The Plaskett Therapy

PLASKETT THERAPY

Dr Lawrence Plaskett is vice chair of the Nutritional Council in Britain.

After a degree in biochemistry at Cambridge, a doctorate at London University and a number of years in food companies and Government agencies, Dr Plaskett turned his extensive knowledge to updating the Gerson Therapy. His argument was simple. Dr Gerson was brilliant but since his death over 40 years ago much more has been learned about nutrition and biochemistry.

A nutritional approach to cancer should be nationally available

It is Plaskett’s firmly held view that a nutritional approach to cancer should be nationally available. More fundamentally he argues that orthodox authorities are already in full acceptance that nutrients can protect against the inception of cancer1. And that various sources indicated that up to 60 per cent of cancers appear to have nutritional cause.

This may or may not be the case. Indeed, cancer development is a multi-stop process and nutrition, or rather poor nutrition, may be a factor in virtually all cancers, even if other factors are more damaging.

As a biochemist he sites research showing, for example, that

1. Flavenoids such as quercetin (onions) stop the proliferation of cancer cells in vitro, especially if vitamin C is present (Kandaswami)
2. Quercetin and genistein (a soya isoflavone) are the most potent anti-proliferating flavenoids in colon cancer (Kno)
3. Quercetin has potential in the treatment of leukaemia (Teofil)
4. Catechins in green tea reduce size of human prostate and mammary tumours (Liao)
5. Beta-carotene and vitamin C influence the survival of women with breast cancer (Ingram BJC 1994)
6. Lycopene (tomatoes) inhibits prostate cell growth, as do beta-carotene, canthavanthin and retinoic acid. Coenzyme Q10 produces good results with breast cancers (Lockwood 1994).

Plasket argues that many recent scientific discoveries have proven that Gerson was, indeed, right and considerably “ahead of his time”. His research into the latest scientific studies has supported, for example, the importance of omega 3 (from fish oils and linseed oil) as an essential element in the good health of cells; the use of coffee enemas to induce raised levels of glutathione S-transferases, the enzymes of liver detoxification; the use of high potassium and digestive enzymes.

There is no need for castor oil, iodine and iodide, dried thyroid, liver juices and liver injections

Where he feels recent studies have added to Gerson is that there is no need for castor oil, iodine and iodide, dried thyroid, liver juices and liver injections. Instead he recommends a very detailed and precise list of supplements, some of which vary according to the cancer (see Appendix).

Plaskett is very open and honest about what is still unknown about the particular ingredients of plants, vegetables and fruits that might be protective probably because he is such a precise man.

He sites carotenoids, flavanoids, indoles, thiocyanates, ellagic acid, commarins and limonaids as protective, but given that there are 4000 flavenoids known to science for starters he is honest enough to conclude that exactly which ones are the best, and how much should be taken of each is imprecise. With quercitin he adds that large quantities of onions might not be too good for the digestion or even breathe, but supplements (which are available) might lack important “assisting” micronutrients.

Plaskett included in his therapy:

1. coffee enemas (but less than Gerson)
2. fruit and vegetables (but less than Gerson)
3. potassium (as Gerson), plus magnesium in addition to ensure that the sodium pump worked effectively
4. linseed oil (as Gerson) plus fish oil
5. digestive enzymes (as Gerson) but supplemented by amino acids
6. bowel flora bacteria (not used by Gerson)
7. aloe vera (not used by Gerson) – it stimulates the immune system and is a glycoprotein (see later)
8. high fruit and vegetables but concentrating on them with scientific evidence
9. adjustment of therapy to certain different cancers – e.g. the use of soya for hormonal cancers
10. the use of very specific levels of certain supplements.

His scientific studies have led him to seven areas for inclusion in his therapy.

1. Antioxidants – using vitamins E, C, curcuminoids from turmeric, Coenzyme Q10, and multiple carotenoids and flavenoids.
2. Anti-proliferating agents to slow down cancer proliferation e.g. flavenoids, carotenoids, vitamin A, curcuminoids.
3. Detoxifying – e.g. organic sulphides from garlic, thiocyanates from brassicas and magnesium to increase glutathione levels.
4. Differentiators – to induce cancer cells to become more “normal” e.g. bromelain (from pineapple), zinc, s-allyl cysteine (from garlic).
5. Inhibitors of metastatis – stopping cancer spreading, e.g. bromelain, soya.
6. Immune stimulation – e.g. aloe vera, bromelain, vitamins and minerals.
7. Angiogenesis inhibitors – inhibiting growth of new blood vessels needed by tumours, e.g. soya bean genistein, garlic.

The therapy is vigorously vegan. Dairy products, eggs, fish and meat are vigorously excluded. A low protein diet has been shown to be effective against cancer (Tannenbaum). All fried foods are avoided, as are processed foods.

The therapy is vigorously vegan

Fresh vegetable intake is high, but uses only those with proven phytonutrients with anti-cancer properties e.g. garlic, cabbage, red-leaved lettuce, carrots, celery, parsnips, parsley, onions (red and green), tomato, aubergine, broccoli, cucumber, kale, cauliflower, sweet potatoes, radishes, Brussel sprouts, endive, watercress, capsicum peppers.

Herbs and spices are used: liquorice, ginger, turmeric, mint, horseradish, oregano, rosemary, sage, thyme, chives, basil, mustard and tarragon (all organic).

Plaskett even provides a list of daily requirements:

1. Garlic 10 gms
2. Fresh onion 100-150 gms
3. Fresh tomato 200 gms
4. Turmeric powder 5 gms
5. Pulses-fresh and dried peas, lentils, chickpeas and beans 40 gms
6. Soya (only included if the cancer is hormonal)
7. Nuts and seeds are avoided to minimize fat and protein intake
8. Oats 50 gms
9. Brown rice 125 gms
10. Buckwheat
11. Barley
12. Fresh sweet corn
13. Occasionally potatoes – bake and boiled – freely used
14. No tea or coffee – but dandelion, organic Japanese green tea, rosibosch tea are allowed
15. Sugar of all kinds (including honey, syrup, jams)
16. Textured soya Confectionary
17. Chocolate Ice cream
18. Fizzy soft drinks
19. Squashes
20. Alcohol
21. Yeasts
22. Oxo
23. Marmite
24. Bovril
25. Modified foods
26. No fats (because it activates carcinogens) other than a limited amount of linseed oil and fish oil (both for omega 3)
27. Dried fruit (it contains sulphite)

Forbidden foods include:

Juices consist of six per day (all freshly squeezed)

• 1 glass of orange juice
• 2 glasses of leaf juice (endive, watercress, lettuce, green peppers, red cabbage)
• 3 glasses of apple and carrot (1:1)
• Some beetroot juice is also used.

Development

Of interest may be the nutritional developments in hand for the Plaskett Therapy.

1. Brassica vegetables possess a number of anti-cancer agents. Even higher levels of some of these are found in germinating broccoli seeds.
2. Some cultivations of garlic produce higher selenium levels and these bulbs have been linked with, for example, effective prevention of mammary tumours (Ip and Lisk). Garlic normally contains sulphide rather than selenium.
3. Saffron has anti-cancer components crocin, picrocin and saframal.
4. Shiitake mushrooms have 1:3 beta-glucan polysaccharide which has shown strong anti-cancer properties.
5. Curcuminoids seem to exhibit more anti-cancer properties, the more research is done!
6. Limonene-rich orange peel oil is also strong in anti-cancer properties although the oil may produce negatives too.

Clearly, here we are looking at a very detailed, disciplined and thoroughly prepared nutritional plan. The detail of supplements down to the exact number of milligrams is very different from the more casual juicing plan of Gerson.

Either way both Gerson and Plaskett fervently believe that nutrition if poor can cause cancer; and nutrition if perfected can restore health.

We would be wise to heed both men…

Outcomes of the Therapy

A full enquiry by an independent nutritional practitioner into the results of the therapy over the 8-year period of use is being mounted using the The Nutritional Cancer Therapy Trust’s records. The first indications are that:

40 full recoveries were obtained (i.e. no diagnosable signs of cancer with the patient being well). These represent 57% of the patients who followed the protocol for the specified period of time. Among those who died there are indications that some had defaulted in continuing to use certain components of the therapy, suggesting that, if there had been fully rigorous control of the treatment the recovery rate could have been higher. In any case, many of those who died did so after surviving well beyond the length of their original prognosis, indicating that the therapy had been a partial success in their cases also. The cases whose records were available for study did not represent all the patients who undertook the therapy, so there could be more than the known 40 recoveries.

The drop out rate for patients was high due to various factors, including the rather strict demands of the therapy, family or financial problems, lack of a home carer, advice given against the therapy by orthodox doctors and the intervention of medical situations making the continued use of the therapy too difficult.

A NUTRITIONAL APPROACH TO INFLUENCE CANCER

By L.G. Plaskett BA, PhD, C.Chem, FRIC

This Newsletter provides details of a nutritional programme for cancer sufferers that has been arrived at after careful analysis of the available scientific research and which has been tested in use over an 8-year period (1998-2006) by the Nutritional Cancer Therapy Trust. Because I designed the therapy for them, the Trust gave it the name “The Plaskett Therapy”. This programme includes many foods and nutrients that are known to have an anti-cancer effect according to research published in reputable scientific and medical journals. The author, a medical research scientist with long knowledge and experience of nutritional medicine, put them together on the basis of published research information. This account specifically avoids making any claim on the part of the author to treat or to cure cancer. It offers information but definitely does not constitute medical advice for any individual cancer sufferer. Nonetheless the programme disclosed and discussed herein will be referred to as a “therapy” because its intent is to help the condition of cancer sufferers by altering the body biochemistry in beneficial ways. The distinct hope is there that this may proceed to the point where the cancerous process is reversed. Observation of those who have used the therapy indicates that this may occur with sufficient frequency to justify real therapeutic interest. Indeed, the author is writing this because of his seriously held opinion that a great many cases of cancer, even cases that are terminal under orthodox medicine, can be reversed with the use of this therapy.

Why Use Nutrition in Cancer?

Serious interest in the potential for nutritional medicine in cancer therapy is more than justified by the severe limitations of current forms of cancer treatment with orthodox medicine. Although there is much that these therapies can achieve, huge numbers of patients are being left eventually with no further treatment options and go on to die. Moreover, there have been repeated and widespread accounts in the scientific and medical literature that nutritional factors powerfully influence the development and growth of cancer. Many would say that, given the full weight of scientific evidence, the health professions have been very remiss in not carefully investigating the potential power of nutrition as cancer treatment. Given the potential of nutritional therapy the determination to avoid investigating it seems tantamount to letting the public down.

Why is Nutritional Treatment not being Used Widely?

Money and decision-making power in cancer research is in the hands of the orthodox medical profession. That profession seems greatly committed to the currently standard techniques of surgery, radiotherapy and chemotherapy and very little else. Those who would like to advance the idea that other forms of therapy, like the nutritional approach, should be given a full and fair trial usually report a very negative response. Government sources of funding and charitable sources alike usually refer applications for such research funds to arbiters who are in the orthodox profession. To those of us who are concerned with advancing new ideas in the field the seemingly inevitable negative outcome of such applications may appear to be determined largely by prejudice. The arbiters involved commonly have little knowledge of nutrition and the extent of its medical possibilities when applied as therapy. The fear may be that vested interests and protectionism within the orthodox profession and the drugs industry really determine these outcomes.

Whatever the cause, the result has been that all attempts to bring scientifically supported nutritional measures into the mainstream of cancer treatment by conducting trials have been consistently thwarted.

Does Nutritional Cancer Treatment have a History?

In the nineteenth and early twentieth centuries there was much trouble with charlatans who would deliberately offer false remedies for cancer in order to profit fraudulently. This quite properly resulted in the UK in the Cancer Act of 1939 that prohibited and provided punishment for offering unauthorised treatment for cancer. However, this Act that was intended to stop charlatans is now being used to suppress genuine and well-intentioned efforts to deal with cancer by means of alternative medicine. One can offer cancer patients nutritional advice designed to improve their health status but must avoid indicating that the advice might cure or alleviate their cancer. This has naturally acted as a deterrent to those who might otherwise try out new cancer treatments, even when they appear to have genuine potential. Similar onerous deterrents exist in the United States.

Nonetheless, some dedicated individuals have continued to put themselves at legal and professional risk in order to apply nutritional therapy to the cancer cause. These are too numerous to enumerate. Instead I list a few of those that are to some degree akin to the Plaskett Therapy in their approach and their medical philosophy. I make particular mention of the therapies of Kelley in the USA and Gerson in the USA and Mexico. I regard both of these as forerunners of my own approach. Both used a thoroughgoing approach to diet and nutrition. Both addressed the problem of protein digestion in cancer patients. Both used proteolytic enzymes for this purpose and Gerson used a very low protein diet. Both employed detoxification procedures, a fact that places both of these therapies into the Naturopathic category. Both included coffee enemas in the list of detoxifying procedures. These are intended to detoxify the liver of the patient and to leave the patient in a better condition to detoxify the body as a whole. Both used “organ flushes”, namely intensive procedures for detoxifying a particular organ. The liver and gallbladder received special attention, with Gerson employing a regular castor oil treatment for this purpose. The Gerson therapy includes twelve or more glasses daily of freshly pressed fruit and vegetable juices, a daily vegetable soup, potassium/iodine supplements and thyroid gland extract. Gerson also used linseed oil (also known as “flaxseed oil). This was a brilliant step suggestive of special insight at a time when the role of Omega-3 fatty acids was not understood. The therapy also includes focusing upon the acid/alkali balance and the sodium/potassium balance of the body, following the leads provided earlier by Cope, Reich and Barefoot. Others have also taken up the issue of the acid/alkali balance from around 1950 onwards.

The Gerson therapy in particular was well written up by its author. His book, “A Cancer Therapy – Results of 50 Cases”, gives full details of the therapy and records some very favourable outcomes. These were often achieved in desperate and advanced cases. Nonetheless several sources have offered me the opinion that this therapy is less effective today than in Gerson’s time and that Gerson’s personal qualities as a caring doctor may have contributed to his level of success. It has also been suggested that today’s cancer patients are more toxic than those of the 1940s or 50s and hence may require different or additional treatment measures. I give every possible credit to Gerson and Kelley for their vision in times when much of today’s nutritional information was unavailable. I have never found it hard to accept the accounts of their success in many cases. These are the therapies that, in my view, constitute the principal nutritional cancer therapies of the past and both are still on offer in the present.

I also mention here the approaches of Dr Contreras in Mexico and Dr Budwig and Issels in Germany. These have little in common with Kelley and Gerson. Contreras, for example, focused upon use of shark cartilage, ozone therapy, ultraviolet blood irradiation, melatonin and laetrile as well as detoxification. The work of Budwig is nutritional but focuses upon using linseed oil in combination with cottage cheese. The latter is used as a source of sulphur amino acids, which it is, but clear evidence that the sulphur amino acids are of specific importance to the therapy seems to be lacking. At any rate this is an example of the very different forms that nutritional cancer therapy can take. Both Contreras and Budwig used some additional dietary provisions. Issel’s treatment is based primarily upon anti-cancer vaccines but also employs a long list of supplementary nutrients and herbs including co-enzyme Q10 and Vitamin C.

The Theory behind the Plaskett Therapy

I have not used agents such as laetrile, melatonin or ozone therapy. I tend to have doubts about therapeutic means of treatment that have nothing to do with the likely reasons for development of the primary tumour. Laetrile appears to have been effectively debunked as an anti-cancer agent and as a vitamin and shown to be severely toxic. Those supporting the concept behind ozone therapy need to explain why the body should require oxidizing therapy and anti-oxidant therapy at the same time, since they appear to have conflicting objectives.

I accept the view that was well stated by both Gerson and Kelley that cancer is a metabolic disease. That is to say that it comes about through faults in metabolism. This implies some degree of failure in the biochemical vitality of cells, resulting in a relative deficiency of cellular energy due to damage to enzyme systems or through a lack of catalysts needed for energy production. Damage to enzyme systems and, indeed, damage to the integrity of cell structure, can be brought about by toxic substances that react chemically with proteins, lipids and nucleic acids. Damage to nucleic acids seems to be a necessary part of the cellular damage that leads to cancer, leading to errors of copying the genetic material during cell division. Above all, the enzyme systems that are dedicated to the repair of DNA (desoxyribonucleic acids, the genetic material) may be compromised, with the result that damaged DNA can no longer be efficiently repaired. The removal of harmful waste materials and environmental toxins that gain access to the cells will obviously be impeded if detoxifying enzyme systems are either damaged, not produced in sufficient quantities, suffer from toxic inhibition or lack the energy supplies needed to detoxify.

Gerson, who passed away, I believe, in 1959, could not have known that the effects of cellular intoxication would, by the end of the twentieth century, be capable of such detailed explanation. Yet his work shows that he already understood the essence of this as if he had inklings of the future. He designed his therapy accordingly. But he did not have available to him all of the specific nutritional tools that are now known to support the energy-producing enzymes systems, support the detoxification enzymes systems (of which we now know several distinct types), minimize the inhibitory effects of toxins and promote the healing of toxic damage.

