(UNDER CONSTRUCTION)

— Saira Riaz 2019/08/04
— Marcos Reyes 2019/08/04

Cancers differ in the causes that lead to the altered cellular replication machinery. Cancer can arise from mutations in proliferation-related genes, including mutated proto-oncogenes and tumor suppressor genes. ¹⁾. Cancer can also arise from epigenetic rearrangement of DNA strands in the chromosomes, and from mitochondrial mtDNA mutations. There are viruses that cause cancer ²⁾. Cancer stem cells form tumors of phenotypic and functional heterogeneity. ³⁾

Just as the cause of a cancer can be unique, the optimal treatment for each cancer can be unique. This article reviews research for optimal treatment in respect to the afflicted organ or anatomy, because that is how cancer has been researched in the past. Additionally, while the molecular cause of every cancer can be independent of location, overall health is affected when one bodily system is not functioning at capacity.

While mainstream treatments use chemo or radiotherapy, our focus is to find treatments that avoid harm and benefit normal cells, and exploit the weaknesses of cancer cells.

Fasting is considered to be effective in protecting normal cell growth and also can induce selective apoptosis in cancer cells. Fasting improves cellular health and reduces lipid peroxidation by reducing oxidative stress. It also induces autophagy, removing muted or damaged proteins, thereby increasing oxidative stress tolerance. Various studies also report that chemotherapy in combination with fasting can help in the reduction of tumor based cells. Fasting also results in decrease of amino acids and low glucose level that enhance anti warburg effect that unable ATP generation that promote oxidative damage. ⁴⁾ Fasting-mimicking diets have also been applied to increase the effectiveness of therapeutic medicines.

Even in an optimal environment, cells are evolving mutations at a slow rate due to imperfections in the maintenance and replication of DNA. Despite safeguards to maintain the original DNA sequence, including programmed self-destruction, multi-cellular organisms become a mosaic of evolved cells, with the cells most fit to survive enduring.

Mutations are random in nature. Most mutations are deleterious. While the cell could continue to survive with some mutation, certain mutations will provide internal signaling to trigger self-destruction. Cells are programmed with a fail-safe to suicide for the overall benefit of the organism, a process known as apoptosis. However, some mutations do not trigger apoptosis. Through mitosis, the mutated cells replenish dying cell neighbors with their own mutated copy.

These very few mutated cells may in some way be able to out-compete neighboring cells. While these cells could have advantage over neighboring cells in terms of competitive survival, they may not necessarily be the most effective towards the overall health of the organism. This is an aspect of the aging process. In the case of cancer, the mutated cell proliferation will likely cause an organism's death.

Mutated cells can happen in different stages of life, and results in clonal mosaicism, including where different regions of the body have differing genomes.

The imperfections in the machinery for DNA maintenance and DNA replication, could be more exact and fault tolerant. However, a certain level of mutation is beneficial for the survival of a species in a changing environment. Cancer and aging are products of the evolutionary process.

Cells have evolved a very intricate and careful internal balance, and once the balance is tipped, additional mutations are more likely to occur, accelerating the evolutionary process.

One of the mutations that may follow, can be the fail-safe that instructs the cell to suicide when internal sensors indicate instability.

Another mutation that may follow, is cell replication without the required signaling to do so. For example, normal cells will not replicate when they are surrounded by neighbors. A mutation may occur where replication / proliferation occurs despite contact inhibition. These mutated cells are said to be cancerous.

Cancer cells may also separate from their original tissue, circulate in the bloodstream, and take up residence elsewhere. The migration is termed metastasis.

Because of accelerated evolution in cancer cells, cancer is not a single disease, and treatment or finding a cure is more challenging. However, because cancer cells have an insatiable appetite, required for proliferation, finding weaknesses in their energy metabolism may be a key to treatment. ⁵⁾

Many types of cancer exhibit the Warburg Effect.

Fasting could be harmful because of mal-nourishment, due to cancer altering the available proteins in the body. In which case, keto with adequate protein could be a solution. Also it has been observed that starving of cancer cells is only observed in the limited mice related studies. If the cancer patients would be exposed to starvation for longer period of time this might increase rate of mortality and risk of prolonged patients care. Many Studies also showed that people who are well nourished have better chances of survival and lesser chances of having cancerhttps://www.ncbi.nlm.nih.gov/pubmed/24269077.

