I-TREAT Cancer Protocol: Adjunctive Cancer Treatments (2025 Edition)

Contents

• Methodology
• Causes of Cancer
• The ACS 2022 Guideline for Cancer Survivors
• Diet and Cancer
• Quit smoking and alcohol
• The Metabolic Approach to Treating Cancer
• Metabolic and Lifestyle Interventions for Cancer Management
• Body Weight and Physical Activity
• Best Anti Cancer Supplements (Evidence-based)

1. Vitamin D3
2. Turmeric (Curcumin)
3. Magnesium and Molecular Hydrogen
4. Vitamin C
5. Green tea (EGCG)
6. Melatonin
7. Omega-3 Fatty Acids
8. Berberine

• Repurposed Drugs in Oncology
1. Ivermectin
2. Fenbendazole
3. Others

• Key Takeaways

Introduction

We are pleased to introduce the I-TREAT CANCER protocol, designed to help individuals and doctors treat cancer based on updated scientific information. 

The i-Treat cancer protocol consists of three basic components (DSR):

1. Individualized Diet program
2. Individualized Supplement program, which includes vitamins, minerals and phytonutrients.
3. Repurposed drugs

This article serves as a consumer guide for complementary cancer treatment, focusing on practical treatment strategies rather than technical theories. Our aim is to summarise relevant, updated, and practical points, providing you with a personal blueprint and resource for cancer survival.

Cancer survivors indicate that nutrition information obtained from providers is often inadequate or conflicting. (Eur J Cancer Care 2021)

The overall 5-year relative survival rate for all cancers combined is now 68%, and there are over 16.9 million survivors in the United States. Evidence from laboratory and observational studies suggests that factors such as diet, physical activity, and obesity may affect risk for recurrence and overall survival after a cancer diagnosis.

The purpose of this guide is to provide evidence-based, cancer-specific recommendations for diet and lifestyle related strategies for reducing recurrence and cancer death. The audiences for this guide are health care providers caring for cancer survivors as well as cancer survivors and their families.

Sources of evidence that form the basis of this guide are systematic literature reviews, meta-analyses and large randomized clinical trials published.

Most cancer survivors prefer to receive information about diet, alcohol, weight management, and physical activity from their health care team and such discussions can positively influence behavior changes. However, relevant resources are often lacking. Furthermore, many oncology care providers cite lack of time as a barrier to providing counseling on these topics and acknowledge that they have inadequate training and knowledge about available resources. (ACS Cancer J 2022)

Evidence-based information on nutrition and physical activity for cancer survivors is available online through sources such as the ACS, ACSM, and AICR. However, there is also a plethora of misinformation on internet sites—and on social media sites in particular. Survivors report difficulty accessing credible nutrition information online and may be especially vulnerable to claims that specific behavior changes can cure their cancer or extend survival. (ACS Cancer J 2022)

One study of cancer-related nutrition and meal planning content in Pinterest found that a substantial proportion claimed a particular food or recipe prevented, treated, or cured cancer. Approximately one-half of those posting content were for-profit, and only 35% of posts included a disclaimer. Without efforts by social media platforms to flag and manage such misinformation, it is likely to flourish and can potentially overwhelm the evidence-based information that exists. (ACS Cancer J 2022)

Methodology

Why evidence-based? A proven method trumps an unproven one. 

We've scoured the internet, unearthed the best references, and reviewed over 1,000 studies so you don't have to. When interpreting and filtering scientific research, it's crucial to consider the hierarchy and quality of evidence. Not all evidence is created equal. So, what is good evidence? 

Cell culture findings carry less weight than results from studies conducted on mice. Similarly, conclusions from mouse studies are surpassed by findings from human studies.

Case studies and preliminary results from small-scale human trials hold less significance than outcomes from umbrella reviews, systematic reviews and meta-analysis*, randomised controlled trials (RCTs), and more extensive, long-term human trials.

*A systematic review is a review that collects, critically appraises, and synthesises all the available evidence to answer a specifically formulated research question. A meta-analysis, on the other hand, is a statistical method that is used to pool results from various independent studies, to generate an overall estimate of the studied phenomenon.

It would be impossible to review all the studies on the internet; rather, we have focused on, curated and evaluated the information that appear to have the greatest clinical utility. 
 

Causes of Cancer

Why is it important to know? By knowing the root causes, we will better understand why we are using certain strategies to prevent cancer.

As depicted below, most of the root causes of cancer are diet and lifestyle related.

AACR Cancer Progress Report 2023

Therefore, it makes sense to improve your diet and lifestyle in order to prevent or to treat early cancer.

From research point of view, cancer is daunting in the breadth and scope of its diversity, spanning genetics, cell and tissue biology, pathology, and response to therapy. 

The hallmarks of cancer (Cancer Discov 2022) is helping to make the complex science of cancer more understandable. 

The Hallmarks of Cancer were proposed as a set of functional capabilities gained by human cells as they transform from normal cells to cancer states.

Biological Changes and Acquired Capabilities (Cell 2000):

1. sustaining proliferative signaling, 
2. evading growth suppressors, 
3. resisting cell death, 
4. enabling replicative immortality, 
5. inducing angiogenesis, and 
6. activating invasion and metastasis.

Emerging Hallmarks (Cell 2011):

1. deregulating cellular energetics
2. avoiding immune destruction

Enabling characteristics (Cell 2011)::

1. Genome instability and mutation
2. Tumor promoting inflammation

Four new hallmarks (Cancer Discov 2022):

1. unlocking phenotypic plasticity,
2. non-mutational epigenetic reprogramming,
3. polymorphic microbiomes
4. senescent cells.

The ACS 2022 Guideline for Cancer Survivors

General recommendations for cancer survivors

• Nutritional assessment and counseling should begin as soon as possible after diagnosis, with the goal of preventing or resolving nutrient deficiencies, preserving muscle mass, and managing side effects of treatments that may adversely affect nutritional status. 
• Physical activity assessment and counseling should begin as soon as possible after diagnosis, with the goal of helping patients prepare for treatments, tolerate and respond to treatments, and manage some cancerrelated symptoms and treatment-related side effects. 

Recommendations to improve long-term health and increase the likelihood of survival

• Avoid obesity and maintain or increase muscle mass through diet and physical activity. • 
• Engage in regular physical activity, with consideration of type of cancer, patient health, treatment modalities, and symptoms and side effects.
• Follow a healthy eating pattern that meets nutrient needs and is consistent with recommendations to prevent chronic disease. 
• Follow the general advice of the American Cancer Society Guideline for Diet and Physical Activity for Cancer Prevention to reduce risk of a new cancer.

In 2020, the American Cancer Society (ACS) published diet and physical activity guidelines for cancer prevention. Nutrition and physical activity recommendations established by the ACS for the primary prevention of cancer are broadly relevant to survivors undergoing and immediately after cancer treatment.

Diet and Cancer

If oral intake does not support adequate nutrient intake to meet energy expenditure, the Recommended Dietary Allowance for vitamins and minerals, and >1 g of protein per kilogram of body weight per day, then the use of an oral nutritional supplement should be implemented.

If intake remains insufficient, consideration should be given to additional nutrition support strategies, such as an enteral nutrition tube feeding regimen; and, if enteral nutrition support is contraindicated, parenteral nutrition support could be considered to meet nutritional needs.

