Cancer: causes and cures

Re: Breast Cancer Treatment?

wisrnow said:
The previous one could not return since it was banned. I learned my "lesson" and I'm "wisrnow." That is all I care to say about the matter.

So you were banned and then created a new account in order to gain access to the forum again. Not kosher. It does not appear you are any wiser, since you decided to sidestep your ban in order to return. Just creating a new account does not eliminate the ban, in fact it is evidence that the ban should continue.
 
Re: Breast Cancer Treatment?

wisrnow said:
The previous one could not return since it was banned. I learned my "lesson" and I'm "wisrnow." That is all I care to say about the matter.
Unfortunately it doesn't work that way here, wisrnow. If someone is asked to leave a house, they don't then try and come back through a window. What's done is if that person wants to return, they come to the door, apologize, do everything they can to make amends and ask to be let back in. Isn't that what you would want for yourself? I suggest that you open a new thread and begin again with why you were banned and what you felt you have learned - in a manner that is honest and respectful of the house rules.
 
Re: Breast Cancer Treatment?

By the way, you didn't answer truth seeker's question:

What was the moniker on your last account and why didn't you feel it was appropriate to use that one upon returning?
 
Re: Breast Cancer Treatment?

wisrnow said:
...Being a member of this forum, I feel sure you are already aware of most of this, and I wish you continued good health on your journey! :)

Yes. On this particular topic, though, I am choosey about what details I post and while I started out to elaborate a little more, I thought the better of it. I don't want someone mining my posts (which are not anonymous), twisting what I say, and using the information against me in the future.
 
Re: Breast Cancer Treatment?

Link: Is there a role for carbohydrate restriction in the treatment and prevention of cancer?

An excerpt from the conclusions, evidence that "the diet" works against cancer (CHOs = "carbs", KD = "Ketogenic Diet"):

(iii) Many cancer patients, in particular those with advanced stages of the disease, exhibit altered whole-body metabolism marked by increased plasma levels of inflammatory molecules, impaired glycogen synthesis, increased proteolysis and increased fat utilization in muscle tissue, increased lipolysis in adipose tissue and increased gluconeogenesis by the liver. High fat, low CHO diets aim at accounting for these metabolic alterations. Studies conducted so far have shown that such diets are safe and likely beneficial, in particular for advanced stage cancer patients.

(iv) CHO restriction mimics the metabolic state of calorie restriction or - in the case of KDs - fasting. The beneficial effects of calorie restriction and fasting on cancer risk and progression are well established. CHO restriction thus opens the possibility to target the same underlying mechanisms without the side-effects of hunger and weight loss.

(v) Some laboratory studies indicate a direct anti-tumor potential of ketone bodies. During the past years, a multitude of mouse studies indeed proved anti-tumor effects of KDs for various tumor types, and a few case reports and pre-clinical studies obtained promising results in cancer patients as well. Several registered clinical trials are going to investigate the case for a KD as a supportive therapeutic option in oncology.
 
Baking soda to cure cancer?

What do you think about this cure?

http://www.youtube.com/watch_popup?v=Yl8Y8I_TsjI

Also his blog:

http://zencat00.blogspot.com.es/
 
Re: Baking soda to cure cancer?

loreta said:
What do you think about this cure?

http://www.youtube.com/watch_popup?v=Yl8Y8I_TsjI

Also his blog:

http://zencat00.blogspot.com.es/
Hi loreta,

The subject of baking soda and cancer has actually been discussed a few times, I believe. A really good practice for you to try is to use the search function in the upper right-hand corner. Because we have so many threads here, quite often we find that something's been discussed already so it's best to try to remember to check before posting. :)
 
Re: Baking soda to cure cancer?

truth seeker said:
Hi loreta,

The subject of baking soda and cancer has actually been discussed a few times, I believe. A really good practice for you to try is to use the search function in the upper right-hand corner. Because we have so many threads here, quite often we find that something's been discussed already so it's best to try to remember to check before posting. :)

You are right! Sometimes I forget to check. Thanks to remind me. :)
 
Re: C is for Cancer

Interesting research here showing that vitamin c can is a good pretreatment therapy for radiation:

http://www.youtube.com/watch?v=Rbm_MH3nSdM
 
Re: C is for Cancer

Kniall said:
Interesting research here showing that vitamin c can is a good pretreatment therapy for radiation:

http://www.youtube.com/watch?v=Rbm_MH3nSdM

Thanks for the link, good discussion by those trying to make a difference with health information for people, yet as the one physician states after sending out 150 press releases, there were no calls, no interest - the fear of saying anything against Tepco is like speaking against the emperor of old, not many dare.
 
Cancer as a Metabolic Disease: Thomas Seyfried

I recently read the book "Cancer as a Metabolic Disease: On the Origin, Management and Prevention of Cancer" by Thomas Seyfried, biochemical geneticist and Professor in Dept Of Biology, Boston College after Hesper mentioned this book in the ketogenic diet thread. Dr Seyfried has had a long career as a cancer researcher and is presently focused on therapeutic and preventive properties of the diet on cancer. His book is well-written; it has a lot of technical details which are suitable for biochemists and geneticists but at the same time he does a good job in making things comprehensible to the layperson. He has taken apart the official stand on cancer research - one that uses billions of dollars in research grants ultimately coming out of public money - while producing little if any useful results for the millions of cancer patients who suffer and die more perhaps from the toxicity of treatment rather than the diease itself, hoping for the next miracle drug which the drug companies promise to be just around the corner. His anguish at the state of cancer research as well as clinical management comes out quite clearly in the book. I will try to provide a somewhat detailed review of the key points in the book.

Synopsis

Seyfried references the research done by Nobel laureate Otto Warburg quite extensively in the book. Warburg postulated in 1924 that cancer was principally a disease of mitochondrial dysfunction.

[quote author=Otto Warburg]
"Cancer, above all other diseases, has countless secondary causes. But, even for cancer, there is only one prime cause. Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar."
[/quote]

Seyfried has slightly modified the above hypothesis put forward by Warburg by including the fermentation of amino acids (glutamine in particular) by mitochondria of cancerous cells as an additional energy producing mechanism along with fermentation of glucose. In this model, the millions of genetic modifications seen in cancer,which are being enthusiastically chased around by countless researchers at the expense of taxpayers while roughly 1500 people die each day from cancer in USA alone, are treated as a downstream epiphenomenon of impaired cellular respiration. He sites hundreds of research publications which essentially support the Warburg hypothesis on cancer and meticulously addresses the key scientific objections raised by dissenters who choose to swim endlessly (but profitably) in the genetic soup.

