor-1 are strongly associated with protection from cancer and diabetes in both mice and humans; however, their role in cardiac function and cardiovascular diseases is controversial. Here, we review the link between growth factors, cardiac function, and heart disease with focus on the cardioprotective and sensitizing effect of growth factors in both model organisms and humans.

Lee et al. 2012

Starvation, detoxification and multi drug resistance in cancer therapy

The selection of chemotherapy drugs is based on the cytotoxicity to specific tumor cell types and the relatively low toxicity to normal cells and tissues. However, the toxicity to normal cells poses a major clinical challenge, particularly when malignant cells have acquired resistance to chemotherapy. This drug resistance of cancer cells results from multiple factors including individual variation, genetic heterogeneity within a tumor, and cellular evolution. Much progress in the understanding of tumor cell resistance has been made in the past 35 years, owing to milestone discoveries such as the identification and characterization of ABC transporters. Nonetheless, the complexity of the genetic and epigenetic rewiring of cancer cells makes drug resistance an equally complex phenomenon that is difficult to overcome. In this review, we discuss how the remarkable changes in the levels of glucose, IGF-I, IGFBP-1 and in other proteins caused by fasting have the potential to improve the efficacy of chemotherapy against tumors by protecting normal cells and tissues and possibly by diminishing multidrug resistance in malignant cells.

Lee et al. 2012

Fasting Cycles Retard Growth of Tumors and Sensitize a Range of Cancer Cell Types to Chemotherapy . Sci Transl Med. 2012 Mar 7; 4(124): 124ra27.

Short-term starvation (or fasting) protects normal cells, mice, and potentially humans from the harmful side effects of a variety of chemotherapy drugs. Here we show that treatment with starvation conditions sensitized yeast cells (S. cerevisiae) expressing the oncogene-like RAS2val19 to oxidative stress and 15 of 17 mammalian cancer cell lines to chemotherapeutic agents. Cycles of starvation were as effective as chemotherapeutic agents in delaying progression of specific tumors and increased the effectiveness of these drugs against melanoma, glioma, and breast cancer cells. In mouse models of neuroblastoma, fasting cycles plus chemotherapy drugs— but not either treatment alone—resulted in long-term cancer-free survival. In 4T1 breast cancer cells, short- term starvation resulted in increased phosphorylation of the stress-sensitizing AKT and S6 kinases, increased oxidative stress, caspase-3 cleavage, DNA damage and apoptosis. These studies suggest that multiple cycles of fasting promote differential stress sensitization in a wide range of tumors and could potentially replace or augment the efficacy of certain toxic chemotherapy drugs in the treatment of various cancers.

Lee & Longo 2012

Oncogene (2011) 30, 3305–3316

The dietary recommendation for cancer patients receiving chemotherapy, as described by the American Cancer Society, is to increase calorie and protein intake. Yet, in simple organisms, mice, and humans, fasting—no calorie intake—induces a wide range of changes associated with cellular protection, which would be difficult to achieve even with a cocktail of potent drugs. In mammals, the protective effect of fasting is mediated, in part, by an over 50% reduction in glucose and insulin-like growth factor 1 (IGF-I) levels. Because proto-oncogenes function as key negative regulators of the protective changes induced by fasting, cells expressing oncogenes, and therefore the great majority of cancer cells, should not respond to the protective signals generated by fasting, promoting the differential protection (differential stress resistance) of normal and cancer cells. Preliminary reports indicate that fasting for up to 5 days followed by a normal diet, may also protect patients against chemotherapy without causing chronic weight loss. By contrast, the long-term 20 to 40% restriction in calorie intake (dietary restriction, DR), whose effects on cancer progression have been studied extensively for decades, requires weeks–months to be effective, causes much more modest changes in glucose and/or IGF-I levels, and promotes chronic weight loss in both rodents and humans. In this study, we review the basic as well as clinical studies on fasting, cellular protection and chemotherapy resistance, and compare them to those on DR and cancer treatment. Although additional pre-clinical and clinical studies are necessary, fasting has the potential to be translated into effective clinical interventions for the protection of patients and the improvement of therapeutic index.