The National Comprehensive Cancer Network (NCCN) and the American Society for Clinical Oncology (ASCO) recently published guidelines for cancer survivors and their clinicians outlining diet, nutrition, and physical activity recommendations.

Highlights include:

• Recommendations to eat a healthy diet pattern, with adequate macronutrient and micronutrient content from both animal-based and plant-based food options but with a preference to plant-based diet patterns; 
• Caution regarding the overuse and misuse of dietary supplements during and after treatment; 
• Adherence to food safety procedures to avoid foodborne illnesses; and 
• Being as physically active as possible.

Source: American Cancer Society nutrition and physical activity guideline for cancer survivors (2022)

Quit smoking

The recommendation to quit smoking, established by the ACS for the primary prevention of cancer are also relevant to survivors undergoing and immediately after cancer treatment.

Cigarette smoking topped the charts as the leading risk factor, contributing to nearly 20 percent of all cancer cases and close to 30 percent of cancer deaths. Smoking comprised 56 percent of potentially preventable cancers in men and almost 40 percent of those in women. (Journal of the American Cancer Society 2024)

Journal of the American Cancer Society 2024

If you are a non smoker, then your risk of cancer will be reduced. Smoking is by far the leading risk factor for lung cancer. In the early 20th century, lung cancer was much less common than some other types of cancer. But this has changed once manufactured cigarette became readily available and more people began smoking.

Avoid tobacco products altogether, including cigarettes, cigars, and smokeless tobacco. About 80% of lung cancer deaths are thought to result from smoking. The risk for lung cancer among smokers is many times higher than among non-smokers. The longer you smoke and the more packs a day you smoke, the greater your risk.

On top of that, you should also try to cut down on your visits to places where people tend to smoke e.g. pubs etc. Passive smoking is just as bad.

Cancer and Physical Activity

Most studies support that exercise is generally safe for individuals undergoing cancer treatment. However, because most of these studies are randomized controlled trials that may include healthier participants than the general population of patients with cancer, it is important for patients who have cancer to seek medical evaluation to inform their individual exercise program during treatment. 

This type of guidance is valuable in creating a safe and effective fitness plan for patients who have cancer with appropriate and tailored modifications related to specific cancer diagnosis or treatment-related issues, such as breast cancer-related lymphedema. Individuals undergoing cancer treatment are encouraged to be active members of their nutrition and physical activity care planning team. Interventions during and immediately after treatment should be individualized and realistic and should have scientific support.

Source: American Cancer Society nutrition and physical activity guideline for cancer survivors (2022)

The Metabolic Approach to Treating Cancer

Although mitochondrial replacement therapy could, in principle, restore a more normal energy metabolism and differentiated state to tumor cells, it is unlikely that this therapeutic approach would be available in the foreseeable future. 

However, if cancer is primarily a disease of energy metabolism, then rational approaches to cancer management can be found in therapies that specifically target energy metabolism. The goal of metabolic adjunctive treatments is to “starve the cancer cell” by modulating energy pathways that are important to the survival of cancer cells and thereby reduce cancer growth and cancer metastases (the cause of death in over 90% of cancer patients). 

An approach to cancer treatment is emerging with research showing impressive results from the use of metabolically targeted drug cocktails alongside conventional chemotherapy. The metabolic protocol is designed to work primarily by restricting the overall ability of cancer cells to take up and use (i.e., ‘metabolize’) energy. By starving cancer cells of energy substrates, metabolic interventions may reduce the capacity of cancer cells to defend themselves against chemotherapy and radiation. 

The metabolic protocol may also act on the many dysregulated signaling pathways within cancer cells helping to enable apoptosis, or “programmed cell death,” allowing chemotherapy and radiation to kill cancer cells more effectively. The most important and central approach to the metabolic treatment of cancers is dietary calorie (glucose) restriction. This is supplemented with pharmacologic and nutraceutical compounds that target specific cancer pathways and interventions that restore “normal” anticancer immunity and prevent metastases.

It is important to emphasize that there is no single “magic bullet” and that multiple interventions act synergistically and simultaneously to promote cancer cell death. The combination of dietary interventions together with multiple repurposed drugs/nutraceuticals that act synergistically is strongly recommended.

However, similar to the work of Jane McLelland, we suggest a more extensive and targeted list of pharmacologic and nutraceutical compounds combined with glucose restriction and a ketogenic diet. 

The metabolic approach to cancer should be considered as adjunctive to more “traditional” approaches to cancer treatment. The metabolic treatments will likely act synergistically with the more traditional approaches, thereby increasing tumor response rate, limiting the toxicities of standard chemotherapy, limiting the risk of metastasis, and leading to an improvement in overall quality of life. This combined approach will allow for reduced dosages of standard chemotherapeutic agents, drastically reducing their toxicity.

Related: Expert Explains Cancer May Be Metabolic Disease, and Shares a Cure

Dietary Caloric Restriction, The Ketogenic Diet, and “Real” Food 

Numerous studies show that dietary energy restriction is a general metabolic therapy that naturally lowers circulating glucose levels and significantly reduces the growth and progression of numerous tumor types, including cancers of the breast, brain, colon, pancreas, lung, and prostate. 

An impressive body of evidence indicates that dietary energy restriction can retard the growth rate of many tumors regardless of the specific genetic defects expressed within the tumor. Hyperglycemia with high insulin levels is associated with tumor recurrence. 

Sugar sweetened beverages are associated with an increased risk of cancer. Both experimental and clinical data suggest that fructose, particularly fructose-corn syrup, is more carcinogenic than glucose. 

As demonstrated by Dr. Otto Warburg, almost all cancer cells are dependent on glucose as a metabolic fuel via aerobic glycolysis, with hyperglycemia being a potent promotor of tumor cell proliferation and associated with poor survival. 

Although the mechanisms responsible for the caloric-restriction-mediated reduction in tumorigenesis have not been unequivocally identified, they may involve caloric-restriction-induced epigenetic changes as well as changes in growth signals and in the sirtuin pathway. 

Insulin resistance plays a major role in the initiation and propagation of cancer. Reversing insulin resistance is therefore a major goal in patients with cancer. Dietary energy restriction specifically targets  several cancer hallmarks (see above, under 'causes of cancer') including cell proliferation, evasion of apoptosis, and angiogenesis. 

Dietary energy restriction targets inflammation and the signaling pathways involved with driving tumor angiogenesis. Indeed, calorie restriction is considered a simple and effective therapy for targeting tumor angiogenesis and inflammation. 

Calorie restriction results in the downregulation of multiple genes and metabolic pathways regulating glycolysis. Besides lowering circulating glucose levels, dietary energy restriction elevates circulating levels of fatty acids and ketone bodies.

Fats, and especially ketones, can replace glucose as a primary metabolic fuel under calorie restriction. This is a conserved physiological adaptation that evolved to spare protein during periods of starvation. Many tumors, however, have abnormalities in the genes and enzymes needed to metabolize ketone bodies for energy. Elevation in ketone bodies is well known to be able to suppress blood glucose levels and glycolysis, which are major drivers of tumor growth. 

