What Causes Cancer

Ted_Hutchinson

\r\n \r\n At ï¿½60 for the kindle version of the book I don\'t think it\'s going to be on my shopping list.
\r\nBut this blog has some extended excerpts of which this will interest some people
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\r\nQuote from: Cancer as a Metabolic Disease
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\r\n \r\n The data show that blood glucose levels remain high in mice that consume the Ketogenic Diet,(KD) in unreduced amounts. If glucose levels remain high, body weights remain stable or increase [36]. When the KD is fed to mice in unrestricted amounts, blood glucose levels remain high and ketones are largely excreted in the urine. We clearly showed, however, that blood ketones were higher in tumor-bearing mice under DER than under AL (unrestricted) feeding [34]. Under DER, ketones are retained in the body for use in metabolism rather than excreted in the urine. This information is critical when designing metabolic therapies for tumor management.
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\r\n This means that it is the amount of the diet consumed rather than the composition of the diet that determines blood glucose levels. Many people have difficulty appreciating this fact because they often think that low carbohydrate diets will produce low blood glucose levels. This is clearly not the case here. We reported similar findings in our previous investigation of glucose and ketones in epileptic mice [36, 48]. Our data show that blood glucose levels are influenced more by the amount of calories consumed than by the composition of the calories consumed. Nutritional oncologists and cancer patients also need to know this information. Although ketone (β-OHB) levels are higher in the mice consuming the KD than in mice consuming the standard diet (SD), the β-OHB levels are even higher in mice that consume the KD in restricted amounts (KC {keto-cal}-R). Why would blood ketone levels be higher in mice that eat less KD than in mice that eat more KD? The answer is simple. Ketones are retained in the body when glucose levels are low. Ketones serve as an energy substitute for glucose. If glucose is not reduced as in the KC-UR (unrestricted keto cal)groups, then most ketones will be excreted in the urine. This is why it is better to measure blood ketone levels than to measure urine ketones as an indicator of ketosis. Cancer cells are placed under metabolic stress when glucose levels are reduced and ketone levels are elevated . The therapeutic action of ketones is best when blood glucose levels are low.\r\n \r\n

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Ted_Hutchinson

\r\n \r\n What Causes Cancer? Part II\r\n

Solstice Goat

\r\n \r\n Interesting. So ketones in the urine aren\'t indicative of blood sugar? Is that what they\'re trying to say?\r\n

Ted_Hutchinson

\r\n \r\n Cancer Part III–Dietary Treatments
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\nYou may want to watch this as an example of how it works out in practice.
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\nHow To Cure Breast Cancer and Modified Ketogenic Diet with Elaine Cantin
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\nHere is a link to her book.
\nThe Cantin Ketogenic Diet: For Cancer, Type I Diabetes & Other Ailments\r\n

Ted_Hutchinson

\r\n \r\n Those who are interested in learning more about the science supporting a ketogenic diet to slow progression or prevent cancer there is a detailed site here
\r\nKetoNutrition Metabolic Strategies for Neurodegenerative Diseases and Cancer\r\n

Ted_Hutchinson

\r\n \r\n The final part of this series.
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\nCancer Part 4: Got Hope?
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\nIt\'s been very interesting. I agree with everything she has suggested but I think in addition to her strategy I would add on Vitamin D3 repletion.
\nI\'d raise my 25(OH)D to nearer the 200nmol/l = 80ng/ml mark by taking at least 10,000iu daily and getting short UVB exposure daily.
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\nI\'d suggest CURCUMIN supplements morning and evening. Curcumin works a bit like Vitamin D3(It activates the Vitamin D receptor) but it also has it\'s own anti cancer actions that are independent of the Vitamin D effect.
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\nI\'d continue with omega 3 and magnesium (anti inflammatory)
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\nResveratrol also improves mitochondrial function.
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\nBasic mechanisms involved in the anti-cancer effects of melatonin.
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\nGREEN TEA
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\nHigher HDL-Cholesterol Levels Associated With Lower Risk of Cancer
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\n Niacin is currently the most potent available agent to increase high-density lipoprotein\r\n