Guevara- Aguirre et al. 2011

Sci Transl Med 3, 70ra13 (2011)

Clues to a Cancer- and Diabetes-Free Life

In the 1958 film Live Fast and Die Young, two reckless sisters threaten to burn out early. Similarly, one theory of aging predicts that a faster metabolism leads to a shorter life. Does this trade-off also apply to age-related disease? A new study by Guevara-Aguirre et al. offers clues that address this seminal question. The authors’ findings stem from studies of a unique group of Ecuadorian people who have a mutation in the growth hormone receptor (GHR) gene and a resulting insulin-like growth factor −1 (IGF-1) deficiency, which stunts their growth. These descendants of Spanish conversos, Jews who converted to Christianity to avoid the Inquisition, almost never get diabetes or cancer as a result, the authors postulate, of the privileged metabolic status that arises from their altered hormonal state. Relative to controls, these subjects show lower insulin concentrations and higher insulin sensitivity, and when stressed, their cells tend to self-destruct rather than accumulate mutations and DNA damage−−all features that are known to promote cell protection in model organisms.

For 22 years, this group of 99 related Ecuadorians−−most of whom are homozygous for an A-to-G splice site mutation at position 180 in exon 6 of the GHR gene−−has been monitored extensively, so that their health details are well documented. From this reservoir of data, plus information about the diseases of family members as well as causes of death of those relatives who have died, the authors deciphered that the Ecuadorian subjects who carried the GHR mutation had an abnormally low incidence of cancer and diabetes. The group showed only one case of nonlethal cancer and no cases of diabetes, whereas the controls −−unaffected relatives−−developed cancer (17%) and diabetes (5%) at rates similar to those of the Ecuadorian population as a whole.

To illuminate the underlying reason for the subjects’ freedom from these diseases, the authors focused on the components carried in their blood. In experiments on cultured human epithelial cells, Guevara-Aguirre et al. found that low concentrations of one of these, IGF-1, was responsible for preventing oxidative DNA damage when the cells were exposed to the oxidizing agent H2O2 and for promoting cell death when stress-related DNA damage did occur, a checkpoint that averts cancer-promoting behavior by abnormal cells. Analysis of the participating cell signaling pathways identified activation of the transcription factor FoxO under conditions of low IGF-1 as a likely mediator of these effects. Further, the lower blood insulin concentrations and higher insulin sensitivity in these subjects likely account for the absence of diabetes in this population.

Although it is difficult to prove that alterations in IGF-1 amounts are responsible for the cancer- and diabetes-free lives of these Ecuadorian people, genetic work from several model organisms suggests that this is so. In yeast, mutations in genes that encode components of a growth-promoting pathway protect against age-dependent genomic instability, and mutations in the insulin/IGF-1−like signaling pathway increase life span and reduce abnormal cellular proliferation in worms. Mice with defects in GH and IGF-1 live exceptionally long lives, with delayed appearance of age-dependent mutations and cancer. The Ecuadorians do not live longer-than-normal lives compared with their compatriots, but rather die in due course from causes of death other than cancer and diabetes complications. Thus, the metabolic inverse of ”live fast and die young”−−a slowed metabolism yields a longer life−−is not supported by the current findings. But a life free from two dreaded diseases may be considered a desirable trade-off.

Raffaghello et al. 2010

Fasting and differential chemotherapy protection in patients

Cell Cycle 9:22, 4474-4476

Chronic calorie restriction has been known for decades to prevent or retard cancer growth, but its weight-loss

effect and the potential problems associ- ated with combining it with chemother- apy have prevented its clinical application. Based on the discovery in model organ- isms that short term starvation (STS or fasting) causes a rapid switch of cells to a protected mode, we described a fasting- based intervention that causes remarkable changes in the levels of glucose, IGF-I and many other proteins and molecules and is capable of protecting mammalian cells and mice from various toxins, including chemotherapy. Because oncogenes prevent the cellular switch to this stress resistance mode, starvation for 48 hours or longer protects normal yeast and mammalian cells and mice but not cancer cells from chemotherapy, an effect we termed Differential Stress Resistance (DSR). In a recent article, 10 patients who fasted in combination with chemotherapy, reported that fasting was not only feasible and safe but caused a reduction in a wide range of side effects accompanied by an apparently normal and possibly augmented chemotherapy efficacy. Together with the remarkable results observed in animals, these data provide preliminary evidence in support of the human application of this fundamental biogerontology  finding, particularly for terminal patients receiving chemotherapy. Here we briefly discuss the basic, pre-clinical and clinical studies on fasting and cancer therapy.