A transition from carbohydrates to ketones for energy is a simple way to target energy metabolism in glycolysis-dependent tumor cells while enhancing the metabolic efficiency of normal cells. Metabolism of ketone bodies and fatty acids for energy requires inner mitochondrial membrane integrity and efficient respiration, which tumor cells largely lack. 

Under fasting conditions, ketone bodies are produced in the liver from fatty acids as the main source of brain energy. Ketone bodies bypass the glycolytic pathway in the cytoplasm and are metabolized directly to acetyl CoA in the mitochondria. 

The ketogenic diet is a high-fat, low-carbohydrate diet with adequate protein and calories originally developed in the 1920s as a treatment for intractable epilepsy. The traditional ketogenic diet is a 4:1 formulation of fat content to carbohydrate plus protein. A classic 4:1 ketogenic diet delivers 90% of its calories from fat, 8% from protein and only 2% from carbohydrate. 

Ketogenic diets of the 1920s and 1930s were extremely bland and restrictive diets and, therefore, prone to noncompliance. In recent years, alternative keto-genic protocols have emerged, making adherence to the diet much easier. Alternatives to the traditional keto-genic diet includes a medium-chain triglyceride (MCT)-based ketogenic diet and the Atkins diet. Compared to long-chain triglycerides, MCTs are more rapidly absorbed into the bloodstream and oxidized for energy because of their ability to passively diffuse through membranes. Another characteristic of MCTs is their unique ability to promote ketone body synthesis in the liver. Thus, adding MCTs to a ketogenic diet would allow significantly more carbohydrates to be included. 

A ketogenic diet has tumor growth-limiting effects, protects healthy cells from damage by chemotherapy or radiation, accelerates chemotherapeutic toxicity toward cancer cells, and lowers inflammation. Altered availability of glucose and induction of ketosis influence all the classically defined hallmarks of cancer.

Weber et al demonstrated that ketogenic diets slow melanoma growth in vivo regardless of tumor genetics and metabolic plasticity. Moreover, ketogenic diets simultaneously affected multiple metabolic pathways to create an unfavorable environment for melanoma cell proliferation. In glioma cancer models a ketogenic diet has been shown to reduce angiogenesis, inflammation, peri-tumoral edema, migration and invasion. 

The ketogenic diet may work in part as an immune adjuvant, boosting tumor-reactive immune responses in the microenvironment by alleviating immune suppression. A meta-analysis on the use of ketogenic diet in animal models demonstrated significantly prolonged survival time and reduced tumor weight and tumor volume. The ketogenic diet was effective across a broad range of cancers. 

The ketogenic diet is an effective adjuvant to radiation therapy for the treatment of malignant glioma.(293) Ketone bodies have been shown to inhibit histone deacetylases and may decrease tumor growth. In addition, the ketone bodyβ-hydroxybutyrate acts as an endogenous histone deacetylase inhibitor, resulting in downstream signaling that protects against oxidative stress.

The randomized controlled trial by Chi et al describes how adhering to a caloric-restricted diet for 6 months can have therapeutic benefits in slowing the growth of prostate cancer.  The men in the control group were instructed to avoid any dietary changes, whereas the men in the calorie-restricted group were coached by a dietician to restrict dietary carbohydrates to <20 grams/day. The authors found that elevated levels of serum ketone bodies at both 3 and 6 months were associated with significantly longer prostate cancer antigen doubling time (p < 0.0001), which is a marker of prostate cancer growth rate. 

Similarly, in a post hoc exploratory analysis of the CAPS2 randomized study the PSA doubling time was significantly longer in the low carbohydrate diet versus control diet (28 vs. 13 months, P = 0.021) arms. These findings support the concept that elevations in ketone bodies are associated with reduced tumor growth. 

In a randomized trial in women with endometrial or ovarian a ketogenic diet was associated with a significant improvement in physical function scores with less fatigue. In this study the ketogenic diet resulted in the selective loss of fat mass, retention of lean mass with lower fasting serum insulin levels. 

In a RCT Khodabakshi et al determined the feasibility, safety, and beneficial effects of an MCT-based Ketogenic diet in patients with locally advanced or metastatic breast cancer and planned chemotherapy. Compared to the control group, fasting blood glucose, BMI, body weight, and fat% were significantly decreased in intervention group (P < 0.001). Overall survival in neoadjuvant patients was higher in the ketogenic group compared to the control (P = 0.04).

A ketogenic diet following completed courses of chemotherapy and radiotherapy was further reported to be associated with long-term survival in a patient with metastatic non-small cell lung cancer.  “Long-term” survival has been reported in patients with glioblastoma on a ketogenic diet. Furthermore, evidence shows that therapeutic ketosis can act synergistically with conventional chemotherapeutic drugs, irradiation, and surgery to enhance cancer management, thus improving both progression-free and overall survival. 

In addition, it is highly likely that therapeutic ketosis acts synergistically with the repurposed anticancer drugs reviewed in this document. Therapeutic ketosis requires a blood glucose < 90 mg/dl and a blood ketone > 2 mmol/l, aiming for a glucose-ketone index (GKI) < 2. 

See the GKI calculator in the section on caloric restriction. There are no known drugs that can simultaneously target as many tumor-associated signaling pathways as can calorie restriction. Hence, energy restriction can be a cost-effective adjuvant therapy to traditional chemo- or radiation therapies, which are more toxic, costly, and generally less focused in their therapeutic action than dietary energy restriction. It should be noted that the medium-chain fatty acids that are present during the consumption of a ketogenic diet directly inhibit glutamate receptors. 

Shukla et al observed reduced glycolytic flux in tumor cells upon treatment with ketone bodies. Ketone bodies also diminished glutamine uptake, overall ATP content, and survival in multiple pancreatic cancer cell lines, while inducing apoptosis. 

According to Dr. Seyfried: “Most human metastatic cancers have multiple characteristics of macrophages. We found that neoplastic cells with macrophage characteristics are heavily dependent on glutamine for growth. We have not yet found any tumor cell that can survive for very long under prolonged restriction of glucose and glutamine. Furthermore, we have not yet found any fatty acid or ketone body that can replace either glucose or glutamine as a growth metabolite. It, therefore, becomes essential to simultaneously restrict both glucose and glutamine while placing the person in nutritional ketosis for successful cancer management.” 

Although dietary energy restriction and anti-glycolytic cancer drugs will have therapeutic efficacy against many tumors that depend largely on glycolysis and glucose for growth, these therapeutic approaches could be less effective against those tumor cells that depend more heavily on glutamine than on glucose for energy. Glutamine is a major energy metabolite for many tumor cells and especially for cells of hematopoietic or myeloid lineage. 

Green tea polyphenol (EGCG) targets glutamine metabolism by inhibiting glutamate dehydrogenase activity under low glucose conditions (see section below). In addition, mebendazole, curcumin and resveratrol inhibit glutaminolysis. Glioblastoma, breast cancer, pancreatic cancer, lung cancer, prostate cancer, and lymphoma may depend on glutamine as a source of energy. 

Real Food: The Banting Diet

Patients are strongly recommended to eat “real food” and not processed food. If it looks like food, it is likely food. If it comes in a box or carton, has a food label, and/or a long list of chemicals and additives with long and complex names it is not food. A high proportion of the population (60-80%) eating a Western diet are addicted to processed food.