My therapy is dedicated to harnessing modern nutritional knowledge to all the above ends. I do not accept the view of those who argue that Dr. Gerson’s therapy should be preserved and used unaltered in today’s world. If Gerson himself had lived longer he would surely have harnessed cutting edge nutritional knowledge himself as more became known. He could not do that and yet it appears essential that someone should do it, creating a brand new therapy. The principles I employ, therefore owe much to the work of Gerson and Kelley but the protocol is based to a great extent upon new known facts in nutritional science. Some parts of Gerson’s protocol now seem not to have stood the test of time and hence, in my opinion, they should be discarded in favour of new measures.

Key Principles in the Design of the Plaskett Therapy

The first principle of my therapy is to provide the cells with luxury nutrition in respect of the well-established minerals and vitamins. I expected this to protect the cellular energy supply, the enzyme systems and the cell structure. Where these things have been compromised as part of the metabolic degradation that led to cancer, this luxury nutrition can be expected to permit and encourage a start to recovery, i.e. to start a shift towards more normal metabolism and a reactivation of the cellular repair mechanisms. Whether or not this in itself can be expected to reverse an established cancer was bound to be uncertain. On the whole the expectation would be, from biochemical considerations, that they would not achieve this unaided. One could have surmised that it would work in a few cases, since even several single nutrients have been shown to be capable of reversing cancer cases but only with a low level of reliability.

A good many of these well-established minerals and vitamins are known, from experiment, to have certain anti-cancer actions. In most cases what has been demonstrated is an ability to inhibit the initiation of cancer. That is different from reversing established cancer. In most cases we now have fairly good knowledge of the mode of action of these minerals and vitamins. This knowledge tells us how these nutrients act as co-factors for specific enzyme systems that play roles in such processes as energy generation, protein synthesis, the formation and maintenance of membranes and the synthesis and/or repair of the DNA. Also, some of these minerals and vitamins act to enhance detoxification or to reduce new toxin formation in the tissues. This is especially true of those that act as antioxidants. These include, among the common nutrients, Vitamins C and E and the mineral selenium.

It has long seemed obvious to me to formulate nutrient cocktails for cancer patients that would combine together agents that support a wide range of different cellular enzyme systems and that help to maintain cellular structure in a number of different ways. The principle here is to improve all systems if possible, prevent all types of intracellular degradation and then promote the repair and healing of the toxic damage that has accumulated. If cell biochemistry is improved in all these ways then the cell may 1) avoid becoming cancerous, 2) return, after suffering (at least) precancerous damage, to relative normality of structure and function (redifferentiation), 3) in the case of immune cells, be reactivated so as to be able to destroy those cancer cells that are beyond being reclaimed.

More than just Vitamins and Minerals

However, it seems clear that we cannot necessarily expect that the common essential micronutrients alone will actually restore the body to normal. Therefore in my therapy I call also upon a diverse group of substances called “phytonutrients”, a name that signifies that they are derived from plants. Some people prefer the name “nutriceuticals”, since that term can include substances derived also from animals or from bacteria or fungi. Some of these, like alpha-carotene for example (a member of the important group of “carotenoids”), are present in normal foods. If we do not get enough alpha-carotene it may be because we do not eat enough carrots or red palm oil. Carrots contain only a little of it, so one needs to eat a lot of them. Red palm oil is a bit of a speciality. Although it is in supermarkets in the UK, not everyone buys it, good tasting though it is. We may or may not even want or need the other components of this particular oil. Another large phytonutrient group are the flavonoids. Some very good flavonoids are present in tea, though there is room for doubt as to whether these are still good after going through the black tea manufacturing process or after the addition of milk to the beverage. Therefore, best advice is to use green tea for this purpose. Other flavonoids occur in other foods, all of which is starting the make the dietary selection very specific and rather complex. It called for a very directive approach (i.e. thou shalt eat this or that fruit or vegetable specifically), not just any type that you fancy. If one is a cancer patient it seems likely to be well worth putting up with this inconvenience for at least the chance to extend one’s life, improve one’s quality of life or even perhaps regain health. In my therapy I provide a diet and supplements programme designed to give a very potent daily input of these phytonutrients. I do not include them in the diet unless the published research literature indicates that the particular phytonutrient has a worthwhile anticancer action. The result is a protocol that provides an absolute abundance of phytonutrients having known anticancer actions. Some, like beta-carotene (which must be of natural origin) are at the same time both vitamin-like and a phytonutrient. There are many other important carotenoids, like lutein, zeaxanthin and lycopene. These, and the flavonoids, together go a long way towards explaining the known anticancer action of diets high in fruit and vegetables.

The Standard of Evidence

I start to take an interest in a particular nutrient or phytonutrient for the therapy if research papers show that it has an anticancer effect. These must be research papers accepted for publication in peer-reviewed scientific journals, not just statements in popular writing or on websites. Remember that anyone can write anything. Unsupported statements upon such matters are valueless unless confirmatory scientific work exists. The best type of research is a trial with human cancer patients. Since these are very hard to organise and there are usually ethical problems about including the necessary controls (patients not receiving the potentially therapeutic nutrients), these are few in number. Moreover, one really needs work with people with established cancers. Work on cancer prevention by nutrients, intensely interesting though that is, is not directly applicable to cancer treatment. The nutrient choices I have made are all supported by good research evidence, not always in human trials but sometimes in reported research in animal cancer or in laboratory trials using cultured cancer cells. That these do not always transfer to the human case is known and recognised, but what I am looking for are strong research indications of likely anti-cancer potency, even if it falls short of proof for individual substances. I have made reference to some of the research evidence for some of the nutrients and foods in the final section below. A full referencing to this literature would be very voluminous.

How do the Nutrients Produce their Effects?

The research literature revealed that there were at least 7 different mechanisms by which nutrients could exert an anticancer effect. They are not all the same with regard to how they act. These are the seven mechanisms below. I have indicated in each case one or more of the nutrients that act in the particular way.

Anti-Oxidant Effect – This comprises quenching free radicals to reduce new damage that can be done to the patients’ body cells, including immune cells, during the treatment. This may make the re-differentiation of cancer cells to normal cells more possible and prevent damage to recently repaired cells. Examples of this are Vitamins C and E, many carotenoids, many flavonoids, co-enzyme Q10 and the curcuminoids from the spice turmeric.

Anti-Proliferative Effect – This comprises slowing down the replication of the cancer cells. Since most tumours are in any case loosing cells at a great rate, this may be decisive in determining whether tumour growth slows down or stops. Examples are flavonoids, multiple carotenoids, Vitamin A and curcuminoids from turmeric.

Induction of Detoxifying Enzymes – This is the effect of increasing production of detoxifying enzymes and, by doing so, reducing toxins levels in the tissues. As a result cell damage will be reduced in the immune system and elsewhere. This may increase immune effectiveness. Moreover, further damage to recently repaired cancer cells will be reduced. Examples of substances working in this way are the organic sulphides from garlic, sulphoraphane and other thiocyanates from vegetables of the cabbage family, many other phytonutrients, coffee enemas to increase glutathione-S-transferase level in the liver and magnesium to increase glutathione levels as well as many minerals and vitamins.

Encouragement of Cell Re-Differentiation – This effect is to encourage genetic repair to cancer cells and thus to encourage tumour cells to become normal cells again. This is very much like encouraging desertion from the enemy’s army. Examples are bromelain – possibly zinc for DNA repair function and S-allylcysteine from garlic.

Inhibition of Metastasis – This is a slowing down of the process (metastasis) by which clumps of cancer cells detach from the tumour and migrate via the blood to establish secondary tumours in other parts of the body remote from the primary tumour. An example of a nutrient with this effect is bromelain.

Direct Immune Stimulant Effects – This is the effect by which nutrients directly stimulate those functions of the immune system that have most to do with the immune attack upon tumour cells. Examples are Aloe vera, bromelain and many minerals and vitamins.

Angiogenesis Inhibitors – This is the effect by which a nutrient inhibits the growth of the new blood vessels that the tumour needs and usually induces as it grows. Hence the result is to deny the tumour its blood supply and cause necrosis (death) of tumour cells. Examples of this effect are seen with the soya bean isoflavone, genistein.

In the design of my therapy I have taken all of these different anticancer actions into account. I have provided a blend of nutrients and phytonutrients that possesses all seven of these anticancer actions in the food and supplements of the therapy. I do not think that this approach has been consciously employed before.

The Cancer Patient Needs to Exclude Unhelpful Foods

There is a long exclusion list comprising textured soya, sugar of all kinds, molasses, honey and syrups, jam or other preserves, salt (except for potassium chloride as a salt substitute), confectionery, ice-cream, chocolate, carbonated beverages or squashes, alcohol, yeast or yeast extract, hydrolysed vegetable or animal protein, savoury liquids, pastes and cubes of whatever brand containing yeast extract or hydrolysed vegetable or animal protein, soy sauce, miso, tamari, and all canned or frozen products. Genetically modified foods are excluded by the requirement for organic produce. The dietary protein intake is kept low in accordance with the early work of Tannenbaum (1940), which received ample support in the 1970’s (e.g. Armstrong & Doll 1975, Hems 1978) and also much more recently (Fontana et al 2006). All fried foods are similarly excluded, to avoid using oil and the hazard of damaging that oil with high temperatures. Processed foods are entirely excluded, as one would expect in any naturopathic programme, to get away from process damage, nutrient depletion, lack of organic origin and salt and other additives. Also, the diet on the therapy is vegan and hence meat, dairy products, eggs and fish are all excluded rigorously. No separated fats or oils are used on the diet apart from those needed to deliver the Omega 3 essential fatty acids. A diet too high in total fat stimulates the production of an extremely unhelpful enzyme known to activate carcinogens and thereby to promote mammary, colonic, pancreatic and pulmonary cancers in animals. Hence, relatively low fat diets with adequate but not excessive polyunsaturated fatty acids would seem to be indicated.

Methods

I detail the methods used below.

Lifestyle and Environment

Although there is no a priori reason to think that removing the factors that cause cancer will necessarily help to reverse it, it was nonetheless decided to remove such factors as a precaution. Both laboratory experiments and the epidemiology of cancer are showing us that multiple factors may work together to generate the cancerous transformation. Lanza et al (1990) stated that 68% of cancer deaths in the USA were accounted for by diet, alcohol and tobacco. When “chemicals and other environmental factors” are also included Simone (1992) estimated that 80-90% of all cancers were accounted for. It seems clear that interaction of these different factors is important and that any anti-cancer programme should avoid known cancer-causing agents. Because carcinogenicity is a common property among chemicals of many types, it was decided to follow a general policy of excluding chemical agents as far as possible.

The following guidelines were therefore issued to all patients joining the programme. What follows is only a summary of those guidelines.

All food used should be organically grown. All tap water to be directly consumed or used for cooking should be treated to remove such contaminants as pesticides, nitrates and nitrites, heavy metals and metallo-organic compounds of heavy metals, chlorine from the Water Company’s treatment plant, organo-chlorine compounds which come from the chlorine treatment of water, PCBs, fluoride, aluminium etc. and for this purpose a reverse osmosis water treatment was recommended. All types of chemical exposure should be avoided. This includes household chemical products, including particularly aerosols, insect sprays, cosmetics that contain chemicals and hairsprays, gardening sprays and garden chemicals and any high concentrations of the vapour of petroleum products, such as oil and petrol. Smoking, alcohol and drugs are similarly excluded, whether the drugs have been medically prescribed or not. This is because this is a detoxifying therapy and cannot be expected to succeed in the presence of constant retoxification. In the case of dependence upon medical drugs, this can be a reason for difficulty or even exclusion from the therapy unless it can be resolved. Patients that are clearly dependent upon drugs should be identified and they should either not follow this therapy or, if practicable, should enter upon a period of gradual and controlled drug withdrawal under the proper supervision. This delicate matter may well depend upon the nature of the drug or drugs and the reason for their original prescription and must be handled professionally. These basic requirements for implementing the therapy entirely preclude patients who are having chemotherapy.

Details of the Therapy Diet

The foods were selected to embody the principles of balanced nutrition within the context of a vegan diet. All foods were grown without agricultural chemicals. The protein and fat intakes were not monitored individually but principles of the diet were applied with an element of choice by each patient. The protein content was normally about 50g/day, in accord with literature already quoted showing a relationship between tumour growth and protein intake. For similar reasons fat intake was controlled to about 25g/day while ensuring provision of essential fatty acids. Fresh vegetables were used (usually not less than 1000g fresh weight per day excluding potatoes), providing at least 80g of vegetable solids/day. Pulses were also used up to a limit of 40g/day. The selection of dietary items was based upon research literature showing that the foods contained anti-tumour biochemicals in significant concentration. Dietary items specifically prescribed included onions or shallots (120g/day) and garlic (10g/day) for their content of flavonoids and organic sulphides, dry powdered turmeric (5g/day) for curcuminoids, cruciferous vegetables (170g/day) for carotenoids (especially lutein and zeaxanthin), isothiocyanates and indoles. In some cases tomatoes (200g/day) were also taken for lycopene and other carotenoids. However, a full list of vegetables known to contain favourable levels of anticancer phytonutrients was provided to the patients.

Juices (minimum 200ml each, six/day) were taken, having been prepared from fresh oranges, apples, carrots and green leaf vegetables. These were selected as sources of multiple anti-tumour biochemicals, most particularly many different forms of carotenoids and flavonoids.

In addition the diet permitted whole grains in which rice and/or millet and also oats, played a prominent part. Buckwheat, barley and fresh sweet corn are used as occasional variations. The only oils used, and provided in measured amounts, were linseed oil and/or fish oil, the latter, which was not always used, being, obviously, a non-vegan item. The advantage of the fish oil is the long chain-length of the fatty acids, which makes them more directly usable.

The Coffee Enemas

Coffee enemas are used (4/day, 560-840ml each) for their naturopathically recognised purpose of increasing the detoxification capacity of the liver. Biochemically their role is to increase the titre of the enzyme family, the glutathione-S-transferases in that organ, as reported by Hildenbrandt in 1990. They comprise an extremely important set of enzymes of detoxification. Four enemas are used, spaced through the day. Each enema is prepared from 25g of organic ground coffee to one litre of treated water. Patients are supplied with a precise preparation method.

Due to the long use of coffee enemas in cancer patients, and also in non-cancer patients with chronic illness, there is little room for doubt about the safety of using these enemas. Those who wish to attack and suppress any nutritional approach to treatment have quoted one report that alleged there was some hazard in their use. However, the standard of proof in that report is so low as to make it unworthy of attention.

The Nutritional Supplements Used on the Therapy

The nutrients given as supplements, with daily intakes, were magnesium, as citrate, 1008mg, nicotinamide (Vitamin B3), 100mg, thiamine (Vitamin B1), riboflavin (Vitamin B2), pyridoxine (Vitamin B6), pantothenate (Vitamin B5), para amino benzoic acid, 50mg of each, cyanocobalamine (Vitamin B12) and biotin, 50µg of each, folic acid, 90µg, iron 30mg, zinc, 63mg, manganese, 63mg, chromium as the GTF form, 198µg, selenium as selenomethionine, 198µg, molybdenum 648µg, boron 5.4mg, silicon 162mg, Vitamin A, 7560 i.u., potassium, as mixed organic salts, citrate, gluconate and acetate, 2.72g, choline as choline bitartrate 1.5g, inositol, 1.5g, calcium ascorbate, 2.25g, ascorbic acid, 2.25g, citrus bioflavonoids, 500mg, beta-carotene, 14.5mg, alpha-carotene, 300µg, lutein, 110µg, zeaxanthin, 55µg, cryptoxanthin, 35µg, 19 different amino acids: individual intakes from 90mg to 450mg: total intake 5.4g, bromelain, 1500mg, co-enzyme Q10, 30mg, pancreatin, 3000mg, selenium as “Food State” form, 200µg, chromium as “Food State” form, 120µg, Vitamin C as “Food State” form, 500mg, Vitamin E as “Food State” form, 200mg, isoflavones of soya or clover (certain patients only): daidzein, 31mg, genistein, 8mg, glycitein, 21mg, fish oil, 5ml, Bifidobacterium bifidus, 4 billion active organisms, Lactobacillus acidophilus and rhamnosus, 10 billion active organisms, betaine hydrochloride, 1944mg, pepsin, 30mg.

The majority of these nutrients, or metabolites derived from them, have been implicated in inhibiting either the genesis or growth of cancer (or both) and reported as such in peer-reviewed scientific journals. Most of them were used in the form of three composite supplement products made up especially for use by the Trust.

Complex Homoeopathic Remedies

Two complex homoeopathic remedies from the German school were used in most versions of the Therapy (Co-enzyme compositum and Ubichinon from Biologische Heilmittel GmbH from Baden-Baden. These are remedies formulated to stimulate the cell-level respiratory and energy-generating processes. They are used in the form of injectable ampoules. The contents of one ampoule of each is injected subcutaneously twice per week in accord with manufacturers’ optimum recommendations. In variants of the therapy adapted to cancer of particular sites, different or additional remedies are used. It is quite widely believed by homoeopaths that low-potency remedies have the strongest effects close to the physical and physiological level and that they therefore have the more direct effects than higher potencies upon biochemical processes in the living cell. Homoeopathic remedies of this type (low-potency complex remedies) are very commonly used medicine in Germany, where they mainly originated, and other European countries but have had much less uptake in the UK. They differ from higher potency “classical” remedies in that they still contain, after dilution and secussion, some small quantities of the remedy materials. They appear to have major advantages over classical single remedies for initiating and maintaining detoxification and healing at the subcellular level as an adjunct to nutritional and naturopathic therapy.

