It is a lovely idea but the more research delves into genes and cancer the more it is becoming increasingly clear that the idea is fundamentally wrong. In recent years, as ‘gene sequencing’ becomes possible at a fraction of the expense, it has been possible to look closely at the genes in a person’s cancer cells and compare them to their healthy cells, the goal being to find those shared genetic mutations that occur, for example, in women with breast cancer, to identify a cancer-causing gene to target with a drug.
The gene theory of cancer, known as Somatic Mutation Theory (SMT for short), proposes that single changes, known as mutations, in genes are passed on to offspring cells, resulting in the rapid growth of cancer cells, forming tumours. Yet, in almost all cases, even people with the same kind of cancer have vastly different mutations in their DNA code strongly suggesting that DNA damage may be the consequence, not the cause, of the disease of cancer as it unfolds.
In recent years, as cloning techniques have evolved, two experiments really put a nail in the coffin of the SMT theory of cancer. A cell has a nucleus in the middle, the yolk, where all the apparently damaged/mutated cancer genes would live, and a cytoplasm, the white, in which various organelles such as the mitochondria, which are the energy powerhouses of the cells, live.
A research group headed by William Schaeffer at the University of Vermont, given that the SMT theory proposes that it is DNA changes in the nucleus of the cell that drive cancer, wondered what would happen if you put the nucleus of a mouses’s cancer cell into a healthy cytoplasm. Out of sixty-eight mice only one developed a tumour.
Then, they did the opposite. They put a healthy cell’s nucleus into a malignant cytoplasm. Almost all, 97 per cent of the mice developed tumours. If damaged DNA in the nucleus of a cancer cell can’t cause the cell to grow and proliferate then how can the ‘cause’ of cancer be in the genes? It must be to do with something going on in the cytoplasm. More on this in a minute.
The real failure of the SMT gene theory has been its inability to make any substantial difference to cancer survival.
The standard treatment for cancer during the first half of last century was surgery and radiation, but these are no good for ‘liquid’ cancers that do not result in one mass of tumour cells such as lymphomas and leukemias. This led to the development of chemotherapy, systemic drugs that poison and kill cancer cells throughout the body.
How effective is chemotherapy?
The first drug used was mustard gas, in 1946, after it had been discovered that the lymph nodes and bone marrow of exposed soldiers were depleted of white blood cells, the cells that proliferate wildly in lymphoma. The second was methotrexate which works by stopping cells getting folic acid since folic acid is needed for cell growth. This drug is still in widespread use, also for auto-immune diseases such as rheumatoid arthritis. It is a dirty drug with nasty side-effects.
More and more toxic drugs were added to the mix until the standard treatment became cocktails of drugs that hammer cancer cells from every angle. The goal is to wipe out all cancer cells, devastating healthy cells in the process as the necessary evil, but hopefully all cancer cells are killed, while most healthy cells recover and the patient survives. It is basic stuff in concept with horrendous side-effects. But does it work?
The overall results are not good. In 1985, when a million people died of cancer in the US, a biostatistician called John Bailer worked out the total benefit of modern treatment, based on surgery, radiation and chemotherapy, and reported that 4% of cancer patients had been saved. However, cancer deaths as such had gone up by 9% presumably due to our increasing exposure to carcinogens from smoking, diet and the environment. He was not popular among those fighting the war on cancer.
In 2004 a meta-analysis of trials of chemotherapy in the US found that “The contribution of chemotherapy to five year survival in adults is 2.1%.” The researchers emphasised that these figures “should be regarded as the upper limit of effectiveness”. Of course, chemotherapy was the only option for ‘liquid’ cancers such as Hodgkins lymphoma, and while initial survival rates of children treated with chemotherapy look good it was then discovered that they were 18 times more likely to develop secondary malignant tumours and girls had a 35 per cent chance of developing breast cancer before age 40 – which is 75 times higher than average. So, long-term survival wasn’t nearly as good as 5 year survival.
Since 1970 the five year survival rate for a person diagnosed with cancer has barely changed from then 49% to now 54%. That means that all the advances in cancer treatment in the past 50 years have saved perhaps 6% of lives. In the US, for example, more than a million are diagnosed each year and a half a million die from it. Given the billions of hours and dollars poured into cancer research that’s remarkably unimpressive.
It is this crossing of the 50% mark that allowed Cancer Research Campaign to boast that ‘more people survive than die from cancer.’ However, it ignored two things. Firstly, with earlier diagnosis people are more likely to survive 5 years. A 10 year survival figure, or simplyoverall mortality, would be a more honest reflection of the effectiveness of treatment. Secondly, more people are getting cancer in their lifetime – namely 1 in 3 women and 1 in 2 men. So, overall, we have more deaths.
