Cancer diet and high calcium levels?

Ian Billinghurst, de schrijver van Give Your Dog A Bone, 1993, was onze gast in september 2007.

Cancer diet and high calcium levels?

Ongelezen berichtdoor Fadadomar » 21 sep 2007 09:00

Dear Dr. Billinghurst,
Thank you so much for being on this forum and for your book GYDAB, which I acquired 7.5 years ago, which helped me start my then 1 year old Boxer Cody on a natural diet. He used to be ill quite often (I fed him premium kibble). He hasn't been sick since I started him on a grain-free, raw meat and bones diet, until 3 weeks ago. He started drinking and consequently peeing a lot and didn't want to play anymore. I took him to an emergency vet, who suspected cancer. She ran some tests and it turned out to be lymphoma. Many types of cancer can be cured nowadays with chemotherapy, but in Cody's case it can't be cured. The cancercells appear to be of the T-type.
He is now on Prednisone and doing fairly well. He does, however, have a craving for all types of food, including grains, cat-droppings, canned food, etc. He regularly refuses to eat raw meaty bones!

I wonder if you would have an idea how to best feed a dog that is apparently craving for all sorts of junk food. I don't think I should fast him, and I think: what the heck? He is dying; give him anything he likes...
He used to get 1 meal a day and 1 fast-day a week. Now I find myself often feeding him small or larger amounts of various types of food (about 5 times a day).

Another question I have for you, if I may, is if you know how to lower the calcium levels in his blood? I suppose feeding him a diet low in calcium will not help in this case?

Thank you very much in advance.
Veel liefs,

Lia, Rui en de katten
Scheveningen

Cody 25-11-1998 - 4-12-2007, voor altijd in mijn hart
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Fadadomar
 
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Ongelezen berichtdoor Dr. Ian Billinghurst » 22 sep 2007 20:10

I have attached a copy of a paper I presented to the Australian Veterinary Association’s annual conference last year.

I am hoping it may help you with some ideas for feeding and supplementing your dog. After having read it, if you have further questions, please get back to me.

Sincerely

Ian B

=========================

THE CRITICAL AND FUNDAMENTAL ROLE OF NUTRITION IN TREATING NEOPLASTIC DISEASE

Ian Billinghurst
Warrigal Publishing/BARF Australia/Durham St Veterinary Clinic
PO Box 9064 Bathurst NSW 2795

“A cell’s “decision” to divide or not is of crucial importance to the organism. When the regulatory mechanisms that limit cell division are defective and cells undergo unregulated division, the result is catastrophic – CANCER.” (Lehninger – Principles of Biochemistry)

Introduction

In the 1970s, Richard Nixon declared war on cancer.6 Today, more is known about neoplastic disease than any other; the mapping of the human genome has produced an explosion of cancer related knowledge. A pivotal piece of knowledge is that most carcinogens are mutagens, with somatic mutations triggering cancer in the individual, and germinal mutations causing hereditary cancer. While less is known about companion animal neoplasia, research shows that the neoplastic process is essentially the same in all species.3

Neoplasia is…?

A Neoplasm is abnormal tissue growing out of control, lacking to varying degrees, structural organisation, functional coordination and expected biochemistry.

Malignant neoplasms (cancers) have the ability to invade and metastasise.

Cancer, a genetic disease, begins with one cell, mutating, in a growth-controlling gene. Most cells, so primed are destroyed by the immune system or they self-destruct. Neoplasia requires further mutations in growth controlling genes, permitting the cell to divide uncontrollably despite contrary signals from the rest of the body. The new tissue no longer grows or functions in response to bodily needs, it is committed only to its own survival. 5

Primary tumours with sufficient mutations, are able to invade and metastasise. The tumour is now malignant. As secondary tumours, malignancies develop a parasitic relationship with their host. In the process they drastically alter host physiology, producing bodily wasting, declining health and energy and in too many cases, death of the host.

To intelligently prevent neoplasia, requires an understanding of basic causes. To successfully treat neoplasia requires an understanding of neoplastic biology and inherent weaknesses. Being understood as a genetic disease has enabled conventional medicine to treat more effectively with chemotherapy and radiotherapy.

To date, similar opportunities to use targeted nutrition therapeutically and prophylactically have been largely ignored by both medical practitioners and veterinarians.