Randomized and un planned fasting can deteriorate the health instead of benefiting the cancer patients. Cancer patients with malnutrition face the more deleterious effects.There is a need of special screening of nutrients for cancer patients and it varies on the basis of cancer stages too. Short term nutritional interventions should be based on some criteria as proposed by European society of clinical nutrients and metabolism https://www.ncbi.nlm.nih.gov/pubmed/12765673.

Diet, nutrition and the prevention of cancer 2004 https://www.who.int/nutrition/publications/public_health_nut6.pdf

check this article contains very comprehensive overview of the diet effects and also contain recommended diet constituents (by WHO-WORLD HEALTH ORGANIZATION).

To fast, or not to fast before chemotherapy, that is the question
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5870384

Let's follow every citation and rewrite this article. Every other line, he's constantly saying remarks like “we think it's not good” “it's our opinion” etc etc. Who cares?! Let's break it down into each article that is cited in this study, and draw conclusions from facts rather than this author's opinions.

Also the citations in this opinion: https://www.quora.com/Whats-better-for-someone-with-cancer-and-doing-chemotherapy-fasting-or-eating-well/answer/Liang-Hai-Sie

This is where studies go, if they don't fit into a specific cancer type

Preliminary clinical data indicates that in cancer patients fasting is not associated with major side effects and may reduce several of the side effects associated to chemotherapy, including a decreased toxicity to lymphocytes. These pre-clinical and preliminary clinical results served as the foundation for randomized trials to test the safety and efficacy of fasting cycles on the effect of chemotherapy on both normal and cancer cellshttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815756/

Many promising cancer drugs being developed will require years to become approved by regulatory bodies and, in most cases, will only be effective for a fraction of patients with specific types of cancer. It is therefore important to develop broader, complementary strategies that can be translated rapidly into effective therapies. Two to 4 days of fasting before chemotherapy treatment is safe and protect animals, and possibly humans, against the side effects of chemotherapy.Experiments in simple organisms, human cells, and mice indicated that these effects of fasting were caused by changes inside and outside cells that increased the death of tumor but not normal cells, a process termed differential stress sensitizationhttps://stm.sciencemag.org/content/4/124/124ra27/tab-pdf.

In another studyhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4102383 it was found that prolonged fasting reduces circulating IGF-1 levels and PKA activity in various cell populations, leading to signal transduction changes in long-term hematopoietic stem cells (LT-HSC) and niche cells that promote stress resistance, self-renewal and lineage-balanced regeneration. Multiple cycles of fasting abated the immunosuppression and mortality caused by chemotherapy, and reversed age-dependent myeloid-bias in mice, in agreement with preliminary data on the protection of lymphocytes from chemotoxicity in fasting patients. The pro-regenerative effects of fasting on stem cells were recapitulated by deficiencies in either IGF-1 or PKA and blunted by exogenous IGF-1. These findings link the reduced levels of IGF-1 caused by fasting, to PKA signaling and establish their crucial role in regulating hematopoietic stem cell protection, self-renewal and regeneration. Main key points are below

• Cycles of prolonged fasting (PF) reduce damage in bone marrow stem and progenitor cells and protect mice against chemotoxicity
• Prolonged fasting cycles promote lineage-balanced hematopoietic regeneration
• Prolonged fasting cycles regulate stem cell populations independently of chemotherapy and help reverse from immunosenescence
• Reduction of IGF-1 or PKA signaling promotes HSC self-renewal

Calorie restriction and cancer prevention: a mechanistic perspective https://cancerandmetabolism.biomedcentral.com/articles/10.1186/2049-3002-1-10

When less may be more: calorie restriction and response to cancer therapy. https://www.ncbi.nlm.nih.gov/pubmed/28539118

A 2014 systematic review of fifty-nine studies on animals found that 91% showed caloric restriction to play an anti-cancer role during intiation, progression and metastasis of cancer. https://www.ncbi.nlm.nih.gov/pubmed/25502434

THE FOLLOWING IS FROM https://osher.ucsf.edu/patient-care/integrative-medicine-resources/cancer-and-nutrition/faq/low-carbohydrate-diet The article was last updated on 2016, so we will be adding research and conclusions available since then. We have messaged UCSF for permission.