The holy grail of chemotherapy is to find something that kills only cancer cells and leaves healthy cells untouched. The dream of SMT is to find a mutated gene and block it with a specific drug to effect a cure. Apart from the problem of finding the oncogene, there is then the problem of finding a way to target it in the nucleus of cancer cells and turn it off.
The first ‘success’, proudly boasted as a proof of principle for SMT,was Herceptin. One in five women with breast cancer have an oncogene called HER-2. It stands for Human Epithelial Receptor and, fortunately is easily accessible as it sits on the outside of cells and tells the nucleus, the bit in the middle with all the DNA instructions, to divide and make another cell. So it was an accessible target.
Most breast cells have 50,000 such HER-Receptors, activated by certain hormones such as oestrogens, but when it was discovered that cancerous breast cells have over a million the race was on to find a drug that would inactivate the HER-2 receptor, stop the growth instructions and thus stop the cancer cells dividing. That drug is Herceptin. Of course, it is only like to be effective for HER-2 positive breast cancer, which is about 20% of cases. But, for these people, is it a cure?
The first trial reported a 150% improvement in response rates. It shrunk half the tumours in women treated with the drug, compared to a third on placebo. However, tumour reduction, while good, doesn’t mean the cancer is cured. This is one of the biggest misconceptions about chemotherapy fuelled by the fact that drugs, to get licensed, only have to show tumour shrinkage, not increased survival. A ten year follow up of the Herceptin treated patients reported a 2.9% increased survival at 4 years and an 8.8% increased survival at ten years, compared to standard chemotherapy.
Obviously, this is good news for the 8.8% but if the best drug that targets what is supposedly the defective gene that supposedly causes the breast cells to become cancerous and grow can only benefit twenty in a hundred women, and of those, save the lives of two of them (10%), that is a vastly disappointing outcome for SMT which supposes that most cancers are caused by faulty genes.
The inheritance of such so-called oncogenes, such as HER-2, BCRA1 and 2, account for 5 to 7% of all cancers, a small part of the overall equation. Even if a person has these oncogenes it doesn’t mean they are necessarily expressed. Take the example of the BCRA ‘breast cancer’ gene. The faulty BRCA gene makes breast cancer cells grow. Angelina Jolie took this thinking to an extreme in first removing her breasts and ovaries despite the fact that only 6 to 12% of BRCA carriers get ovarian cancer. The rate of breast cancer is higher, 46-52%, however that means that half of all BRCA gene carriers get neither. Why?
Not having dairy products inhibits breast cancer cell growth, as does a higher intake of soya in those with the BRCA gene, according to a study which found that a higher soya intake cut breast cancer risk by 60% in BRCA carriers. This illustrated that it is the environment around a nucleus that drives the genes and cancer cell growth, more than the presence of oncogenes. These genes do not cause cancer, they just make it more likely under certain circumstances – circumstances that are under our control.
Cells have an outer membrane and an inner environment called the cytoplasm, containing various mini-organs called organelles, including mitochondria which make energy, ribosomes which make proteins, lysosomeswhich clear away garbage and, in the middle, the nucleus which contains the genetic material encoded in the DNA.(see the diagram in the article Super Cell Me)
The idea that the cytoplasm was the ‘home’ of whatever goes wrong wasfirst proposed back in the 1920’s by a brilliant medical scientist and recipient of a Nobel Prize, Dr Otto Warburg, a good friend of Albert Einstein. He observed that cancer cells make a lot of lactic acid compared to normal cells.
The Metabolic Theory of Cancer
Cells turn glucose into energy in a highly efficient way, called aerobic metabolism, that needs oxygen to ‘light the fire’. This produces lots of ATP which is the energy currency of our cells. Although this was unknown at the time, this process happens in the mitochondria, the energy factories in the cell’s cytoplasm.
But, in the absence of enough oxygen, for example in sprinters whose rapid burst of activity exhausts the cell’s ability to make enough energy aerobically, a secondary mechanism of making energy through fermentation, called anaerobic metabolism, kicks in. It doesn’t need oxygen, and consequently doesn’t generate oxidants, the exhaust fumes of oxidative metabolism, but is much less efficient, creating much less ATP and creates lactic acid as a by-product. That’s the stuff that makes muscles sore after exercise.
Warburg went on to show that if you starved a healthy cell of oxygen it would become cancerous but then giving the cancer cell enough oxygen wouldn’t reverse the process. Cancer, he reasoned was caused by the permanent alteration of the cell’s respiratory machinery, reverting the cell to anaerobic metabolism. But he didn't know why this led to the rapid proliferation of cancer cells.
