Ketogenic diet

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In cancer studies glucose can be seen aiding in celleur growth. Both healthy and cancerous cells.

There was recently a write up in NCBI pondering on and suggesting reconsidering the way cancer is perceived.
It began with "Although cancer has historically been viewed as a disorder of proliferation, recent evidence has suggested that it should also be considered a metabolic disease.

The ending statement is-
"Are the changes in metabolism in cancer cells a consequence of the changes in proliferation or a driver of cancer progression? Can cancer metabolism be targeted to benefit patients?"

http://www.ncbi.nlm.nih.gov/pubmed/24139946

Next article -
"Is there a role for carbohydrate restriction in the treatment and prevention of cancer?"

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3267662/

With that being said lets look at Ketogenics

A great article that describes Ketogenics and what areas its being used in--all the way from weight loss, epilesy and post trials on cancers.
The diet can be adjusted by a qualified nutrionist to perform alot of metabolic reactions.

http://io9.com/what-you-should-know-abo ... -489267213

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Brain tumors and Ketogenics diet
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819381/

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Olgas posting in 2013

http://www.cureasps.org/forum/viewtopic.php?f=53&t=718

Certainly a good thing to remember--

Nutrition During Cancer Treatment and Recovery


Prior to the identification of effective cancer screening and treatment, many people were diagnosed with cancer in a late stage, when they may have already experienced the weight loss and cachexia that was common among patients with late-stage cancer. In addition, patients undergoing cancer treatment often experienced significant untreated nausea and vomiting, which led to further weight loss. Because of these clinical experiences, cancer was considered to be a disease associated with weight loss, rather than obesity. However, many patients now being diagnosed have early stage disease and treatments are more effective. Therefore, with growing numbers of patients beginning the cancer treatment process already overweight or obese,7 additional weight gain is a frequent complication of treatment.8 While highly variable depending on the type of cancer and stage at diagnosis, cancer can cause profound metabolic and physiological alterations that can affect the nutrient requirements for macro- and micronutrients.9 Symptoms such as anorexia, early satiety, changes in taste and smell, and disturbances of the bowel are common side effects of cancer and cancer treatment and can lead to inadequate nutrient intake and subsequent malnutrition. Substantial weight loss and poor nutritional status can still occur early in the course of some cancers, although the prevalence of malnutrition and weight loss varies widely across cancer types and stage at diagnosis.10 Consuming enough calories to prevent additional weight loss is therefore vital for survivors at risk of unintentional weight loss, such as those who are already malnourished or those who receive anticancer treatments affecting the gastrointestinal tract.10, 11
All of the major modalities of cancer treatment, including surgery, radiation, and chemotherapy, can significantly affect nutritional needs; alter regular eating habits; and adversely affect how the body digests, absorbs, and uses food.9, 12 Nutritional assessment for survivors should therefore begin as soon after diagnosis as possible and should take into consideration treatment goals (curative, control, or palliation) while focusing on both the current nutritional status and anticipated nutrition-related symptoms.12


During active cancer treatment, the overall goals of nutritional care for survivors should be to prevent or resolve nutrient deficiencies, achieve or maintain a healthy weight, preserve lean body mass, minimize nutrition-related side effects, and maximize quality of life. Studies confirm the benefit of dietary counseling during cancer treatment for improving outcomes, such as fewer treatment-related symptoms, improved quality of life, and improved dietary intake.13-16 Suggestions for finding an oncology nutrition expert to provide dietary counseling are provided in Table 1.

My concern with the diet?

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My concern with the diet? Loosing weight when you can't afford it as a cancer patient..

Had to search under low carb diets to locate this article

http://www.livestrong.com/article/16260 ... -diabetic/

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It has come to our attention that the recent news of lactate being a possible driver, fuel if you will of Alveolar soft part sarcoma ,to reconsider the ketogenic diet and low glycemic thought for now.

Be well our friends
Love
Debbie

http://www.cureasps.org/forum/viewtopic.php?f=2&t=980

Thank you Jolie for the wonderful article !

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https://robertanagourney.wordpress.com/ ... t-sarcoma/

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The Case for Metabolic Cancer gains Traction

Researchers from the Huntsman Cancer Institute at the University of Utah reported an interesting finding with far-reaching implications.