Ted_Hutchinson

\r\n \r\n Here is another recent paper that adds to the story though somewhat at a tangent to earlier posts in this thread.
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\nObesity-driven inflammation and cancer risk
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\r\n \r\n Obesity increases circulating estrogen, insulin, IGF, and cause chronic low-grade inflammation.
\nThese diverse pathways directly or indirectly converge to induce accumulation of myeloid derived suppressor cells, while programming macrophages to the alternatively activated M2 phenotype.
\n MDSCs and M2 macrophages are a major source of immunosuppression that allows for tumor-escape from effective anti-cancer responses.
\n The induction and preferential tilting of macrophages towards the M2 phenotype may be a primary physiologic and metabolic response to insulin insensitivity, as well a secondary consequence of an immune process to control overt, chronic, low grade inflammation. In any event, these processes may be inadvertently modulated by tumor cells to promote angiogenesis, metastasis and overall poor outcome.\r\n \r\n

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\r\n \r\n Another area of potential therapeutic targeting is the use of anti-inflammatory agents to reduce the low grade chronic inflammation that leads to the insulin insensitivity and subsequent physiologic response of MDSC and M2 macrophage induction. Some of these anti-inflammatory therapies are already in use for cardiovascular disease prevention in obese individuals\r\n \r\n

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In addition to the suggestions made in Post 7 above I should mention that correcting the omega 3 omega 6 ratio, by increasing sources of omega 3 and decreasing sources of omega 6 is probably a good idea, not only does this improve the actions of vitamin D3 but omega 3 itself is an anti-inflammatory agent when it\'s not being overwhelmed by excess intakes of omega 6.\r\n

Ted_Hutchinson

\r\n \r\n Treatment-induced secretion of WNT16B promotes tumor growth and acquired resistance to chemotherapy
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\r\n \r\n Innate or acquired resistance to chemotherapy presents an important and predictable challenge in cancer therapy.
\n Malignant tumors consist of both neoplastic and benign cells such as stromal fibroblasts, which can influence the tumor\'s response to cytotoxic therapy.
\n In a recent article in Nature Medicine, Sun et al. show that increased expression of Wnt family member wingless-type MMTV integration site family member 16B (WNT16B) by the tumor microenvironment in response to cytotoxic damage and signals through the canonical Wnt pathway to promote tumor growth and chemotherapy resistance.
\nSuch findings outline a mechanism by which cytotoxic therapies given in cyclical doses can actually augment later treatment resistance and may open the door to new areas of research and to the development of new therapeutic targets that block the DNA damage response program.\r\n \r\n

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This paper shows how chemotherapy drugs may enable cancer cells to replicate and spread faster.
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\nTreatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B.
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\r\n \r\n Acquired resistance to anticancer treatments is a substantial barrier to reducing the morbidity and mortality that is attributable to malignant tumors.
\nComponents of tissue microenvironments are recognized to profoundly influence cellular phenotypes, including susceptibilities to toxic insults.
\n Using a genome-wide analysis of transcriptional responses to genotoxic stress induced by cancer therapeutics, we identified a spectrum of secreted proteins derived from the tumor microenvironment that includes the Wnt family member wingless-type MMTV integration site family member 16B (WNT16B).
\n We determined that WNT16B expression is regulated by nuclear factor of κ light polypeptide gene enhancer in B cells 1 (NF-κB) after DNA damage and subsequently signals in a paracrine manner to activate the canonical Wnt program in tumor cells.
\nThe expression of WNT16B in the prostate tumor microenvironment attenuated the effects of cytotoxic chemotherapy in vivo, promoting tumor cell survival and disease progression.
\n These results delineate a mechanism by which genotoxic therapies given in a cyclical manner can enhance subsequent treatment resistance through cell nonautonomous effects that are contributed by the tumor microenvironment.\r\n \r\n

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If we know "Components of tissue microenvironments are recognized to profoundly influence cellular phenotypes, including susceptibilities to toxic insults." surely changing the available fuel source and PH of that microenviroment in ways that are known to prevent or slow the growth of cancer cells is an obvious way to reduce the capability of cancer cells to replicate in chemoresistant forms?\r\n

