Life Goal to Prevent Cancer

[Arielle2]

RE: Has anyone tried fasting before chemotherapy? (Dr. Valter Longo study)
by Lillylover on Thu Oct 06, 2016 08:11 PM

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Today I had my 5th round of chemo for bc. I have fasted for each round--48 hours before, 24 hours after. I take in nothing but water or if I really need something different I have black coffee or green tea, but usually not more than 2 cups during the fasting period. While there are some fast-mimicking diets out there I figure the more I keep out of my body,, the better. If I can do it. So far, it hasn't been that difficult. When I feel hungry I distract myself. I truly believe it has worked well for me. My side effects are minimal with the exception of hair loss. I have had no nausea, no mouth sores, my taste, while off for a couple weeks, was back to normal after the 3rd round, my white blood count has stayed up, although my hemoglobin and platelets dropped after the 3rd round, necessitating a decrease in the dosage of one of my drugs, but today's lab showed them back up. My appetite is good, I haven't lost weight. I'm happy with my decision to try fasting. If you choose to try it, I hope it works as well for you. Good luck with your treatment.

 

[Arielle2]

RE: Has anyone tried fasting before chemotherapy? (Dr. Valter Longo study)
by chriscrossan on Thu Oct 06, 2016 09:25 PM

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That is great news, Lilly. I fasted only 36 hours total each time I had chemo, and I saw the benefits. Since that time five years have passed, and my body is the picture of health for a 61-year-old man. When I contacted Dr. Valter Longo, he encouraged me even after the chemo therapy was complete, to fast several times a month. The reason is that fasting itself causes the cancer cells to become starved, and they will go into apoptosis (self-destruction), so although I have one remaining form of cancer left (Follicular Lymphoma), the tumors have remained stationary for the last three or four years. I think this is in part due to fasting 32 hours once or twice a month. In any case, I congratulate you for exercising such discipline in your own treatment. May heaven look down with favor on you...

 

[Arielle2]

The above has been from

https://cancercompass.com/message-board/message/all,73866,2.htm

 

[Arielle2]

One mans journey thru several rounds of treatment and his experience both not fasting, and fasting.

https://adventuresinlivingterminallyoptimistic.com/2016/09/29/chemo-in-the-fast-lane/

Prof. Longo’s preclinical research incorporates fasting both pre-infusion (to given benign cells a chance to slow down and hibernate before chemo attacks) and post-infusion (to make sure benign cells don’t come out of hibernation & wake up in the midst of chemo).

 

[Arielle2]

http://yaletownnaturopathic.com/fasting-before-chemotherapy/

Fasting Before Chemotherapy
Home / Blog / Fasting Before Chemotherapy
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Fasting Before Chemotherapy
By Yaletown Naturopathic / In Blog / Comments(5)
Written By: Dr. Adam McLeod, ND, BSc

There has been a major movement lately for cancer patients to fast before and after an infusion of chemotherapy. When first hearing this, it sounds dangerous to encourage a patient to fast when their body is already stressed with chemotherapy. Fasting before chemotherapy has been used safely in several clinical trials1,4. It turns out that there is a significant amount of scientific data to support this therapy when the patient is properly supervised. This is a very interesting shift in thinking because the conventional approach in the past has been encouraging patients to get as many nutrients into their body as possible.

There are a number of metabolic reasons why fasting may increase the effectiveness of chemotherapy while reducing the side effects2,3. Fasting triggers normal cells to enter into a protective mode. They rapidly become more efficient and this triggers a reduction in glucose and IGF-1 levels by more than 50%3. This rapid metabolic shift would be very difficult to achieve even with a very potent mixture of drugs. Cancer cells are unable to shift into this protective mode and this makes them more vulnerable to the chemotherapy than normal cells5. This is referred to as differential protection and it has the potential to transform conventional cancer care.

The length of fasting before chemotherapy varies significantly depending on which study that you look at. The most commonly recommended fasting period is 48 hours before chemotherapy and this continues until 24 hours after the chemotherapy infusion. During this fasting period ideally the patient should only have water. It should be as close to complete fasting as possible.

Although it is clearly uncomfortable not eating for a total of 72 hours, the research is indicating that this is a worthwhile sacrifice. The discomfort from hunger will actually decrease the severity of the side effects from the chemotherapy. It is also important to keep in mind that this starvation state is triggering a powerful metabolic shift in your cells that protects your cells while making the cancer cells more vulnerable to the chemotherapy.

As fasting before chemotherapy is further researched it is likely that other mechanisms will be discovered that explain this differential protection. Even without a fully defined biochemical mechanism for this protection, it is clear that fasting does make a substantial difference. Do not implement a fasting protocol before chemotherapy without the supervision of a qualified health professional. It is essential that you are monitored during this process because fasting is not safe for everyone.

If you are currently doing chemotherapy make sure that you contact a Naturopathic Physician who focuses on oncology. There are many different naturopathic therapies which not only increase the effectiveness of the chemotherapy but they can act to reduce side effects from the chemotherapy. These natural approaches are safe to use with chemotherapy when they are used under the supervision of an experienced Naturopathic doctor. A Naturopathic Doctor that works with oncology will take the time to look at your case and help you effectively integrate these approaches into your program.