Malignant cells use glucose and amino acids like glutamine as their energy source through the process of fermentation even in the presence of oxygen. So cutting off glucose and glutamine should help in starving cancer cells of their fuel. That is where the energy restricted ketogenic diet comes in which drastically lowers supply of carbs as well as proteins and generates ketone bodies through fat metabolism. While healthy cells can switch to ketone bodies for their energy requirements, cancer cells are unable to make the transition and consequently die. In a nutshell, this is the essence of the book's message.
 
Re: Cancer as a Metabolic Disease: Thomas Seyfried

Cellular Respiration

In order for cells to live and perform their programmed functions, they must produce energy. This cellular energy is governed by ATP (adenosine triphosphate ) molecules. ATP is synthesized inside the cell during cellular respiration. Hydrolysis (breakdown of ATP under the action of water) of ATP releases energy stored in its phosphate bonds. The standard energy of ATP hydrolysis under physiological conditions is tightly regulated in all cells between − 53 and − 60 kJ/ mol. Energy from ATP is used to gate ion channels and maintain cell membrane potential.

[quote author=Cancer as a Metabolic Disease]
There are several sources of ATP synthesis that can be used to maintain membrane potentials. The mitochondria produce most of the energy in normal mammalian cells. In cells with functional mitochondria, ATP is derived mostly from oxidative phosphorylation (OxPhos) where approximately 89% of the total cellular energy is produced (about 32/ 36 total ATP molecules during the complete oxidation of glucose). This value can differ among different cells depending on which shuttle systems are used in the transport of cytoplasmic reducing equivalents (nicotinamide adenine dinucleotide (reduced form), NADH) from the cytoplasm to the mitochondria. Through OxPhos, mitochondria produce the bulk of intracellular ATP, and hence are considered the cell's “power plants.” In addition, mitochondria regulate Ca2 + homeostasis and modulate several other metabolic circuitries including the Krebs cycle, the urea cycle, gluconeogenesis, ketogenesis, heme biosynthesis, fatty acid β-oxidation, steroidogenesis, metabolism of certain amino acids, and the formation of iron/ sulfur clusters. .....

Besides OxPhos, approximately 11% (4/ 36 total ATP molecules) of the total cellular energy is produced through substrate-level phosphorylation.
[/quote]

In oxidative phosphorylation, ATP is produced through electron transfer reactions in the presence of oxygen, using a gradient of protons across the inner mitochondrial membrane. Substrate level phosphorylation on the other hand, generates ATP through addition of phosphates to ADP from the substrate or an intermediate reaction product. There are two main pathways in mammalian cells for substrate level phosphorylation:

a) glycolysis in the cyptoplasm of the cell where glucose (substrate) is broken down generating net 2 ATP molecules

b) succinyl-CoA synthetase reaction in the TCA (tricarboxylic acid cycle or Kreb's cycle) cycle which takes place in the mitochondrial matrix and generates 2 ATP molecules.

Unlike OxPhos, substrate level phosphorylation does not require oxygen.

[quote author=Cancer as a Metabolic Disease]
The number of ATP molecules produced from TCA cycle, substrate-level phosphorylation would need to increase if OxPhos were insufficient to maintain energy homeostasis. This would be similar to the increase in the number of ATP molecules produced through glycolysis when OxPhos is reduced. Nonoxidative energy production through amino acid fermentation and substrate-level phosphorylation has been documented in developing mammalian embryos, in diving animals, and in heart and kidney tissue under hypoxia.
[/quote]

An important point to consider is that the standard energy of ATP hydrolysis under physiological conditions is tightly regulated in all cells as mentioned earlier. Energy production in heart and liver which contain many mitochondria is largely through OxPhos while the red blood cells (erythrocytes) which do not have a nucleus or mitochondria produces energy through glycolysis. The membrane potentials for these cells are
heart : -86mV
liver: -56mV
red blood cells: -6mV

Despite the differences in resting membrane potentials as well as mechanism of energy production among various cells in the body, the free energy of ATP hydrolysis is maintained around -56 KJ/mol. This indicates that the balance of energy consumption and production (energy homeostasis) is independent of the energy source and the total amount of ATP produced. . Any disturbance in this energy homeostasis affects cell function and cell viability. Normal cells have the capacity to balance the energy use and production with respiration and substrate level phosphorylation thus maintaining the free energy of ATP hydrolysis. However, energy dysregulation is the characteristic of cancer cells.



Energy regulation in cancer cells

If OxPhos becomes compromised in a normal cell through some injury, then substrate level phosphorylation must increase to maintain the stable free energy of ATP hydrolysis and cell viability. The cell could reduce energy expenditure to balance the reduced energy production. The cell could also die through apoptosis (programmed cell death) or necrosis (stress induced uncontrolled cell death).

[quote author=Cancer as a Metabolic Disease]
It is important to recognize that prolonged reliance on substrate-level phosphorylation for energy production in previously normally respiring cells produces genome instability, disorder, and increased proliferation, that is, the hallmarks of cancer. Entropy refers to the degree of disorder in systems and is the foundation of the second law of thermodynamics . Szent-Gyorgyi described cancer as a state of increased entropy, where randomness and disorder predominate . Protracted OxPhos insufficiency coupled with persistent compensatory fermentation increases entropy. Cells that do not increase fermentation energy to compensate for insufficient OxPhos simply die off and never become neoplastic. Adaptation to fermentation allows a cell to bypass mitochondrial-induced senescence. Cancer arises in those cells that bypass mitochondrial-induced senescence (akin to programmed cell death).
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Warburg was the first to describe in detail the dependence of cancer cells on glucose and glycolysis in order to maintain viability following irreversible respiratory damage. He considered respiration and fermentation as the sole producers of energy within cells, and energy alone as the central issue of tumorigenesis. “We need to know no more of respiration and fermentation here than that they are energy-producing reactions and that they synthesize the energy-rich adenosine triphosphate, through which the energy of respiration and fermentation is then made available for life” [Warburg] . Warburg considered fermentation as the formation of lactate from glucose in the absence of oxygen. This type of energy is also produced in mammalian embryos and in our muscles during strenuous exercise.