Ted_Hutchinson

\r\n \r\n In order to discover just how possible it is to do a water fast to get into a ketogenic state quickly Dr Ede has experimented on herself and reports on the experience here.
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\r\nKetogenic Diets for Cancer and Beyond
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\r\nIt\'s a pity those ketone blood testing strips are so expensive.\r\n

jesichashope

\r\n \r\n This study was known for sometime and has been suppressed and ignored by conventional doctors, hence the normal media channels as well. Who wants the truth being told? Is it any wonder why cancer seems to spread very quickly when patients are given mega doses of chemo? And all we can do is say the patient is putting up a good fight; how can doctors live with themselves knowing what they are doing?
\nOf course there is another recent article that states, most doctors have no idea what side effects the chemo drug they use will have, in fact, most drug companies fail to put that out for everyone to see, its hidden or forgotten somewhere deep in all the white papers. Doctors read only the leaflets, and we trust what they are doing and giving us? This may explain why doctors did not know or care that the chemo was prolonging and spreading the cancer.\r\n

Ted_Hutchinson

\r\n \r\n A Diet for Chemotherapy.
\r\nThis is a reasonable approach that includes many of the ideas discussed earlier in this thread.\r\n

newlife

\r\n \r\n Looking for a facebook-style "like" button.

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TrinB

\r\n \r\n Is it possible to do the ketogenic diet when someone has cachexia?\r\n

Ted_Hutchinson

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\r\n Originally Posted by TrinB\r\n

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Is it possible to do the ketogenic diet when someone has cachexia?

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I think most of the work on ketogenic diets as a cancer treatment have been done on people for whom NO EFFECTIVE CONVENTIONAL TREATMENT is available.
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\r\nWhile there is a possible that a conventional medical intervention is available or possible, it\'s thought unethical to use unconventional or experimental treatments, so most of our knowledge is based on the work with no-hoper\'s who have exhausted every other possibility for treatment.
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\r\nCancer & Sugar - Strategy for Selective Starvation of Cancer
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\r\nStarving Cancer: Ketogenic Diet a Key to Recovery
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\r\nI appreciate it is counter-intuitive to suggest a carbohydrate free diet for someone with cachexia but surely it\'s better to feed the patient with food that isn\'t also promoting the growth of the cancer?
\r\nWhen babies are relying on breast milk only we aren\'t concerned they may not be getting all the nutrients they require, so why do we voice those concerns when adults with cancer or children with epilepsy are given a ketogenic diet?\r\n

TrinB

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\r\n Originally Posted by Ted_Hutchinson\r\n

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What Causes Cancer
\r\nThis looks like it will turn into an interesting series of blogs.
\r\nIt may help if you watch this video first.
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\r\nThomas Seyfried, Ph.D.ï¿½Targeting Energy Metabolism in Brain Cancer [AHS12 Talks]

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Is it Ok for someone with Cachexia to try this diet?\r\n

TrinB

\r\n \r\n Thanks so much for that. I think we\'ll keep with the dairy for now as the diet is restrictive enough. For the past 6 months or so we have been trying a macrobiotic diet but obviously although parts of the diet are good ie lots of vegetables and seaweed there are too many grains in it. Do you know much about ALP (Alkaline phosphotase)? This level has been consistently high, we have been told its a cancer marker. Last time it was taken it was 300.\r\n

Solstice Goat

\r\n \r\n You two could probably fit these pieces together better than I;
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\r\n \r\n Randomized clinical trials need to be done to test the vitamin D theory of influenza. With what we know now, however, perhaps an annual shot of 600,000 IU of vitamin D (Med J Aust 2005;183:10–12) would be more effective in preventing influenza than a jab of flu vaccine.\r\n \r\n