While nothing actually contradicted Warburg’s discovery other theories just overtook his because, at least conceptually, they had an explanation for the growth of cancer cells, even if it would later be proved wrong. The discovery that cancer cells had messed up chromosomes, which are the spirals that contain DNA, coupled with the increasing number of discoveries of certain compounds, called carcinogens, that could trigger cancer, fitted neatly with the idea that the carcinogens were responsible for the chromosomal damage. This provided the basis for SMT theory, which took off like a vengeance when Watson and Crick won the race with Linus Pauling and discovered the structure of DNA in 1953. The hunt was on for which bit of genetic code was programming cancer cells to proliferate uncontrollably.
Shortly before his death, in 1970, when Warburg was invited to give a lecture to other Nobel Laureates he stated: “Cancer, above all other diseases, has countless secondary causes. Almost anything can cause cancer, but even for cancer, there is only one prime cause. The prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by fermentation of sugar.” But no-one was listening. Like Linus Pauling’s ramblings about vitamin C, Warburg’s ‘metabolic theory of cancer’ was side-lined as the ramblings of an otherwise brilliant scientist gone off the rails. Cancer was caused by carcinogensdamaging genetic material, which then sent unchecked ‘growth’ signals –or so most believed.
But, step by step, Warburg has been proved right. Cyril Darlington, an English researcher, made an interesting discovery in the 50’s that the most potent carcinogens damaged cytoplasm, the ‘white’ of the cellular egg, more than the DNA. This discovery was ignored because it didn’t fit the SMT.
The next piece of the jigsaw was to come from Pete Pederson, an American scientist at John Hopkins School of Medicine in Baltimore. He wondered why some tumours would grow fast and others slowly. He discovered that the faster a cancer cell grew the less mitochondria were in the cell, and the more they fermented sugar. With less mitochondria, he reasoned, it was the only way the cancer cell could survive and the ‘switch’ that would shunt glucose into fermentation was permanently openin the cancer cells. The ‘switch’, he discovered, was an enzyme called hexokinase which, in cancer cells was slightly different, called hexokinase II, and hyperactive. As a result there was a build up of lactic acid which leaked out and damaged and weakened surrounding material, paving the way for the cancer cell to divide and spread. Hexokinase II, he discovered, also switched off the normal cell-suicide signal, called apoptosis, which makes badly behaving cells die. And, on top of that, it became parasitic and would steal energy, ATP, from neighbouring healthy cells to keep itself alive. This was a whole new story for how cancer cells survive and spread into healthy cellular space that has nothing to do with oncogenes.
The fact that this messed up sugar metabolism is key to cancer is illustrated by PET scans, which heralded the big breakthrough in diagnosis in the 1970’s. While previous scans could detect tumour masses they couldn’t say if the cells were actively cancerous. For that you need a ‘marker’ for an active cancer cell. Hexokinase II is the marker used in PET scans today for detecting active cancer cells. After fasting for six hours, the patient is injected with a fluoridated glucose solution (FDG). This binds only to hexokinase II, the aberrant enzyme found only in cancer cells. That’s how PET scans for cancer detection work. Sugar metabolism is at the heart of it.
New Approaches to Cancer
So, if messed up sugar metabolism is what makes cancer cells grow, how do you stop this? Since cancer cells do not appear to revert to healthy cells the strategy still remains to create an environment that healthy cells can survive in and cancer cells cannot.
Since cancer cells have far fewer mitochondria, and thus struggle to generate enough energy from sugar by fermentation, two ways to give cancer cells a hard time is to deprive them of fuel, namely glucose, and bombard them with oxidants. Linus Pauling’s group had demonstrated that it is oxidants, the by-products of aerobic metabolism, that ages and damages mitochondria. This is also the likely basis by which radiation weakens and destroys cancer cells, by bombarding them with oxidants.
Dr Thomas Seyfried, inspired by Pedersen’s research, was also convinced that cancer was a metabolic disease, and wrote a book about it in 2012 (Cancer as a Metabolic Disease). He proposed that chronic and persistent damage to the cell’s ability to produce energy aerobically triggered emergency signals from the mitochondria to the nucleus’s DNA, thus switching on all sorts of ‘oncogenes’ and triggering uncontrolled cell division. But these oncogenes were the consequence, not the cause of cancer. He noticed that fasting, or severe calorie restriction, shrank tumours. In the absence of glucose healthy cells have another way of producing energy, by burning ketones, generated from fat. This back-up system isn’t available to cancer cells, and it also produces oxidants, so only healthy mitochondria, with plenty of antioxidants, can generate energy smoothly in this way.