Fontana et al. 2010

Extending Healthy Life Span—From Yeast to Humans 5976/321.

When the food intake of organisms such as yeast and rodents is reduced (dietary restriction), they live longer than organisms fed a normal diet. A similar effect is seen when the activity of nutrient- sensing pathways is reduced by mutations or chemical inhibitors. In rodents, both dietary restriction and decreased nutrient-sensing pathway activity can lower the incidence of age-related loss of function and disease, including tumors and neurodegeneration. Dietary restriction also increases life span and protects against diabetes, cancer, and cardiovascular disease in rhesus monkeys, and in humans it causes changes that protect against these age-related pathologies. Tumors and diabetes are also uncommon in humans with mutations in the growth hormone receptor, and natural genetic variants in nutrient-sensing pathways are associated with increased human life span. Dietary restriction and reduced activity of nutrient-sensing pathways may thus slow aging by similar mechanisms, which have been conserved during evolution. We discuss these findings and their potential application to prevention of age-related disease and promotion of healthy aging in humans, and the challenge of possible negative side effects.

Lee et al. 2010

Cancer Res; 70(4); 1564–72

Reduced Levels of IGF-I Mediate Differential Protection of Normal and Cancer Cells in Response to Fasting and Improve Chemotherapeutic Index

Inhibitors of the insulin-like growth factor-I (IGF-I) receptor have been widely studied for their ability to enhance the killing of a variety of malignant cells, but whether IGF-I signaling differentially protects the host and cancer cells against chemotherapy is unknown. Starvation can protect mice, but not cancer cells, against high-dose chemotherapy [differential stress resistance (DSR)]. Here, we offer evidence that IGF-I reduction mediates part of the starvation-dependent DSR. A 72-hour fast in mice reduced circulating IGF-I by 70% and increased the level of the IGF-I inhibitor IGFBP-1 by 11-fold. LID mice, with a 70% to 80% reduction in circulating IGF-I levels, were protected against three of four chemotherapy drugs tested. Restoration of IGF-I was sufficient to reverse the protective effect of fasting. Sixty percent of melanoma-bearing LID mice treated with doxorubicin achieved long-term survival whereas all control mice died of either metastases or chemotherapy toxicity. Reduc- ing IGF-I/IGF-I signaling protected primary glia, but not glioma cells, against cyclophosphamide and protected mouse embryonic fibroblasts against doxorubicin. Further, S. cerevisiae lacking homologs of IGF-I signaling pro- teins were protected against chemotherapy-dependent DNA damage in a manner that could be reversed by ex- pressing a constitutively active form of Ras. We conclude that normal cells and mice can be protected against chemotherapy-dependent damage by reducing circulating IGF-I levels and by a mechanism that involves down- regulation of proto-oncogene signals

Longo & Fontana 2010

Trends Pharmacol Sci. 2010 February ; 31(2): 89–98Calorie restriction and cancer prevention: metabolic and molecular mechanisms

An important discovery of recent years has been that lifestyle and environmental factors affect cancer initiation, promotion and progression, suggesting that many malignancies are preventable. Epidemiological studies strongly suggest that excessive adiposity, decreased physical activity, and unhealthy diets are key players in the pathogenesis and prognosis of many common cancers. In addition, calorie restriction (CR), without malnutrition, has been shown to be broadly effective in cancer-prevention in laboratory strains of rodents. Adult-onset moderate CR also reduces cancer incidence by 50% in monkeys. Whether the anti-tumorigenic effects of CR will apply to humans is unknown, but CR results in a consistent reduction in circulating levels of growth factors, anabolic hormones, inflammatory cytokines and oxidative stress markers associated with various malignancies. Here, we discuss the link between nutritional interventions and cancer prevention with focus on the mechanisms that may be responsible for these effects in simple systems and mammals with a view to developing chemoprevention agents.