Processed food addiction is a recognized “substance use disorder” (SUD) and should be treated as such. Animal experiments demonstrate that sugar and fructose are more addictive than cocaine and heroin and that carbohydrate addicts demonstrated many of the behaviors of those with an SUD. 

Results from the NutriNet-Santé prospective cohort study demonstrated that a 10% increase in the proportion of ultra-processed foods in the diet was associated with a significant increase of greater than 10% in risks of overall and breast cancer.

The EPIC Cohort study investigated the association between dietary intake according to amount of food processing and risk of cancer at 25 anatomical sites using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. In this study, in a multivariate model, substitution of 10% of processed foods with an equal amount of minimally processed foods was associated with reduced risk of overall cancer (hazard ratio 0·96, 95% CI 0·95-0·97), head and neck cancers (0·80, 0·75-0·85), oesophageal squamous cell carcinoma (0·57, 0·51-0·64), colon cancer (0·88, 0·85-0·92), rectal cancer (0·90, 0·85-0·94), hepatocellular carcinoma (0·77, 0·68-0·87), and postmenopausal breast cancer (0·93, 0·90-0·97). 

A low carbohydrate-high fat (LCHF) dietary pattern is especially important for patients with cancer. As already discussed, a low carbohydrate ketogenic diet is essential to control blood glucose levels. Furthermore, a real food diet high in both soluble and insoluble fiber and fermented foods is critical to normalize the microbiome. Alterations in the microbiome play an important role in both tumorigenesis and tumor propagation. Altered gut microbiota is associated with resistance to chemotherapeutic drugs while restoration of a normal microbiome improves the response to the anticancer drugs. 

Antibiotics cause severe dysbiosis which is associated with an increased risk of cancer and reduced response to chemotherapy. The Banting Diet comes close to meeting the criteria of the ideal real-food diet. William Banting (1796-1878), a Victorian undertaker, is regarded as the father of the low carbohydrate diet. In 1863, Banting wrote a booklet called Letter on Corpulence, Address to the Public, which contained the particular plan for the diet he followed. 

It was written as an open letter in the form of a personal testimonial. Banting described all of his unsuccessful fasts, diets, spa visits, and exercise regimens all of which had been advised by various medical experts. He then described the dietary change that finally had worked for him, following the advice of another medical expert. "My kind and valued medical adviser is not a doctor for obesity, but stands on the pinnacle of fame in the treatment of another malady, which, as he well knows, is frequently induced by [corpulence]." 

His own diet consisted of meat, greens, fruits, and dry wine. The emphasis was on avoiding sugar, saccharine matter, starch, beer, and milk. Banting's pamphlet was popular for years to come and would be used as a model for modern diets. The Banting diet consists mainly of animal protein (including poultry, eggs, and fish), saturated animal fats (including lard, duck fat, and butter), coconut oil, olive oil, and macadamia oil, some cheeses and dairy products, some nuts and seeds, fresh vegetables grown mainly above the ground and a few berries. 

The Banting diet excludes all processed package foods and fast foods. It also excludes all foods with sugar, fructose, and maltose as well as grain products (wheat, barley, oats, rye) and soy products. Soy products are genetically modified, toxic non-foods. Replace all seed oils (canola, sunflower, safflower, cottonseed, soy) with healthy saturated fats, extra virgin olive oil and virgin coconut oil are freely encouraged. High fat dairy products are suggested but not skimmed or fat-free dairy products.

Intermittent Fasting, Autophagy, and Cancer

Fasting has a profound effect on promoting immune system homeostasis, improving mitochondrial health, and increasing stem cell production. Fasting stimulates the clearing of damaged mitochondria (mitophagy), misfolded and foreign proteins, and damaged cells (autophagy). Intermittent fasting/time-restricted eating is the single most effective method to activate autophagy. 

However, the role of intermittent fasting and autophagy in cancer is complex. The 2016 Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for his initial elucidation of the morphological and molecular mechanisms of autophagy in the 1990s. Macroautophagy (herein referred to as autophagy) is a conserved lysosomal degradation pathway for the intracellular recycling of macromolecules and clearance of damaged organelles and misfolded proteins to ensure cellular homeostasis. 

During autophagy, cytoplasmic constituents (damaged proteins, misfolded proteins, foreign proteins) are engulfed within double-membrane vesicles called autophagosomes, which subsequently fuse with lysosomes to form autolysosomes, where the cargo is degraded or recycled.

Autophagy occurs at basal levels under physiological conditions and can be upregulated in response to stressful stimuli such as hypoxia, nutritional deprivation, DNA damage, and cytotoxic agents. The molecular machinery that mediates the autophagic process is evolutionarily conserved in higher eukaryotes and regulated by specific genes (ATG genes), which were initially characterized in yeast. 

The process of macroautophagy can also lead to cell death or “autophagic cell death,” as a result of the accumulation of autophagosomes and autolysosomes in the cytoplasm. The effects of fasting, autophagy and cancer are still under study, but many researchers propose that intermittent fasting could help with the treatment and eradication of tumors and cancer cells.

Intermittent fasting/time-restricted eating is the most effective therapy for the treatment of insulin resistance, metabolic syndrome, and type II diabetes. Intermittent fasting has additional benefits in prolonging health span, alleviating the symptoms/curing many chronic diseases, as well as preventing cardiovascular disease, Alzheimer’s disease and cancer. To gain the maximum benefits of intermittent fasting, it is thought that feeding times should be scheduled to align with circadian rhythms and activities so that timely nutrient metabolism favors healthy physiology.

The metabolic effects of intermittent fasting are numerous and include increasing insulin sensitivity, decreasing blood glucose levels, decreasing insulin levels, decreasing insulin-like growth factor, activating the sirtuin pathway, and activating autophagy. Intermittent fasting is the most effective means of activating autophagy and accounts for many of its beneficial effects. These effects likely explain the benefits of intermittent fasting in patients with cancer. 

There has been some concern that while autophagy may play an important role in preventing the development of cancer, it may paradoxically promote cancer cell proliferation. Once a tumor is established, the main function of autophagy is to provide a means to cope with cellular stressors, including hypoxia, nutritional and growth factor deprivation, and damaging stimuli, thus allowing tumor adaptation, proliferation, survival, and dissemination. While autophagy may theoretically promote cancer cell proliferation multiple studies have demonstrated that autophagy leads to cancer cell death. 

Almost all the repurposed drugs listed in this monograph have been demonstrated to enhance tumor cell death by activating the autophagy pathway. Limited rodent studies and human studies have evaluated the independent effects of intermittent fasting/time restricted eating in modulating cancer progression. In a study of a high-fat driven, postmenopausal breast cancer mouse model, intermittent fasting markedly inhibited tumor initiation, progression, and metastasis compared with mice fed ad libitum in the absence of calorie restriction or weight loss. 

This beneficial effect of intermittent feeding was probably mediated, at least in part, by reduced insulin signaling because systemic insulin infusion through implanted pumps reversed the intermittent fasting-mediated cancerprotective actions. Additional animal models have demonstrated the benefit of intermittent fasting on cancer progression.