Dr. Adam McLeod is a Naturopathic Doctor (ND), BSc. (Hon) Molecular biology, First Nations Healer, Motivational Speaker and International Best Selling Author. He currently practices at his clinic in Vancouver, British Columbia where he focuses on integrative oncology. http://www.yaletownnaturopathic.com

References:

1) Safdie, Fernando M., et al. “Fasting and cancer treatment in humans: A case series report.” Aging (Albany NY) 1.12 (2009): 988.

2) Raffaghello, Lizzia, et al. “Fasting and differential chemotherapy protection in patients.” Cell Cycle 9.22 (2010): 4474-6.

3) Lee, C., and V. D. Longo. “Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients.” Oncogene 30.30 (2011): 3305-3316.

4) de Groot, S., et al. “Abstract P4-16-12: CARE: A pilot study of the effects of short-term fasting on tolerance to (neo) adjuvant chemotherapy in breast cancer patients.” Cancer Research 73.24 Supplement (2013): P4-16.

5) Laviano, Alessandro, and Filippo Rossi Fanelli. “Toxicity in chemotherapy—when less is more.” New England Journal of Medicine 366.24 (2012): 2319-2320.

 

[Arielle2]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4215472/

In this regard, dietary modifications, such as high-fat, low-carbohydrate ketogenic diets that enhance mitochondrial oxidative metabolism while limiting glucose consumption could represent a safe, inexpensive, easily implementable, and effective approach to selectively enhance metabolic stress in cancer cells versus normal cells.
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The most notable and well-studied use of a ketogenic diet is for the treatment of obesity popularized by Dr. Robert Atkins (see Fig. 1) (Dr. Atkins Diet Revolution 1972). Ketogenic diets have also been shown to be beneficial in the treatment of patients with glucose transporter defects and other inborn metabolic disorders [24]. The diet is reported to show promise in slowing the progression of amyotrophic lateral sclerosis [25], and there is a growing body of evidence suggesting ketogenic diets may be beneficial in other neurodegenerative diseases including Alzheimer’s disease and Parkinson’s disease [26]. In addition, there are case reports and small case studies indicating improvement in patients with autism [27] depression [28], polycystic ovary syndrome [29], and type 2 diabetes mellitus [18].
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Recently, ketogenic diets have been studied as an adjuvant to cancer therapy in both animal models and human case reports. As early as 1987, Tisdale et al. saw decreased tumor weight and improved cachexia in mice with colon adenocarcinoma xenografts eating a ketogenic diet [30]. Additional studies have shown that ketogenic diets reduce tumor growth and improve survival in animal models of malignant glioma [31–33], colon cancer [34], gastric cancer [35], and prostate cancer [36–38]. Furthermore, ketogenic diets have been hypothesized, with some supporting evidence, to potentiate the effects of radiation in malignant glioma models [39] as well as in non-small cell lung cancer models [5]. Fasting, which also induces a state of ketosis, has been shown to enhance responsiveness to chemotherapy in pre-clinical cancer therapy models as well as possibly ameliorating some of the normal tissue side effects seen with chemotherapy [40]. Fasting cycles are also reported to retard the growth of tumors and sensitize a range of cancer cell types to chemotherapy [40,41].

Some of the clinical results include a case report of two female pediatric patients, with advanced stage malignant astrocytoma who demonstrated a 21.8% decrease in tumor SUV when these patients were fed a ketogenic diet, as determined by uptake of 2-deoxy-2[18F]fluoro-d-glucose (FDG) using positron emission tomography (PET) [42]. A more recent case report showed improvement in a 65 year old female patient with glioblastoma multiforme treated with calorie-restricted ketogenic diet together with standard treatment [43]. Importantly, a quality of life study in patients with advanced cancer found that a ketogenic diet had no severe adverse effects, improved emotional functioning, and reduced insomnia [44].

 

[Arielle2]

from the above site
[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4215472/figure/f0010/']
Comparison of normal cell and tumor cell metabolism on an American diet and a ketogenic diet. Relative to normal cells, tumor cells have been hypothesized to have increased mitochondrial DNA mutations as well as alterations in the expression of nuclear encoded mitochondrial proteins, resulting in increased production of reactive oxygen species (ROS) during mitochondrial respiration. Increased tumor cell ROS increases tumor cell dependence upon glucose metabolism, resulting in generation of NADPH and pyruvate via the pentose phosphate shunt and pyruvate from glycolysis. NADPH and pyruvate reduce hydroperoxides. Ketogenic diets decrease the capability of tumor cells to produce NADPH because, in most tissues, fat metabolism is unable to undergo gluconeogenesis to form glucose-6-phosphate (G-6-P) necessary to enter the pentose phosphate shunt. Thus, ketogenic diets should further increase the oxidative stress in tumor cells relative to normal cells by limiting NADPH regeneration.
[/URL]