However, there are effective nutritional strategies to supplement and/or replace the “cut” “poison” and “burn” approach to cancer therapy. These can be used as weapons with considerable power, little harm and rigorous scientific validation. This paper outlines the biology of cancer, both as a genetic and epigenetic disease. Its epigenetic features are vital in relation to particular foods, nutrients, herbs etc., which are able to target specific aspects of cancer biology, reducing or sometimes eliminating the tumour and/or its impact on the host.

Carcinogens - Sources

Environmental mutagens/carcinogens include radiation (including radiation therapy) and numerous ‘foreign’ chemicals (including chemotherapy) polluting food and the environment generally. However, the most serious cause of mutations is damage by free radicals, commonly produced during aerobic metabolism. Mostly this is not a problem, unless the DNA that is damaged, codes for DNA repair proteins. Both DNA and RNA viruses also cause cancer. Finally, growth-controlling genes may undergo spontaneous mutation. 1

In all of this, diet plays a critical role, particularly with respect to maintaining a strong immune system and the presence or absence of anti-oxidants and other ‘protective’ nutrients in the diet.

There are also carcinogens that are not mutagens, including inflammatory processes and anything, which will compel a cell to divide with greater frequency, including constant irritation/cellular damage. These factors are critical, particularly during promotion and progression. 5

Carcinogens work with and are critical components of poor nutrition.

The ideal nutritional program for any species is the food that species evolved to require. Modern humans and their companion animals have strayed far from that ideal. 9

Modern western (human) diets provide sub-optimal levels of anti-carcinogens and protective factors. Food-refining eliminates/reduces many anti-carcinogenic nutrients and concentrates cancer promoters. Statistics and epidemiological evidence support this. 4

Modern processed pet foods are similarly carcinogenic, with their total lack of fresh foods, poor quality proteins, minimal levels of essential nutrients, almost total lack of protective factors, together with excessive levels of soluble carbohydrates and Omega 6 EFAs and low levels of Omega 3’s. These foods surely play a critically significant role in companion animal carcinogenisis, on many fronts. 7

Initiation

The initiating step in neoplasia involves damage to a critical growth-controlling gene, usually an oncogene. This initial damage primes the cell, for further mutations that may eventually produce neoplasia. If the cell resists further critical mutations or it is destroyed/inactivated by the immune system or self-destructs; there is no cancer.


Promotion…

Involves on-going exposure to carcinogenic agents, which cause further mutations (up to six or seven), taking the cell into uncontrolled cell division; the formation of a primary tumour.

The mutations/factors that take a tumour to the metastatic phase usually include the following…

1) Formation of oncogenes
2) Resurrection of telomerase
3) Faulty DNA repair genes.
4) Increased rates of cell division.
5) Faults in/loss of tumour suppressor genes
6) Lost or declining apoptotic ability
7) Acquisition of angiogenic ability5

A primary tumour will often be amenable to surgical excision. However, it is now ready to evolve further.

Progression

This is the invasion/metastatic phase. It involves overcoming many obstacles. Each obstacle requires a further mutation.

First, the production of proteases allows invasion of adjacent tissues. Tumour cells then loosen their connections with the tumour mass and invade the blood/lymph. Here they must overcome barriers presented by the immune system. Having evaded the immune system, they next develop receptors and revamp their adhesive abilities and attach to the new tissue to be parasitised. Once established in their new home (bone, lung, liver or brain etc), they develop a blood supply (angiogenesis) and recommence growth. At this point, they are de-differentiated and largely anaerobic. 4, 5

Progression occurs because successive mutations occur with continual bombardment by mutagens/carcinogens and each mutation promotes genetic instability, making successive mutations more likely; an accelerating process. As the tumour ‘pumps’ out a continual stream of mutated cells, by chance, neoplastic cells with the appropriate mutations (as above), to allow invasion and metastasis, are eventually produced. 5

With 80% of all human cancer deaths (and almost certainly the same for companion animals) being metastasis related, metastasis is a vital aspect of carcinogenesis. 4, 5

“Any approach or strategy that limits or interferes with metastasis should result in some clinical benefit.” (Henry Osiecki.)