A dependence on glucose with lactate production in the presence of oxygen later became known as the Warburg effect, which is essentially aerobic glucose fermentation or the continued production of lactic acid in the presence of O2. Why would cancer cells continue to ferment glucose in the presence of O2? Warburg attributed the aerobic fermentation in tumor cells to respiratory damage or respiratory insufficiency. Tumor cells grown in the presence of O2 behave as if they were abnormal facultative anaerobes in continuing to ferment in the presence of O2.
[/quote]

Here it may be worthwhile to understand the difference between respiration and fermentation. From a cellular perspective, fermentation is evolutionarily older than respiration. Fermentation is linked to relatively uncontrolled cell proliferation and less differentiation. Respiration in the presence of oxygen on the other hand is a characteristic of more complex, differentiated structures. So in the presence of injury to the mitochondria which disrupts respiration, cells which do not die but revert to fermentation as their main source of energy can eventually transform into malignant cancer cells.

There is considerable experimental evidence of mitochondrial injury in cancer cells. Mitochondria in tumors differ in number, size and shape from regular mitochondria. There is experimental evidence to show that OxPhos capability is closely linked to the structural integrity of healthy mitochondria; conversely when OxPhos capability is impaired, the morphology becomes abnormal. It has been reported that greater the degree of mitochondrial morphological abnormality, greater is the degree of malignancy of the tumour.



Disputes about Warburg's Theory

One insufficiently rigorous criticism of Warburg's theory comes from the observation that cancer cells do use O2. This is then taken as an indication of normal respiration in cancer cells. However, there is experimental evidence to show that is not true.

[quote author=Cancer as a Metabolic Disease]
Indeed, O2 consumption increases with increased malignancy in some tumor cells. Does this mean that respiration is normal or increased in such cells? Not necessarily. Warburg has attributed this phenomenon to defects in the coupling of respiration to ATP production . In other words, some cancer cells produce CO2 and consume O2, but produce insufficient energy through respiration.
Defects in the inner mitochondrial membrane of tumor cells dissipate the proton motive gradient, thus uncoupling the linkage between electron transport and ATP production through OxPhos.
[/quote]

When such uncoupling occurs between the electron transport mechanism (where oxygen is utilized as in OxPhos ) and usable energy production ( ATP synthesis as in OxPhos), there is often a production of heat. More aggressive tumours are known to be "hot". The author's hypothesis ties the heat produced in aggressive tumours to the mechanism of mitochondrial uncoupling.

Role of amino acid fermentation
One of the criticisms of Warburg's hypothesis was that not all cancer cells showed elevated lactic acid production through glycolysis. The author provides evidence which supplied the missing link in Warburg's hypothesis.

[quote author=Cancer as a Metabolic Disease]
Although many tumor cells have active TCA cycles and might appear to respire, in that they consume oxygen and produce CO2 and ATP in the mitochondria, I will present data showing that this is pseudo respiration in some cases. In other words, pseudo respiration has all the characteristics of respiration, but does not involve ATP synthesis through OxPhos. I propose that this apparent respiratory energy is derived from amino acid fermentation. Just as tumor cells ferment glucose in the presence of O2, some tumor cells also ferment glutamine and possibly other amino acids in the presence of elevated glucose and O2. Glucose and glutamine interact synergistically to drive tumor cell fermentation. Fermentation is the bioenergetic signature of tumor cells.
..............
Mitochondrial amino acid fermentation is known to maintain metabolic homeostasis under hypoxia in several species of diving animals. Mitochondrial amino acid fermentation can also maintain metabolic homeostasis in the heart and kidney under low glucose and low O2 conditions. The possibility that tumor cells might also obtain energy through amino acid fermentation has not been considered previously as an alternative energy source to OxPhos. Although Warburg considered respiration and glucose fermentation as the sole producers of energy within cells, amino acid fermentation in the mitochondria can also produce energy through substrate-level phosphorylation.

We were the first group to report that Krebs cycle substrate-level phosphorylation might compensate for insufficient respiration in metastatic cancer cells . On the basis of preliminary studies, I suggest that energy through glutamine fermentation could compensate for insufficient or suppressed respiration in those tumor cells that can use glutamine for energy. While it is well known that glucose can be fermented, less is known about amino acid fermentation. Lactate is the by-product of glucose fermentation, whereas succinate, alanine, and aspartate are by-products of glutamine or amino acid fermentation under hypoxia (insufficient oxygen availability). ...........

The expression of lactate in the presence of O2 is abnormal and would indicate that the cells are fermenting. The degree of fermentation (lactate production) is positively correlated with the degree of malignant growth . Also, the less is the respiration, the greater is the fermentation.
....If the cells consume oxygen, it is unlikely that succinate would accumulate. Under high glucose, amino acid fermentation can occur whether or not succinate accumulates. Hence, it is important to account for the multiple variables required to assure that cells are actually using OxPhos alone or are using some combination of OxPhos and mitochondrial substrate-level phosphorylation to maintain their viability.
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Using a bioluminescent-based in vitro ATP assay, we found that ATP production and cell viability were similar in the metastatic cells grown in media containing either glutamine alone or glucose alone. Shelton also showed that lactate production was significantly lower in the metastatic cells grown in glutamine than in the cells grown in glucose, indicating that these cells produce little lactate from glutamine alone. ...However, ATP synthesis and lactate production were significantly greater in the VM-M3 tumor cells grown in glucose and glutamine than that for the tumor cells grown in either glutamine alone or glucose alone . These findings show that glucose and glutamine work synergistically to enhance ATP synthesis, lactate production, and growth..... The synergy we found in the VM-M3 tumor cells was due to glutamine, as neither aspartate nor alanine (alternative nitrogen sources) could replace glutamine for the effect.
....

In other words, mitochondria are capable of metabolizing glutamine in these tumor cells. The question arose as to whether these cells were using the glutamine to produce energy through OxPhos or through mitochondrial fermentation. The role for glutamine in energy production would be in addition to the known role of glutamine in replenishing TCA cycle metabolites (anapleurosis).