Variations of the Therapy

The protocol of the therapy was not varied after the start except in cases where some disability prevented individual measures from being applied or where the intensity of the therapy had to be relaxed for a time due to patient responses. However, differences or additional measures for cancers of certain sites were specified where the research literature indicated special benefit. Some particular nutrients or foods are likely to be helpful with regard to the particular forms of cancer (e.g. isoflavones in oestrogen-related cancers, extra lycopene or tomatoes in pancreatic or cervical cancer). Variations in the homoeopathic element of the therapy were mentioned above.

Results and Conclusions

A full enquiry by an independent nutritional practitioner into the results of the therapy over the 8-year period of use is being mounted using the Trust’s records. The first indications are that:

40 full recoveries were obtained (i.e. no diagnosable signs of cancer with the patient being well). These represent 57% of the patients who followed the protocol for the specified period of time. Among those who died there are indications that some had defaulted in continuing to use certain components of the therapy, suggesting that, if there had been fully rigorous control of the treatment the recovery rate could have been higher. In any case, many of those who died did so after surviving well beyond the length of their original prognosis, indicating that the therapy had been a partial success in their cases also. The cases whose records were available for study did not represent all the patients who undertook the therapy, so there could be more than the known 40 recoveries.

The drop out rate for patients was high due to various factors, including the rather strict demands of the therapy, family or financial problems, lack of a home carer, advice given against the therapy by orthodox doctors and the intervention of medical situations making the continued use of the therapy too difficult.

The patients admitted to the therapy by the Trust have been, in the main, those who had no orthodox treatment currently on offer, or who opted to eschew orthodox therapy for reasons connected with their own personal belief systems. The doctors of the majority of the patients joining the therapy rated them as terminal.

This therapy should be offered to patients as a nutritional programme that is thought likely to benefit their general condition and quality of life rather than as a means to stop the cancer. Nonetheless, the results obtained so far in the application of the Therapy do suggest rather strongly that a modification of that view would be justified and that the method could well be offered as therapy for advanced cancer, quite openly and honestly, if the Law permitted it. That one cannot do that is due to a now archaic Law that should be altered as soon as possible.

In whatever country the therapy is applied the relevant Law of that country should always be followed. It is my understanding that all the patients who were admitted to the therapy came forward spontaneously to request it. My advice to the Trust was to follow that procedure and ensure that patients had a correct understanding of the position and, in the UK, to always follow the provisions of the Cancer Act (1939). At the same time I always felt that the UK Cancer Act should be amended so as to allow more scope for nutritional treatments to be developed by those who back them. The Cancer Act (1939) has, in fact been used to suppress the Nutritional Cancer Therapy Trust even though that body was run as a charity and did not engage in commerce. The community is now considerably poorer for that act of folly.

The Act was clearly put in place, quite correctly, to prevent trickery. But in this case it has had and is having a very suppressive effect upon a potentially very important area of work, in which the science indicates there is much serious potential.

Appendix 1 – Literature Evidence of the Anti-Cancer Activities of Important Dietary Items, Nutrients and Herbs Included in Therapy

Some readers may be satisfied to be assured that this work is based upon appraisal of the relevant research literature. For those who would like evidence to be specifically cited I offer the following section that names authors and literature references. My book “The Nutritional Therapy of Cancer (in preparation) gives far more extensive coverage of this.

Many natural products and foods have been shown to have quite powerful effects in the prevention of carcinogenesis. These have been reviewed by many authors including Wattenberg (1986), Block et al (1992), Stavric, (1994), Wargovich (1997), Ren & Lien (1997). Some of the biochemical substances involved would be classed as food constituents and others as herbal products. Many of these are also the subjects of a less voluminous but nonetheless impressive literature showing that they exert an anti-tumour effect upon established cancers (See for example, Pettit 1977).

A low protein diet is advocated for cancer patients and is known to activate some important immune system functions (Tannenbaum, 1940, Good and Jose 1973, Franceschi et al., 1989, Hildenbrand 1990, Buiatti et al. 1990, Böing et al. 1985). Werbach (1993) lists five studies that disclose an advantage, with regard to cancer incidence, for following a vegetarian diet. There are many reports of the negative effect of meat diets upon cancer; for example, Day et al. (1994) report that meat specifically (rather than just protein), was one of the factors that increased the development of a second primary tumour in patients who already had one.

The paper by Lindblad et al (1997) refers to previous studies on diet and renal cell cancer, which found “an inconsistent positive association with meat, milk, and protein”. Overall the evidence incriminates milk less than meat, but the link to total protein intake appears to be strong.

The case for use of onions and garlic in connection with cancer has been reviewed by (Ernst 1997) and the selenium compounds of garlic have been much implicated in its anti-cancer actions (el-Bayoumy et al, 1996, Lea, 1996).

Curcuminoids have been the subject of many reports showing an anti-cancer effect, e.g. Nagabhushan & Bhide (1992). Broccoli, and its anti-cancer active principal, sulforaphane, was the subject of a very careful investigation by Fahey et al (1997). There have been many studies of the anti-cancer effects of carotenoids, for example, Nishino, (1995), who studied several carotenoids apart from beta-carotene, including alpha-carotene and also fucoxanthin, a carotenoid dominant in the Phaeophyta or brown algae.

Aloe vera has been implicated in the possible treatment of cancer through several research reports. Aloe’s high molecular weight polysaccharide (in the form of a separated proprietary preparation, Acemannan) has been used to treat cancer in animals (Peng et al, 1991, Harris et al, 1991, Tizard, 1991, King et al, 1995) and effects of Aloe extracts upon human cancer tissue cells have been demonstrated (Winters et al 1981). The effect of Aloe vera juices, either gel or whole leaf products, upon established cancers in vivo has not been documented to the same extent but many anecdotal accounts of apparently successful human treatment have been recorded (Ritter, 1993, Ritter 1998). However, the ability of Aloe preparations to stimulate the animal and human immune system in vivo seems to be beyond doubt (Karaca, 1995, t’Hart et al 1989, Pulse TL & Uhlig, 1990).

Notwithstanding the previously published anecdotal accounts of success in cancer treatment with Aloe treatment alone, it was considered unlikely that this could provide a realistic and worthwhile cancer treatment on its own. Moreover, Aloe extracts taken by mouth could not be expected to fulfil the same function as the injected Acemannan employed by United States researchers in animals. It was therefore important that the Aloe should comprise just one constituent within a multi-component therapy.

Bromelain, an enzyme preparation obtained from pineapple stem juice, matches Aloe vera in that it also possesses both anti-inflammatory and anti-tumour properties as well as other benefits. Taussig and co-workers, in particular, studied the anti-tumour effects (Goldstein et al, 1975, Taussig et al 1985, Taussig et al 1988, Taussig et al 1991).

Evidence has continued to accumulate that certain flavonoids from natural products can discourage the growth of established tumours. Kandaswami (1993) demonstrated that flavonoids such as quercetin exert an antiproliferative effect upon squamous cell carcinoma in-vitro that is enhanced by Vitamin C. Kuo (1997) showed that quercetin and genistein were the most potent anti-proliferative flavonoids against cells of colon cancer. Armand (1988) carried out a study that included the screening of 200 naturally occurring flavonoids and found that quercetin enhanced the lifespan of mice with P-388 leukemia. Teofili (1992) demonstrated that quercetin was potentially useful in the treatment of acute leukemias. Liao et al (1995) found that catechins in green tea reduced the size of human prostate and mammary tumours growing in mice.

The same is true of the carotenoids and terpenoids. Beta-carotene and Vitamin C (or possibly other nutrients consumed within the diet that yielded these) appear to very strongly influence the survival of women with breast cancer (Ingram 1994). Wattenberg et al (1986) showed that “high doses of D-Limonene can cause regression of mammary tumours that have already reached a size that can be palpated grossly”. Rock et al. (1996) also found that a carotenoid-rich diet improved the prognosis after diagnosis of breast cancer. From this work it appears that the carotenoid lutein was particularly important. Hall (1996) found that beta-carotene, canthaxanthin and retinoic acid could inhibit the growth of human DU145 prostate cancer cells to the extent of 45, 56 and 18%, respectively. Lycopene was also found to inhibit cell growth.

The literature concerning the anti-tumour activities of vitamins, minerals and vitamin-like substances is too complex and voluminous to quote here. However, an example is that of Co-enzyme Q10. Following some work which showed that administration of high doses of Co-Enzyme Q10 (Lockwood et al 1994a) could favourably influence the progression of established cancer of the breast, Lockwood and colleagues (1994b) set out to find out the effect of combining this co-enzyme with a wide range of other vitamins and minerals. The trial involved 32 women with breast cancer. In a period running from 1992 to 1995 none of the women died of the disease, none of the women showed signs of the development of distant metastases, whilst six showed some degree of remission, extending in two cases to actual disappearance of the tumour. Further results from continuation of this study are awaited, but at this stage it appears from the above work that nutritional supplements alone, whilst not a complete therapy in themselves, have a markedly favourable influence even upon actively growing tumours.

Weiner (1986) reviewed the positive effects upon the immune system performance from using a wide range of mineral and vitamin supplements. Werbach (1993) reviewed the effects of such supplements upon the immune system and also upon carcinogenesis and cancer.

This work, which has been touched upon here only briefly, indicates that it is absolutely unsupportable to maintain today that nutrients do not influence both carcinogenesis and the growth of established tumours. That being the case it should be incumbent upon all oncologists to study the subject and to at last move away from the habit of advising cancer patients, as they often do, to take no special measures with their diets.

References and Bibliography

Armand (1988) In “Progress in Clinical and Biological Research 280, Ed. Cody, V., Middleton, E. Harborne, JB., Beretz, A. Pp235-241 Alan R. Liss New York (1988). Armstrong, B & Doll, R., (1975), “Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practice”, Int. J. Cancer 15 617-631.

Block, G., Patterson, B. & Subar, A., “Fruit, vegetables, and cancer prevention: A review of the epidemiological evidence”, Nutrition and Cancer, 18 1-29 (1992).

Böing et al. “Regional nutritional pattern and cancer mortality in the Federal Republic of Germany”, Nutr. Cancer 7 (3) 121-130 (1985).

Buiatti E., et al., “A case controlled study of gastric cancer and diet in Italy: association with nutrients” Int. J. Cancer 45 899-901 (1990).

Day GL; Shore RE; Blot WJ; McLaughlin JK; Austin DF; Greenberg RS; Liff JM; Preston-Martin S; Sarkar S; Schoenberg JB; “Dietary factors and second primary cancers: a follow-up of oral and pharyngeal cancer patients.” Nutr. Cancer, 21 (3): 223-32 (1994).

el-Bayoumy K; Chae YH; Upadhyaya P; Ip C., Anticancer Res (59L),; 16 (5A): 2911-5, (Sep-Oct 1996).

Ernst, E., “Can allium vegetables prevent cancer?” Phytomedicine 4 (1) 79-83 (1997).

Fahey, J.W., Zhang, Y., and Talalay, P. “Broccoli Sprouts: An Exceptionally Rich Source of Inducers of Enzymes that Protect against Chemical Carcinogens”, Proc. Natl. Acad. Sci. USA 94 10367-10372 September (1997).

Fontana, L., Klein, S., Holloszy, J.O., (2006), “Long-term low-protein, low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk”, American Journal of Clinical Nutrition, 84 1456-1462.

Franceschi, S., et al. “Dietary factors and non-Hodgkin’s lymphoma: a case controlled study in the north eastern part of Italy”, Nutr. Cancer 12 333-341 (1989). Gerson, M, “A Cancer Therapy – Results of 50 Cases”, Gerson Institute, Bonita, CA 92002 U.S.A. (1958).

Goldstein, N., Taussig, S., Gallup, J., & Koto, V. “Bromelain as a Skin Cancer Preventative in Hairless Mice”. Hawaii Medical Journal 34 (3), 91-94, 1975. Good and Jose, D., The Journal of Experimental Medicine 137 (1973).

Hall A. K., Anti-Cancer Drugs Vol: 7, Issue: (3), Pages: 312-320 (1996). Harris, C., Pierce, K., King, G., Yates, K.M., Hall, J., Tizard, I., “Efficacy of Acemannan in treatment of canine and feline spontaneous neoplasms”, Mol. Biother. 3 207-213 (1991).

t’Hart LA, Van Den Berg AJ, Klus L, Van Dijk & Labadle RP “An anti-complementary polysaccharide with immunological adjuvant activity from the leaf parenchyma gel of Aloe vera.” Planta Med 55 (6) 509-12 (1989).

Hems, G., (1978), “The contributions of diet and childbearing to breast cancer rates”, Brit. J. Cancer 37 974-982

Hildenbrand, G. (Editor), Gerson, M, “A Cancer Therapy – Results of 50 Cases”, Gerson Institute, Bonita, CA 92002 U.S.A. (1986).

Hildenbrand, G. “How the Gerson therapy heals”, Transcript of a Lecture, The Gerson Institute, California, USA (1990).

Ingram D. “Diet and subsequent survival in women with breast cancer.” Br J Cancer, 69 (3): 592-5 Mar; (1994).

Kandaswami C; Perkins E. Soloniuk D S; Drzewiecki G; Middleton E Jr., Anti-Cancer Drugs Volume: 4, Issue: (1), Pages: 91-96 (1993).

Karaca, K., Sharma, J.M. & Nordgren, R., “Nitric Oxide production by chicken macrophages activated by Acemannan, a complex carbohydrate extracted from Aloe vera”, Int. J. Immuno pharmacol. 17 (3) 183-8 (1995).

King, G.K., Yates, K.M., Greenlee, P.G., Pierce, K.R., Ford, C.R. McAnalley, B.H. & Tizard, I.R., “The effect of Acemannan immunostimulant in combination with surgery and radiation therapy on spontaneous canine and feline fibrosarcomas.

Kuo, S.M., Morehouse, H. F. Jr., Lin C.P., “Effect of antiproliferative flavonoids on ascorbic acid accumulation in human colon adenocarcinoma cells”, Cancer Letters 116, (2) 131-137 (1997).

Lanza, E., Mostow, E.N. & Winick, M., “Diet and Cancer”, in “The Metabolic and Molecular Basis of Acquired Disease”, Cohen, R.D., Lewis, B., Alberti, K.G.M.M. & Denman, A.M. Bailliere Tindall, (1990) p19.

Lea, M.A., “Organosulfur compounds and cancer”, in “Dietary Phytochemicals in Cancer Prevention and Treatment”, Am. Inst. Cancer Res., Plenum Press, NewYork, (1996). Liao S; Umekita Y; Guo J; Kokontis J M; Hiipakka R A., Cancer Letters 96, (2) 239-243 (1995).

Lindblad P; Wolk A; Bergstrom R; Adami HO., “Diet and risk of renal cell cancer: a population-based case-control study.” Cancer Epidemiol Biomarkers Prev., (4): 215-23 Apr; 6 (1997).

Lockwood, K., Moesgaard, S., & Folkers, K., “Partial and Complete Remission of Breast Cancer in Patients in Relation to Doses of Co-enzyme Q10”, Biochem. Biophys. Res. Comm. 199 1504-8, (1994a).

Lockwood, K., Moesgaard, S., Hanioka, T. & Folkers, K., “Apparent Partial Remission of Breast Cancer Patients Supplemented with Nutritional Anti-Oxidants, Essential Fatty Acids and Co-Enzyme Q10”, Mol. Aspects Medicine, 15 Supp, s231 – s240, (1994b).

Nagabhushan, M. & Bhide, S.V., “Curcumin as an Inhibitor of Cancer”, J. Am. Coll. Nutr. 11 (2) 192-198 (1992).

Nishino, H., J Cell Biochem, Suppl, 22 231 -5 (1995).

Peng, S.Y., Norman, J., Curtin, G., Corrier, D., McDaniel, H.R. & Busbee, D., “Decreased mortality of Normal Murine Sarcoma in mice treated with the immunomodulator, Acemannan”, Mol. Biother. 3 79-87 (June 1991).

Pettit, G.R., “Biosynthetic Products for Cancer Chemotherapy”, Vol 1 Plenum Press (1977).

Plaskett, L.G., “Nutritional therapy to the aid of cancer patients”, Intl. J. Alternative and Complementary Medicine, Dec. (1999).

Pulse TL & Uhlig E., “A Significant Improvement in a Clinical Pilot Utilizing Nutritional Supplements, Essential Fatty Acids and Stabilized Aloe Vera Juice in 29 HIV Seropositive, ARC and AIDS Patients.” J Adv Med 3 (4) 209-30 (1990).

Ren, S. & Lien, E.J., “Natural products and their derivatives as cancer chemopreventative agents”, Progress in Drug Research, 48 147-171 (1997). Ritter, L. “Aloe vera – A Mission Discovered”, Triputic (1993).

Ritter, S. & Ritter, L., “21st Century Medicine”, Triputic, Carrollton, Texas (1998).

Rock C L; Saxe G A; Ruffin M T IV; August D A; Schottenfeld D., Nutrition and Cancer Vol: 25, Issue: (3), Pages: 281-296 (1996).

Simone, C. B., “Cancer and Nutrition”. Avery Publishing Group Inc. New York (1992).

Stavric, B., “Role of chemopreventers in the human diet”, Clinical Biochemistry, 27 (5) 319-332 (1994).

Tannenbaum, A., “The initiation and growth of tumours. Introduction “1 Effects of underfeeding” Am. J. Cancer 38 335 (1940).