Mouse models of glioblastoma demonstrate treatment enhancement when mice were fed a ketogenic diet in combination with chemotherapy and/or radiation.8 9 Additionally, studies showed that mice fed a ketogenic diet, some with a liquid ketogenic supplement and calorie restriction, have prolonged survival and significantly decreased tumor growth.9, 10, 11, 12 These studies provide a promising backdrop for the human trials.

A study published in 2014 reported results of a retrospective review of 53 patients being treated for glioblastoma with concurrent chemo-radiotherapy and adjuvant chemotherapy.13 Of these 53 patients, six followed a ketogenic diet during treatment. The diet was well tolerated and without any adverse effects. Serum glucose levels were significantly lower for those on the ketogenic diet than for those on a standard diet, despite the use of high dose steroids.

In 2014, researchers published data on the ERGO Trial,14 which was a pilot, non-randomized feasibility study (n=20) of a ketogenic diet in recurrent glioblastoma. The results suggest that although the ketogenic diet alone does not seem to extend median survival, when combined with chemotherapy, there was enhanced progression-free survival. These findings were seen again in another pilot study (n=2) published in 2015.15 Although no benefit was seen from following a ketogenic diet alone, remission rates were improved when the diet was used in combination with treatment. Both of these studies demonstrated the safety of following a ketogenic diet. There are currently several active clinical trials looking at the potential benefit of using a ketogenic diet or modified Atkins Diet in patients with brain tumors.

In mouse models of prostate cancer, researchers have been evaluating varying amounts of carbohydrate intake. In 2008, researchers were able to show that mice on a no-carbohydrate diet (0 grams) had significantly reduced tumor growth and prolonged survival versus mice on a 72% carb diet (standard) or 44% carb diet (low).16 Similar results were found in other studies.17 Another study showed that mice following a no-carbohydrate diet had significantly prolonged survival, as well as lower levels of inflammation, insulin and obesity, along with increased apoptosis of cancer cells.18

Although these findings are interesting, they do not readily transfer to humans, given the difficulties of following a 0 gram carbohydrate diet. In 2010, another study showed that mice fed a 10-20% carbohydrate diet had similar survival to mice consuming a 0% carbohydrate diet.19 Two more studies showed similar results, and actually one determined that mice on a 20% carbohydrate diet had the slowest rate of tumor growth.20, 21

So far, we only have research on two human trials looking at prostate cancer and low carbohydrate diets, with three clinical trials currently recruiting. Lin and colleagues recruited eight men with newly diagnosed prostate cancer and randomized them to a low fat, low glycemic load intervention arm (<20% fat & <100 glycemic load) or a “standard American” control arm (35% fat & >200 glycemic load).22 The men on the low fat/low glycemic load diet lost more weight and showed significant gene expression changes in prostate epithelium on biopsy; suggesting the possibility of a therapeutic value. Many of these gene changes could conceivably alter the proliferation, metabolism and redox potential of prostate epithelial cells. In 2011, data was published from a cohort study of 566 Swedish men, which showed that adherence to a low carbohydrate, high protein diet was associated with a decreased risk of prostate cancer.23

Most of the research on carbohydrate restriction and breast cancer investigated its effects on prevention. Only two mouse model studies of breast cancer have evaluated a low carbohydrate diet and tumor growth. One study found that tumor growth was suppressed by a ketogenic diet.24 Another study showed that cancers grew slower in mice fed a low carbohydrate, high protein diet.25 A further reduction in growth in the primary tumor and metastasis was observed when the ketogenic diet was combined with a COX-2 inhibitor.

The Shanghai Women’s Health Study (79, 942 Chinese women between the ages of 40-70) showed an association between a high carbohydrate, high glycemic load diet and an increased risk of pre-menopausal breast cancer.26 The Nurses’ Health Study (included 86,621 American women between the ages of 30-55) found lower risk for ER negative postmenopausal breast cancer with a diet high in fruits, vegetables, plant proteins, and plant fats with a total carbohydrate intake <50% and a glycemic load <100. 27

The remaining studies looked at the ability of a low carbohydrate diet to lower metabolic markers associated with breast cancer risk. In one study, 115 overweight or obese women with increased risk for breast cancer followed either a calorie restricted, low carbohydrate diet (650 kcal, <50 grams carb x 2 days/week) or ad lib calorie, low carbohydrate diet (<50 grams carb x 2 days/week) or a 1500 kcal/day diet with normal carbohydrate intake for 7 days/week.28 They found that those in either of the carbohydrate restricted groups had greater weight loss, lower body fat, and less insulin resistance.