We showed that tumor cell viability and ATP production were robust in either anoxia or cyanide as long as both glucose and glutamine were present in the media. Since anoxia (95% N2, 5% CO2) or cyanide (an inhibitor of complex IV respiration) inhibits OxPhos, the robust synergy seen for glucose and glutamine is unlikely due to significant energy from OxPhos.

We propose that the glucose/ glutamine energy synergy observed in our metastatic mouse cells arises from linked fermentation redox couples in the cytoplasm and mitochondria that synthesize ATP largely through nonoxidative substrate-level phosphorylations.
[/quote]
 
Re: Cancer as a Metabolic Disease: Thomas Seyfried

Genetic Theory of Cancer

[quote author=Cancer as a Metabolic Disease]

How was it possible for the gene theory to gain precedence over Warburg's metabolic theory for the origin of cancer? As with most man-made fiascos, there is usually a convergence of several mishaps. The same can be said for why the gene theory displaced the Warburg metabolic theory for the origin of cancer.

First, the appearance of normal respiratory function in cancer cells leads many to question Warburg's central hypothesis that injury to OxPhos was the origin of cancer. As discussed in Chapter 4, the attacks of Weinhouse and other investigators were especially effective in discouraging investigation into the respiratory origin of cancer. Moreover, how could cancer cells arise from injured respiration if so many investigators working in the cancer metabolism field have reported that OxPhos is normal in many tumor cell types? I have addressed the shortcomings of these arguments in Chapters 4, 5, and 8. The experimental evidence linking the origin of cancer to defective energy metabolism appeared to be confused to many investigators working both within and outside the metabolism field. It was also difficult to see how defective respiration could cause gene mutations or metastasis. The failure to craft a cohesive cancer theory based on defective energy metabolism raised the possibility that other explanations of cancer might be more credible than any metabolic hypothesis. The gene theory gained momentum over the viral theory of cancer once the perceived molecular mechanisms of viral action were revealed. A mechanistic linkage between gene defects and viruses was convenient, as viruses had long been recognized as the origin of cancer. It gradually became recognized that viruses might cause cancer by turning on certain cancer-causing genes called oncogenes, or by turning off other genes that prevented cancer, that is, tumor suppressor genes. Oncogenes are those that are assumed to cause cancer. This accounts for the attention given to these kinds of genes in the cancer field. According to James German, a pioneer in cytogenetics, 1981 was the turning point when scientific evidence overwhelmingly supported the mutational origin of human cancer. Stratton and colleagues have considered 1982 as this turning point with the seminal discovery that the human HRAS oncogene could transform normal mouse NIH3T3 cells into cancer cells . In 1994, Harold Varmus was quoted as saying “there's incontrovertible evidence that cancer is a genetic disease” . Dr. Varmus now heads the NCI (National Cancer Institute).
..........................................

Although there is incontrovertible evidence that genomic instability is found in most cancers, this does not mean that cancer is primarily a genetic disease. According to Gibbs, “No one questions that cancer is ultimately a disease of the DNA” . I must apologize to Dr. Gibbs, but I seriously question this notion. I consider the majority of gene defects described in tumor cells as downstream epiphenomena of insufficient or damaged respiration. This includes the majority of recognized oncogenes and tumor suppressor genes. Alterations in these genes are required in order to enhance nonoxidative energy metabolism. In other words, the genetic damage seen in cancer arises as an effect of damaged respiration with compensatory fermentation rather than as the direct cause of cancer. If oncogene upregulation does not follow respiratory injury, the cell will die. Oncogenes are needed to maintain cellular viability following protracted respiratory insufficiency. There is growing evidence supporting this concept.

How would the genomic instability theory of cancer be viewed if there were evidence showing that nuclear genomic stability is dependent on normal respiratory function? How would the genomic instability theory of cancer be viewed if there were evidence showing that oncogene upregulation and suppressor gene downregulation are required for maintaining cell viability following respiratory damage? How would the genomic instability theory of cancer be viewed if there were evidence showing that tumor suppressor gene mutations and viruses damage respiration? I will review evidence showing that genomic instability, DNA damage, and abnormal expression of many oncogenes and tumor suppressor genes arise as secondary downstream effects of abnormal respiration rather than as primary causes of most cancers. I will review evidence showing that inherited cancer genes damage respiration, which then produces cancer. Once genomic defects become established in the tumor cell, they can contribute to the irreversibility of the disease. The persistent view of cancer as a DNA disease is largely responsible for the failure to develop effective cancer therapies. It is difficult to develop an effective therapy for a disease when the origin of the disease is misunderstood.
[/quote]


Inconsistencies in the genetic theory of cancer

[quote author=Cancer as a Metabolic Disease]
It is important for readers to carefully consider the multiple inconsistencies supporting the gene theory of cancer.

Soto and Sonnenschein state:

“the emergence of conflicting data within the SMT (somatic mutation theory) did not result in the rejection of premises and hypotheses. For example, an oncogene could be ‘dominant’ and express a gain of function with respect to the non-mutated homologue, and its biological effect could be contextual at the same time. That is, a mutation that should have produced uncontrolled cell proliferation resulted in cell death or arrest of cell proliferation. Again, ad hoc explanations were proposed to resolve conflicting evidence, leading to a situation whereby any possible conclusion is valid because no alternative concept is ever disproved and abandoned. The lack of fit is attributed to the unfathomable complexity of nature/ biology. In short, something can be anything and its opposite” .


Support for the Soto and Sonnenschein argument was recently highlighted regarding mutations in the gene for isocitrate dehydrogenase 1 (IDH1) [50]. Some investigators suggest that the IDH1 gene acts as a tumor-provoking oncogene, whereas others suggest that IDH1 acts as a tumor-inhibiting suppressor gene. The problem becomes even more confusing with suggestions that IDH1 can act simultaneously as an oncogene and as a tumor suppressor gene . In other words, when it comes to the SMT (somatic mutation theory) of cancer, “something can be anything and its opposite.”

Rous may have hit the nail on the head regarding the SMT as early as 1959 when he stated: “Most serious of all the results of the somatic mutation hypothesis has been its effect on research workers. It acts as a tranquilizer on those who believe in it”.