Fasting seems to improve the response to chemotherapy by several mechanisms including: 

• Enhances DNA repair in normal cells but not in malignant cells 
• Improves autophagy mechanisms as a protection against damage to organelles 
• Promotes apoptosis by both increasing tumor cell susceptibility to apoptotic stimuli, and averting apoptosis-mediated damage to normal cells 
• Decreases regulatory T cells and enhances stimulation of CD8 cells.

Interestingly, fasting in combination with cytotoxic agents elicited differential responses in normal and cancer cells, a phenomenon known as differential stress resistance (DSR). For DSR, normal cells prioritize maintenance pathways and inactivate growth factor signaling when nutrients are absent. In contrast, cancer cells, due to oncogene activation, do not inhibit stress resistance pathways, thus becoming vulnerable to cytotoxic treatment. 

The role of intermittent fasting and the enhancement of autophagy in patients with cancer is complex. While animal models demonstrate a benefit of intermittent fasting in several tumor models, clinical data in humans is limited. While time-restricted feeding (intermittent fasting) may theoretically promote cancer cell proliferation, this concept has not been observed in patients with cancer. Furthermore, more prolonged fasting of 24-96 hours has been well tolerated in patients with cancer and appears to improve quality of life and disease symptoms.

This data suggests that the approach to intermittent fasting should be individualized in patients with cancer according to each patient's response. Data from small trials in humans suggest that many types of intermittent fasting regimens positively affect risk factors for poor breast cancer outcomes, such as glucoregulation, inflammation, obesity, and sleep. Experimental animal models and human data support the hypothesis that a prolonged nightly fasting interval (time restricted eating) could reduce cancer risk and improve cancer outcomes. 

Marinac et al investigated whether the duration of nightly fasting predicted recurrence and mortality among women with early-stage breast cancer. Data were collected from 2413 women with breast cancer but without diabetes mellitus who were aged 27 to 70 years at diagnosis and participated in the prospective Women’s Healthy Eating and Living study. Nightly fasting duration was estimated from 24-hour dietary recalls collected at baseline, year 1, and year 4. The mean fasting duration was 12.5 ± 1.7 hours per night. In repeated-measures Cox proportional hazards regression models, fasting less than 13 hours per night was associated with an increase in the risk of breast cancer recurrence compared with fasting 13 or more hours per night (HR 1.36; 95% CI, 1.05-1.76).

Source: https://covid19criticalcare.com/wp-content/uploads/2023/06/Cancer-Care-FLCCC-Dr-Paul-Marik-v2.pdf

Metabolic and Lifestyle Interventions for Cancer Management

1. Glucose Management and the Ketogenic Diet

A carbohydrate-restricted diet (less than 25 g of carbs per day) that is high in saturated fat and Omega-3 fatty acids (ketogenic diet) is suggested. Avoid all processed food. Contrary to current dogma, saturated fatty acids are “healthy,” but avoid processed omega-6 vegetable oils or linoleic acid (see below).

Avoid foods that are high on the glycemic index and follow the “hacks” to flatten the blood glucose curve (see below). A continuous glucose monitor (CGM) is essential to track changes in blood glucose levels. Patients must keep accurate records to identify (and avoid) any food that might spike blood glucose. Target a baseline blood glucose of 60-80 mg/dl (3.3 – 4.4 mmol/l) and a postprandial (after a meal) glucose of less than 120 mg/dl (6.6 mmol/l). The ideal is a flat blood glucose curve; the blood glucose should not increase by more than 20 mg/dl after a meal. In addition, a blood ketone meter (blood level of beta-hydroxybutyrate) is recommended to confirm that the patient has entered ketosis (normal level < 0.5 mmol/l). Ideally, the blood ketone level should be over 2 mmol/l. The optimal therapeutic range is between 3 and 5 mmol/l. It is important to track changes in blood glucose and ketones with both fasting and exercise. Therapeutic ketosis requires a blood glucose < 90 mg/dl and a blood ketone > 2 mmol/l, aiming for a GKI of < 2. 

The GKI can be calculated at: https://keto-mojo.com/glucose-ketone-index-gki/ and https://perfectketo.com/glucose-ketone-index-calculator/ 

The Glycemic Index 

The glycemic index (GI) is a value assigned to foods based on how quickly those foods cause increases in blood glucose levels and how high they spike. The glycemic index ranks food on a scale from 0 to 100. Pure glucose is arbitrarily given a value of 100, which represents the relative rise in the blood glucose level after two hours (see Figure 7). The GI of a specific food depends primarily on the quantity and type of carbohydrate it contains (see Table 4). Foods that are low on the GI scale tend to release glucose slowly and steadily. Foods that are high on the glycemic index release glucose rapidly. It should be noted that the glycemic index varies among individuals. (360, 361) A continuous glucose monitor allows for the individual assessment of the glucose excursion (GI) of various foods.

What To Eat and What Not to Eat 

The most important intervention to reduce obesity, metabolic syndrome, type II diabetes, cancer, cardiac disease, neurodegenerative diseases, autoimmune diseases etc., is to eat real food and not processed food. Telling the difference is quite simple. If it looks like food, it is real. If it comes in a box or has a food label, it’s likely processed. The more ingredients listed on a product’s label and the more chemicals you see with strange and unpronounceable names, the more processing the product has undergone. Recent evidence suggests that processed foods in themselves can cause insulin resistance. 

Healthy foods include: 

• All vegetables, especially avocados, and cruciferous and leafy vegetables. 
• Fish (wild caught fresh fish especially Alaskan/Pacific salmon and sardines) 
• Eggs (they’ve been giving a bad rap!); free range “organic” eggs are suggested.
• Chicken breast (free range, no hormones, no antibiotics) 
• Nuts especially almonds, brazil nuts, cashews, and pistachios. 
• Unsweetened Peanut butter (but avoid the white bread and grape jelly!) and Chia seeds 
• Meat (grass-fed, no hormones, avoid processed meats) 
• Blueberries (limit volume if insulin resistant) 
• Coffee, with heavy cream or coconut oil; choose Stevia (without erythritol) over sugar or artificial sweeteners. 

Flattening the Glucose Curve 

Apart from carbohydrate restriction/ketogenic diet and time-restricted eating, several simple interventions (or hacks) prevent the high glucose spikes that fuel cancer. The book “Glucose Revolution” by Jessie Inchauspe is highly recommended and provides more details on interventions to flatten the blood glucose curve, such as. 

Eat Foods in the Right Order 

Veggies (greens/fiber) should be eaten first, protein and fat second, and starch (sugars) last; this slows gastric emptying, as well as the breakdown and absorption of glucose. Eat fruit last; always preceded by fiber. Don’t begin a meal with bread (starch). 