He figured that a ketogenic diet could seriously weaken cancer cells,without harming healthy cells. The fastest way to switch the metabolism of healthy cells from sugar to ketones is to fast for 2 or 3 days, followed by a period of a very low GL diet, strictly avoiding carbs, but increasing fat, may be an effective cancer treatment. This kind of diet can include vegetables, fish, especially fatty fish in preference to meat, nuts, seeds such as chia and a few berries, plus olive oil, coconut butter, avocados, but no sugar or grains. Beans, which also contain carbs, need to also be limited.
While many forms of chemotherapy deliver toxic oxidants which the cancer cell is unable to deal with, vitamin C, in high doses, ideally given intravenously, but certainly at maximum tolerated levels, up to ‘bowel tolerance’, has been shown to act as an oxidant within cancer cells, however without any harm whatsoever to healthy cells. In this respect it achieves the holy grail of chemotherapy.
Another discovery involving oxygen may also prove another piece in a ‘metabolic’ approach to cancer treatment, and that is oxygen. Dominic D’Agostino, a professor at South Florida University, discovered that cancer cells cannot deal with an overload of oxygen. When he placed them in a hyperbaric oxygen chamber they rapidly died. The combination of a ketogenic diet, hyperbaric oxygen therapy (HBOT), intravenous vitamin C has yet to be tested but early results with HBOT and a ketogenic diet are looking very promising.
There are also drugs that target cancer cells’s inability to deal efficiently with glucose that might prove promising in a metabolic approach to cancer such as 2-deoxyglucose (2DG), a molecule that looks like glucose but cannot be metabolised, rapidly bringing fermentation in cancer cells to a halt. Another is 3-bromopyruvate (3-BP) which looks like pyruvate, an essential chemical that cells readily take up, but 3-BP makes the faulty enzyme, hexakinase II, grind to a halt.
These may be the next frontier in the pharmaceutical industry’s fightagainst cancer however a recent study of cancer stem-like cells found vitamin C was 10 times more effective than 2DG . There are so many less toxic and natural ‘chemotherapy’ agents which I have written about in my book Say No to Cancer. However, knowing which ones will be most effective for a specific patient’s type of cancer is the key, and the research focus of a laboratory in Greece called the Research Genetic Cancer Centre. They have developed the ability to test a comprehensive panel of natural remedies, as well as chemotherapy drugs if required, against a person’s specific kind of cancer, from a blood sample containing their
cancer cells. Among the natural agents they test for efficacy are artemesia, vitamins A, C and D, mistletoe, indole-3-carbonol (broccoli extract), quercitin (red onions), curcumin (turmeric), green tea extract, sodium bicarbonate, ganoderma, maitake, acemannan (aloe), resveratrol and salvestrols.
This kind of targeted cancer therapy allows a person to create an environment that makes it very difficult for cancer cells to survive, with minimal if any harm on healthy cells. With the suppression of cancer cell’s ability to ferment sugar, lactic acid levels drop and neighbouring cells become stronger, resisting invasion.
Prevention is better than cure
But, of course, none of this would be necessary if we all did the right things in the first place to stop healthy cells switching over to fermenting sugar for their survival. The first right move is to eat a low GL diet, to prevent insulin resistance and keep your cell’s ability to process glucose healthy. This means choosing whole foods, limiting carbohydrate intake, and combining with protein.
The second is to have a high intake of antioxidants and polyphenols, from berries and vegetables, that help healthy cells process oxygen efficiently. Fruit, especially fruit juices, might be better to limit unless you are slim and doing plenty of exercise, especially in cases of active cancer. Specific antioxidants that help keep mitochondria healthy include Co-Q10, glutathione or NAC, alpha-lipoic acid, plus vitamin A,C and E. I supplement all of these every day in an antioxidant formula.
The third is to minimise hormonal growth signals. This means losing weight, since fat cells make oestrogens, limiting or avoiding dairy products, which increase insulin-like growth factor (IGF-1) a known promoter of cancer cell growth, as are the oestrogens present in milk.
The fourth is to avoid obvious carcinogens, from smoking and pollution, to xenoestrogens in plastics in contact with food and other non-biodegradable carcinogens, alcohol and burnt fat found in meat and nitrosamines in cured meats. Also best avoided are pesticides and herbicides in non-organic food. Monsanto’s Roundup, a widely used glyphosate, is classifed as carcinogenic by the WHO.
To dig deeper read Tripping Over the Truth by Travis Christofferson, available on Amazon.
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