Sadie et al. 2009

Fasting and Cancer Treatment in Humans: A Case series report

AGING, December 2009 Vol.1 No 12 1-18

Abstract: Short‐term fasting (48 hours) was shown to be effective in protecting normal cells and mice but not cancer cells against high dose chemotherapy, termed Differential Stress Resistance (DSR), but the feasibility and effect of fasting in cancer patients undergoing chemotherapy is unknown. Here we describe 10 cases in which patients diagnosed with a variety of malignancies had voluntarily fasted prior to (48‐140 hours) and/or following (5‐56 hours) chemotherapy. None of these patients, who received an average of 4 cycles of various chemotherapy drugs in combination with fasting, reported significant side effects caused by the fasting itself other than hunger and lightheadedness. Chemotherapy associated toxicity was graded according to the Common Terminology Criteria for Adverse Events (CTCAE) of the National Cancer Institute (NCI). The six patients who underwent chemotherapy with or without fasting reported a reduction in fatigue, weakness, and gastrointestinal side effects while fasting. In those patients whose cancer progression could be assessed, fasting did not prevent the chemotherapy‐induced reduction of tumor volume or tumor markers. Although the 10 cases presented here suggest that fasting in combination with chemotherapy is feasible, safe, and has the potential to ameliorate side effects caused by chemotherapies, they are not meant to establish practice guidelines for patients undergoing chemotherapy. Only controlled‐randomized clinical trials will determine the effect of fasting on clinical outcomes including quality of life and therapeutic index.

Jennifer Couzin – News of the Week

Can Fasting Blunt Chemotherapy’s Debilitating Side Effects?

SCIENCE VOL 321 1146-7

Raffaghello et al. 2008

Starvation-dependent differential stress resistance protects normal but not cancer cells against

high-dose chemotherapy cgi doi 10.1073 pnas.0708100105

Strategies to treat cancer have focused primarily on the killing of tumor cells. Here, we describe a differential stress resistance (DSR) method that focuses instead on protecting the organism but not cancer cells against chemotherapy. Short-term starved S. cerevisiae or cells lacking proto-oncogene homologs were up to 1,000 times better protected against oxidative stress or chemotherapy drugs than cells expressing the oncogene homolog Ras2val19. Low- glucose or low-serum media also protected primary glial cells but not six different rat and human glioma and neuroblastoma cancer cell lines against hydrogen peroxide or the chemotherapy drug/ pro-oxidant cyclophosphamide. Finally, short-term starvation pro- vided complete protection to mice but not to injected neuroblas- toma cells against a high dose of the chemotherapy drug/pro- oxidant etoposide. These studies describe a starvation-based DSR strategy to enhance the efficacy of chemotherapy and suggest that specific agents among those that promote oxidative stress and DNA damage have the potential to maximize the differential toxicity to normal and cancer cells.

The China Study re-visited




So why don’t we know about The China Study? I say we – I didn’t – until 2015. Why hadn’t I read this book? I kept myself up-to-date, read the BMJ and Lancet. But this type of research just doesn’t feature heavily in the mainstream medical press. Anyway, no use crying over spilled milk!! Back to 2015 – The Victory family were visiting Florence in May of that year. Hungry, and looking for a healthy eatery we came across a “fast-food” vegan restaurant.

Quite yummy and I noticed on a shelf, multiple copies of a book named “The China Study”. I got up from my seat and leafed through the pages – it looked really interesting. As time has passed and I have researched dietary solutions, The China Study is mentioned often. However, as often as it is cited I see web articles describing how the study has been de-bunked. Debaters describe the China Study as flawed. At first glance it looks to me like a major piece of science. So, finally I listened to “The China Study” on Audible.