Factors, which promote or favour metastasis include: inflammation; platelet aggregation; infection; reduced number of immune cells or immunosuppression; impaired oxygenation of tissues and/or the tumour; any generalised nutrient deficiency, specifically a zinc deficiency; copper excess; stress; anything which promotes coagulation; trauma; surgery; irradiation; chemotherapeutic drugs; pain; toxins; endothelial cell injury; hormones such as oestrogen, progestins, androgens, insulin-like growth factor; NF-Kappa B and activated matrix metalloproteins (proteases). Most of these are amenable to nutritional control (see below) and/or standard veterinary drugs. 4

Cell Cycle Control and Carcinogenesis 1, 4, 5

The Cell Cycle clock (CCC) is the cell’s decision-maker. Based on information received from the rest of the body and its own state of health, the CCC will issue appropriate instructions to the cell: divide, commit suicide, rest or differentiate.

The Cell Cycle itself

The G1 phase (RNA and protein synthesis. Restriction point towards end of G1

S phase (or DNA synthesis phase). Most cancer related defects occur here; ERORS made in copying DNA.

G2 phase. Preparation for cell division, Correction of Errors phase. Last chance for damaged DNA to repair or cell to commit suicide.

M phase or Mitosis.

The CCC is run by…

Cyclins and cyclin-dependent kinases (CDKs), respond to cellular signals and control cell division by attaching phosphate groups to target proteins, switching them either on or off. Each kinase controls a wide range of processes, associated with and controlling DNA transcription and cell division. The kinases depend on the cyclins (which appear and disappear during the various phases of the cell cycle), to direct them to the appropriate proteins.

The cyclins and the CDKs are controlled by proto-oncogenes and tumour suppressor genes, which respond to a range of growth promoting and inhibitory factors, including nutritional factors. Mutations to proto-oncogenes and tumour suppressor genes, cause loss of control of the cell cycle, that allows cancer initiation and promotion.

Mistakes made copying DNA causes cell death by apoptosis. If the mistake survives, we may see cancer. Anything, which speeds up the cell cycle, increases the risk/incidence of cancer, by allowing transcription errors to be preserved. 5

Oncogenes are mutant forms of genes for proteins that regulate (accelerate) the cell cycle. The proteins include growth factors, transmembrane receptors, G proteins, protein kinases and nuclear transcription factors (e.g. Jun, Fos). 1

Tumour suppressor (TS) genes encode proteins that restrain cell division. Defects in TS genes can lead to cancer. TS genes are genetically recessive; tumours only form if both chromosomes of a pair contain a defective gene. 1

The retinoblastoma protein (pRb) is the cell’s master braking system. Tumour cells, either lacking or with a damaged pRb protein, proceed into DNA copying (the S phase) in an uncontrolled fashion.

DNA damage is detected by the protein kinases ATM and ATR. They activate p53, which stimulates the synthesis of p21, which jams itself into all the cyclin-CDK partner complexes, shutting down the cell cycle, which is arrested in G1. This allows time to repair DNA before entering the S phase. If the damage is too great, apoptosis follows.

Mutated P53’s are present in about 50% of all human cancers. There is little reason to believe the animal situation is much different.

Every aspect of the cell cycle clock is amenable to epigenetic factors, principally targeted nutrition – see below. 10

Changes in biochemical status of cancer cells 1

“Glucose Catabolism is deranged in cancerous tissue.”

Normal tissue utilises aerobic metabolism as its principle source of energy. Most tumours use anaerobic glycolysis for ATP production, with glucose uptake being much increased compared to normal tissues. Tumour cells have small numbers of (or no) mitochondria. Oncogenes and tumour suppressor genes (e.g. p53 and ras) force the cell into anaerobic glycolysis. This highly inefficient process produces only 2 ATP per glucose molecule, as opposed to 36 aerobically. Hence patients with advanced neoplastic disease lack energy, and with insufficient protein/fat in the diet, lose lean body mass as bodily protein is converted to sugar to feed the tumour. Additionally, with lactate being the end product of anaerobic glycolysis, the system becomes/remains damagingly acidic. 1

However, anaerobic glycolysis is a major ‘Achilles heel’ for tumours and may be exploited with a ketogenic diet to starve the tumour. Supplementing with citrate may further starve the tumour. High intracellular citrate levels signal that the cell is meeting its current needs for ATP and biosynthetic intermediates. It regulates enzymes to reduce the flow of glucose through glycolysis. 1

One of the most powerful nutritional strategies is to instigate a ketogenic diet and supplement with citric acid. 4

E.g. Ketosis – particularly useful in the treatment/reduction of Brain Cancer 10

The British Journal of Cancer – October 2003 – pp 1375 – 82 is quoted as follows … “Brain tumours lack metabolic versatility and are dependent largely on glucose for energy. This contrasts with normal brain tissue that can derive energy from both glucose and ketone bodies.” It is proposed that ketone bodies reduce stromal inflammatory activities while providing normal brain cells with non-glycolytic high-energy substrate. This fuel starves cancer cells but not normal cells. The results shown with a mouse astrocytoma suggest that malignant brain tumours are potentially manageable with dietary therapies that reduce glucose and elevate ketone bodies.