• Begin all meals with a salad or green vegetables. Use olive oil and vinegar as salad dressing.
• Avoid starchy foods with no fiber.
• Avoid fruit juices and smoothies, which cause a large glucose spike.
• Skip breakfast. Breakfast is the worst time to eat sugar and starches; this results in a large glucose spike. Cereal for breakfast causes a rapid spike in glucose.
• Avoid snacking throughout the day.
• Drink a tablespoon of vinegar stirred into a tall glass of water before eating starch or something sweet. Apple cider vinegar is recommended. The acetic acid in vinegar decreases the enzymatic breakdown of starch, increases glycogen synthesis (and glucose uptake), and increases fatty acid oxidation. Vinegar may be beneficial even if consumed up to 20 minutes after a starchy food. Apple cider vinegar is usually unpasteurized and should be avoided in pregnancy.
• If vinegar is not readily available, consume a few fiber tablets (esp. glucomannan tablets) before eating a starchy/sweet treat.
• Go for a 20-minute walk within an hour of eating/having starchy food. During exercise, muscles take up glucose for energy while increasing mitochondrial oxidative capacity. Going to the gym or doing resistance exercise is an alternative. Climbing a few stairs is an option at work. If sedentary, do sitting calf raises (the soleal pump). The soleal pump is strongly recommended; it has been demonstrated to reduce postprandial glucose by about 50%, reduce hyperinsulinemia, and improved lipid metabolism. When engaging in fasted exercise (before eating), the liver releases glucose into the bloodstream to fuel the mitochondria in the muscles causing a glucose spike. This is mediated by an increased release of cortisol, epinephrine, and norepinephrine (with decreased glucagon); i.e., release of harmful stress hormones. If exercising before eating, we suggest instead of a regular protein shake, consider a shake with ‘superfoods,’ e.g., Ka’Chava ™ or 310 Shakes.™ Shakes should include ingredients like plant protein, a super green, omega-3 fatty acids, vitamins, adaptogenic herbs, probiotics, fiber, super mushrooms, and berries.

Establishing/Restoring a “Normal” Microbiome 

The microbiome has a remarkable effect on blood sugar levels and insulin sensitivity. (372-378) Establishing a normal microbiome is important for regulating blood glucose levels and improving insulin sensitivity. Furthermore, alterations in the microbiome play an important role in both tumorigenesis and tumor propagation. Follow these suggestions to help establish a “normal microbiome”: 

• Eat a diverse range of foods. 
• Eat lots of vegetables, legumes, and beans. • Eat fermented foods like yogurt (unsweetened), kefir, apple cider vinegar, kombucha, pickles, sauerkraut, tempeh, and kimchi. 
• Eat foods rich in polyphenols (dark fruits). Include resveratrol supplements. 
• Eat prebiotic fiber. Glucomannan is a dietary fiber (soluble and insoluble) made from the root of the konjac plant. 
• Eat chia seeds, high in insoluble and soluble fiber.
• Eat less sugar and sweeteners. 
• Reduce stress. 
• Avoid taking antibiotics unnecessarily. 
• Stop snacking. 
• Exercise regularly. 
• Spend time outdoors in the natural world to get exposure to millions of microbes, many of which can benefit microbiome diversity. 
• Get enough sleep. 

The consumption of fermented foods may be particularly important in restoring/maintaining a normal microbiome. Large cohort studies as well as limited interventional studies have linked the consumption of fermented foods with weight maintenance and decreased diabetes, cancer, and cardiovascular disease risks. 

The Saturated Fat-Cholesterol Hoax 

The Cholesterol-Saturated fatty acid hoax began to proliferate in the 1960s. Dr. Ancel Keys popularized the notion that saturated fats and high cholesterol were the primary causes of atherosclerotic heart disease — the so-called Diet-Heart Hypothesis. This concept has been vigorously studied, including in many RCTs, and has been convincingly proven to be false. (357, 384, 385) Indeed, replacing saturated fats with a diet high in vegetable oils (linoleic acid) was associated with higher rates of death, cardiovascular and coronary heart disease as well as a significantly increased risk of cancer. (386)

Healthy and Unhealthy Oils Avoid seed oils high in linoleic acid. Linoleic acid is an Omega-6 fatty acid that our bodies require in small amounts. Unfortunately, many people eat up to 10 times the desired amount of linoleic acid, because of excess consumption of foods made with seed oils. Too much linoleic acid is associated with inflammation, obesity, heart disease, and other unfavorable conditions. Therefore, avoid the following oils: 

Soybean oil, Corn oil, Cottonseed oil, Sunflower oil, Sesame oil, Grapeseed oil, Safflower oil, Rice bran oil, Margarine.

Instead, opt for healthy oils and fats such as the ones listed below. Use only high-quality products and check production and expiration dates. 

• Olive oil (oleic acid, omega-9 monounsaturated fatty acids); never heat olive oil to the point where it produces smoke. 
• Avocado oil (oleic acid, omega-9 monounsaturated fatty acids) 
• Coconut oil (medium chain fatty acid) 
• Flaxseed oil (alpha-linolenic acid, ALA omega-3) 
• Walnut and pecan oils; should be refrigerated to avoid spoilage 
• Butter (saturated fat)

Source: https://covid19criticalcare.com/wp-content/uploads/2023/06/Cancer-Care-FLCCC-Dr-Paul-Marik-v2.pdf

 

Breast cancer women with lifestyle intervention 56% less likely to have died from breast cancer compared to women in the control group

A landmark prospective, randomized study evaluated the short- and long-term effects of a comprehensive lifestyle intervention on women with stage II or stage II breast cancer who had undergone surgery. (ACS Journal 2008)

The intervention included techniques to reduce stress, improve “quality of life,” and promote healthy behaviors including guidance on diet, exercise, relaxation techniques, social support and healthy living.

Patients in the intervention group attended regular sessions with follow-up appointments to ensure compliance with the lifestyle program. Eleven years later, women who participated in the intervention had a 45% lower risk of cancer recurrence than those in the control group and were 56% less likely to have died from breast cancer compared to women in the control group. Intervention patients were also 49% less likely than women in the control group to die from any cause. 

The study also demonstrated that women who took part in the intervention had significantly improved psychological, behavioral, and health outcomes, as well as improved immune function compared with patients in the control group. 

Best Cancer Fighting Supplements: Evidence Based

What vitamins minerals etc can help fight cancer?

We have ranked the top cancer fighting supplements to help you with your research. We have also organised and summarised relevant and salient research information in one place. Below, we look at the most published and studied categories.

Important Note: This information is for educational purposes only and should not be interpreted as medical advice.

Here is the list (listed in order of importance):

1. Vitamin D3

Is vitamin D the most powerful anti cancer supplement? Vitamin D can absorb calcium and help the immune, muscle, and nervous systems function properly. There are more than 12,000 search results on vitamin D and cancer on PubMed. 

A vitamin D level > 30 ng/mL is widely considered “normal” while a level between 20-30 ng/mL is considered vitamin D insufficient and a level <20 ng/mL is considered vitamin D deficient. However, more recent data suggests that a level > 50 ng/mL is desirable, and ideally targeting a level of 55- 90 ng/mL is preferable.

It may take many months or even years to achieve optimal levels in patients with low vitamin D levels (< 20 ng/mL) taking the standard recommended dose of 5,000 IU/day. It is therefore important that the optimal regimen for vitamin D supplementation be followed to achieve adequate circulating levels (see Table below).

Since the highest dose of commercially available vitamin D3 is 50,000 IU capsules, and due to its affordability and better gastrointestinal absorption, we recommend using 50,000 IU D3 capsules for community setups. Together, a number of these capsules can be taken as a bolus dose [i.e., single upfront doses such as 100,000 to 400,000 IU]. However, the liver has a limited 25- hydroxylase capacity to convert vitamin D to 25(OH)D: thus, taking 50,000 IU capsules over a few days provides better bioavailability.