In their study of the rare tumor known as alveolar soft part sarcoma (ASPS), they examined the well-established chromosomal translocation that occurs between chromosomes 17 and X. This results in the production of a fusion protein dubbed ASPSCR1-TFE3. Like other fusion proteins described in malignancies such as lymphoma, acute pro-myelocytic leukemia and chronic myelogenous leukemia, a novel function occurs when two disparate genomic elements are spliced together.

In this instance, the ASPSCR1-TFE3 gene product functions as a lactate transporter. Strikingly, every mouse in which the gene was up regulated developed a tumor. The locations of tumor, in the skull and near the eye, both represented areas of high lactate concentration. In humans, this tumor occurs in skeletal muscle, also associated with high lactate production.

Since 1930, when Otto Warburg first described increased glycolysis (preferential use of sugars) in tumor cells, investigators have pondered the implication of inefficient glucose metabolism in the face of adequate oxygenation.

Human metabolism relies upon mitochondrial function to efficiently liberate the maximum amount of energy in the form of ATP from each glucose molecule. Glycolysis occurring in the cell cytoplasm is highly inefficient and produces only 1/18 of the amount of ATP that a full molecule of glucose can produce through mitochondrial oxidative phosphorylation. Recent molecular biological studies have established that the preferential use of glycolysis may represent the cells need to direct glucose away from energy production and toward the creation of essential structures like amino acids, lipids, and nucleic acids. With the rapid turnover of glucose, cells produce an overwhelming amount of lactate, which is then transported out of the cell. At least this has been the working hypothesis over many years.

More recently, investigators have begun to examine how lactate metabolism may represent the interplay between stromal fibroblast cells and tumor cells. Indeed, many tumor cells are now known to increase lactate uptake reflecting increased lactate production by fibroblasts that have been commandeered in the tumor microenvironment.

Lactate uptake is under the control of a family of transporters known as monocarboxylate transporters, of which nine have been described. These are expressed differently in various tissues, have different affinities for lactate and transport in one direction or another. These processes appear to be under the control of the major regulator of oxygen metabolism known as HIF-1 alpha. As cancer cells adapt to a high lactate environment, they can survive in low oxygen tension.

The preferential use of lactate as a source of energy is contrary to many dictates of current metabolic research that suggest that tumor cells preferentially use glucose and have limited capacity to utilize non-glucose energy sources like the ketone bodies acetoacetate and beta-hydroxybutyrate. Substantial literature on ketogenic diets suggests that these ketone bodies deprive cancer cells of needed nutrition and energy. The current discovery by the Utah investigators, as well as interesting work conducted by researchers in Italy on the prostate cancer, provide a new angle on some of these principles of cancer metabolism.

As the investigators from Utah note, the alveolar soft part sarcoma is a rare tumor, but the implications of these findings could be profound, as they force us to re-think tumorigenesis and the metabolic basis of cancer.

https://robertanagourney.wordpress.com/ ... t-sarcoma/

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Lactate uptake is under the control of a family of transporters known as monocarboxylate transporters, of which nine have been described. These are expressed differently in various tissues, have different affinities for lactate and transport in one direction or another. These processes appear to be under the control of the major regulator of oxygen metabolism known as HIF-1 alpha. As cancer cells adapt to a high lactate environment, they can survive in low oxygen tension.

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Lactate and Ketone Bodies Act as Energy Substrates as Well as Signal Molecules in the Brain

Abstract

Astroglia or astrocytes, the most abundant cells in the brain, are interposed between neuronal synapses and the microvasculature in the brain’s gray matter. This unique anatomical location allows astroglia to play pivotal roles in brain metabolism as well as in the regulation of cerebral blood flow. In particular, astroglial cellular metabolic compartmentation exerts supportive roles in dedicating neurons to the generation of action potentials and protects neurons against the oxidative stress associated with their high energy consumption. Key products of astroglia include lactate and ketone bodies (beta-hydroxybutyrate and acetoacetate), which can also be produced avidly by muscle and liver, respectively. Therefore, brain cells, skeletal muscles, and hepatocytes constitute a metabolic compartmentation in the whole body. In this chapter, I will focus on brain cells, especially astroglia, since the impairment of normal astroglial function can lead to numerous neurological disorders including stroke, neurodegenerative diseases, and neuro-immunological diseases. I will also discuss the metabolic responses of brain cells in terms of food consumption and exercise. A better understanding of the astroglial metabolic response is expected to lead to the development of novel therapeutic strategies for diverse neurological diseases.



https://www.intechopen.com/chapters/75814