The Ketogenic Diet 4

Is high fat, moderate protein, and extremely low carbohydrate. It does not include any trans fatty acids. It may include cream, coconut milk, olive oil, cold pressed macadamia oil, fish oil, medium chain triglycerides, fish, chicken, butter, etc. It omits intake of refined vegetable oils, particularly those rich in Omega 6 fatty acids. Carbohydrate rich foods are strictly avoided. Fibre intake is maintained with (low glycaemic load/index) fruit/vegetable fibres, e.g. from salad type vegetables – cabbage, raw beetroot, lettuce, cucumber, celery, broccoli etc. Fluid intake is maintained and the body requires to be alkalised, e.g. NaHCO3. This diet should be followed for at least two months to induce apoptosis or possibly cell necrosis.

Once the tumour is under control, the diet changes to a preventative approach and depends upon the type of tumour that is present. Patients with blood or immune type malignancies do better on a high protein, high fat diet, while patients with epithelial or solid tumours tend to do better on a plant, low glycaemic index based diet.

Maintaining the Immune System

A vigilant healthy immune system protects against cancer by seeking out and destroying cells with damaged DNA. High quality, ‘optimal protein level’ diets, with all other nutrients in evolutionary balance, fulfil those requirements. Additionally, many of the specific supplements and herbs (Vitamins A, E, C etc.) powerfully support immune system health in many ways, such as the activation of NK cells etc.

Any stress factor including surgery, psychological or physical stress, pain, etc (excessive release of cortisol) – will influence the activity of the immune system, especially by reducing or inhibiting NK cell activity.

Omega 3 oils reduce stress-induced immunosuppression, especially following surgery.

Bromelain – (orally) has a generally good immune enhancing effect, and together with pancreatic enzymes (orally) has been shown to help (human) mammary cancer.

Vitamin E succinate enhances humoral and cell mediated immunity, augments phagocytosis, enhances cell surface expression of Fas on cancer cells, and makes cancer cells more susceptible to Fas ligand. Reduces oxidation of cell membranes associated with chemotherapy (especially doxorubicin and bleomycin).

Co Enzyme Q 10 has powerful immune enhancing properties. Increases phagocytosis by macrophages, improves cellular energetics. Increases IgG levels and Polymorphs if there is an infection.

Supplement with Arginine – improves tumour killing – a precursor of NO. NO, when released is tumouricidal

The bottom line: an evolutionary diet, suitably supplemented, fulfils immune boosting requirements in stark contrast to unsupplemented modern processed (carcinogenic/pro-inflammatory) western style diets, rampant in today’s world.

Minimising Oxidative Damage
10

Oxygen is a two edged sword. While anaerobic conditions protect and confer biological advantage to neoplastic tissue (oxygen therapy is a recognised treatment for cancer),4 uncontrolled oxygen species are carcinogenic. Oxidation of glucose to produce ATP, produces free radicals, which attack working proteins, unsaturated fats and DNA. Maintaining antioxidant status using vitamins E, C and many of the B vitamins, phytonutrients, the minerals selenium and zinc etc., and limiting glucose precursors in the diet, all contribute to minimising oxidative (free radical) damage. Oxidative damage is a major player in ageing and senescence, with damage to DNA, initiating carcinogenesis. Selenium and vitamin E are especially important. Selenium works by increasing the activity of glutathione peroxidase, which increases the levels of glutathione. Additionally, selenium is a good agent for detoxifying heavy metals (carcinogens). There is much research to demonstrate that selenium reduces the risk of developing most cancers. Selenomethionine is the best form in which to supplement. For humans, a good safe level is 300 ug/day (ten times what is ‘recommended’), with 25 ug being suitable for a 4 year old child and 100 ug for a 10 year old. It is recommended that companion animals receive pro-rata dosing.