The concerns raised over the years regarding the SMT as a rational explanation for the origin of cancer are so profound that it is remarkable that this theory has persisted for as long as it has. How many more patients must die before the cancer field abandons the failed therapies based on the SMT of cancer?
...............................
Just because the majority of cancer researchers do not question the theory that guides their work does not mean that the theory is correct. Indeed, it appears that the average cancer researcher is not guided by any grand theory, rather they formulate restricted hypotheses for the next few experiments and tend to go on collecting data without reference to the problem of carcinogenesis (Ponten J. In: Iversen OH, editor. New Frontiers in Cancer Causation. Washington, DC: Taylor & Francis; 1992. p. 59). More disturbingly, many investigators pursue their research in areas considered to be “hot” simply because well-known researchers have defined the area as such. Many correctly surmise that it is easier to get papers published and grants funded in hot areas than in areas not considered hot. Cancer is one of the few fields where research areas are consistently hot, but progress toward the cure is consistently cold.

The cancer research field has drifted off course for too long in my opinion. It is now time for all cancer researchers to pause, and to reconsider the foundation upon which their views rest. In light of the compelling counterarguments against the gene-based theories of cancer together with our extensive in vivo studies in brain cancer [53– 55], it has become clear to me that genetic theories are wanting in their ability to explain the origin of cancer. I do not dispute the overwhelming evidence that defects in DNA, genes, and chromosomes occur in all cancers. The evidence is massive. What I do question, however, is whether these defects actually cause the disease. I will review evidence showing that most of the genomic defects seen in tumor cells can be linked directly or indirectly to insufficient respiration.
[/quote]

This should sound familiar to the readers of this forum as a consequence of ponerization of society at large and science in this particular case .

Here are just some experimental results reviewed by the author that supports his pov about the genetic origins of cancer.

[quote author=Cancer as a Metabolic Disease]

If respiratory insufficiency is the origin of cancer, then tumor nuclei should not induce malignancy when placed in cytoplasm containing respiration competent normal mitochondria. Alternatively, if mitochondrial dysfunction is the origin of cancer, normal nuclei should be unable to prevent tumorigenesis when placed into the tumor cytoplasm. I refer to these types of experiments as nuclear– cytoplasm transfer studies.
...................
In a more extensive series of experiments, Israel and Schaeffer showed that suppression of the malignant state could reach 100% in cybrids containing normal cytoplasm and tumorigenic nuclei. The unique aspect of their study was that all of the cells utilized, both normal and transformed, were derived from an original cloned progenitor [4]. They also showed that nuclear/ cytoplasmic hybrids derived by fusion of cytoplasts from malignant cells (nucleus absent) with karyoplasts from normal cells (nucleus present) produced tumors in 97% of the animals injected. These findings showed that normal cell nuclei could not suppress tumorigenesis when placed in tumor cell cytoplasm. In other words, normal nuclear gene expression was unable to suppress malignancy.
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It is also well documented that nuclei from cancer cells can be reprogrammed to form normal tissues when transplanted into normal cytoplasm despite the continued presence of the tumor-associated genomic defects in the cells of the derived tissues.
[/quote]

Experimental evidence shows that "Normal mitochondria suppress respiratory dysfunction and tumorigenicity, whereas abnormal mitochondria cannot suppress respiratory dysfunction or tumorigenicity."

(a) Normal cells beget normal cells.

(b) Tumor cells beget tumor cells.

(c) Delivery of a tumor cell nucleus into a normal cell cytoplasm begets normal cells despite the persistence of tumor-associated genomic abnormalities.

(d) Delivery of a normal cell nucleus into a tumor cell cytoplasm begets tumor cells or dead cells, but not normal cells.

The results show that nuclear genomic defects alone cannot cause tumors and that normal mitochondria can suppress tumorigenesis. .

[quote author=Cancer as a Metabolic Disease]

In summary, the origin of carcinogenesis resides with the mitochondria in the cytoplasm, not with the genome in the nucleus. How is it possible that so many in the cancer field seem unaware of the evidence supporting this concept? How is it possible that so many in the cancer field have ignored these findings while embracing the flawed gene theory? Perhaps Payton Rous was correct when he mentioned “the somatic mutation theory acts like a tranquilizer on those who believe in it”.
[/quote]

[quote author=Cancer as a Metabolic Disease]

Emerging evidence indicates that a persistent retrograde response can link respiratory injury to the genomic instability seen in tumor cells [5– 7]. The RTG response is the general term used for mitochondria-to-nuclear signaling and involves cellular responses to changes in respiration and the functional state of mitochondria [6, 8– 14]. The RTG response is initiated following interruption in the respiratory energy production. Genomic stability is dependent on the integrity of the mitochondrial function. If respiratory insufficiency is not corrected, the RTG response will persist, thus producing the Warburg effect, genomic instability, and the path to tumorigenesis.
[/quote]



Metastasis

[quote author=Cancer as a Metabolic Disease]

Metastasis is the general term used to describe the spread of cancer cells from the primary tumor to surrounding tissues and to distant organs and is the primary cause of cancer morbidity and mortality [1– 8]. It is estimated that metastasis is responsible for about 90% of cancer deaths [9]. This estimate has not changed significantly in more than 50 years [10, 11]. Although systemic metastasis is responsible for 90% of cancer deaths, most research in cancer does not involve metastasis in the in vivo state [5]. That about 1500 people continue to die each day from cancer further attests to the failure in managing the disease once it spreads to other organs. Metastasis involves a series of sequential and interrelated steps. In order to complete the metastatic cascade, cancer cells must detach from the primary tumor, intravasate into the circulatory and lymphatic systems, evade immune attack, extravasate at distant capillary beds, and invade and proliferate in distant organs [1– 4, 7, 12, 13]. Metastatic cells also establish a microenvironment that facilitates angiogenesis (development of new blood vessels) and proliferation, resulting in macroscopic, malignant secondary tumors.