Another study showed similar results. Post-menopausal breast cancer survivors consumed a ketogenic diet (<40 grams carb, 800-1200 kcal) and successfully achieved weight loss and improvement in metabolic markers (lower CRP levels, lower fasting insulin levels, and lower circulating estrogen levels).29 In another study, administration of a low-carbohydrate diet to patients with hormone responsive breast cancer on anti-estrogen or anti-aromatase therapy resulted in weight loss with improved lipid profiles and a decrease in signs of non-alcoholic hepatic steatosis.30 There is currently one active clinical trial looking further at a ketogenic diet in a breast cancer rehabilitation program.

In 1995, a case study of two female pediatric patients with advanced stage astrocytoma showed a decrease in glucose uptake at the tumor site when following a ketogenic (10% carbohydrate) diet.31 Of the two, one continued the diet remaining free of disease progression for an additional 12 months.

In head and neck cancer, it’s been hypothesized that carbohydrate restriction and ketosis can be supportive treatments by protecting normal tissue while sensitizing tumor tissue to radiation and chemotherapy while simultaneously supporting body and muscle mass maintenance.32 There is currently an active clinical trial looking at a low carbohydrate diet in head and neck cancer patients.

A study published in 2014 showed that endometrial cancer survivors following a ketogenic diet (<40 grams/day) had statistically significant decreases in weight, estrogenic markers and fasting insulin levels thereby reducing their risk for recurrence.33

One study found increasing risk for various colon cancers with increasing intake of fat, sucrose, lactose, glucose and fructose.34 While no reduction in cancer risk was seen from following a 39% carbohydrate diet in a prospective cohort study of 62,582 Swedish people.35 Based on a review of the other studies referenced in this article, a 39% carbohydrate diet may not be considered low enough to elicit the benefits seen in some of the other studies.

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In the treatment of metastatic advanced cancers, a ketogenic diet has shown promise in mice models for reducing tumor growth and spread while prolonging survival.36, 37 In a human study of 10 patients, those with the highest degree of ketosis showed disease stabilization or partial remission, with no adverse effects.38 Another study of 16 patients following a ketogenic diet (<70 grams/day) showed improved emotional functioning and less insomnia in those who were able to maintain the diet.39 The remaining cancers have at least one mouse study available, but no human data looking at low carbohydrate diets and that specific type of cancer.

In mice with melanoma, researches have observed tumor inhibition at a 20% carb and 2% fat diet.40 And interestingly, when these same mice are given a phytonutrient supplement in addition to the low-carbohydrate or moderate-carbohydrate diet, they see even fewer tumor modules, plus increased survival times.41

In mice with liver cancer, researchers have observed tumor inhibition and even regression when fed a 12% carb diet.42

Mouse models have shown tumor inhibition, treatment enhancement, and prolonged survival in lung cancer, pancreatic cancer, and neuroblastoma. 43, 44, 45, 46

In mice, fasting before radiotherapy offers a protective effect on normal cells, while simultaneously having a mild increase in pancreatic tumor cell death. ⁷⁾

https://www.npr.org/sections/health-shots/2016/03/05/468285545/fighting-cancer-by-putting-tumor-cells-on-a-diet

https://www.quora.com/How-does-a-ketogenic-diet-help-in-fighting-cancer/answer/Ellen-Davis-9

https://www.quora.com/Are-there-hospitals-that-are-using-the-ketogenic-diet-as-management-therapy-for-cancer/answer/Ellen-Davis-9

— Sobia Syed 2019/07/30
— Marcos Reyes 2019/08/01

Statements need to be well supported by research. Marijuanadoctors, medicalnewstoday, Healthline, cancer.gov, fda.gov, and harvard.edu: while they may be great sources worthy of inclusion, there also needs to be peer reviewed research articles that support the same statements. You can have multiple sources backing up a statement as follows. 1) 2) 3) Another statement. 4) 5)

Cannabis oil is booming as the cure of cancer for the past few years and it has become a treatment option for many. The mechanism by which cannabis oil treats cancer involves a partnership between the immune system and the endocannaboid system.