Source: Nutrients – Special Issue: “Vitamin D – Calciferol and COVID”. Reproduced with permission from the author. 

Treatment

A 2024 post hoc analysis (Nutrients 2024) of the AMATERASU trial (UMIN000001977), a randomized controlled trial (RCT), included 302 patients with digestive tract cancers divided into two subgroups stratified by median serum levels of omega-3 into higher and lower halves. The 5-year relapse-free survival (RFS) rate was significantly higher in the higher half (80.9%) than the lower half (67.8%). In the patients in the lower omega-3 group, the 5-year RFS was significantly higher in the vitamin D (74.9%) than the placebo group (49.9%). In patients with digestive tract cancers, these results suggest that vitamin D supplementation may reduce the risk of relapse or death by interacting with marine omega-3.

Vitamin D and Chemotherapy

Multiple studies indicate that a significant proportion of cancer patients are vitamin D-deficient (level < 20 ng/mL) and that higher plasma 25-hydroxyvitamin D levels are associated with improved survival in colorectal, breast, gastric, and lymphoma cancer patients [Systematic Review 2014]. Meta-analyses and clinical trials demonstrate that vitamin D supplementation may reduce cancer mortality and improve survival in cancer patients, especially when used in combination with chemotherapy (Meta-analysis 2023). SUNSHINE (JAMA 2019), a clinical trial on metastatic colorectal cancer patients, showed that “high-dose” vitamin D3 (aiming for a level of >50 ng/mL) combined with standard chemotherapy resulted in improved progression-free survival compared to standard-dose vitamin D3.

Caution: The dosage for vitamin D in prevention (1,000 to 2,000 IU daily) is very much different from the high dose treatment dosage i.e. 20,000 to 50,000 IU daily. Always consult your doctor first! 

Clinical studies 

Data suggest that the majority of patients with cancer are vitamin D deficient (level < 20 ng/mL). Several prospective observational studies have shown that higher levels of plasma 25-hydroxyvitamin D were associated with improved survival among patients with colorectal cancer.

Similarly, elevated 25-OH D levels were associated with better overall survival in patients with breast and gastric cancer and lymphoma. In a population-based study of patients with cancer of the breast, colon, lung, and lymphoma a 25- OHD level below 18 ng/mL at diagnosis experienced shorter survival.

In a meta-analysis of 19 studies Robsahm et al reported an inverse relationship between 25-hydroxyvitamin D and cancer survival. Chen performed a meta-analysis of observational cohort studies and randomized trials which assessed the role of post-diagnosis vitamin D supplement intake on survival among cancer patients. The meta-analysis included 11 publications consisting of 5 RCTs and 6 observational cohort studies. The summary relative risk (SRR) for overall survival of vitamin D supplement use vs. non-use, pooling cohort studies and randomized trials, was 0.87 (95% CI, 0.78–0.98; p = 0.02). 

Vaughan-Shaw et al performed a meta-analysis of 7 studies evaluating the use of supplemental vitamin D in patients with colorectal cancer. The study reported a 30% reduction in adverse outcomes and a beneficial effect on progression-free survival (HR = 0.65; 95% CI: 0.36–0.94). In a meta-analysis by Kuznia et al, subgroup analysis revealed that vitamin D3 administered daily, in contrast to bolus supplementation, reduced cancer mortality by 12 %. It should be recognized that a daily dose of between 800 IU and 4000 IU was administered in the studies included in this meta-analysis and that vitamin D levels were not monitored. A more dramatic reduction in mortality would likely be realized if patients were dosed more appropriately.

SUNSHINE was a double-blind, multicenter, randomized clinical trial designed to evaluate the efficacy of “high dose” vitamin D3 compared with standard-dose vitamin D3 given in combination with standard chemotherapy in patients with metastatic colorectal cancer. 

The high-dose group received a loading dose of 8,000 IU per day of vitamin D3 (two 4,000 IU capsules) for cycle 1 followed by 4,000 IU/d for subsequent cycles. The standard dose group received 400 IU/d of vitamin D3 during all cycles. In this underpowered (n=139) RCT, multivariable HR for progression-free survival or death was 0.64 (95% CI, 0-0.90; p = .02) in favor of the high dose group. Comparison of progression-free survival between the high-dose and standard-dose vitamin D3 groups using a log-rank test stratified by ECOG performance status was statistically significant (p = .03). At baseline, median plasma 25-hydroxyvitamin D levels were deficient in both the high-dose vitamin D3 group (16.1 ng/mL [IQR, 10.1 to 23.0 ng/mL]) and in the standard-dose vitamin D3 group (18.7 ng/mL [IQR, 13.5 to 22.7 ng/mL]). Only 9% of the total study population had sufficient levels (≥30 ng/mL) of 25-hydroxyvitamin D at baseline. 

At treatment discontinuation, patients in the high-dose vitamin D3 group had a median 25-hydroxyvitamin D level of 34.8 ng/mL (IQR, 24.9-44.7 ng/mL), whereas those in the standard-dose vitamin D3 group were still deficient in vitamin D and had a median 25- hydroxyvitamin D level of 18.7 ng/mL(IQR, 13.9-23.0ng/mL) (difference, 16.2 ng/mL [95% CI, 9.9-22.4 ng/mL]; P < .001). It is important to note that based on these levels the “high dose” group was profoundly underdosed. As indicated above, vitamin D dosing should be based on a serum level aiming for a level of > 50 ng/mL (target 55-90 ng/mL). Based on the data from this study we would suggest a daily dose of vitamin D3 of 20,000 to 50,000 IU/day until a vitamin D level is obtained. It is possible that patients with cancer may require an even higher level, approximating 150 ug/dL.

Wang et al demonstrated that postoperative vitamin D supplementation in esophageal cancer patients undergoing esophagectomy was associated with improved quality of life and with improved disease-free survival. Similarly, vitamin D use post-diagnosis was found to be associated with a reduction in breast cancer-specific mortality. Two recent clinical trials in prostate cancer patients suggest that vitamin D supplementation may prevent prostate cancer progression. Vitamin D has additive or synergistic effects when combined with conventional chemotherapy. Zeichner et al demonstrated that the use of vitamin D during neoadjuvant chemotherapy in HER2-positive nonmetastatic breast cancer was associated with improved disease-free survival (HR, 0.36; 95% CI, 0.15-0.88; p=0.026). 

Types of cancers that Vitamin D may be beneficial for Vitamin D supplementation is likely beneficial in most cancers, but particularly in patients with breast, colorectal, gastric, esophagus, lung, and prostate cancer as well as those with lymphomas and melanoma. Dosing and cautions As almost all patients with cancer are severely vitamin D deficient, a high loading dose of vitamin D is suggested followed by dose titration according to vitamin D blood levels, aiming for a level of > 50 ng/mL (target 55-90 ng/mL). 

However current data suggest that levels up to 150 ng/mL are necessary for certain types of cancer to stop growth and metastasis. Vitamin D intoxication is observed when serum levels of 25-hydroxyvitamin D are greater than 150 ng/mL (374 nmol per liter). (554) Hypercalcemia will usually not occur until levels exceed over 250 ng/mL. We, therefore, suggest a daily dose of 20,000 to 50,000 IU until a vitamin D level is obtained. With the suggested doses, serum 25(OH)D concentrations rise above 100 ng/mL within a week or two, but unless a suitable higher maintenance dose is used (~ 10,000 IU/day), the level will start to drop to baseline after three weeks or so, and the benefit of vitamin D will be lost. 