A difficulty in characterizing the cellular origin of metastasis comes in large part from the lack of animal models that show systemic metastasis. As I have mentioned in Chapter 3, tumor cells that are naturally metastatic should not require intravenous injection to initiate the metastatic phenotype. The key phenotype of metastasis is that the tumor cells spread naturally from the primary tumor site to secondary locations. Nevertheless, numerous investigators use intravenous tumor cell injection models to study metastasis. While these models can provide information on tumor cell survival in the circulation, it is not clear if this information is relevant to survival of naturally metastatic tumor cells.
[/quote]

Cellular origin of metastasis

Epithelial to Mesenchymal Transition (EMT) (from genetic theory of cancer)

[quote author=Cancer as a Metabolic Disease]

The epithelial to mesenchymal transition (EMT) posits that metastatic cells arise from either epithelial stem cells or differentiated epithelial cells through a stepwise accumulation of gene mutations that eventually transform the epithelial cell into a tumor cell with mesenchymal features [8, 9, 16– 20]. This idea comes from findings that many cancers arise in epithelial tissues where abnormalities in cell– cell and cell– matrix interactions occur during tumor progression. Eventually, neoplastic cells emerge that appear as mesenchymal cells, which lack cell– cell adhesion, are dysmorphic in shape, and eventually spread to distant organs.
.....
The idea for the EMT arose from attempts to draw parallels between the behavior of normal cells during metazoan morphogenesis and the behavior of cancer cells during tumor progression [9, 16]. Adaptation of the EMT into the gene theory of cancer suggested that metastasis is the endpoint of a series of genomic alterations and clonal selection. This then provided the neoplastic cells with a growth advantage over normal cells [17, 20, 24, 25]. It is difficult to understand how a collection of gene mutations, many of which are random, could produce cells with the capacity to detach from the primary tumor, intravasate into the circulation and lymphatic systems, evade immune attack, extravasate at distant capillary beds, and recapitulate epithelial characteristics following invasion and proliferation in distant organs. This would be quite a feat for a cell with a disorganized genome.

The recapitulation of epithelial characteristics at distant secondary sites is referred to as the mesenchymal– epithelial transition (MET) and is thought to involve a reversal of the changes responsible for the EMT [9, 16, 17]. No explanation has appeared on how the genomic instability and multiple point mutations and chromosomal rearrangements responsible for the neoplastic mesenchymal phenotype could be reversed or suppressed when the tumor cells recapitulate the epithelial phenotype at distant sites.

If many of the nuclear genomic mutations are not reversed, how is it possible that they could be responsible for EMT in the first place? I think the imagination must be stretched to the limits in order to accept the EMT/ MET as a credible explanation for metastasis. The changes in cell behavior and morphology linked to this explanation of metastasis and their dramatic reversibility are similar in some ways to those of the werewolf.
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Myeloid Cells as the origin of metastasis


The myeloid cell ( a blood cell which is not a lymphocyte, having its origin in the bone marrow or spinal cord) origin of metastasis proposes that metastatic cancer cells arise from myeloid cells regardless of tissue origin [26]. Myeloid cells are already mesenchymal cells and would therefore not require the complicated genetic mechanisms proposed for the EMT in order to metastasize. Macrophages (big eaters which engulf and digest cellular debris and pathogens in a process called phagocytosis) arise from the myeloid lineage and have long been considered the origin of human metastatic cancer [15, 26,42– 45] . Macrophages can fuse with epithelial cells within the inflamed microenvironment, thus manifesting properties of both the epithelial cell and macrophage in the fusion hybrids [29, 46]. The origin of metastatic cancer from hematopoietic stem cells (which makes cellular components of blood) , derived from bone marrow cells, is also consistent with the myeloid hypothesis. In his recent excellent review on metastasis, David Tarin states:

“Hence, it would appear that tumor metastasis first appears in the lower chordates in parallel with the origin of lymphocytes and this may indicate that metastasis cannot occur until an organism has evolved the genes for lymphocyte trafficking.”

According to our hypothesis, it is hematopoietic stem cells themselves or their lineage descendants that become the metastatic cells either through direct transformation in the inflamed microenvironment or through their fusion with neoplastic tumor cells. The idea that transformed myeloid cells can give rise to invasive and metastatic cells within tumors is not widely recognized. Rather than being recognized as part of the neoplastic cell population, many investigators consider macrophages and other myeloid cells as part of the tumor stroma.
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What are the properties of macrophages that would make them prime suspects for the origin of metastasis? Macrophages are among the most versatile cells of the body with respect to their ability to migrate, to change shape, and to secrete growth factors and cytokines [36, 60– 62]. These macrophage behaviors are also the recognized behaviors of metastatic cells.
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Phagocytosis involves the engulfment and ingestion of extracellular material and is a specialized behavior of M2 macrophages and other professional phagocytes [62]. This process is essential for maintaining tissue homeostasis by clearing apoptotic cells, cellular debris, and invading pathogens. Like M2 macrophages, many malignant tumor cells are phagocytic both in vitro and in vivo. Tumor cell phagocytosis was first described over a century ago from histopathological observations of foreign cell bodies within in the cytoplasm of cancer cells, which displayed crescent-shaped nuclei [44]. This cellular phenotype resulted from the ingested material pushing the nucleus to the periphery of the phagocytic cell. These cells were commonly referred to as either bird's-eye or signet-ring cells [144, 158]. While this phagocytic/ cannibalistic phenomenon is commonly seen in feeding microorganisms, cell cannibalism is also seen in malignant human tumor cells [120, 144, 158, 159]. Fais and colleagues provided dramatic evidence of tumor cell phagocytosis in showing how malignant melanoma cells eat T-cells. This is remarkable as T-cells are thought to target and kill tumor cells.


There is also evidence that some tumor cells can eat NK cells [159]. If macrophage-derived metastatic cells can eat T-cells and possibly NK cells, then it is possible that immune therapies involving these cells might not be effective for long-term management of some metastatic cancers. Indeed, cancer immunotherapies have had little impact in reducing the yearly death rate from advanced metastatic cancers.


Fusogenicity is the ability of a cell to fuse with another cell through the merging of their plasma membranes [29, 154]. This process can arise in vitro as is seen with the formation of antibody-producing hybridomas. However, fusion in human cells is a highly regulated process that is essential for fertilization (sperm and egg) and skeletal muscle (myoblasts) and placenta (trophoblast) formation [183]. Outside of these developmental processes, cell-to-cell fusion is normally restricted to differentiated cells of myeloid origin (reviewed in Ref. 148).