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\r\n \r\n Vitamin D (25-hydroxyvitamin D) blood levels, the barometer for vitamin D status, are measured in nanograms per milliliter (ng/ml) or nanomoles per liter (nmol/l), where ng/ml = 0.4 nmol/l. Children and adults need a vitamin D blood level >8 ng/ml to prevent rickets and osteomalacia (demineralization and softening of bones) respectively. It takes a concentration >20 ng/ml to keep parathyroid hormone levels in a normal range. A level >34 ng/ml is required to ensure peak intestinal calcium absorption. Finally, neuromuscular performance steadily improves in elderly people as vitamin D levels rise up to 50 ng/ml. Accordingly, a vitamin D blood level <8 ng/ml is regarded as severely deficient; 8–19, deficient; and 20–29, insufficient, i.e., too low for good health. A level >30 ng/ml is sufficient, but experts now consider 50–99 ng/ml to be the optimal level of vitamin D. Levels 100–150 ng/ml are excessive and >150 ng/ml, potentially toxic.
\n A majority of Americans have insufficient or deficient vitamin D blood levels. In veterans undergoing heart surgery at the Seattle VA hospital, I found that 78% had a low vitamin D level: 12% were insufficient; 56%, deficient; and 10% were severely deficient.
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\n In order to enjoy optimal health, we should maintain a vitamin D blood level of ≥50–99 ng/ml. Without sun exposure, to reach a level of 50 ng/ml requires taking a 5,000 IU/day vitamin D supplement. There are two kinds of vitamin D supplements: vitamin D3 (cholecalciferol), the kind our skin makes, and vitamin D2 (ergocalciferol), a synthetic variant made by irradiating plants. Vitamin D2 is only 10–30% as effective in raising 25-hydroxyvitamin D blood levels compared to vitamin D3, leading the authors of a recent study conclude, "Vitamin D2 should not be regarded as a nutrient suitable for supplementation or fortification" (Am J Clin Nutr 2006;84:694–697).
\n Concerns about vitamin D toxicity are overblown, along with those about sun exposure. As one researcher in the field puts it, "Worrying about vitamin D toxicity is like worrying about drowning when you’re dying of thirst." The LD50 of vitamin D in dogs (the dose that will kill half the animals) is 3,520,000 IU/kilogram. One can take a 10,000 IU vitamin D supplement every day, month after month safely, with no evidence of adverse effect. (Am J Clin Nutr 1999;69:842–856). A person must consume 50,000 IU a day for several months before hypercalcemia (an elevated calcium level in the blood, which is the initial manifestation of vitamin D toxicity) might occur. Vitamin D in a physiologic dose (5,000 IU/day) prevents the build up of calcium in blood vessels. (Circulation 1997;96:1755–1760). If one takes 10,000 IU of vitamin D a day and spends a lot of time in the sun, it would be prudent to check vitamin D blood level to ensure that it does not exceed 100 ng/ml.\r\n \r\n

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\nhttps://www.lewrockwell.com/miller/miller25.html\r\n

Ted_Hutchinson

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\r\n \r\n Randomized clinical trials need to be done to test the vitamin D theory of influenza. With what we know now, however, perhaps an annual shot of 600,000 IU of vitamin D (Med J Aust 2005;183:10ï¿½12) would be more effective in preventing influenza than a jab of flu vaccine.\r\n \r\n

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That is a ludicrous idea.
\r\nThe last thing we want is to replete Vitamin D status with an annual jab.
\r\nWe know from earlier work that increasing vitamin D status suddenly can lead to a loss of immune function as the "Set point" for immune function is adjusted following a change in level. We know what the half life of vitamin D is so why not keep intakes as close to natural as possible with Daily or weekly intakes. When people get to the point they are no longer able to manage their own oral intakes then perhaps a monthly oral supplement may be justified but really the idea of just a single annual intake is not sensible at all IMO.
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\r\nI don\'t think flu jabs are the answer either.
\r\nI\'ve never had one and never intend to either.\r\n

Solstice Goat

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\r\n Originally Posted by Ted_Hutchinson\r\n

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That is a ludicrous idea.
\nThe last thing we want is to replete Vitamin D status with an annual jab.
\nWe know from earlier work that increasing vitamin D status suddenly can lead to a loss of immune function as the "Set point" for immune function is adjusted following a change in level. We know what the half life of vitamin D is so why not keep intakes as close to natural as possible with Daily or weekly intakes. When people get to the point they are no longer able to manage their own oral intakes then perhaps a monthly oral supplement may be justified but really the idea of just a single annual intake is not sensible at all IMO.
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\nI don\'t think flu jabs are the answer either.
\nI\'ve never had one and never intend to either.

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\nI don\'t think it was suggested as optimum, but a much better alternative than a flu shot.
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\r\n \r\n Levels 100ï¿½150 ng/ml are excessive and >150 ng/ml, potentially toxic.\r\n \r\n

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\nUntil someone can post something besides conjecture to the above limit, I will take it as gospel.\r\n

Ted_Hutchinson

\r\n \r\n Ketogenic Diet May Be Key to Cancer Recovery\r\n

Ted_Hutchinson · ï¿½ #1 ï¿½ 01-20-2013, 09:06 AM

What Causes Cancer
This looks like it will turn into an interesting series of blogs.
It may help if you watch this video first.

Thomas Seyfried, Ph.D.ï¿½Targeting Energy Metabolism in Brain Cancer [AHS12 Talks]

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