Taussig, S., Batkin., S., Oishi, N., Vaught, L. & Szekerczes, J., “Bromelain — its Tumour Growth Inhibiting Properties”, Presented at: SWOG Meeting by N. Oishi in Detroit, Michigan, Sept., 1985.

Taussig, S.J., Batkin, S., & Stanley, “Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical applications”, J. Ethnopharmacol. 22 (2) 191-203 1988. Taussig, S., Batkin., S.,Szekerczes, J., Yoshizawa, C. & Kimura, L. “Effect of Bromelain on Lung Metastases induced by Lewis Lung Carcinoma in C57 Black Mice.

Chem. Abs. 115 1991 Abstr. 64750.

Teofili L; Pierelli L; Iovino MS; Leone G; Scambia G; De Vincenzo R; Benedetti-Panici P; Menichella G; Macri E; Piantelli M; et al., Leuk Res, 1992; 16 (5): 497-503 (1992).

Tizard, I., “Use of immunomodulators as an aid to clinical management of feline leukemia virus-infected cats”, JAVMA 199 (10) 1482-1484 (1991).

Wargovich, M.J., “Experimental evidence for cancer preventative elements in foods”, Cancer Letters, 114 11-17 (1997).

Wattenberg, L. W., Hanley, A.B. Barany, G., Sparnins, V.L., Lam, L.K.T. Fenwick, G.R., “Inhibition of Carcinogenesis by Some Minor Dietary Constituents.” “Diet Nutrition and Cancer” Y. Hayashi et al. (Eds.) Japan Sci. Soc. Press, Tokyo, Sci. Press Utrecht pp193-203 (1986).

Weiner, M.A., “Maximum Immunity”, Gateway Books, 1986.

Werbach, M.R., “Nutritional Influences on Illness – A Sourcebook of Clinical Research”, Third Line Press, California, U.S.A. (Second Edition) (1993).

Winters, W.D., Benavides, R. & Clouse, W.J., “Effects of Aloe Extracts on human normal and tumor cells in vitro”, Economic Botany 35 (1) pp 89-95 1981.

Copyright: L.G. Plaskett May 2007

About the Book

SPECIAL FEATURES

• The book presents a new approach to cancer treatment never published before
• This treatment is nutritional and naturopathic, based upon an intensive programme of diet and supplementary nutrients, the avoidance of toxins and the use of naturopathic elimination
• The predecessor of this new treatment is the reasonably well-known therapy devised and published by Dr. Max Gerson in the 1940’s and 1950’s
• Compared to the Gerson Therapy, the new treatment adds a huge amount of new nutritional knowledge and measures that have become available since Gerson died in 1959. It omits aspects of the Gerson Therapy no longer thought useful in a modern context
• The first half of the book prepares the thought processes of the reader for an open mindedness towards the general concept of the therapy and its background
• In the process of 5 above it sets out principles that are of very wide potential application to the whole subject of understanding and treating chronic illnesses, not just cancer, though it focuses most particularly on cancer throughout
• The greatest space is given to explaining in detail the exact basis of the therapy and the medical philosophy that lies behind it. The very strong element of naturopathy runs throughout. However, the scientific research that supports this approach to chronic illness and cancer is examined with unprecedented depth with the objective of convincing the sceptical and giving added credence to this sort of work generally
• The overriding philosophy behind the therapy is embodied in “The Theory of General Chronicity”, which is a theory developed by the author himself and expounded in this book. This theory is unique to the book and could only be formulated by someone with both naturopathic understanding and very detailed and up to date knowledge of the medical sciences, including biochemistry
• The overall double message of the book is:
  • This is the best way to treat cancer in future, subject to some concessions to the orthodox
  • “The Theory of General Chronicity” is an important blueprint for future medicine to follow
• No other book on cancer has ever been written to examine the subject in this manner
• No “alternative” book on cancer has ever included so much detailed and informed analysis of the scientific literature

SUMMARY LIST OF CHAPTERS

1. Cancer, the Individual and Society
2. A Body Made up of Cells
3. Factors which Threaten the Life of the Cell
4. The Causes, General Nature and Biology of Cancer
5. Orthodox Treatment and its ay Forward
6. The Theory of General Chronicity – its Relationship to Cancer
7. So what causes Chronic Illnesses?
8. The Nature of the Cancerous Change
9. Detoxification Mechanisms
10. Preventing the Cancerous Change Through Food and Nutrients
11. Anti-Cancer Actions of Groups of phytonutrients
12. How does knowledge of Anticancer Action impinge upon treatment
13. The Rationale of Nutritional Cancer Therapy
14. The Full Protocol of the Therapy
15. Results of the therapy
16. Index

SYNOPSIS OF CHAPTERS

1. Cancer, The Individual and SocietyWhat leads people to fear cancer so particularly over other illnesses? The exchange of information between the patient and the doctor. How the nature of cancer relates to the image people have of it – how it impinges upon patient psychology. Seeing the cancer as being separate from ourselves. How orthodox treatment bears upon the above subjects. To operate or not to operate on the primary tumour. What does orthodox treatment do for the patient’s underlying condition? What to do after an operation. How do recurrences occur? How do detoxication and nutrition fit into this process? The prospects of recovery once the primary tumour has given rise to metastases.
2. A Body Made up of CellsThis deals with the concept of cells as units of life. The book deals throughout with cancer as a cellular and dynamic phenomenon. It is important to impart to the reader a basic understanding of the structure and activities of cells. The following topics are covered. The history of discovering and understanding them – The Cell Theory. The Nature of cells. Their need for materials and energy. The inner structure of cells – organelles. Bechamp and Lindlahr. Bacterial cells. The nucleus. Cell division. Cell membranes, including internal membranes. The biochemical activities of cells – metabolism – the breakdown of bulk nutrients, fat, carbohydrate and protein. Cell Communication and Control Mechanisms. Cell surface receptors. Different cell types in the human body. The organization of cells into tissues and organs. Pharmacological Action of Dietary Components and Herbal Remedies – where Nutrition begins and ends.
3. Factors which Threaten the Life of the CellToxins that affect Energy Production and Protein Synthesis. Toxins that affect Nucleic Acids (DNA). Toxins that affect Membranes. Free Radicals. The Glycosylation of Proteins. Ingress of Sodium and Water into the Cell. How Nutritional Deficiencies and Imbalances Increase the Problem. The Body’s Eliminatory Processes at the Biochemical Level. The Processes of Cell Death. The Prevention of Cell Death. Apoptosis.
4. The Causes, General Nature and Biology of CancerThe Causes of Cancer – Diverse Causes – Just One Principle. Chemical Carcinogenesis. The Outlook of Orthodoxy. Naturopaths have no such Inhibitions. The Role of Nutrients. Back to Naturopathic Theory. Viruses and Radiation Also Cause Cancer. The Nature of the Malignant Tumour and its Growth and Spread. The Nature of Cancer Cells. Cell Division. Differentiation and Anaplasticity. The Growth of Tumours and Survival of the Fittest Amongst Cancer Cells. Cell Division and the Grow Rate of Tumours. The Spread of Tumours.
5. Orthodox Treatment and its Way ForwardSurgery – the compatibilities and conflicts between the surgeon’s position and that of the naturopath are examined carefully. The Likely Outcome from Orthodox Cancer Treatment – an examination of survival rates after surgery. Radiotherapy – when it is likely to be applicable and useful. Chemotherapy – in view of the naturopathically destructive nature of chemotherapy it is very important to identify when chemotherapy has a reasonable chance of success and when it does not. The Mode of Action of Chemotherapy Drugs – this passage offers an understanding of chemotherapy drugs by classifying them according to their different modes of action. Ways to make Chemotherapy more Effective – a view of future perspectives in the orthodox chemotherapy field – where might the break-through come? Biomolecules for Chemotherapy – this passage examines chemotherapy agents that can be derived from living organisms. It seeks to draw a distinction between these cytotoxic natural substances and the ‘phytonutrients’ from plants that can help by raising the person’s immune resistance and similar, more benign effects. Immunotherapy – the place where orthodox and alternative treatment could well meet one day!
6. The Theory of General Chronicity – Its relationship to CancerA Specialized Meaning of ‘Chronicity’. The Nature of Toxic Damage ‘ Non-Specific Cell Toxicity. Enzymes and Metabolism. Enzymes in Relation to Protein Structure. The Vulnerability of Enzymes to Toxins. How Does the Body Cope with Damaged Enzyme Proteins? The Nature of Membranes. Mechanisms of Protein Synthesis and their Vulnerability to Toxins. Damage to Mitochondria and the Endoplasmic Reticulum. Relationship of General Cellular Damage to Cancer. The Nucleus, DNA and their Vulnerability to Toxins. DNA Repair Mechanisms. The Nature of Toxic Damage – Specific Cell Toxicity. Cell Damage and the ‘General Chronicity’ Theory. Theory.
7. So What Causes Chronic Illnesses?There are Only Limited Candidates for the Ultimate Causes of Chronic Illnesses. Do Nutritional Deficiencies Cause Chronic illnesses? A Sensible Response to Recognizing the Role of Toxins. Effects of Stress. Microbial Infections. Genetic Defects. The Constitution – Confluence of Genetic and Naturopathic Viewpoints. ‘Biochemical Naturopathy’ – envisaging that naturopathy and biochemistry can work together. Subtle Energies – the role of energy forces that may be undetected by science. Indicators that Micronutrients Promote Cell Activity and Performance. So What Direction for Therapy: How to Cure Chronicity?
8. The Nature of the Cancerous ChangeThe Control of Cell Division. Mitogens, Mutagens, Clastogens, Recombinogens, Carcinogens and Teratogens. Which Substances Act as Mutagens? Carcinogenesis – A Multiphase Process. Carcinogenesis – Its Relation to the Normal Processes that Control Cell Division. Carcinogenesis – The Nature of the Underlying Changes. Synergism: Co-Mutagens and Co-Carcinogens.
9. Detoxification MechanismsThis is a key chapter that aims to give an understanding of how the body detoxifies itself and delivers a scientific explanation. It also demonstrates the complete compatibility of that explanation with naturopathic principles. Scavenging of Free Radicals by Vitamins and Vitamin-Related Nutrients. Scavenging of Free Radicals by Enzymes. Detoxifying Toxins by Oxidation – Cytochromes P-450. The Effects of Nutrition upon Cytochromes P-450. Nutritional Effects upon Other Oxidative Enzymes. Detoxifying Toxins by Conjugation – and their Nutritional Requirements. Rhodanese. Detoxifying the Products of Reactions between Toxins or Free Radicals and Cell Constituents. The Cell pays a Heavy Price for Detoxification Failure. The Inhibition of Detoxifying Enzymes.
10. Preventing the Cancerous Change through Food and NutrientsThis Chapter is devoted to analyzing the merits of giving attention to diet and taking regular nutritional supplements for the purpose of avoiding cancer. Each of the following section is accompanied by presentation of scientific evidence plus naturopathic comment. Fruit and Vegetable Intake. Consumption of Animal-Derived Protein and Total Protein. Dietary Fat Levels. Different Types of Fat. Sodium and Potassium Intakes. Sugar Consumption. Dietary Fibre. Methionine and Choline. Anti-Oxidant Vitamins. Magnesium. Trace Elements.
11. Anti-Cancer Actions of Groups of PhytonutrientsThis chapter begins to delve into what lies behind the known fact that fruit and vegetable consumption inhibits cancer. What are the substances within them that are responsible for such an important protection of the human body? Each of the main groups are examined – carotenoids – flavonoids of different classes – organic sulphides – thiocyanates – glucosinolates – ellagic acid – curcuminoids – terpenoids etc. The main purpose here is to familiarize the reader with these substances and to offer the scientific evidence that these substances really do inhibit carcinogenesis.
12. How Knowledge of Anticancer Action Impinges upon Treatment?This is a pivotal or focal chapter of the book. We turn here from understanding cancer and prevention of cancer towards the main question of treatment. The main purpose here is to appreciate why it is that many of the factors that help to prevent cancer can also be used to get rid of it once it has formed. In the process one has to consider the different routes by which the therapeutic measures can work.
13. The Rationale of Nutritional Cancer TherapyThis Chapter examines the requirements and priorities for building an assemblage of knowledge about anti-cancer measures into a coherent therapeutic approach. This involves narrowing down the options and making choices. It looks closely at the criteria for including particular natural medicine actions into a therapy and highlights the differences between these and the criteria that must be used for pharmaceutical medicines.
14. The Full Protocol of the TherapyThis gives the details of the way in which the Trust carried out the Therapy. It lists the requirements for Lifestyle, Diet and Nutritional Supplements. Where appropriate it gives details of the adjustments that were made for cancer of particular sites. This data is presented for information only and not as medical treatment for any particular case. It is not the intention of this book to recommend or prescribe.
15. Results of the TherapyThis chapter presents a write-up of the actual results that were achieved in practice by the Nutritional Cancer Therapy Trust
16. Index

REVIEWS OF THE BOOK

“Lawrence Plaskett has done us all a tremendous service by going close up, at a cellular level, to describe exactly what has to happen for a normal cell to become a cancer cell, and how to undo the process using natural medicine. There is a massive medical blindspot that struggles to recognise that by understanding what causes cells to become cancerous, and there are many contributive factors, lies the secret to their undoing. The rising incidence of cancer, and the ineffectiveness of chemotherapy which, according to meta-analyses optimistically reduces fatality by less than 3%, means anyone with cancer really needs to look outside the conventional medicine box, to natural and non-toxic medicine. This book provides invaluable guidance for health professionals.”

Patrick Holford

“Dr Lawrence Plaskett has made a life-long study of the relationship of cancer and nutrition and his book ‘The Nutritional Therapy of Cancer’ is of great relevance to any serious student of nutrition or integrative cancer medicine. When starting my career in this field in 1985, I was told by some doctors that the idea that cancer and nutrition were linked was ridiculous and that it was irresponsible of me to suggest to my patients that they change their diet once diagnosed with this illness. Since then bad nutrition has been found by leading epidemiologists Doll and Peto to be responsible for 35% of all causes for cancers with infections, excess alcohol and environmental toxicity accounting for another 25%. As our ability to deal successfully with all these factors also comes down to good nutrition, it is likely that as many as 60% of cancers start because our Western lifestyle leaves us overfed, under-nourished and toxic. However, the big breakthrough in understanding just how vital nutrition is in the treatment as well as prevention of cancer has come from the 2007 San Diego study showing that women with breast cancer who change to a healthy diet and exercise daily have a 50% survival advantage over those who do not 9 years post diagnosis! There is no conventional cancer treatment which comes close to producing this level of survival benefit for women with breast cancer. It is becoming clear that Dr Plaskett’s theories are of major health and economic importance as this terrific improvement in outcome has been achieved at minimal cost to the health provider by providing proper focus on the nutritional guidance and fitness support of those with cancer. His book is extremely well referenced, very detailed and academically thought provoking. It is an excellent starting place for those wishing to practice, study and research further this vital area of nutritional healthcare for the benefit of mankind. Thank you, Lawrence, for making the fruits of your study and research available to us all in the Integrative Medicine community in such a clear and scholarly way.”

Dr Rosy Daniel BSc MBBCh
Integrative Cancer Consultant

“Dr Plaskett’s book is an exhaustive and carefully compiled study which fills a huge gap in the general understanding of cancer and other chronic diseases and deserves wide attention. Orthodox medical practitioners should heed its contents.”

Michael Finucane

About the Author

DR LAWRENCE PLASKETT

Early career

Lawrence graduated from Cambridge University in 1956 as a biochemist and then completed a PhD at University College Hospital Medical School, London in 1960. He then became a Lecturer in Medical Biochemistry at Edinburgh University Medical School (1960-65). At this time he was a specialist in thyroid biochemistry and thyroid diseases.

Changing to the food industry, he was Research Director for an international group (1965-74) and subsequently established his own Biotechnology Consultancy Company (1975-82) serving the Food and Bio-Energy Industries and contributing to the bio-energy policies of UK, EU and Brazil.

Later

From the later 1970’s he developed his interest in unorthodox approaches to clinical nutrition and Chinese medicine and he established a multi-disciplined alternative medicine clinic in the South West of the UK and a practice in London’s Upper Harley Street.

He was first in the UK to set up a College for training Nutritional Medicine Practitioners in 1982, teaching a holistic approach. His College of 700 students took up a leading position in the UK and now licences his training courses to colleges in 37 countries, covering Nutritional Medicine, Iridology and Slimming Consultancy.

Lawrence has in all some 80 publications consisting of research papers, UK and US patent applications and scientific reports on his research and consulting assignments. He has written many articles and newsletters on nutritional issues and designed a range of nutritional supplement products. He is known for having produced a nutritional cancer therapy protocol (that includes use of Aloe vera) that has been applied in the UK.

Now

Partly retired from teaching students and from practice, he concentrates upon writing and research. His long experience working in the borderlands between nutrition and medicine enables him to offer a synthesis between many fields that are not often brought together: nutrition, pathology, biochemistry, toxicology, pharmacology, cell biology, naturopathy and homoeopathy.

Outcomes of the Therapy

A full enquiry by an independent nutritional practitioner into the results of the therapy over the 8-year period of use is being mounted using the The Nutritional Cancer Therapy Trust’s records. The first indications are that:

40 full recoveries were obtained (i.e. no diagnosable signs of cancer with the patient being well). These represent 57% of the patients who followed the protocol for the specified period of time. Among those who died there are indications that some had defaulted in continuing to use certain components of the therapy, suggesting that, if there had been fully rigorous control of the treatment the recovery rate could have been higher. In any case, many of those who died did so after surviving well beyond the length of their original prognosis, indicating that the therapy had been a partial success in their cases also. The cases whose records were available for study did not represent all the patients who undertook the therapy, so there could be more than the known 40 recoveries.