During differentiation, subsets of macrophages fuse with each other to form multinucleated osteoclasts in bone or multinucleated giant cells in response to foreign bodies [43]. Osteoclasts and giant cells have increased cell volume that facilitates engulfment of large extracellular materials [43]. Macrophages are also thought to fuse with damaged somatic cells during the process of tissue repair.
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Mekler et al. and Warner proposed that fusion of committed tumor cells with host myeloid cells would produce tumor hybrids capable of migrating throughout the body and invading distant organs [149, 187]. Recent studies from Wong and coworkers described how macrophages fuse with tumor epithelial cells [29, 188]. Besides inflammation, radiation also increases the fusion hybrid process [188]. Is it possible that decreased long-term survival in some irradiated cancer patients results from enhanced production of macrophage– epithelial fusion hybrids? We have stated that the human brain should rarely if ever be irradiated [189]. It is my opinion that radiation will contribute to brain tumor recurrence.
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Although radiation therapy can help some cancer patients, radiation therapy will also enhance mitochondrial damage and fusion hybridization, thus potentially making the disease much worse.
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As respiration is responsible for maintaining genomic stability and the differentiated state, respiratory insufficiency will eventually induce the default state of unbridled proliferation. If this occurs in cells of myeloid origin such as macrophages, then emergence of cells with enhanced metastatic potential would be a predicted outcome. Macrophages are genetically programmed to exist in the circulation and to enter and exit tissues [221]. While cells of myeloid origin can serve as the body's best friend during wound healing and in killing pathogenic bacteria, these same cells can become the body's worst enemy if they become transformed during tumorigenesis.

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Thus according to the author's hypothesis, both immunotherapy and radiation therapy have the potential to cause more damage in metastatic cancers.


It is also worthwhile to note that metastatic tumor cells do not invade distant organs randomly. Lung, liver and bone are some of the most common sites of metastasis. The myeloid cell origin of metastasis can provide an explanation for this phenomenon - which has been called the "seed and the soil" hypothesis for breast cancer where the tumor cells (seed) are found to have an affinity for certain organs (soil).

[quote author=Cancer as a Metabolic Disease]

Basically, respiratory insufficiency in cells of myeloid origin can explain the seed and soil phenomenon. This comes from findings showing that mature cells of monocyte origin (macrophages) enter and engraft tissues in a nonrandom manner [224]. Macrophages are genetically programmed to exist in the circulation and to preferentially enter various tissues during wound healing and the replacement of resident myeloid cells [221, 224]. Some macrophage populations in liver are regularly replaced with bone marrow-derived monocytic cells, whereas other macrophage populations are more permanent and require fewer turnovers [225]. It is reasonable to assume that metastatic cancer cells derived from macrophages or fusions of monocytic cells with epithelial cells will also preferentially home to those tissues that naturally require regular replacement of resident macrophages.

This prediction comes from findings that many metastatic cells express characteristics of macrophages [29]. Macrophage turnover should be greater in tissues such as liver and lung where the degree of bacterial exposure and the wear-and-tare on the resident macrophage populations is considerable [226]. This could explain why these organs are a preferred soil of many metastatic cancer cells. Bone marrow should also be a common target of metastatic cells because this site is the origin of the hematopoietic stem cells, which give rise to myeloid cells. Liver, lung, and bone are also preferential sites for metastatic spread for the VM mouse tumor cells [36]. This is one reason why the natural tumors in the VM mouse, which preferentially home to these tissues, are an excellent model for metastatic cancer.
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In addition, any unhealed wound is an ideal "soil" for macrophage infiltration. In a phenomenon called inflammatory oncotaxis, mechanically injured tissues (eg tooth extractions) are sometimes found to be susceptible to cancer metastasis.

The crown-gall disease in plants share many features with tumours in animals and is referred to as a form of plant cancer. It shares all the important aspects of animal cancer except for the property of metastasis.

[quote author=Cancer as a Metabolic Disease]
The crown-gall tumors do not metastasize because they do not have macrophages or myeloid cells as part of their immune system [249]. The findings in crown-gall are also consistent with Tarin's [1] hypothesis, “that metastasis cannot occur until an organism has evolved the genes for lymphocyte trafficking.”
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Re: Cancer as a Metabolic Disease: Thomas Seyfried

Prevention/Management/Healing of Cancer


What causes damaged cellular respiration

[quote author=Cancer as a Metabolic Disease]

Any unspecific condition that damages a cell's respiratory capacity, but is not severe enough to kill the cell, can potentially initiate the path to a malignant cancer. Reduced respiratory capacity could arise from damage to any mitochondrial protein, lipid, or mtDNA. Some of the many unspecific conditions that can damage a cell's respiratory capacity thus initiating carcinogenesis include inflammation, carcinogens,radiation (ionizing or ultraviolet), intermittent hypoxia, rare germline mutations, viral infections, and age.
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Chronic inflammation is said to be one of the most common causes of damage to mitochondria and cellular respiration. Several cellular mechanisms can be at play in the process - one of which is "persistent nitric oxide expression in the inflamed microenvironment. "


Metabolic Management of Cancer

[quote author=Cancer as a Metabolic Disease]
If we know what cancer cells can and cannot eat, we can kill them. Ketone bodies and fatty acids can provide alternative metabolic fuels to glutamine for mitochondrial ATP synthesis. As these alternative fuels also require O2 for metabolism, death should occur quickly for any cell in the absence of both glucose and O2, especially if ketone bodies and fatty acids are the only available fuels. If cells maintain viability in O2 using either ketone bodies or fatty acids as the only energy substrates, then these cells are likely using OxPhos for survival. As far as I know, ketone bodies and fatty acids are not fermented for energy [4].
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Because tumor cells ferment rather than respire, they are dependent on the availability of fermentable fuels (glucose and glutamine). Normal cells shift metabolism from glucose to ketone bodies and fats when placed under energy stress. This is dependent on genomic stability. Ketone bodies and fats are nonfermentable fuels in mammalian cells. Tumor cells have difficulty in using ketone bodies and fats for fuel when glucose is reduced. Because tumor cells lack genomic stability, they are less able than normal cells to adapt to changes in the metabolic environment.
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Such a metabolic approach to cancer therapy is applicable to the majority (if not all) types of cancer irrespective of tissue origin.


Therapeutic Fasting

There are numerous studies which show that dietary energy restriction (DER) is a general metabolic therapy that significantly reduces growth and progression of various types of tumour - including cancers of brain, breast, colon, pancreas, lung and prostrate. DER reduces circulating glucose levels on which many tumours depend for survival and growth. Such therapeutic fasting promotes a new state of energy homeostasis in the cells where stored fat and protein in the body is used to generate glucose through the process of gluconeogenesis (new glucose generation) as well as increase in blood ketones. Respiratory insufficiency and genomic instability prevents tumor cells from entering this new energy state. This is most effective for people who are just diagnosed with cancer.