It is fascinating, such a great story. A plausible biological mechanism to explain why cancer rates are lower in certain areas of the world and higher in others. Broadly speaking ,cancer rates are much higher in urban areas, industrialised countries. T Colin Campbell and his research team postulate that animal protein, particularly the milk protein casein provide a set-up for the development of cancer.

I am aware of the criticisms – the researchers used a proxy indicator of animal protein intake – the serum cholesterol. After all most of the cholesterol we eat comes from animals and the rest is made by the liver. So the China Study – which is actually a book not a peer-reviewed paper cannot show direct causation or even a direct correlation. However, the big picture here is so striking, so profound, so important: there are hotspots and cold spots around the world for disease. In some areas of the world there is simply no cancer or heart disease. None. Conclusions must be drawn from this and other studies that some aspect of the western diet is involved in the initiation, and promotion of atherosclerosis and also tumours. It seems to me that the critics are concentrating on the minutiae and ignoring the big picture.

This research does not deserve to be suppressed, ignored or hidden. And it is the big picture which has biological plausibility! This should be feeding future research. There is so much more evidence now supporting T Colin Campbell’s hypothesis – migration studies for instance. Natives of rural areas (and their descendants) migrating to urban areas where the Standard American Diet is prevalent eventually succumb to the Western chronic diseases. Lactose intolerant individuals appear to have markedly lower rates of breast, prostate and ovarian cancer – why? – well they get tummy ache when they eat lactose-containing dairy – so they tend to avoid dairy produce….

Whatever you do – choose to make some change – the status quo appears to be creating a sick population! The balanced diet, eat in moderation etc. – how effective has that been? The answer – it hasn’t  – the balanced diet is feeding the epidemic of diabetes, obesity, cardiovascular disease and cancer in the West and now in the Eastern countries that are becoming industrialised. I have been following a plant based diet for several years now. My dietary history has been of a tendency to reduced animal and dairy intake over the last 25 years. Initially I cut out meat, but did not become vegan until recently. The source of protein in my diet switched from meat to fish and dairy, with ever increasing amounts of milk and cheese based foods. I realise now this was a mistake and I should have taken the plunge to become vegan a lot earlier. For me – I was given an extreme diagnosis and have needed to take extreme measures. Does this suit everyone? Perhaps not – but if you cannot give up animal protein altogether there are still ways to make the diet more healthy – eating organic meat that is not factory-farmed (free of hormones and antibiotics). Perhaps eat meat less often. Perhaps switch to a non-dairy milk that is palatable. Or switch from cow’s milk to sheep or goat products (there are many healthy centenarians in Sardinia where pecorino cheese is a staple – you would need to do your own research on the risks / benefits of different types of alternative dairy).

Just to finish, here is a Dr. Michael Greger video that just about clinches the argument for me:

How much Curcumin??


The king or queen of spices – Turmeric. A common ingredient of curry powder this spice is the subject of much scientific interest. It appears to protect against cancer and may have a role in treatment of the disease. When I asked my orthodox oncologist what else I could do to improve my chances, the answer was to eat as much turmeric – or rather the active ingredient curcumin –  as I could tolerate. I love curry but turmeric is not well absorbed so a little thought was needed to elucidate the best way to get this lifesaving spice into my system.

It appears that curcumin absorption is increased by eating with fat and also by black pepper. Hence the very wonderful Golden Paste:

The recipe I use:

But how much should I take and with what precautions?

This website describes a protocol for slowly increasing the dose. A slow increase is needed to allow the bowels to get used to the idea!!

One can use supplements and I do supplement my intake of the whole spice with some turmeric capsules. However, I have found that at high supplement doses my liver starts to hurt, so I tend to concentrate on using the golden paste made up with non-dairy milk such as almond or cashew.

There are side effects and interactions to consider. For instance turmeric can trigger gallstone formation. There is also some evidence that turmeric thins the blood, so care is needed if one is taking aspirin or blood thinners. Also some people will get abdominal discomfort if eating a lot of golden spice. One also needs to be aware that curcumin can stain work surfaces. But on the whole curcumin is well tolerated and the health benefits can be very rewarding…

However, eliminating dairy may be even more efficacious – more about that later!