Epigenetic Factors, which Drive Neoplasia5

Rapid Growth Rates8

These promote carcinogenesis
by accelerating the cell cycle, increasing the chance of preserving mutations. Think of bone cancers in giant breed dogs. Such cancers are common and possibly increasing, together with many other canine cancers, most especially in the larger breeds. This leads us to consider why? A possible scenario is as follows.

To produce a giant breed pup requires more cell divisions than the production of a toy pup. Giant breed pups are commonly fed high carbohydrate, low fat dry foods. These promote accelerated growth, inflammation, lack protective factors and almost certainly have a high level of mutagenic factors such as BHT etc. It would appear we have developed an excellent way to increase the possibility of cancer, most particularly bone cancer in large breed dogs.

Inflammation – the silent killer - Drives Cancer 10

“If genetic damage is the match that lights the fire of Cancer, some types of inflammation may provide the fuel that feeds the flames.” (Lancet 2001)

Any factor which forces the production of metabolites from Arachidonic acid down the inflammatory pathway promotes cancer, including metastasis.

Inflammation is involved in every aspect of carcinogenesis, particularly cancer progression. Inflammation promotes angiogenesis, proteolytic enzymes production, metastasis, malignant cell survival, decreasing apoptosis, cellular proliferation and adhesive factors that facilitate secondary tumour implantation/growth.

Chronic inflammation in particular, promotes cancer. This includes a broad range of immunological disorders; infections, especially repeated infections, (bacterial, helminth, viral etc.); chronic conditions such as gastritis, Inflammatory Bowel Disease, cystitis, Ulcerative Colitis, Crohn’s Disease etc.; surgery; radiotherapy; any irritants, and of course – chemo and radiotherapy.

Unfortunately, modern diets (for both domestic pets and their human carers) are pro-inflammatory in a number of ways. Most importantly, having strayed far from evolutionary requirements, they ‘encourage’ the development of degenerative disease. They are high in grain-based carbohydrates and sugar, and are therefore insulin promoting. This drives delta 5 desaturase and the pro-inflammatory cascade through arachidonic acid. Lacking sufficient Omega 3’s with excessive levels of Omega 6 essential fatty acids is also a major driver of the inflammatory cascade. 7, 8, 9, 10

Inflammation encourages cell cycle progression, inhibits apoptosis, and promotes tumour angiogenesis. Its production is stimulated by cytokines, mitogens, toxic metals, stress, viral products, UV light, oxygen free radicals and HYPOXIA. Activation of the transcription factor, NF kappa B by chemotherapy or radiotherapy blunts the effectiveness of these treatments. (So reduce its activity during chemotherapy!) Unfortunately, the entire inflammatory cascade is initiated by NF-kB, which induces appropriate genes to produce enzymes that assist production of the whole range of inflammatory mediators, such as TNF-alpha, cytokines (IL-1, IL6, IL8) and eicosanoids (prostaglandins, leukotrienes, thromboxanes). All of these promote cancer and the whole cascade can be down regulated by an evolutionary approach to diet. 10

Use targeted nutrition and supplements to beat inflammation! 10

DHA/EPA compete with AA for enzyme sites, reducing inflammatory eicosanoids and therefore reducing cancer progression. Feed meat that is white or wild, avoid red meat, avoid grain fed meat, avoid grains, avoid sugar, feed masses of raw crushed low GI/GL vegetables.

Inhibition of PAF – achieved with ginko biloba, quercetin, rutin, zinc, and vitamin A. Platelets are made less sticky by PGE1 (from GLA – Evening Primrose oil.) and by PGE3 (from alphalinolenic acid (linseed) and EPA (fish).

Research shows NSAIDS significantly reduce levels of cancer.

Flax oil, evening primrose oil, marine oil and reducing AA containing foods (e.g. red meats), reducing Omega 6 oils and reduction in carbohydrates, all help reduce cancer by reducing inflammation. Carbohydrates promote inflammation by pushing the production of AA via insulin’s promotion of delta-5 desaturase.

Foods that reduce inflammation include Ginger, Fish oil and Turmeric. Clearly, these are healthier to use than NSAIDs, because they are kind to, probably support rather than destroy, organs such as the gut and the kidneys.