Restricted Ketogenic Diet

Studies have been conducted on the effect of cancer from following a restricted ketogenic diet (KD-R). KD-R has been shown to produce similar anti-tumor effects as that in DER. The key factor observed in studies with mice was that the KD had no therapeutic effect on tumor growth if consumed in unrestricted amounts.

[quote author=Cancer as a Metabolic Disease]
The data [] show that blood glucose levels remain high in mice that consume the 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.
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This validates the usefulness of the ketogenic diet with intermittent fasting discussed in the main ketogenic diet thread. Since only cells with normal mitochondrial respiratory capacities can effectively use ketone bodies for energy, tumor cell viability is lost in the presence of ketone bodies resulting in death of tumor cells. On the other hand, glucose is directly implicated in tumour growth: higher blood glucose levels lead to faster growth.


* Malignancy and invasiveness of tumours are directly related to vascularity (blood vessel development or angiogenesis). Reduced availability of glucose has been observed to reduce vascularity and cell proliferation. DER and KD-R have both shown anti-angiogenic properties in both mouse and experimental human brain tumors. These therapies target angiogenesis naturally in contrast to toxic anti-angiogenic drugs.

[quote author=Cancer as a Metabolic Disease]
In light of our findings, it is surprising that the cancer field would persist in treating cancer patients with toxic antiangiogenic drugs such as bevacizumab and cediranib, which show marginal efficacy and appear to enhance the invasive behavior of tumor cells [121– 123]. Compared to bevacizumab (Avastin), which targets angiogenesis, while producing adverse effects and enhancing tumor cell invasion [112, 122, 124– 126], DER targets angiogenesis, while improving general health and inhibiting tumor cell invasion [34, 45]. Is it better for oncologists to target tumor angiogenesis using toxic drugs with marginal efficacy or is it better to use nontoxic metabolic strategies such as DER with robust efficacy? Oncologists should consider this question. Patients with advanced cancers should be presented with therapeutic options.[/quote]


* DER also promotes cell apoptosis (programmed cell death). Apoptotic cell death is different from necrotic cell death which is usually associated with inflammation. Apoptotic tumor cell death is preferred over necrotic tumor cell death as it is less harmful for the tumor microenvironment since tissue inflammation is less in apoptosis than in necrosis. Radiation as well as toxic chemotherapy kills tumor cells through necrosis and inflammation which often hurt long-term prognosis of the disease.


* DER also directly suppresses multiple pro-inflammatory pathways in tumours.

[quote author=Cancer as a Metabolic Disease]
There are no oncology drugs known to my knowledge that can simultaneously target inflammation and angiogenesis, while, at the same time, killing tumor cells through an apoptotic mechanism.
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* The author advocates a suitable combination of drugs and dietary therapies for advanced cases.

[quote author= Cancer as a Metabolic Disease]
Although DER is effective in reducing tumor growth and invasion, this therapeutic approach alone is unlikely to completely eradicate all types of malignant cancers [51, 229]. I believe that metabolic diet therapies will be enhanced when combined with drugs that also target glucose energy metabolism. Support for my hypothesis comes from our study showing that the nonmetabolizable glycolysis inhibitor, 2-DG, works synergistically with the KD-R to reduce CT-2A astrocytoma growth [30].
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Few studies have evaluated the therapeutic efficacy of antiglycolytic or anticancer drugs in combination with DER [51]. Recent studies from Safdie and the Longo group suggest that CR and fasting can enhance patient health during chemotherapy [26, 232, 233]. We were the first to show that the KD-R supplemented with 25 mg/ dl of 2-DG was effective in reducing intracerebral tumor growth to a greater extent than was either 2-DG 2-DG or KD-R when administered alone. These findings showed a powerful synergistic interaction between 2-DG and the diet.
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Combinations of CR mimetics (drugs which try to produce the same physiological state as achieved by calorie restriction) with the restricted KD could open new avenues in cancer drug development, as many drugs that might have minimal therapeutic efficacy or high toxicity when administered alone could become therapeutically relevant and less toxic when combined with energy-restricted diets. ....CR mimetics will also be more effective against advanced cancer if administered with drugs that also target glutamine, a major fuel for metastatic cancer [229].
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* Targeting glutamine is important as experimental results showed that DER alone was unable to stop metastasis in some cases. This led the author to direct his attention towards the role of glutamine in systemic metastasis.

[quote author=Cancer as a Metabolic Disease]
Although DER reduces blood glucose levels, it does not reduce blood glutamine levels. Indeed, blood glutamine levels might increase under DER in mice, as moderate physical activity can increase blood glutamine [72]. Mice increase physical activity food foraging under DER. We knew that the VM-M3 tumor cells shared several characteristics with macrophages and that glutamine is a major fuel of immune cells, including macrophages. We also knew that transformed macrophages or their fusion hybrids are the origin of metastatic cancer cells. Hence, it would be important to determine if glutamine restriction might reduce systemic metastasis. We found that the DON (a glutamine antagonist) prevented metastatic spread to the liver, lung, and kidney. In addition, we examined liver histology because liver becomes heavily infiltrated with VM-M3 cells. Indeed, liver metastasis was found in 100% of the control mice. Liver is also a common site for many metastatic human cancers. Histological analysis confirmed the lack of tumor cells in the liver of the DON-treated mice in comparison to the control AL (unrestricted feeding) nontreated mouse and control and CR-treated CR-treated groups.
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* Finaly, inflammation is the cause of many diseases in humans in addition to cancer. Switching energy metabolism from glucose to ketones has been shown to have powerful anti-inflammatory effects. Hence, according to the author, KD is under consideration for numerous neurological and neuro-degenerative diseases (like Alzheimers) where inflammation is a part of the pathology.
 
Re: Cancer as a Metabolic Disease: Thomas Seyfried

A very interesting and very readable (now -- after all the other reading) book. I want one! At $74.25 for the Kindle edition, and $111.52 for hardcover, however, a little more about what you personally learned and found of value from reading the book could be helpful.

I haven't yet finished reading the excerpts above; that might help too. :)
 
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