And here is a spicy song! I was never a great fan of the Spice Girls but this was the spiciest song I could find on YouTube!!

POMI-T. More Broccoli please!

I love juicing! However a recent talk by an integrative oncologist emphasised the importance of diet rotation. I needed a bit of that to prevent the tumour outflanking my defences!

I decided to cut back on carrot and beetroot juice – the sugar content was a concern – I would juice with less sugary fruit and vegetables. What could I juice then? As luck would have it I came across the POMI-T study ( which in my opinion is massive:


This randomised controlled trial investigated patients with prostate cancer. The patients in the active treatment group took a pill containing:

  • broccoli powder (Brassica oleracea) 100 mg,
  • turmeric powder (Curcuma longa) 100 mg,
  • pomegranate whole fruit powder (Punica granatum) 100 mg,
  • green tea 5:1 extract (Camellia sinensis) 20 mg equivalent to 100 mg of green tea and
  • bulking agent (di-calcium phosphate), anti-caking agents (modified maize-based starch, maltodextrin and magnesium stearate) removed post trial.

The change in prostate specific antigen (PSA) over six months was studied. A control group was given placebo. Well – you certainly wouldn’t want to have been in the placebo group! Even in this small-ish study involving 200 patients a highly significant benefit was seen in patients who took the POMI-T pill. The PSA rise was pretty small whereas in the untreated group a massive 78% rise occurred. The anti-cancer effect does not seem to be mediated through a hormonal mechanism.

What does this mean? Well it is not a clinical outcome study so we don’t really know if the findings correspond to a real benefit to the patients. HOWEVER! All the ingredients may be purchased down my local high street – the wonderful Gloucester Road. Difficult not to buy some pomegranates, curcumin root, broccoli and juice away to my heart’s content. Green tea mid afternoon and Bob’s your uncle, as they say…

Here is a link to a web-page concerning POMI-T with a very excellent youtube clip of Professor Robert Thomas who led the trial:

A word of caution: Curcumin has side effects and can thin the blood and may rarely trigger gallstones in susceptible individuals. Also broccoli can affect vitamin K metabolism – patients taking blood thinners need to be careful. So best to discuss with one’s doctor if considering this treatment.

Today marks 3 years since I found a lump..



A 3 year Cancer-versary! I am feeling positive and everything seems stable. All power to the NHS for putting the fire out! But then it’s been over to natural chemotherapy – curcumin, artemisinin, vitamin D, a vegan low sugar diet and much much more. The orthodox docs still see me as a good advert for chemo but I am outside the 95% confidence intervals for survival for this rare as hen’s teeth condition. At times – following some of the cancer stories – there has been sadness as others have not been so lucky….

Currently I am concentrating on the emotional side – wow! I really rate EFT (Emotional Freedom Technique) and hypnotherapy. A real eye opener!


So – to celebrate here is an uplifting song!!!!

Can’t stop the Feeling!!!

Would write more but it’s sauna time….

Chemoprevention of colorectal cancer in individuals with previous colorectal neoplasia: systematic review and network meta-analysis


A wordy title! No wonder patients feel confused when conversing with doctors!

This was the first article that caught my eye in December’s issue of the BMJ:

Chemoprevention of colorectal cancer in individuals with previous colorectal neoplasia: systematic review and  network meta-analysis:

BMJ 2016355 doi: (Published 05 December 2016)Cite this as: BMJ 2016;355:i6188

Meta-analysis is a research method that pools results of similar small studies creating a large body of data from numerous patients – this makes for much more powerful statistics in the right hands. Unfortunately, this paper is very difficult to read and understand. The authors use a lot of abbreviations, acronyms and medical jargon. When I was reviewing papers I would have used a lot of red ink on this one!! This paper looks at patients followed over a 3-5 year period.