Note – it is well recognised that a diet supplemented alpha and gamma linolenic acid can retard or inhibit tumour growth

Modulation of the enzymes cyclooxygenase and lipoxygenase can be achieved using Omega 3 EFAs, bromelain, quercetin, boswellic acid, zinc, vitamin E and B6. This approach will result in the reduction of tumour growth.

Antagonists to NF kappa B

Green tea polyphenol, genistein, aspirin, lipoic acid, melatonin, vitamin C, quercetin and Vitamin E succinate, antioxidants, omega 3 oils and monounsaturated fatty acids.

Note: Anti-inflammatories and antioxidants affect the expression and the function of several cell-cycle-regulating proteins. In other words, they don’t ONLY stop inflammation and mutation in their anti-cancer roles.

Obesity has been linked to mortality from the majority of cancers. The insulin/insulin-like growth factor (IGF) system may partly explain this effect. It is important to keep insulin levels down, as hyperinsulinaemia is an important factor, not only in ageing, but also in the development of cancer. A study using various rodents demonstrated that Insulin Sensitivity determines longevity. The rodents were given cancer. The half that was treated with Phenformin (used to decrease blood sugar in NIDDM by increasing sensitivity to insulin), showed a significantly increased lifespan. By disposing of the sugar, they produced less insulin, which was correlated with longevity. Combining these results with other research it has become clear that anything that Increases Insulin Sensitivity Inhibits Cancer! This provides further support for the use of ketogenic/real food diets as opposed to modern artificial carbohydrate based diets. 7

Angiogensis and Cancer

Failure to develop a blood supply will stop tumour growth and prevent tumour dissemination. Angiogenesis is a prime activity of most tumours.

Inhibitors of Angiogenesis…

GLA, EPA, bromelain, pancreatin, trypsin, quercetin, rutin, African bush willow, Currumbin, baicalein, vitamin E succinate, zinc and extract of bovine cartilage.

Metastatin is the active ingredient in bovine tracheal cartilage. Bovine tracheal cartilage was found to decrease vascular endothelial growth factor (VEGF). This factor is a major stimulant to new blood vessel growth. 10

Vascular Endothelial Growth Factor (VEGF) is the key mediator of tumour vascularisation.
Other nutrients that down regulate VEGF…
1) Vitamin E – long term supplementation produces decreased serum VEGF
2) Green tea extract – inhibits angiogenesis by decreasing the expression of VEGF receptors
3) Baiclin decreases MMP-2 and basic fibroblast growth factor and this produces a reduction in angiogenesis activity
4) DHA/EPA and quercetin both reduce the levels of Cox 2 and VEGF

MMPs and Cancer

Matrix Metalloproteinases (MMPs) are Zinc Dependent Endopeptidases, which digest protein. They are from stromal cells and/or inflammatory cells. They destroy the collagen matrix barrier, which surrounds the tumour, allowing the tumour to invade. Proinflammatory cytokines can induce MMP production. This is inflammation causing the spread of cancer. 10

MMPs have a range of activities that include modulation of cell death, cell proliferation, cell differentiation, tumour-associated angiogenesis and malignant conversion. While their major function in metastasis is to attack the cellular matrix, they also act on chemokines, growth factor receptors, adhesion molecules and apoptotic mediators.

In other words, MMPs contribute to multiple steps in tumour progression, angiogenesis, and the establishment and growth of metastatic lesions at different sites.

Inhibitors of various MMPs include…
Vitamin A (retinoids), genistein, green tea polyphenols, curcumin, quercetin, luteolin, ursolic acid, EPA/DHA, glucocorticoids, interleukin 10, N-Acetyl cysteine, shark cartilage extract and tetracycline analogue.

Conclusion

To prevent and treat cancer, I suggest that the patient be fed an evolutionary diet,(7,8, 9, 10) and be supplemented at the very least with Omega 3 essential fatty acids, selenium, vitamin E and bovine tracheal cartilage. This is a programme, which supports the immune system, reduces inflammation, oxidation and angiogenesis. Clearly there is much more that can be done with additional supplements and/or herbs.

In addition to the foods/supplements mentioned above, there is a veritable avalanche of nutritional and supplemental products that have been shown to influence both the genetic (prevent mutations) and epigenetic (favourably aid gene expression) controls on neoplasia. All of these and more we could use to treat cancer.