The drop out rate for patients was high due to various factors, including the rather strict demands of the therapy, family or financial problems, lack of a home carer, advice given against the therapy by orthodox doctors and the intervention of medical situations making the continued use of the therapy too difficult.

PUBLISHED ARTICLES

Published articles are available here in Word Document format. To save the article to your computer right-click the ‘download this article’ button, then select ‘save target as’ from the menu – save the article to your computer and open it with Word (or another Word-compatible program such as Works).

---

CLINICAL APPLICATION OF A NUTRITIONAL CANCER THERAPY WITH PRESCRIBED DIET AND NUTRIENTS

First published at the International Aloe Science Council Seminar of September 2000 in Dallas, Texas and recorded in the proceedings of that Council. This was written well before the full outcome of the Trust’s work was known (2006-7) Provides further rationale of the Therapy and more supporting literature references.

Extract…

An important issue of the day is whether foods, nutrients and natural products can play a significant part not only in the prevention of cancer but also in its treatment. Many natural products have been shown to have quite powerful effects in the prevention of carcinogenesis. These have been reviewed by many authors including Wattenberg (1986), Block et al (1992), Stavric, (1994), Wargovich (1997), Ren & Lien (1997). Some of these materials would be classed as food constituents and others as herbal products. Many of these are also the subjects of a less voluminous but nonetheless impressive literature showing that they exert an anti-tumour effect upon established cancers…

---

GERSON TRUST PROJECT TO PRODUCE AND USE CONCENTRATED PHYTONUTRIENTS IN CANCER THERAPY

First published in the Journal of Alternative and Complementary Medicine Jan 1998. At the time the Gerson Trust had not yet changed its name to Nutritional Cancer Therapy Trust.

Extract…

The Gerson Trust was formed on the basis of a dedication to the use of holistic nutrition principles and naturopathic principles in the treatment of cancer. In particular, as the name of the Trust implies, the initial dedication was to the use of the Gerson Therapy which embodies those principles. These principles are based upon providing conditions in which the body can adequately reject the tumour from its own resources. This is in complete contrast with the techniques of orthodox medicine, drugs, surgery and radiation, designed to “attack” the tumour by wholly external influences without much regard to the resulting cost to the natural resources of the body…

---

NUTRITIONAL THERAPY TO THE AID OF CANCER PATIENTS

First published in the Journal of Alternative and Complementary Medicine December 1999

Extract…

It is my firmly held view that the nutritional approach should take its place in a short time among the general nationally available treatments. Orthodox oncologists seem set to fight that concept all the way. The reason they give (if any is offered at all) is that nutritional treatment is “not proven”. Since it appears churlish to oppose any reasonable call for proof the matter is supposed to end there. However, that belies the fact that the only people likely to have access to the very large funds needed for convincing clinical trials are the orthodox oncologists and they are also the only people likely to obtain the necessary ethical approvals for planned trials. They therefore have the power to simply block any trials of nutritional treatment, just because its underlying medical philosophy clashes with orthodoxy….

---

THE EXPERIENCE OF THE NUTRITIONAL CANCER THERAPY TRUST IN APPLYING THE PLASKETT THERAPY 1997-1999

First published in the Journal of Alternative and Complementary Medicine Jan 2000

Extract…

Patients using the therapy are assessed in depth including a detailed clinical history, to ensure that they are suitable and that they fully understand all that is entailed in following the therapy and what they should expect to achieve in their own case. Particular attention is paid to not raising false hopes. In order to follow the therapy patients must be able to ingest the normal quantities of food for their age, be able to swallow the daily quantities of supplements and have a reasonable level of initial physical fitness. They will probably have a life expectation above 3 months combined with strength of character and the determination to fight on to remission. Family relationships are of paramount importance and severe tensions and disruptions have a catastrophic effect. The mental stability and capability to deal with personal traumas are important for the success of the patient. The patients come from a wide range of social backgrounds, ranging in age from 2 years to those in their 70s….

This website (http://www.therapyofcancer.co.uk/) has been created to present an alternative approach to the treatment of cancer

The site offers information only and none of the content should be construed as constituting an effective treatment for any individual person or as a ‘cure’ for any complaint. This detailed information given is in the interest of promoting more active research and enquiry into the nutritional, herbal and homoeopathic approaches to the alleviation, control and therapy of cancer.

Serious interest in the potential for nutritional medicine in cancer therapy is more than justified by the severe limitations of current forms of cancer treatment with orthodox medicine. Although there is much that these therapies can achieve, huge numbers of patients are being left eventually with no further treatment options and go on to die. Moreover, there have been repeated and widespread accounts in the scientific and medical literature that nutritional factors powerfully influence the development and growth of cancer. Many would say that, given the full weight of scientific evidence, the health professions have been very remiss in not carefully investigating the potential power of nutrition as cancer treatment. Given this potential, the determination to avoid investigating it seems tantamount to letting the public down.

Dr. Lawrence Plaskett is a biochemist, medical researcher, food industry expert, practitioner of nutritional, herbal and homoeopathic medicine and founder of the prestigious Plaskett Nutritional Medicine College. His methods are both science-based and naturopathic and he is noted for producing a synthesis of these approaches. For 30 years his advice was sought after by cancer-sufferers wishing to practice the best possible nutrition, even though he never promised or implied specific results.

Recently Dr. Plaskett reviewed and recorded the scientific research literature that bears upon the influences of nutrition upon cancer. He distilled the outcomes into a protocol for cancer-sufferers (which became known as the “Plaskett Therapy”) that combines together “state-of-the-art” nutritional measures expected to influence cancer.

The results are in his published articles, an article written especially for this Website, and his book “The Nutritional Therapy of Cancer”.

Chapter 6

The Theory of General Chronicity – Its Relationship to Cancer

1 A Specialized Meaning of ‘Chronicity’

What is to be presented in this Chapter is pertinent to the whole question of the initiation of chronic diseases – not just cancer. If we look in the pathology texts and consult the chapters there on individual types of chronic disease we usually find an explanation of cause (aetiology) on a superficial level. However, when we begin to probe into the cause of the causes, we soon hit an impenetrable wall of ‘not knowing’. So, osteoarthritis is ’caused’ by inflammation, according to these books, or is ’caused’ by joint damage. What caused the inflammation? What caused the joint damage in those cases where it was not started by physical trauma? Here is where the orthodox pathologist runs into terminal trouble with his explanations. Quite obviously ‘wear’ of joints and physical knocks to the joints are likely to exacerbate any problem that already exists, but why, then, do some people who experience knocks and wear to the joints not develop osteoarthritis? The case seems overwhelming that there is such a thing as an underlying condition that predisposes the person to osteoarthritis. Naturally, then, if a person with such a predisposition suffers from wear and knocks the joints, he or she is likely to be sent down a road towards developing osteoarthritis when a person free from the predisposition would withstand these stresses without consequence.

Similarly, one can look in these same books at the ‘aetiology’ of Type 1 Diabetes (IDD – Insulin-dependent diabetes). A prime ’cause’ can be said, quite obviously, to be something that goes wrong with the beta cells of the Islets of Langerhans in the pancreas, the cells that normally produce insulin. Since the appearance is that chronic inflammation occurs in and around these beta cells, it is possible to go a stage further and to assert that the ’cause’, very likely, is inflammation that gets out of control and results in the destruction of these important cells. The obvious question is what causes this inflammation in the first place, and what prevents it from being brought under normal controls. Pathologists note that there is an immune response being mounted in the body against the beta cells of the pancreas. An immune attack upon any of the body’s owns tissues amounts to a sort of allergy to ‘self’ and has been termed ‘auto-immunity’. Useful term though this may be, it soon becomes apparent that the coining of a name has actually done nothing to add to the explanation of a cause for the condition. So what causes the auto-immunity? At this point genetic factors that add to susceptibility are pointed out. These do not appear, however, to amount to a ’cause’, since they only change the probability of the disease occurring in an individual. Specific triggers to the development of Type 1 Diabetes may be mentioned, one of which is the consumption of cow’s milk. So is cow’s milk a specific cause of the disease? Whilst this may be getting a little closer to the idea of a cause, there are good reasons for thinking that some cellular damage has to be done first. Both virus damage and chemical damage are invoked at this point. They are considered to produce some initial harm to cells, either in the immune system or in the pancreas. So far as chemical damage is concerned, the orthodox position seems only to be able to envisage one toxin exposure, so that the only cases to be considered in this context are fairly unusual cases of single toxin exposure. This is as far as we can go in conventional texts in understanding the cause of this disease.

Now if we look at these two chronic illnesses from the standpoint of an ‘alternative’ position, we find that one is drawn irresistibly towards underlying cellular damage being the common pathway in both cases. Looking back at osteoarthritis, we need to identify a ‘predisposing underlying factor’ to account for the observed incidence of the disease. It is inherently difficult to envisage one that will not amount to some defect of cell biochemistry and metabolism. Joints depend heavily upon cartilage tissue to maintain their structure. They also depend upon the lubricating fluid of the joint spaces (synovial fluid). Both cartilage and synovial fluid depend upon a constant supply of newly synthesized mucopolysaccharides (now more often called glycosaminoglycans) for full maintenance of their functions. These provide both the tough resilience of cartilage and the slipperiness of the synovial lubricant. It seems to follow, then, that in health, the cartilage tissue or the cells in the synovial membrane around the joint space, will be active in synthesizing these important glycosaminoglycans. If the synthesis of glycosaminoglycans falters, then joint function will be jeopardized. This idea is supported by the observation that supplements of glucosamine sulphate, which are precursors of glycosaminoglycans in the body, alleviate osteoarthritis by supporting the synthesis of fresh glycosaminoglycans. It is therefore reasonable to at least hypothesize that it is active joint cells – joint cells with a high capacity for performing their biochemical functions which protect the body against osteoarthritis. If we maintain their metabolism at a good and active level, especially their ability to synthesize new glycosaminoglycans, then we probably have joints that will resist wear and trauma quite well. If, on the other hand, their metabolism is slow and hindered, then glycosaminoglycans will not be well produced, and joint functions will be jeopardized.

This sort of conclusion focuses attention upon what it is that might be able to keep joint cells in a state of competent and active metabolism. Deliberating about this inevitably results in the conclusion that two things that are likely to get in the way of the activity of enzyme systems in these cells. These are (1) intracellular concentrations of enzyme-inhibiting toxins and (2) a degree of intracellular deprivation of the trace catalysts required by enzyme systems. The trace catalysts are, of course, mainly minerals and vitamin derivatives that become adapted for use as co-enzymes. Ensuring that these damaging conditions do not occur obviously calls for the body to be shielded from exposure to harmful toxins from the environment. Efficient detoxification is required of those toxins that are able to enter the body, as well as an abundant nutritional input of trace catalysts. Suddenly we find that biochemistry is leading us to a conclusion that coincides with the conclusions reached by naturopaths and vitalists during many past decades. Those were times when little input from biochemistry was available. Inexorably, these thought processes lead one in the direction of preventative medicine. It becomes rather obvious what sort of preventative measures would be effective in stopping the disease if the theory is correct. The application of these now obvious preventative measures after the disease has once developed is likely to ameliorate the disease but may fail to cure it completely. The lack of complete recovery will be due to the long intervening toxic damage and physical damage to joint structure.

Turning back now to Type 1 Diabetes, we had noted that orthodoxy would encompass the view that single specific toxins might be a rare underlying cause of the condition. Medical scientists have long known about specific toxins, such as alloxan, which induce diabetes. Here again we can apply the principle that the ‘general metabolic competence’ of the beta cells is being compromised by a toxin that targets them more than other cell types. It is very important for the patient that enough of them retain the ability to synthesize and release insulin. However, in Type 1 Diabetes most of them are in fact even failing to stay alive. Those cells that are dying must have suffered severe blows to their metabolic competence and hence to their stability. It seems that if just a few cells are damaged enough for them to die, or just release, through pathology, some of their contents, then they may give rise to a centre of inflammation. This will be because immune cells may begin to attack the now somewhat altered antigens of the dying cells. Once the inflammation is set up it fails to be dampened down and many more beta cells are killed. The initial problem was almost certainly that toxins damaged some beta cells though it was almost certainly not just a single toxin in most cases. The chronic inflammation and the auto-immunity that flowed from the initial damage were then self-perpetuating. We have to focus our attention upon just why some beta cells were initially affected by toxins. As in the case of the cells of the joints, these cells needed shielding from excessive levels of toxicity from outside or inside. They also needed to have efficient detoxifying mechanisms and generous internal levels of trace catalysts. Had all these more favourable conditions applied, then, in all probability the original exposure of these cells to toxins would not have occurred or, had it occurred, the cells would have been equipped to survive. Then auto-immunity would have been avoided.

Once again, this focuses attention upon preventative measures. The conclusion that the development of Type 1 Diabetes was ‘unavoidable bad luck’ is no longer tenable. It now seems entirely avoidable, even in susceptible individuals, by applying the correct protective measures. Some ‘alternative medicine sources’ have long allowed themselves to be overawed by the strident presentation of the arguments of orthodoxy in relation to diabetes, especially Type 1 Diabetes. Others have not allowed this. So long as it remains viable to do so, the wholistic approach has to be to encourage the production of the patient’s own insulin, or better still, prevent the problem from developing in the first place. Underlying the whole of this medical philosophy is the insistence that the key to stopping chronic illnesses is the maintenance of adequate levels of cellular activity, including the efficient discharge of any specialized cell functions. This is a vitalistic outlook, but it also has a firm basis in cell biochemistry.

Orthodox pathologists suspect that virus damage has a significant part to play in causing several chronic diseases, including Type 1 Diabetes. This presents no conceptual problem in conjunction with the above philosophy. Any long-standing damage from past viral infection is likely to be damage to DNA in the cell nucleus. That has the effect of altering genetic information. It is likely to block the production of some enzymes or result in the production of defective enzymes. In either case the result will be metabolically compromised cells that are going to suffer from increased vulnerability to any kind of stress. Such cells will be toxin-susceptible, may have poor toxification mechanisms, may well take up trace catalysts less effectively and may generate altered antigens that attract autoimmune attack from immune cells. Seen in this light, viral damage is not so much a completely separate cause of chronic disease, but a contributory cause of reduced cellular metabolic competence.

This reduced cellular metabolic competence is what the present author terms ‘chronicity’. Its dictionary definition is ‘the state of being chronic’, though it will be helpful in the present context to better define exactly what that means. It is, perhaps, the ‘final common pathway’ to all chronic disease states, or nearly all.

We have seen that naturopaths generally view ‘the cause’ of chronic diseases to be toxic deposits in the tissues. What is frequently overlooked by people who adopt naturopathic ideas, or by alternative therapists of various disciplines, not fully trained in the naturopathic art, is that the present toxic burden of the body is only a part of the problem. The other main component, apart from the nutritional deficiencies and imbalances that may be corrected with various degrees of difficulty, is the toxic damage that these toxins have done to the cells while they were residing in the tissues. The ‘toxic burden’ of the body, or of a particular tissue, is the sum total of all the toxins that have affected the body, either now or in the past, plus the accumulated damage that they have wrought. The toxins themselves may be (or have been) of various kinds. Some will be from external environmental sources, including from food, some will have been produced by bowel bacteria, some will be waste products of metabolism, while still others will have been formed by the interaction of environmental toxins with tissue components.

Toxic exposure itself can be acute or chronic. That is to say, a large exposure to an individual and identifiable toxin may happen through an occupational accident in a job involving hazardous chemicals or it could be the regular sheep-dip on a farm. That is an acute exposure. It could also happen domestically through the misuse of some chemical product. What then happens depends largely upon the nature of the toxin and the status of our body’s detoxification mechanisms. If the toxin happens to be one of a more forgiving kind, then the deposits might be largely cleared from our system fairly quickly. If we are lucky, this may result in little toxic damage being done. It will have amounted to a high dose / short time exposure. The extent of toxic damage will always be a dose / time effect. For a particular toxin the damage effect will be measured as units of toxin (parts per million, for example) multiplied by years of exposure at that given concentration. In practice one recognizes that the concentration of toxin in the tissue is unlike to be steady over the years. One is then into determining how the toxin level varies with time. The total toxic exposure (which gives rise to the toxic damage effect) will be equal to the area under the graph plotted of toxin level against time. Mathematically, these areas are determined by integrating the results. The toxic damage effect will be the integral of concentration with time.

This is why one may get away with little trouble from a single acute toxic accident. However, in the nature of such an accident the dose may be very high. If the toxin is not of a forgiving type and the dose is an extraordinary one, then of course, the detoxifying mechanisms and eliminatory mechanisms of the body may be overwhelmed by the dose and may prove to be unable to remove the toxins at all well. The problem here would be that the detoxification enzyme systems and the organs of elimination are themselves poisoned to the point of ineffectiveness.