One of the functions of the immune system is to get rid of the dying cells. When it comes to fighting cancer the immune system on its own is only moderately effective, because cancer cells are essentially modified endogenous cells which the immune system doesn’t recognize as harmful. Cancer cells hide from the immune system by hiding the ID that signals something is wrong. However some of the chemicals in cannabis are able to circumvent this disguise. One of those chemicals is THC, a cannabinoids in cannabis. When THC meets the endocannabinoid receptors on cancer cells, they produce ceramide which kills them. Ceramide is the agent the immune system uses to kill dead or dying cells. Once the immune system recognizes that the DNA of the cancer cells is abnormal, it sends the ceramide in and kills the cancerous cells.⁸⁾

Another useful cannabinoid is CBD ( cannabidoil oil) that suppresses the gene that allows the cancer to metastasize and divide. THC and CBD kills the cancer cells and the tissue is left immunized for any over cancer growth, there is nothing else that does this and it works with all types of cancer no matter where the cancer is.

Cannabidiol is mostly confused with marijuana and thought of as a drug. while it is just a second most prevalent of the active ingredients of cannabis (marijuana). While CBD is an essential component of medical marijuana, it is derived directly from the hemp plant, which is a cousin of the marijuana plant. While CBD is a component of marijuana (one of hundreds), by itself it does not cause a “high.” According to a report from the, World heath organization “In humans, CBD exhibits no effects indicative of any abuse or dependence potential to date, there is no evidence of public health related problems associated with the use of pure CBD.” ⁹⁾ (Needs additional citations. One doctor's blog is insufficient proof.)

According to American Society of clinical oncology journal a research was performed on 283 patients with advanced cancer to compare the effects of cannabis extract, THC and placebo on appetite and quality of life in patients with cancer-related anorexia-cachexia syndrome (CACS). The research concluded that there was no differences in patients' appetite or quality of life were found either between cannabis extract, THC, and Placebo or between cannabis extract and THC at the dosages investigated. If we see, this study doesn’t support cannabis treatment or that maybe because all the patients here had advanced stage cancer. ¹⁰⁾

Here are some promising studies performed that suggests that cannabinoids help cure cancer. which is medically reviewed by Alan Carter. ¹¹⁾

• Team worked with a mouse model of pancreatic cancer, which they treated with CBD alongside a typical chemotherapy drug, the team found that, following this combination treatment, the rodents survived almost three times as long as mice from a control group, which had only been treated with typical chemotherapy drugs. ¹²⁾

• A study indicated that CBD could provoke cell death and make glioblastoma cells more sensitive to radiation, but with no effect on healthy cells. ¹³⁾

• Men’s Health Study cohort found that using cannabis may be inversely associated with bladder cancer risk. However, a cause and effect relationship hasn’t been established. ¹⁴⁾

• A study in experimental models of colon cancer suggests that CBD may inhibit the spread of colorectal cancer cells. ¹⁵⁾

• Other research demonstrated the efficacy of CBD in pre-clinical models of metastatic breast cancer. The study found that CBD significantly reduced breast cancer cell proliferation and invasion. ¹⁶⁾

Studies on the role of cannabinoids in the development of cancer have produced mixed results. A 2010 study using a mouse model found that cannabinoids can trigger suppression of the immune system. That could make users more susceptible to some types of cancer. ¹⁷⁾

However, we need more rigorous studies into the potential benefits and risks of CBD, dosing, administration, and how it affects other cancer therapies. ¹⁸⁾ Currently, there are no FDA-approved CBD products for cancer. Patients have been using it on their own.

When it comes to cancer prevention, CBD research has a long way to go and a lot more research is required to bring it to mainstream. Scientists will have to conduct long-term studies of people using specific CBD products, controlling for frequency of use, dosing, and other variables.

https://www.cancervic.org.au/cancer-information/treatments/treatments-types/medicinal-cannabis