Early on in my journey I asked my oncologist what else I should be doing to prevent the tumour returning. Were there some commonly available medicines which might help me? The oncologist mentioned aspirin. Early stage research suggested that aspirin can protect against cancer and possibly its recurrence. However, large randomised trials were not available to give a definitive answer. My oncologist looked at me sidelong while discussing this and tempered his remarks by saying that I was probably at risk of bleeding from the bowel, so on balance best to avoid aspirin.

So, is it possible to prevent colorectal cancer in individuals with a previous history by using some commonly available medicines – NSAIDS or non-steroidal anti-inflammatory drugs (celecoxib and sulindac which are similar to ibuprofen were used in these trials), low and high dose aspirin, calcium and vitamin D, folate? More importantly does the benefit outweigh the risk?

The meta-analysis includes adult patients with previous colorectal neoplasia (i.e. tumours – could be simple or metaplastic polyps or cancer – the paper itself does not specify). Studies were randomised controlled trials of placebo versus an active medication or combination of drugs.

I am unable to reproduce the figures due to copyright but summarising the findings:

NSAIDs were most effective at preventing colorectal cancer but gave most side effects. Of course the most feared side effects of drugs like these (serious side effects are significant but thankfully infrequent) are gastro-intestinal bleeding and kidney failure – so not to be taken lightly.

Aspirin was also very effective especially at the high doses of 160mg. The lower dose 81mg was also effective and had a better track record for side effects.

Calcium supplementation was not very effective and gave a lot of side effects

Folate was not very effective but there were few side effects

Vitamin D was not very effective and there were few side effects. The study doesn’t give the vitamin D doses. One has to delve into the individual referenced papers. The two papers studying vitamin D were quite small and the doses were also rather minute – 20 IU  dailyin Baron et al 2015 and 1000 IU daily in Pommegard et al. 2016. Due to the small numbers of patients given vitamin D alone, I don’t think any real conclusions can be drawn.

Summarising NSAIDs were the most effective but the risks are high. Low dose aspirin had the best risk:benefit profile. However, I don’t feel this paper is sufficiently powered to allow conclusions to be made about calcium, vitamin D or folate.

An Alternative Partridge


I was rather late with Christmas cards this year – so here is a late Christmas message to everyone:

On the First day of Christmas my true love sent to me a mug full of golden milk. 


On the Second day of Christmas my true love sent to me, two ginger roots and a mug full of golden  milk. 


On the Third day of Christmas my true love sent to me three raw salads, two ginger roots and a mug full of golden milk. 

On the Fourth day of Christmas my true love sent to me 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk. 


On the Fifth day of Christmas my true love sent to me, five Brussels sprouts, 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk.



On the Sixth day of Christmas my true love sent to me, six sauna sessions, five Brussel sprouts, 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk.


On the Seventh day of Christmas my true love sent to me seven chaga mushrooms, six sauna sessions, five Brussel sprouts, 4 garlic cloves, three raw salads, two ginger roots and a a mug full of golden milk.chaga-mushroom


On the Eighth day of Christmas my true love sent to me eight healers healing, seven chaga mushrooms, six sauna sessions, five Brussel sprouts , 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk.


On the Ninth day of Christmas my true love sent to me nine juicers juicing, eight healers healing, seven chaga mushrooms, six sauna sessions, five Brussel sprouts, 4 garlic cloves, three tofu chunks, two ginger roots and a mug full of golden milk.


On the Tenth day of Christmas my true love sent to me ten chilli peppers, nine juicers juicing, eight healers healing, seven chaga mushrooms, six sauna sessions, five Brussel sprouts, 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk.


On the Eleventh day of Christmas my true love sent to me Low Dose Naltrexone, ten chilli peppers, nine juicers juicing, eight healers healing, seven chaga mushrooms, six sauna sessions, five Brussel sprouts, 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk.  


On the Twelfth day of Christmas my true love sent for me twelve thoughtful prayers, Low Dose Naltrexone, ten chilli peppers, nine juicers juicing, eight healers healing, seven chaga mushrooms, six sauna sessions, five Brussel sprouts, 4 garlic cloves, three raw salads, two ginger roots and a mug full of golden milk.