 

[Arielle2]

Non-Toxic Metabolic Management of Metastatic Cancer in VM Mice: Novel Combination of Ketogenic Diet, Ketone Supplementation, and Hyperbaric Oxygen Therapy.
Poff AM1, Ward N1, Seyfried TN2, Arnold P3, D'Agostino DP1.
Author information

Abstract
The Warburg effect and tumor hypoxia underlie a unique cancer metabolic phenotype characterized by glucose dependency and aerobic fermentation. We previously showed that two non-toxic metabolic therapies - the ketogenic diet with concurrent hyperbaric oxygen (KD+HBOT) and dietary ketone supplementation - could increase survival time in the VM-M3 mouse model of metastatic cancer. We hypothesized that combining these therapies could provide an even greater therapeutic benefit in this model. Mice receiving the combination therapy demonstrated a marked reduction in tumor growth rate and metastatic spread, and lived twice as long as control animals. To further understand the effects of these metabolic therapies, we characterized the effects of high glucose (control), low glucose (LG), ketone supplementation (βHB), hyperbaric oxygen (HBOT), or combination therapy (LG+βHB+HBOT) on VM-M3 cells. Individually and combined, these metabolic therapies significantly decreased VM-M3 cell proliferation and viability. HBOT, alone or in combination with LG and βHB, increased ROS production in VM-M3 cells. This study strongly supports further investigation into this metabolic therapy as a potential non-toxic treatment for late-stage metastatic cancers.

PMID:

26061868

PMCID:

PMC4464523

DOI:

10.1371/journal.pone.0127407

 

[Arielle2]

ibe study looking at ketogenic diet on colon cancer in mice
Asian Pac J Cancer Prev. 2015;16(5):2061-8.
Growth of human colon cancer cells in nude mice is delayed by ketogenic diet with or without omega-3 fatty acids and medium-chain triglycerides.
Hao GW1, Chen YS, He DM, Wang HY, Wu GH, Zhang B.
Author information

Abstract
BACKGROUND:
Tumors are largely unable to metabolize ketone bodies for energy due to various deficiencies in one or both of the key mitochondrial enzymes, which may provide a rationale for therapeutic strategies that inhibit tumor growth by administration of a ketogenic diet with average protein but low in carbohydrates and high in fat.

MATERIALS AND METHODS:
Thirty-six male BALB/C nude mice were injected subcutaneously with tumor cells of the colon cancer cell line HCT116. The animals were then randomly split into three feeding groups and fed either a ketogenic diet rich in omega-3 fatty acids and MCT (MKD group; n=12) or lard only (LKD group; n=12) or a standard diet (SD group; n=12) ad libitum. Experiments were ended upon attainment of the target tumor volume of 600 mm3 to 700 mm3. The three diets were compared for tumor growth and survival time (interval between tumor cell injection and attainment of target tumor volume).

RESULTS:
The tumor growth in the MKD and LKD groups was significantly delayed compared to that in the SD group.

CONCLUSIONS:
Application of an unrestricted ketogenic diet delayed tumor growth in a mouse xenograft model. Further studies are needed to address the mechanism of this diet intervention and the impact on other tumor-relevant parameters such as invasion and metastasis.

 

[Arielle2]

the purpose of this study was to find an alternative because most poele dont want to live on a keto diet.....

Cancer Res. 2014 Dec 1;74(23):6991-7002. doi: 10.1158/0008-5472.CAN-14-0385. Epub 2014 Oct 10.
Long-chain fatty acid analogues suppress breast tumorigenesis and progression.
Gluschnaider U1, Hertz R1, Ohayon S1, Smeir E1, Smets M1, Pikarsky E2, Bar-Tana J3.
Author information

Abstract


Obesity and type 2 diabetes (T2D) are associated with increased breast cancer incidence and mortality, whereas carbohydrate-restricted ketogenic diets ameliorate T2D and suppress breast cancer. These observations suggest an inherent efficacy of nonesterified long-chain fatty acids (LCFA) in suppressing T2D and breast tumorigenesis. In this study, we investigated novel antidiabetic MEDICA analogues consisting of methyl-substituted LCFA that are neither β-oxidized nor esterified to generate lipids, prompting interest in their potential efficacy as antitumor agents in the context of breast cancer. In the MMTV-PyMT oncomouse model of breast cancer, in which we confirmed that tumor growth could be suppressed by a carbohydrate-restricted ketogenic diet, MEDICA treatment suppressed tumor growth, and lung metastasis, promoting a differentiated phenotype while suppressing mesenchymal markers. In human breast cancer cells, MEDICA treatment attenuated signaling through the STAT3 and c-Src transduction pathways. Mechanistic investigations suggested that MEDICA suppressed c-Src-transforming activity by elevating reactive oxygen species production, resulting in c-Src oxidation and oligomerization. Our findings suggest that MEDICA analogues may offer therapeutic potential in breast cancer and overcome the poor compliance of patients to dietary carbohydrate restriction.