This view of toxicity and the damage that results from it is pretty much a medical hypothesis. It is a working hypothesis, though, for wholistic nutritional practitioners, that serves them in good stead and usually matches up to the task of interpreting clinical observations. It is usually the toxic damage factor that gives us chronic diseases rather than just the presence of toxin in the tissues. The toxins themselves will only kill us in acute dosage and in that case will usually do so in the short term. When we are dealing with chronic diseases, whether they are osteoarthritis, diabetes or cancer, we are usually concerned with gradually accumulating tissue toxicity over years and not with chronic dosage. Obviously, the differences in effect between a 3-day residence time in the tissues and a 30-year residence time will be crucial. The latter is more the kind of duration with which we may be dealing in chronic diseases, although the concentrations of individual toxins may be low.

Therefore, therapists working from a naturopathic standpoint need to distinguish between the toxins themselves that may be removed from the body by intensive detoxification and the toxic damage associated with those toxins, which cannot. Correcting the effects of toxic damage is quite distinct from detoxification and it calls for the healing responses of the body to be activated. Given that toxic damage usually results in some cell death and that the cells around the dead cells may well be moribund, initiating that healing response may well require us to ‘pull out all the stops’. Moreover, we have to recognize that there are degrees of toxic damage that surpass the limits of the body’s ability to heal itself. In this Chapter we look closely at the nature of toxic damage and its effects. We shall look at it both generally and also in specific connection with cancer. Meanwhile, the term chronicity, in the manner in which it is to be used here, may be defined in a way that elaborates upon the simplest dictionary definition. It could well be defined as ‘the sum total of the body’s present and historical toxic burden and the residual cellular and tissue damage it has caused’.

2 The Nature of Toxic Damage – Non-Specific Cell Toxicity

The nature of toxic damage has been explained in outline in Chapter 3. This Chapter examines it in rather more detail. This is necessary if one is to fully understand the nature of ‘Chronicity’ as defined above.

Enzymes and Metabolism

Of course, it is not the object of this book to provide a textbook explanation of the many facets of medical science that underpin the understanding of cell function in relation to cancer. Space will not permit that and there are many good texts available. However, the lay reader needs a broad explanation of what is involved in the various aspects of cell deterioration according to the ‘general chronicity’ theory.

In order to live and thrive the cell needs to take in the bulk nutrients, protein, carbohydrate and fat (lipid), or at least, the digestion products from these, respectively amino acids, sugars and fatty acids. It needs to break these down into simple products, carbon dioxide, water, and ammonia, with the release of energy. That energy is trapped for further use in the form of the high-energy compound ATP (short for adenosine triphosphate). Once formed the ATP acts as a short-term energy store for the cell and its energy can be harnessed to any energy-using process within the cell. In that sense, it is often described as a kind of ‘energy currency’ within the cell. The uses to which it is put include movement, maintaining the intracellular environment by ‘pumping’ some types of molecules or ions into the cell and others out, producing functional secretions, such as the digestive enzymes or hormones. Finally, the cell uses the energy of ATP to synthesize its own constituents, consisting of human-type proteins, carbohydrates and lipids, from those of the amino acids, sugars and fatty acids that have not been broken down for energy. In this way is gains material needed for growth, reproduction and repair and replacement of its own substance.

The breakdown of amino acids, sugars and fatty acids is achieved through complex multistage processes. So also is the synthesis of human proteins, carbohydrates and lipids from simple amino acids, sugars, fatty acids and ATP. Cells must also synthesis and breakdown nucleic acids, the breakdown building blocks of these being ‘nucleotides’. Many cells must also remain capable of producing messenger substances (hormones and ‘cytokinins’) that migrate or are carried to other cells to exert a physiological influence. These too are complex, multistage, operations.

Almost all such processes are brought about inside cells by the action of enzymes. The function of enzymes is to act as catalysts. Since they are of entirely biological origin, they are usually called biological catalysts. . The dictionary defines catalysis as “the chemical influence of a substance which is not itself permanently changed”. To understand a catalytic effect, imagine a chemical reaction in which substance A reacts with substance B, altering them both and giving rise to two different substances, C and D, as the products.

A + B leads to C + D

If, in the laboratory, we take substances A and B and mix them, nothing happens. We can maybe heat them together and shake them, but still without effect. Now we add a minute trace of substance E, perhaps it might be, for example, platinum, whereupon all the substances A and B convert rapidly into substances C and D. At the end of the reaction the substance E, be it platinum or whatever, remains unchanged in the same tiny amount that was put there to start the reaction. To initiate the reaction, and during the reaction, it may have combined temporarily with the substances A and B, then releasing C and D and itself returning to its original state. Having done so, it can repeat the process indefinitely and, in this way, a vanishingly small amount of E can bring about the transformation of a very large quantity of A and B. This is catalysis and the reaction is a catalytic reaction. Platinum is a commonly used catalyst in industrial processes, as is palladium. Nickel is used as a catalyst in the manufacture of margarine. Yet these are examples of non-biological catalysts. These are not the catalysts that normally operate very extensively in the body. The chemical nature of the body’s enzymes is that they are proteins. They are not just any old protein. They are not structural proteins like collagen, one of the proteins that form strong structural fibers in connective tissues, nor are they like the gluten of the wheat seed or the zein of maize, which are plant storage proteins. They are, rather, specific functional proteins that have an active role in cellular metabolism.

In general, each enzyme protein catalyses only one specific reaction that is special to it – or at most, they may catalyze a group of very closely similar reactions. For a particular enzyme, the substance or substances it works upon is, or are, referred to as its substrate or substrates. As the body chemistry is very complex indeed, there are thousands of enzymes catalyzing reactions with different substrates; sometimes more than one enzyme act upon a single substrate, converting it into different products. If one considers in detail the process by which the body converts one important substrate, such as glucose, into specified end products, like carbon dioxide and water, one is certainly looking at a complex multistage process. In this example, one has three subdivisions of the process, called ‘Glycolysis’, the ‘Citric Acid Cycle’ and ‘The Respiratory Chain’. Depending slightly upon just how one defines each sub-process or each step within these sub-processes, we may define the number of steps as follows, giving a 34-step overall process.

Glycolysis – 12 Steps
Citric Acid Cycle – 9 Steps
Respiratory Chain – 13 Steps

The position is actually more complex than this if one also takes into account the existence of side-reactions which connect these pathways to others. Each of these separate steps is catalyzed by it’s own enzyme. Sometimes there will even be several slightly different enzymes for a single step. These are called ‘isozymes’. The sub-processes described above are referred to as ‘metabolic pathways’. This is because the pathway from substrate X to end product Y is defined, with fixed intermediate substances (‘metabolites’) that represent the given number of intermediate stages on the pathway. There can easily be more than one pathway to a given product, but each of the pathways will be defined.

The number of step-specific enzymes in the cell is huge. This becomes clear when one looks at the number of pathways leading to and from all the different cell components that are capable of being either synthesized or broken down. This first step, then towards the concept of ‘general chronicity’ is to understand that enzymes are absolutely crucial to everything that exists, moves, changes or happens inside the living cell. From that realization that enzymes underlie all the phenomena of life and all life activities, one can begin to see how the integrity of one’s thousands of cellular enzymes can determine one’s state of health.

Next one needs to add that a very high proportion of all enzymes require co-factors with which to work. These are substances that could not catalyze the reaction on their own but whose presence is absolutely necessary for the action of the enzyme itself. These co-factors are various. Most typically, though, they are either minerals or co-factors fabricated from vitamins. Many enzymes require both these types of co-factor. Obviously, then, possessing sufficient enzyme is not enough in itself. To have the pathways operating, each co-factor-requiring enzyme must be adequately furnished with its co-factors. The minerals and vitamins are micronutrients in the diet. If they are not adequately present in the diet there can scarcely be any other source of them except by injection or, in a few cases, fabrication of a vitamin by the bacterial flora of the intestines. Immediately, then we face the probability of a huge impact upon enzymic integrity and therefore upon health, from the adequacy and balance of the supply of minerals and vitamins (‘trace nutrient catalysts’) in the diet. What is it that modern processed food diets most often lack – answer – ‘trace nutrient catalysts’. This fact has great implications not only directly upon health but also upon the interactions between toxins and trace nutrients. These interactions will need to be understood in gaining a grasp of ‘general chronicity’.

Enzymes in Relation to Protein Structure

The fact that enzymes are proteins has a profound effect upon their properties as catalysts. It is responsible, for example, for the thermolability of enzymes, that is to say, the fact that enzyme activity does not survive heating.

All proteins are made up of chains of amino acids linked together by chemical bonds called peptide bonds. As this book will not be seeking to probe the chemical background to these subjects, the structure of the amino acids themselves will not be discussed beyond mentioning that there are 20-plus different kinds. These are, therefore, the ‘building blocks’ from which proteins are made, some of them being nutritionally essential. A protein may be built up from one or more chains. The sequence of the 20 types of amino acid in each chain is fixed and definite for a particular protein. This chain of amino acids is then thrown into a coil, typically in some regions of the chain but not others. This coil is termed the ‘alpha helix’. The chain is then folded on itself to form a 3-dimensional shape characteristic of the protein. This folded structure is stabilized by cross-linkages between different regions of the chain. The regions so linked may well be far removed from each other along the amino acid sequence of the chain, but will have been brought into close physical proximity by the folds to which the chain has been subject. There may be several or a good many of these cross linkages in any one protein. Their chemical nature is that they involve atoms of sulphur and they are called ‘disulphide bridges’. These structural arrangements are illustrated 2-dimensionally in Figure 1 – but are depicted 3-dimensionally in Figure 2

The second of these figures shows that although the protein, by fundamental nature, is a linear chain or chains, the folding and/or the bunching together of chains creates more of a globular structure. The fact that the protein contains some 20 different types of amino acid is important. These give rise to variation of electrical charge patterns distributed over the protein’s surface. These charges vary with the degree of acidity or alkalinity of the medium (pH), but over a certain range of pH values will have the effect of attracting certain smaller molecules to the protein surface.

The sole function of an enzyme, as we have seen, is usually to catalyze a particular biochemical reaction. That reaction has to take place in a particular location on the enzyme surface. This means that every enzyme has on its surface a selected special location, apparently designed to attract the substrate to it. That special location is termed the ‘active centre’. The substrate molecule is attracted to it by its pattern of electrical charge, by the shape and size of the substrate molecule and by the conformation (shaping) of the enzyme surface at the active centre. Once located on the active centre the substrate molecule may be split into smaller product molecules through stresses imposed upon it at the active site. Alternatively, if the reaction is a synthesis reaction, the substrate molecule may be induced to combine with a second substrate molecule, which is often of different identity, giving a product molecule of increased size. Some enzymes simply alter the chemical structure of the substrate molecule without either splitting it or enlarging it. Figure – shows a diagrammatic representation of an enzyme molecule with a substrate molecule bound to its surface at its active centre. Note that if a mineral or co-enzyme and/or a second substrate are also involved in the reaction, then it too may well bind at the enzyme’s active centre.

The Vulnerability of Enzymes to Toxins

Now that we have in mind a concept of the mechanism of enzyme action, one can begin to see the vulnerability of enzymes to toxins. The likely result from interaction between an enzyme and a toxin is the inactivation of the enzyme. The enzyme protein remains but the enzymic activity has been lost. Some toxins merely inhibit enzymes reversibly. That is to say, while the toxin remains in the medium with the enzyme, the enzyme’s activity cannot occur, or will be much diminished. This is a rather ‘forgiving’ type of toxin, because as soon as the toxin can be cleared from the body, the original enzyme regains its activity. It does not then have to be broken down and replaced by synthesis of new enzyme. This type of toxin will only exert effects that are apparent during the time when the toxin is present in the tissues in significant concentrations. Of course, such a toxin may well cause death when administered in acute doses. However, most toxins that are involved in directly causing chronic damage are not of this type. The reversible enzyme inhibitor may be a substance that resembles the normal enzyme substrate quite closely. Such a substance may well bind to the active centre and yet be incapable if undergoing the reaction that the enzyme usually performs. By remaining adhering to the active centre it prevents the enzyme from binding with its normal substrate and therefore stops the normal reaction from proceeding. Enzyme inhibitors of this kind are called ‘antimetabolites’ because their effect is to ‘antagonize’ the normal substrate or metabolite. Sometimes they are called ‘analogues’, a name, which stresses their structural resemblance to the normal substrate. Many drugs are antimetabolites, especially those that work upon the nervous system. Another type of inhibitor may combine with a mineral co-factor for the enzyme, rendering it unavailable for its usual role in the reaction. This happens in the case of cyanide poisoning, where the cyanide reacts with the copper atoms that are indispensable to the action of the respiratory enzyme cytochrome oxidase. Still further inhibitors may be antimetabolites for the non-mineral co-enzymes or their associated vitamins. An example would be a thiamine analogue which inhibits the normal utilization if thiamine (Vitamin B1). In these cases the enzyme protein and its potential function are in order, but actual expression of that activity is prevented by the absence of an essential thiamine-containing co-factor.

However, many more toxins that affect enzymes cause irreversible inhibition. This comes about because the toxin reacts with some portion of the enzyme protein causing irreversible changes that are incompatible with its biological activity. This may amount to an unfolding of the precisely folded protein chain or chains of the enzyme – a process called ‘denaturation’ because the protein is not longer in its biologically natural or ‘native’ state. This shows that the exact 3-dimensional conformation of the protein is quite indispensable for the biological activity. This can be easily demonstrated using special more gentle sulphur-containing reagents (such as beta-mercaptoethanol) that cause the protein to unfold without permanent damage. Upon removal of the reagent the protein then re-assumes its ‘native’ state. However, toxins that cause irreversible denaturation clearly cause permanent loss of activity. A good example of a toxin producing irreversible denaturation is mercury. The same effect is produced if the toxin is reactive with some part of the enzyme protein, altering its chemical structure. To do that it will normally involve reacting with one or more of the protein’s amino acid building blocks. We can rely upon it that if this reaction occurs at the active centre, then the active centre will be eliminated. Even away from the active centre, the enzymic activity is still likely to be destroyed because the all-important local patterns of electrical charges on the enzyme surface will be disrupted. Among substances that can damage or destroy enzyme activity by reacting with amino acid groups along the protein chain are alkylating agents, such as those already cited as anti-cancer drugs, melphalan, chlorambucil, ifosfamide, carboplatin and procarbazine and, of course, the nitrogen mustards, such as the notorious mustard gas. Strong oxidizing agents, such as the chlorine in drinking water can react with proteins (as, indeed, it can react with most types of biomolecule) and this is clearly one way in which it unleashes its cytotoxic action against bacteria. Free radicals from any source are likely to do the same, the sulphur groups of the sulphur amino acids cysteine and methionine being vulnerable to conversion to sulphoxides – forms that do not occur at all in ‘native’ proteins. Direct evidence of this kind of reaction being involved in causing cancer does not appear to be available, though altered proteins of this type have been found in rheumatoid arthritis and in diabetes. Carcinogenesis, however, is primarily an event within the nucleus of the cell and directly affects the DNA.

How Does the Body Cope with Damaged Enzyme Proteins?

A damaged enzyme protein is not only useless in the cell, but rather, it will be an encumbrance, a kind of metabolic obstacle, because it takes up intracellular space that should be filled with active enzyme. The body has no choice but to either put up with this encumbrance for a time or else to break the protein down, release its amino acid building blocks and to synthesize new enzyme. All this has very high-energy costs for the cell. The original enzyme had been good and did not need replacing. It needs replacing only because of toxic action. ATP expended in re-synthesis would be better expended on other things, especially upon the elimination of the toxins to very low levels. The amino acid sulphoxides – direct products of the toxin’s action, will call for more expenditure of ATP in the course of their removal. The cell’s output of ATP may or may not be normal; its potential for new protein synthesis may or may not be normal, but if quantities of these precious cell resources are to be expended repairing cell damage, then they are not available for other important activities. In addition it may have to tolerate a lack of the damaged enzyme for a time, with whatever hindrance that may be to its metabolism. Hence the cell that has to cope with toxins and toxic damage is nonetheless a compromised cell. All that contributes to its state of ‘chronicity’.

The Nature of Membranes

This topic has been only introduced in Chapters 1 and 3. To follow the chronicity theory one needs to appreciate the fine structure of cell membranes and to realize the nature of the damage that may befall them. The reader is referred back to Chapter 1 with its description of the structure of membranes with their principal basic structure being a very fine phospholipid bilayer. As previously stated, cholesterol and glycolipid are also present, but phospholipid is the predominant type of lipid present in these layers. When it comes to cell membranes being affected by toxins, we must bear in mind that these can profoundly affect enzyme proteins and receptors that are embedded in the membrane. Here though we focus upon factors’ affecting the lipid bilayer that constitutes most of the area of the membrane.

The phospholipids that it contains are made up of:

1. Glycerol – a non-fatty moiety that, however, loses its non-fatty character when combined into lipid molecules
2. Saturated fatty acids – mainly hydrophobic (water hating) but with one hydrophilic end that is lost upon combination with glycerol
3. Unsaturated fatty acids – same comment as 2 above
4. Phosphate – which retains some ionizable hydrophilic tendency even when combined into phospholipid
5. A nitrogen containing substance such as choline, ethanolamine or serine: sometimes the non-nitrogenous inositol instead. These may carry a charge and contribute toward hydrophilic character

Clearly, then the phospholipid molecules of the cell membrane possess one hydrophilic part only, which is that associated with the phosphate group and the adjacent, mainly nitrogenous special groups. It is this part of the molecule that faces outward from the membrane towards the aqueous medium on both sides, i.e. both inside and outside surfaces. The long carbon chains of the fatty acids are directed into the membranes hydrophobic interior. This has the effect of aligning them parallel with each other throughout the entire area of the membrane. Several factors control the average closeness of these aligned fatty acid chains. These factors determine the fluidity of the membrane because the more closely packed these chains the less fluid the membrane will be and factors that tend to spread them increase fluidity.

