At �60 for the kindle version of the book I don't think it's going to be on my shopping list.
But this blog has some extended excerpts of which this will interest some people
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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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.
It'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.
I'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.
I'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.
I'd continue with omega 3 and magnesium (anti inflammatory)
That inflammation-induced cell growth and division promotes cancerous growth has long been known, the best known example being the generation of gastric cancers by inflammation resulting from growth of Heliobacter pylori.
Equally pertinent are the highly life-threatening qualities of “inflammatory cancers.” Massive infiltration of inflammatory cells, for example, makes it especially difficult to cure breast cancers.
Hence the stress I place on ensuring EVERYONE irrespective of whether or not they have a cancer diagnosis attains and maintains an optimal natural 25(OH)D level around 125nmol/l 50ng/ml and also supplements with MAGNESIUM and OMEGA 3 so they are able to benefit from this combination to optimize their anti inflammatory potential.
Quote:
Distinguishing cancer cells from normal cells is their inherently higher levels of glucose breakdown (glycolysis) and secretion of copious amounts of lactic acid even in the presence of oxygen (aerobic glycolysis)—a phenomenon first observed in the early 1920s by the great biochemist Otto Warburg, who received the Nobel Prize in 1931 for his insights about respiratory enzymes. Now we know that glycolytic breakdown of glucose and the glutaminolysis of the amino acid glutamine provide the cellular building blocks for the protein, nucleic acids, carbohydrates, and lipids needed for new cell growth. Cancer cells, in fact, break down sugar sources at even faster rates than their normal equivalents because one or more of their growth-promoting oncogenes are always on
Knowing this it should be obvious to everyone that REDUCING availability of glucose and foods metabolised to glucose should be the first strategy to deploy even immediately you begin to suspect that cancer may be a potential diagnosis.
A carbohydrate fast with limited protein sources, prior to cancer diagnosis and while waiting for treatment to start, may make the potential cancer more vulnerable to effective treatment. If this is combined with efforts to raise ph with an alkalising diet to combat acidosis then so much the better.
Obesity increases circulating estrogen, insulin, IGF, and cause chronic low-grade inflammation.
These diverse pathways directly or indirectly converge to induce accumulation of myeloid derived suppressor cells, while programming macrophages to the alternatively activated M2 phenotype.
MDSCs and M2 macrophages are a major source of immunosuppression that allows for tumor-escape from effective anti-cancer responses.
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.
Quote:
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
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.
Innate or acquired resistance to chemotherapy presents an important and predictable challenge in cancer therapy.
Malignant tumors consist of both neoplastic and benign cells such as stromal fibroblasts, which can influence the tumor's response to cytotoxic therapy.
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.
Such 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.
This paper shows how chemotherapy drugs may enable cancer cells to replicate and spread faster.
Acquired resistance to anticancer treatments is a substantial barrier to reducing the morbidity and mortality that is attributable to malignant tumors.
Components of tissue microenvironments are recognized to profoundly influence cellular phenotypes, including susceptibilities to toxic insults.
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).
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.
The expression of WNT16B in the prostate tumor microenvironment attenuated the effects of cytotoxic chemotherapy in vivo, promoting tumor cell survival and disease progression.
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.
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?
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.
What Causes Cancer
Linear Mode