In no particular order, in addition to the above mentioned foods/supplements, these might include: probiotics, resveratrol in berries, allicin in garlic, cruciferous vegetables, Astragalus, folate, iodine, conjugated linolenic acid, beetroot, aloe vera, flaxseed, lipoic acid, vitamin K, melatonin, D-limonene, mushrooms, mixed carotenoids, soy, molybdenum, olive oil, calcium, boron, ginseng, spirulina, vitamin D, genistein and many more including a vast array of single and mixed herbs, such as the sheep sorrel mixture, or the powerful wormwood.

Every one of these has been documented as influencing positively, various aspects of the cell cycle, tumour biochemistry, inflammation, redox reactions etc. Clearly, time and space, places limits to their discussion in this paper.

It is my hope that this paper will provide enough information and interest to stimulate further investigation into the use of nutrition and nutritional supplements as powerful, safe and potentially highly effective ways of dealing with neoplasia, both with and without the traditional cut, burn and poison approach.

References

Nelson, D.L. and Cox, M.M. (2000). Lehninger Principles of Biochemistry. Third Edition. Worth Publishers, New York.
Stedman’s Medical Dictionary. (2000). 27th Edition. Lippincott Williams & Wilkins, Baltimore, Maryland.
Morrison, W.B. (2002) Cancer in Dogs and Cats. Second Edition. Teton NewMedia, Jackson, Wyoming.
Osiecki, H. (2002) Cancer A Nutritional/Biochemical Approach. Second Edition. Bio Concepts Publishing, Australia.
Weinberg, R. (1999). One Renegade Cell. Phoenix, London.
Ridley, M. (2000). Genome. HarperCollins Publishers inc., New York. First Perennial Edition.
Billinghurst, I.G. (1993). Give Your Dog a Bone. Warrigal Publishing, Australia.
Billinghurst, I.G. (1998). Grow Your Pups With Bones. Warrigal Publishing, Australia.
Billinghurst, I.G. (2001). The BARF Diet. Warrigal Publishing, Australia.
Billinghurst, I.G. (2006). Pointing the Bone at Cancer. Warrigal Publishing, Australia.
Dr. Ian Billinghurst
 
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Geregistreerd: 17 sep 2007 21:34

Ongelezen berichtdoor Fadadomar » 25 sep 2007 09:45

Dear Dr. Billinghurst,

Thank you so much for your very interesting and extensive reply.

I hope you will still read this, as I didn't have access to the internet until today.

I only have two questions (sofar):

1) you recommend to "avoid grain fed meat", and I wonder what exactly you mean by that? To me white meat is usually chicken, but chicken are grain-fed. I do actually feed quite a lot of chicken, as that is the best available raw food-source I have. I do feed other types of meat, but the bulk I feed is chicken. Both my dogs are not fond of hare, rabbit or duck (about the only "wild" foodsources available here). Pork is not safe to feed raw in Europe, as we run the risk of pork being contaminated with Aujeszky's disease, which kills dogs.

2) What about green tripe? Both my dogs are very fond of green tripe and I do feed that quite often.

Thank you very much again for your helpful reply.

Will you allow me to share your paper with the oncologists who saw my dog and with my own vet?

Sincerely yours,

Lia de Ruiter
Veel liefs,

Lia, Rui en de katten
Scheveningen

Cody 25-11-1998 - 4-12-2007, voor altijd in mijn hart
Afbeelding
Fadadomar
 
Berichten: 32
Geregistreerd: 29 maart 2004 20:39
Woonplaats: Scheveningen, Den Haag, Nederland

Ongelezen berichtdoor Dr. Ian Billinghurst » 05 nov 2007 02:55

Hi Lia,

In answer to your question, that little bit about grain fed meat was referring to grain fed beef – which may be a little too pro-inflammatory for the cancer patient. . Don’t worry about the chicken. It is OK. In Australia there is no Aujesky’s and there should be no Aujesky’s in factory farmed pork. Green tripe is brilliant!!!

Cheers

Ian B
Dr. Ian Billinghurst
 
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Geregistreerd: 17 sep 2007 21:34

Ongelezen berichtdoor Dr. Ian Billinghurst » 05 nov 2007 03:07

Oops

Yes – pleas do share the paper with your oncologist and vet

Cheers once again

Ian B
Dr. Ian Billinghurst
 
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Geregistreerd: 17 sep 2007 21:34


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