To have cell membranes of adequate fluidity one needs adequate dietary supplies of the essential fatty acids belonging to the two groups Omega 3 and Omega 6. These unsaturated fatty acids do not have chains that are conformed straight. They have kinks where the unsaturations occur, giving the molecule of bent form that takes up extra space when the molecules of phospholipid are arranged in the membrane. This separation is beneficial to function, increasing fluidity. The steroid cholesterol is also part of the membrane structure. Today many bad things have been said about the health effects of cholesterol. To a great extent this is justified because too high a blood cholesterol level is undoubtedly associated with an unhealthy condition. However, to develop a balanced picture, one does need to recognize that cholesterol fulfills important functions within the body and that we could not do without it in the correct amounts. It is also important that the body should have enough nutritional balance in respect of other nutrients to enable it to handle the cholesterol correctly. That is a condition frequently not fulfilled in today’s society and this is largely connected with modern western diets and lifestyles. The effect of cholesterol in cell membranes is to decrease fluidity. Since saturated fatty acids also decrease fluidity, there need to be a balance here. To have simultaneously high levels of saturated fatty acids and high levels of cholesterol promotes decreased membrane fluidity and an unbalanced unhealthy condition. These two factors often do coincide in today’s conditions entailing high intakes of animal fats and/or hydrogenated vegetable fats. The condition is made worse by relative lack of many trace catalyst nutrients needed to properly handle cholesterol and fatty acids.

At one time, perhaps 50 years ago, the western diet provided quite inadequate supplies of unsaturated fatty acids of either the Omega 3 or Omega 6 types. Today a great deal of Omega 6 is provided by vegetable oils but there is a relative dearth of Omega 3 except among regular fish eaters. Also the quality of these often leaves much to be desired, since they suffer chemical damage so readily during processing and cooking. So far this discussion has not mentioned toxins. We see, though, that there is much that can go wrong with the body’s cell membranes without having to consider definable toxins because there is plenty that can go wrong with the food supply to disrupt them. In any case, when unsaturated fatty acids undergo chemical changes during processing or cooking the substances that are thereby generated from them can be fairly classed as toxins. It is a subject to which orthodox medical science has been amazingly inattentive. This author recalls reading a scientific report on the health effects of used fish-and-chip shop oil upon laboratory rats. The report recounted how these animals that were fed the used oil ceased to reproduce and developed afflictions of the liver. The conclusion that was drawn by the authors – that these oils were non-toxic, beggars belief.

The reaction products that are formed when fat is used for frying are, for example, epoxides, hydroperoxides and polymeric products derived from these. These same products may be formed from unsaturated fatty acids even when they are in situ as part of the phospholipid molecules within the cell membrane. This is caused, essentially, by free radical damage. Inevitably these adverse toxic products from fatty acids will have their effect upon the fluidity and even the stability of the membrane and upon the membrane’s functionality. Ultimately, we should remember, that the functions of the membrane have to do with permitting or not permitting certain molecules of ions to pass through and providing a working environment for many enzymes and cell surface receptors. These are the functions that appear vulnerable as soon as any significant amount of oxidation of unsaturated fatty acids occurs. Within the membrane these fatty acids are protected against this kind of attack by lipophilic antioxidants such as beta-carotene, possibly other related carotenoids, and Vitamin E (the tocopherols). In the face of free radical attack, what actually happens by way of damage depends to a large degree upon the concentration of these protective substances in the membrane. Once again we find out that cellular damage and its control are the consequence of whatever is the prevailing balance between to damage-inflicting toxins and the protective nutrients. The obvious strategy – that of minimizing the toxic input and maximizing the protective nutrients is one which few people follow. This is so notwithstanding overwhelming scientific and medical evidence about the necessity for doing so. The question is, will the medical orthodoxy ever seriously consider this evidence? Will governments even give a serious thought to this way of protecting the population from illness and reducing their hospital budgets?

Erasmus in his book ‘Fats that Heal – Fats that Kill’ on pages 120-125 of the 2nd edition emphasizes the way in which interactions between unsaturated fatty acids and free radicals can easily turn out to be chain reactions. One molecule of the highly reactive fatty acid, having been raised to an excited energy state by a free radical, may interact with another such fatty acid molecule. Erasmus estimates that this process can go on for up to 30,000 cycles before the free radical effect is quenched. Obviously, if this should happen in the membrane of a cell, then a considerable area of the cell membrane may be wiped out so far as its normal structure and function are concerned. It is clearly likely that the death of cell can be caused quite rapidly in this manner.

We have not yet considered one of the biggest sub-topics in this field. The manufacture of margarines – that is to say, solid spreading-fats – from plant oils requires a procedure for solidifying liquid fat. The one adopted generally is hydrogenation. This is the treatment of the plant oil with hydrogen gas in the presence of a (non-biological) catalyst – nickel. This process converts the unsaturated fatty acids in the oil into saturated ones. When the process is carried to completion the result is hard margarine containing virtually no unsaturated fatty acids. Obviously such a product suffers from the disadvantage that it contributes only saturated fatty acids to human nutrition, with all the disadvantages that that entails. In the realization that unsaturated fatty acids were important, margarines have become soft and now usually contain significant levels of Omega 6 fatty acids. These embody a number of serious disadvantages. Firstly, they quite clearly suffer from the high risk of producing a body imbalance between Omega 6 fatty acids and the Omega 3 fatty acids that are so often in short supply in the diet. Secondly, and perhaps even more seriously, when unsaturated fatty acids are put through the hydrogenation process and allowed to survive the process, many of them are converted into a highly unnatural and harmful chemical form. The natural essential fatty acids of the Omega 6 and Omega 3 series exist in the form of molecules with a particular conformation (or shape) termed the cis configuration. During hydrogenation many of them are converted into the unnatural trans configuration. The change has a profound effect upon molecular shape and hence upon their ability to fit into the packing at the cell membrane. They are also most certainly enzyme inhibitors – almost certainly of the competitive type. Although they are apparently able to exert only reversible inhibition upon enzymes, the reversibility hardly helps if the inhibitors are going to be present in the tissues continually, as they will be in people who eat soft margarine or consume ready-made food products containing hydrogenated oils.

The negative metabolic effects of trans fatty acids are summarized by Erasmus in his book ‘Fats that Heal – Fats that Kill’ on page 112 of the second edition. They include many aspects that have to be considered most seriously in relation to cancer, such as altering the activities of the different types of immune cells and reducing the capacity of the liver to detoxify toxins, including carcinogens. It is easy to conclude that no one who intends to be cancer-conscious should even consider using hydrogenated fats or oils. It would seem likely that if these trans fatty acids were not so closely related to food fats, they would attract an official ban in food as toxic substances.

In all discussion of damage to membranes one should keep in mind that it is not just the outer cell membrane that is at risk, important though this is. All of the internal membranes that bound the organelles inside the cell are similarly vulnerable. One such organelle type, which seems to be very important in receiving damage and then damaging the cell is the lysosome. These little vesicles are full of enzymes for the breakdown of cell constituents. They are, of course, essential to the life of the cell, since all types of cell constituents ‘turn over’, that is, they are broken down and re-synthesized. However, if these breakdown enzymes are released from the little sacs that normally contain them they will begin to break down the normal structural parts of the living cell and render it moribund or non-viable. Hence, toxins that damage lysosomal membranes may be particularly potent. Two human diseases clearly involve damage to lysozomes and the release of their contents, these being gout and silicosis. Experimentally, gross excess of Vitamin A and injected papain (a protein-digesting enzyme from papaya) have been found to do the same thing and release of contents from macrophage lysosomes is postulated as a disease mechanism in rheumatoid arthritis.

Individual toxins that appear to target lysosomes are beryllium, phosphorus, carbon tetrachloride, ethionine, the pyrrolizidine alkaloids, such as occur in plants of the family Boraginaceae, e.g. borage itself and comfrey, and the toxin of the highly poisonous toadstool, Amanita phalloides.

Mechanisms of toxic membrane damage, other than those described above, are often unclear. It seems obvious, though, that the membrane damage may be either primary or secondary. Primary membrane damage occurs when the membrane itself is attacked directly by the toxin. Secondary membrane damage occurs when some other primary toxic effect sets in motion a chain of events which ends up by compromising membrane structure. An example of this is the loss of phospholipids from the membrane that often precedes overt membrane damage. This may be caused by the release of internal phospholipase enzymes (enzymes that break down phospholipids). There may be different ways in which this release of enzymes may be brought about, but increase in intracellular calcium level is one serious candidate. A good many different toxic actions can bring about and increase in the normally extremely low calcium concentration in the internal cell solution (cytosol).

Finally, before leaving this important topic, one should note again that the functioning of the enzymes and receptors embedded in the membrane depend upon and are influenced by the integrity of the cell membrane itself. The state of fluidity and the stability of the bilayer affect their biological activities. For example, it is known that the activity of the sodium pump enzyme is affected by the supply of phosphatidyl choline to act as a component of the phospholipids in the bilayer. This should be born in mind. Relative lack of phospholipids or the ability to make them, imbalances of Omega 6 and Omega 3 fatty acids, excess of dietary cholesterol and saturated fatty acids all affect these functions. These are often just dietary influences, though very important. But toxic effects can also upset these nutritional balances and, indeed, exert their toxic influence in this manner. These toxins often exacerbate the effects of an already existing nutritional imbalance. Note again that toxins and nutrients are interacting. It would appear that the toxic effects of trans fatty acids must be high on this list in the context of current western lifestyles.

Mechanisms of Protein Synthesis and their Vulnerability to Toxins

It is clear that some types of toxin target the protein synthesis mechanism of the cell. This must result in the inability to replace or increase cellular structural protein or to replace enzyme proteins that have been inactivated.

Protein synthesis is a complex biochemical process in which molecules of the twenty or so different kinds of amino acid must come together in the correct numbers and sequence to form a new protein chain. The DNA of the nucleus contains the necessary encoded information to specify the protein sequence. This has to be ‘read off’ as a copy in the form of a special kind of RNA called ‘messenger RNA’. This migrates from the nucleus into the cytoplasm of the cell, carrying the encoded data to the very small RNA-rich intracellular bodies called the ribosomes, where the protein molecules are assembled. The individual amino acids that are to be used in this assembly become attached to a different form of RNA, transfer RNA, and are thus carried to the ribosomes for assembly. The finished protein chain is “peeled off” from the ribosome and carried via the endoplasmic reticulum to the part of the cell for which it is destined. This information – about the destination of the different protein molecules is also encoded, this time in short sequences of sugar units temporarily attached to the protein for the purpose. Being complex probably makes the whole protein synthesizing mechanism particularly prone to toxic damage. This type of damage can clearly occur in any cell, and each cell must make protein. However, liver cell, because they are called upon to make so much protein, are especially vulnerable.

Liver cells suffer this form of toxicity from several toxins acting in different ways on different parts of the system. Ethionine is an ‘antimetabolite’ of the amino acid methionine, which it resembles in structure. In this role it traps much of the cell’s reserves of adenine – the nitrogen base needed to make ATP. Hence ATP formation suffers. But adenine is also needed to make RNA and the cellular deficiency of RNA would obviously inhibit the synthesis of protein either with or without the concomitant ATP deficiency. Dimethylnitrosamine is thought to inhibit synthesis of proteins by causing a loss of messenger RNA. Carbon tetrachloride is thought to damage the ribosomes, which are the very site of protein assembly. Galactosamine works by yet another mechanism, since it sequesters uridine, another nitrogen base. Uridine is much involved in the synthesis of many biomolecules, especially those involving complex carbohydrate structures. The result of this upon protein synthesis is indirect but nonetheless effective. This sequestering probably damages cell organelles, but one can also speculate that the ‘labeling’ of newly formed proteins for their target destinations within the cell, via bound sugar units, may be disturbed.

Damage to Mitochondria and the Endoplasmic Reticulum

Some toxins are more specifically damaging to mitochondria and therefore inhibit cell energy production. The toxins that either inhibit or destroy enzymes have already been discussed, but some toxins may actually damage the structure of the mitochondrion organelle via its membranes or the organization of its enzyme assemblies. Acetaminophen, 1,1-dichloroethane and hydrazine belong in this group. Others attack the structure and function of the endoplasmic reticulum and therefore exert secondary effects upon protein synthesis that enhance the effects described in the last passage above. These include allyl formate, galactosamine and thioacetamide. Other toxins attack the cytoskeleton – the internal fibrous element of cell architecture – and these include toxins called norethandrolone and cytochalasin B.

Relationship of General Cellular Damage to Cancer

Toxins of the various classes described above, attacking the structure and function of non-nuclear components of the cell cannot in themselves represent primary and direct causes of cancer. As will be clearly understood from future chapters, the cancerous change is necessarily a nuclear event, involving changes to the chromosomes and the DNA they contain. The passage below, which concerns the effects of toxins upon the nucleus, is therefore much nearer to the core of our subject. The orthodox ‘wisdom’ of our day tends, therefore, to accord little importance to non-nuclear events so far as carcinogenesis is concerned. The ‘theory of general chronicity’ differs from this and it does accord considerable importance to non-nuclear toxic events.

The basis of this aspect of the theory is that the more generally toxic the cell is, or the more toxic damage it may have suffered, the more likely the cell is to succumb to the actions of a carcinogen.

This is held to be true regardless of whether the toxins concerned are nuclear or non-nuclear in their effects. Toxic damage or toxic inhibition exerted by upon the plasma membrane or upon enzymes or organelles in the cytoplasm is held to have repercussions upon the nucleus and its ability to afford protection to the DNA contained in it, and therefore upon the likelihood of carcinogenesis occurring. It is upon this understanding that we now turn to look at the nuclear DNA.

The Nucleus, DNA and their Vulnerability to Toxins

The reader is familiar already with the nucleus as an intracellular body bounded by a double membrane. Obviously, that membrane is susceptible to alterations in its properties by toxins, and to toxic damage, just as the other membranes are. Some types of toxin are reported as affecting the nucleus of cells in particular, without necessarily having the capacity to do direct damage to the DNA within the nucleus. Here, we have to focus most especially upon the DNA and damage that can be done to it because this is where carcinogens exert their key effects. The situation also obliges us to focus upon the ability of mechanisms within the nucleus to protect the DNA and the encoded information contained within it.

Obviously, substances, such as the anti-cancer drugs mentioned and discussed in Chapter 5, act mainly to prevent or arrest cell division, or to exploit the vulnerability of cells caught in the process of dividing to kill them. Since the processes of cell division centre upon the nucleus and the DNA, the anti-cancer drugs generally work upon the nucleus, the chromatin that forms the chromosomes, and the biochemicals that go into making DNA. This deliberate nucleus-orientated form of cell damage does not appear, in itself, to be strongly carcinogenic. The anti-cancer drugs are not, on the whole, noted carcinogens and it would be ironic if they were. Their purpose is to kill cancer cells, perhaps to arrest their multiplication, but most particularly to kill them. A cell that has its DNA lethally damaged is obviously not going to be a cancer cell, since to give rise to a tumour a cell must be viable. Therefore, effective cell-killing agents are not usually carcinogens. Clearly then, nuclear and DNA damage can take more than one form. The question as to what form of DNA damage is involved in actual carcinogenesis will be discussed in a later chapter.

Here, in order to put flesh onto the bones of the ‘theory of general chronicity’ we have firstly to understand that carcinogenesis consists essentially of a form of DNA damage. Then we should consider the cell’s ability to prevent such damage, and the possibility of that protective ability being eroded through toxic events that may occur outside of the nucleus.

All this cannot be very well appreciated without first understanding the nature of DNA itself and the nature of the damage that can happen to it. Earlier, some explanation was given of the structure of proteins and the fact that the primary structure of proteins is based upon chains of amino acids linked into specific sequences. Most biological macromolecules are built up from large numbers of very much smaller ‘building blocks’ in this manner and the nucleic acids are no exception. In the case of RNA these building blocks are called ‘ribonucleotides’ and in the case of DNA ‘deoxyribonucleotides’. Focusing upon the DNA, each of the deoxyribonucleotides is itself made up of three units, namely, phosphate, the sugar deoxyribose and a nitrogen base. The first two are the same for all the deoxyribonucleotides and the phosphate and deoxyribose moieties link together in sequence to form the backbone, or core, of the chain. The nitrogen bases are, therefore, attached to this core and they project from it. There are, for the most part, just four types of nitrogen base in DNA, named adenine, guanine, thymine and cytosine. Since the role of the DNA is to store information and permit its retrieval, it follows that this information cannot be stored in the ‘core’ part of the chain, since that is of the same composition throughout its entire length. It follows that the information stored in DNA is stored in the sequencing of the four nitrogen bases. An illustration of the overall structure of a section of DNA is shown in Figure 1

Note that its molecular configuration naturally throws the whole molecule into a coil. This can be compared with the alpha helix of proteins, but in DNA the whole of the chain is coiled, not just parts of it. Since the DNA is very acid, its electrical charges need balancing, so the nucleus contains a lot of very basic (‘alkaline’) special proteins called ‘histones’.

The information stored within the sequence of bases in DNA is in the form of a code. The information is ‘read’ or interpreted through translation first into an RNA chain (messenger RNA) and then translated again into a sequence of amino acids in protein, during the process of protein synthesis on the ribosomes. It is interesting to note that there are only four different kinds of nitrogen bases in DNA but at least 20 different amino acids in proteins. It is obvious, then, that a single nitrogen base cannot possibly encode for a single amino acid. It must take more than one nitrogen base to define an amino acid in protein. Indeed, it must also take more than two bases to do this, since combinations of only two bases could only provide, at most, 16 unique structures from which to identify an amino acid. Indeed, the coding units, or ‘codons’, that specify the amino acids in proteins consist of three bases, as illustrated in Figures X and Y. Note that Figure X gives the form of the code as it appears in DNA and also in RNA (which has a complementary code) and that Figure Y just quotes the form of the code that appears in messenger RNA.

It follows, then that the stability of the sequencing of the bases in DNA is crucial to the stability of the genetic information. Any factors that alter that sequence or render it unrecognizable will eliminate or change some aspect of the cell’s genetic make-up. That will destroy the ability of that cell to give rise in future to daughter cells with the characteristic genetic make-up for the person concerned. Thereafter, that changed cell and its entire offspring will be different from other cells in the body. Assuming that the cell is still capable of surviving and reproducing, it will give rise to a new and different type of cell in the body. All the cell’s offspring will be the same, unless, as in the case of cancer, the change that has occurred has also rendered the cell’s genetic make-up subject to further instability in the future. Assuming further instability does not occur, the offspring of the altered cell will constitute a new ‘clone’ of cells within the body. A clone is a population of cells all with the same genetic origin and structure.

Therefore, armed with this knowledge, one needs to be on the look-out for toxic effects in the cell that damage DNA in such a manner that the base sequence is altered. That alteration could take the form of deletion of a section or sections, even just of one codon. It could take the form of alteration to bases to give modified and therefore ‘unreadable’ code instructions. It could take the form of the substitution of sections with new and different sections containing different information. Or it could take the form of chromosome breakage. This may not alter the amount and nature of information present in the code, but it may alter its expression. This is because the expression of encoded information is dependent upon the immediate genetic environment (i.e. what other sequences are in close proximity). Since chromosome breakage changes the environment of those parts of the sequence that are near the break, genetic changes do occur.

It is necessary then, to look at the types of toxic damage that can be suffered by the nitrogen bases of DNA. The attempt is being made here to communicate to the reader some idea of the nature of such damage without writing out chemical formulae or calling upon chemical knowledge that the reader does not have. This is not so easy when one is speaking about the structure of DNA, an immensely long biomolecule containing building blocks that comprise nitrogen rings. The damage itself that we want to consider is inherently chemical in nature. To follow some part of the story it is first necessary to understand that the structure of DNA comprises, not one chain (or ‘strand’), but two. The helical coiled structure has been described and is illustrated in Figure ### but it can be seen that there are two strands coiled together. This is referred to as the ‘double helix’ of DNA. Within that double helix there are some weak chemical linkages between the nitrogen bases that are arranged along the lengths of the paired strands. In other words, the bases themselves are paired. These two strands of DNA replicate themselves during cell division. During the special kind of cell division that is necessary for the formation of sperm and ovum, the two strands separate, and the sperm and ovum only carry single-stranded DNA. These recombine to form double-stranded DNA again at fertilization.

The reason why this is important is that anything that inhibits base pairing disturbs the regular helical structure of DNA. That is true whatever the reason for the base pair inhibition. It may arise because one of the bases has been subjected to an alteration of chemical structure, or a substance has been inserted in an interfering way between the strands.

Not all alterations to DNA are necessarily the result of toxic action. There is a certain very low frequency of mismatching of bases that occurs spontaneously. This may occur because the base molecules have a low inherent tendency to alter their conformation spontaneously. The bases altered in this way tend to pair with the wrong base partner, causing a mismatch. What results is the misplacing of a normal base rather than the production of any abnormal base. Nonetheless, the cell needs to be able to correct the fault if it is to avoid producing a mutated cell line. The risk of this type of spontaneous mispairing, is essentially irreducible under any given set of conditions, though it does depend upon the pH, temperature and composition of the medium inside the nucleus. The evolution of new species of organisms would never occur if there were no mutations at all, at least in the germ cells.

Apart from this, mutations can be caused by chemicals, referred to as mutagens, by ionizing radiation or, at the surface of the body, by ultraviolet light. Again, looking at it from the evolutionary standpoint, these factors have always been present in the environment and can be presumed to have always played their role in evolutionary change. Ultraviolet light is present in sunlight, ionizing radiation is experienced everywhere on earth from cosmic rays and radioactivity in the rocks. Mutagenic substances have always been present in food. What we have to be concerned about is any major increase in the levels of these environmental factors through radioactive pollution or through toxins in our food, water and general environment.

The considerable length given in the previous Chapter to anti-cancer drugs shows just what a wide range of chemicals can work to block cell division. Yet there is only the thinnest of dividing lines between those that stop cell division and those that disrupt cell division significantly enough to give rise to changed or abnormal daughter cells. In some cases it may only be a question of dose and length of exposure. This is not true of a substance like colchicine, which disrupts the action of the ‘spindle’ – a part of the nucleus that is not DNA. Nor is it true of substances, which just inhibit DNA synthesis, like azaserine and the antagonists of the vitamin, folic acid. But where the blockage of cell division is through an action that alters DNA the outcome for any particular cell may be either death or transformation.

Commonly recognized mutagens include dyes of the acridine group, alkylating agents, some antibiotics, urethane, hydroxylamine and nitrous acid.

However, some mutagens are actually analogues of the common nitrogen bases of DNA, adenine, guanine, thymine and cytosine. One needs to recall that an ‘analogue’ substance is one having a chemical structure that is close to one of these normal bases. Indeed, its structure may be close enough for it to become incorporated into DNA but, having been incorporated, to cause trouble, through not functioning in a perfectly normal manner. Hence, at best, some of these analogues may inhibit DNA synthesis and therefore act as anti-cancer agents. But their incorporation into either DNA or RNA, leads to abnormality of these nucleic acids and the protein-synthesizing code, and perhaps the genetic code, are altered. If their incorporation is into RNA, not DNA, then this has the effect of altering part of the message that is transcribed from DNA to RNA without altering DNA itself. Protein synthesis will still be adversely affected. These ‘analogues’, then are altered versions of the bases themselves that may be incorporated in place of the normal base, changing the pattern of base pairing. One such compound is bromodeoxyuridine, which also renders the DNA chain very liable to breakage. Another base analogue, 2-aminopurine, may also be incorporated and cause mismatching.

Alkylating agents as mutagens were discussed in the last Chapter, where several were listed anti-cancer drugs. They notably include the sulphur mustards and nitrogen mustards. They get their name because they add ‘alkyl’ groups to the base molecules that are present in the DNA. Notably they add methyl and ethyl groups. Several of the altered bases that are formed from the reaction between DNA and these reagents cause mispairing and therefore also cause miscoding in the DNA. Most particularly, the guanine base becomes modified, adding a methyl group onto an oxygen atom of the guanine, forming O6 methylguanine. In some cases, therefore, we do have overlap between the growth arresting or lethal actions of these agents and carcinogenic effects on the other. To some extent, therefore, we do have the enigma of a carcinogen being used for cancer therapy.

Ionizing radiation is noted for causing single strand breaks in DNA. Ultraviolet light causes cross linkages between the strands of the DNA double helix, especially cross linkages between thymine bases. These are referred to as cyclobutane: thymine dimers. Such a cross-linking blocks the action of the enzymes that must bring about the replication of DNA at cell division. It also physically bonds the two strands together and prevents them from separating at cell division as they do in their normal function. Another important action of ionizing radiation, especially gamma rays, is to open the nitrogen ring structure of the bases adenine or guanine. This produces an open ring compound called a ‘formamidopyrimidine’.

Given such a wide range of different types of damage and quite a few possible causes, there is no doubt that great importance attaches to the cell’s ability to repair the damage suffered. When damage has occurred, it must be repaired before the next cell division or else the abnormality will be passed on the future generations of cell, producing a new line of abnormal cells.

DNA Repair Mechanisms

The DNA repair mechanisms of the cell will not be described in great detail, even though they are among the most awe-inspiring of cellular mechanisms for their intricacy and beauty. We can recognize, however, different classes of these mechanisms and see, in principle, how they perform.

In bacteria the cyclobutane: thymine dimers that result from UV exposure and cross-link the DNA, can be reversed by the action of visible light working with a special photo-activating enzyme. However, in the human body only the extreme surface can be affected either by UV or by visible light, so this mechanism is of limited significance.

Where alkylating agents have added a methyl group to a guanine base, an enzyme called DNA methyltransferase acts to remove the unwanted and damaging methyl groups.

Where gamma ray damage has left a ‘formamidopyrimidine’, an enzyme called ‘formamidopyrimidine cyclase’ can regenerate the original base in the DNA, i.e. an enzyme that reforms the ring that was broken. Some of the simpler DNA strand breaks may be reversed by what is effectively a ‘rejoining enzyme’, called DNA ligase. Other, more difficult types of strand breaks, that often occur when gamma rays are responsible for the damage, have to be repaired by ‘excision repair mechanisms’ described below.

The ‘excision repair mechanisms’ can be used by the cell to repair DNA damage that is not easily repaired by simple mechanisms. Basically, excision repair consists of cutting out the ‘bad’ or jumbled section of the DNA strand and replacing it with a renewed section of DNA that is identical with the original undamaged version and which therefore carries the same coded messages. In this process an enzyme called an endonuclease first nicks the strand a few nucleotides away from the damage. A second enzyme then excises a short stretch of DNA including the damaged region. Thirdly the enzyme DNA polymerase synthesizes a replacement strand. It does this by using the intact and complementary second strand of the original DNA as a template. That is to say, the original (and correct) genetic message for the section concerned is still available on that second strand and the data from it are used to reconstruct the original strand correctly. Finally, in a fourth step, the repair is completed by DNA ligase joining up the new section to the original strand. This is surely an incredibly beautiful biochemical mechanism that is intricate but marvelously adapted from the evolutionary standpoint to preserve the organism and the genes it contains.

Another mechanism of repair involves a set of enzymes called ‘glycosylases’. These enzymes, as a broad group, are capable of splitting a particular type of substance from its chemical binding with a sugar. Where damage to the DNA involves chemical alteration to an individual base, so that it no longer corresponds to any of the four bases that have a proper place in DNA, then one of the glycolysases can remove that aberrant base. Specific glycosylases have been identified for removal of the following altered bases that have no proper place in DNA strands.

Uracil
Hypoxanthine
3-Methylguanine
3-Methyladenine
7-Methylguanine
5:6 hydrated pyrimidine
Urea or pyridine dimers
Formamidopyrimidine

Naturally, when these abnormal bases are cleaved off, this leaves a gap, a section of the sugar-phosphate ‘core’ of the DNA, without an accompanying base. However, an apparently enzymic activity has been found which places such bases as either adenine or guanine into such gaps. It seems clear that this activity does not work randomly, but instead, works sensitively to re-form the original base pairs and hence maintain the genetic information.

There are other types of error within DNA that are brought about by simple mismatching of bases. That is to say that the bases concerned are not in any way abnormal bases, but they are wrongly matched. Hence repair mechanisms, to deal with that situation, have to have the ability to recognize the wrong identity of bases rather than abnormal types of base. These modes of enzymic repair also exist. They are extremely finely designed because they have to have the ability to detect which base within a pair is the one carrying the incorrect information. If these repair enzymes were to wrongly identify this, they would, of course, compound the problem and compound the genetic damage instead of helping. Instead, they seem to have the ability to identify the recently wrongly incorporated base of the pair, leave intact the one which has the correct identity and replace the aberrant base of the two.

3 The Nature of Toxic Damage – Specific Cell Toxicity

All the forms of toxic damage that have been discussed above are non-specific as to cell type. That is to say, a toxin that affects mitochondria is likely to affect them regardless of the type of cell concerned and one that affects an enzyme will probably do so within any tissue. However, we also note here that many types of toxin are highly specific as to the cell types they affect and the biochemical processes they affect.

For example, a great many plant poisons, drugs and war gases work by altering, and in some cases disabling the nervous system. These quite often work at synapses, which are the communication junctions between one nerve cell and another. The synapses are characterized by the fact that communication across them is not electrical, as it is when the nerve impulse is conveyed along a nerve fiber, but is chemical. It depends upon the release of a special chemical from the end of one nerve cell, which diffuses across the junction to elicit the start of a new impulse in the other fiber. The chemicals, which are different in different types of nerve junction, are called ‘neurotransmitters’. They are to a greater or lesser degree specific to the nervous system, at least in this type of role. The toxins concerned are either ‘antagonists’ to neurotransmitters, in which case they block the normal action of the synapse to various degrees, or ‘agonists’ of the neurotransmitters, in which case they increase and over-emphasize the normal action of the synapse. Many mood-affecting drugs, such as diazapam and the tricyclic anti-depressants, and the pre-operative medication atropine, work in this manner.

Such actions have little direct effect upon general body toxicity levels and therefore do not have a very large effect upon ‘general chronicity’ unless, through their action upon the nervous system other systems of the body are caused to function less efficiently.

There are many examples of forms of toxicity that are more or less specific to particular organs. For example, certain toxins are very specific to individual endocrine glands, such as alloxan and the antibiotic streptozotocin, which are toxic to the beta cells of the Islets of Langerhans in the pancreas and cause a chemically induced diabetes. Another example is thiourea, as specific toxin to the thyroid gland, and this is employed as an anti-thyroid drug. Such actions may have little direct effect upon general body toxicity levels unless the substance concerned also exerts some less severe degree of toxicity to non-endocrine cells. Where this does not happen, these substances may not have a very large effect upon ‘general chronicity’ unless, through their action upon the endocrine system and consequential hormonal repercussions, other systems of the body are caused to function less efficiently.

Bone marrow and liver are very metabolically active and are especially vulnerable to toxins. Effects on the normally rapid cell replication in bone marrow may lead to ‘aplastic anaemia’ in the case of toxicity from anti-cancer drugs or from the anti-bacterial drugs chloramphenicol and the sulphonamides. The liver suffers badly from carbon tetrachloride, chloroform or paracetamol poisoning. These substances are unquestionably toxic to all tissues, so what we are speaking of here is simply a greater susceptibility in the tissues of bone marrow and liver.

The drug phlorrhizin specifically targets the renal tubules, affecting the re-absorption of glucose. The drug thalidomide was specifically toxic to the foetus (which is not an uncommon form of specific toxicity, due to the sensitivity of the foetus) and methanol clearly targets the eyesight. The subject of specific toxicity is mentioned here mainly to recognize its existence, which is often important, though its significance to ‘general chronicity’ is limited to any residual ‘non-specific’ toxic action the substances may have, or to the possible wider consequences of their local inhibitory action.

4 Cell Damage and the ‘General Chronicity’ Theory

If ‘General Chronicity’ is ‘the sum total of the body’s present and historical toxic burden and the residual cellular and tissue damage it has caused’, then it is perhaps not difficult to see how the state of ‘General Chronicity’ promotes a wide range of non-malignant chronic diseases. The presence of toxins and toxic damage to membranes and organelles outside of the nucleus will tend towards cell debility, morbidity and eventually cell death. The tissues and body parts affected by these processes will firstly underfunction and then degenerate. Whole functional groups of cells may be deleted, with serious symptoms and syndromes resulting. All this seems biochemically obvious. It is a puzzle just why orthodox medical people are often so strongly opposed to such ideas about toxins and their effects, when they themselves can cite no other ‘ultimate cause’ of chronic illnesses. Because orthodox medicine has virtually no contribution to make as to the ultimate causes of internally generated, primarily non-genetic, chronic illnesses, there is a virtual absence of any serious argument against the long held naturopathic view that toxins and toxic damage are responsible. Even where genetic pre-dispositions are known to exist towards contracting given chronic illnesses, toxins and toxic damage have still to be invoked as the triggers which turn those pre-dispositions into reality.

However, cancer is special because its initiation requires that cells must be damaged within the nucleus. Orthodox ‘wisdom’ has it that only certain quite specialized toxins can actually trigger cancer – toxins that generate nuclear damage – and ‘carcinogens’ in particular. Yet it seems clear that only a low proportion of human cancers can be fairly attributed to known exposure to those particular and specific substances known at the present time as carcinogens.

So, against the orthodox view, the ‘Theory of General Chronicity’ as it applies to cancer rather than other diseases, postulates that general toxicity throughout the cell leads towards at least a semi-moribund condition of the cell and that semi-moribund cells cannot repair their DNA properly. The ability to maintain an active DNA repair mechanism must depend upon an active enzyme-synthesizing capability and that is synonymous with protein-synthesizing ability. Cell energy must be available in sufficient amounts. It also seems likely that correct sodium / potassium ratio within the cell may also be needed along with intact membranous structures and adequate levels of micronutrients catalysts, such as zinc. These conditions are unlikely to be met in semi-moribund cells affected by ‘general chronicity’. The theory tends to predict, therefore that non-nuclear cell toxicity and cell damage can lead onward quite readily to nuclear damage and carcinogenic transformation and then that, once cancer is established, the generally chronic condition will inevitably prevent the body from throwing off the threat presented by the malignant cells.

http://www.plaskett-international.co.uk/