If measuring vitamin D levels is not feasible/possible, we would suggest a loading dose of 100,000 IU followed by 10,000 IU/day. Doses of 10,000 IU of vitamin D3 per day for up to 5 months were reported to be safe and without toxicity. It should be noted that dosages of vitamin D up to 80,000 IU/day have been reported to be safe. We recommended vitamin D3 over D2 as vitamin D2 is approximately 30% as effective as vitamin D3 in maintaining serum 25-hydroxyvitamin D levels. 

Furthermore, vitamin D3 should be dosed daily rather than large intermittent bolus dosing. It is best to include both vitamin K2 (menaquinone [MK4/MK7] 100 mcg/day, or 800 mcg/week) and magnesium (250-500 mg/day) when doses of vitamin D > 8 000 IU/day are taken. Patients taking coumadin need to be closely monitored and the need to consult with their PCP before taking vitamin K2. Further, we suggest measuring PTH (parathyroid) levels and calcium levels and titrating the dose of Vitamin D according to the PTH levels as follows (Coimbra Protocol): (607, 608) i) if the PTH level is below the lower end of the reference range, reduce the dose of vitamin D ii) if the PTH level is at (or close too) the lower end of the reference range, maintain dose, iii) if PTH is within the reference range but not near to the low end of the reference range increase the dose of vitamin D.

Source: https://covid19criticalcare.com/wp-content/uploads/2023/06/Cancer-Care-FLCCC-Dr-Paul-Marik-v2.pdf

 

2. Turmeric (Curcumin)

What about turmeric and cancer? 

Curcumin, popularly called "curry powder" or turmeric, is a polyphenol extracted from Curcuma longa. Curcumin has antioxidant, anti-inflammatory, antimicrobial, antiviral, and anticancer properties.  

Interestingly, curcumin has displayed antitumor properties both in vitro and in vivo, and has been shown to act through multiple cellular pathways. It is one of the few compounds that has progressed to clinical trials (source).

Curcumin is one of the nutrients with the most evidence-based literature supporting its use against cancer. There are more than 7,000 search results on curcumin and cancer on PubMed and more than 50 clinical trials with curcumin, most of which are still ongoing. The spice turmeric can be extremely helpful when it comes to fighting cancer. 

The use of fenbendazole and curcumin, has achieved much attention due to the reported experience of Joe Tippens. In 2016, Tippens was diagnosed with non-small-cell lung cancer with extensive metastatic disease. At the advice of a veterinarian friend, he took Fenbendazole together with nanocurcumin, and three months after starting these drugs his PET scan was completely clear. 

A review paper published in 2022, analysed 21 human studies. Sixteen out of 21 clinical trials were associated with the effectiveness of curcumin or turmeric on various types of cancer, and the other five clinical trials were related to the evaluation of the efficacy of curcumin or turmeric in relieving the side effects of cancer chemotherapy and radiotherapy. The emerging data from the clinical trials confirm that curcumin has the potential for cancer prevention and intervention. Interestingly, curcumin appears to be universally useful for just about every type of cancer (Arslan 2022), which is really odd since cancer consists of a wide variety of different molecular pathologies.

Both curcuminoids and related turmeric products have been sanctioned by the U.S. Food and Drug Administration (FDA) as safe.

Clinical studies 

Despite the broad anticancer activities of curcumin in experimental models, its clinical use has been limited by its poor bioavailability. Its oral bioavailability is low due to its poor absorption, extensive phase I and II biotransformation, and rapid elimination through the gall bladder. Due to its low solubility in water and poor absorption, it is traditionally taken with full-fat milk and black pepper, which enhance its absorption. To improve the bioavailability, various curcumin analogs and novel drug delivery systems (e.g., phospholipids, nanoparticles, and liposomes) are under investigation. 

Curcumin and Chemotherapy Combination

While a few case series describing the use of curcumin in cancer have been published, the clinical efficacy of curcumin has been evaluated in a limited number of studies. 

In a pilot randomized clinical trial in patients with multiple myeloma, the addition of curcumin (4 g twice daily for 28 days) to treatment with melphalan and prednisone increased the rates of remission ([75% vs. 33.3%, p=0.009]. In this study NF-ΚB, VEGF, and TNF levels were significantly lower in the curcumin group with TNF levels being strongly correlated with remission [OR=1.35; 95% CI=1.03-1.76, p=0.03]. In a phase IIa, open-labeled trial patients with metastatic colorectal cancer were randomized to fluorouracil/oxaliplatin chemotherapy (FOLFOX) compared with FOLFOX + 2 g oral curcumin/d (CUFOX). 

In a prospective, single-arm phase II study, Pastorelli et al evaluated the use of a phytosome complex of curcumin (2 g/day) as adjunctive therapy with gemcitabine in patients with advanced pancreatic cancer. (715) The median overall survival of patients treated with gemcitabine as a single agent is 5.7 months. (716) These investigators reported a 27.3% response rate with 34.1% of cases having stable disease, with a total disease control rate of 61.4%. The median progression-free survival and overall survival were 8.4 and 10.2 months, respectively. Saghatelyan et al randomized 150 women with advanced metastatic breast cancer to receive either paclitaxel plus placebo or paclitaxel plus curcumin once per week for 12 weeks with 3 months of follow-up. (717) In this study, the curcumin was given intravenously. The intention-to-treat analysis revealed that the objective response rate of curcumin was significantly higher than that of the placebo (51% vs. 33%, p<0.01) at 4 weeks of follow-up. The difference between the groups was even greater when only patients who had completed the treatment (61% vs. 38%, odds ratio =2.64, p<0.01) were included.

In dose escalation studies, up to 10 g of curcumin taken daily has been shown to be well tolerated. Patients with breast cancer taking 6 g/day of curcumin for 7 weeks, and patients with prostate cancer who took 3 g/day of curcumin for 9 weeks exhibited no adverse effects. Types of cancers that curcumin (turmeric) may be beneficial for Curcumin (turmeric) may be beneficial for the following types of cancer: colorectal, lung, pancreatic, breast, prostate, chronic myeloid leukemia, liver, gastric, brain tumors, ovarian, skin, head and neck, lymphoma, esophageal and myeloma. Drug formulations and cautions The use of curcumin has been limited by its poor solubility, absorption, and bioavailability. The manipulation and encapsulation of curcumin into a nanocarrier formulation can overcome these major drawbacks and potentially may lead to a far superior therapeutic efficacy. In a murine Hodgkin’s Lymphoma model, formulating curcumin in solid lipid nanoparticles exhibited greater anticancer activity compared to curcumin alone. Nano-curcumin preparations or formulations designed to enhance absorption are therefore recommended.

In the U.S., a large share (55%) of the turmeric dietary supplement market is comprised of products formulated to enhance curcumin bioavailability, including proprietary products where curcuminoid extracts are often combined with some type of lipophilic carrier to increase absorption, or products combining curcumin with piperine to decrease metabolism. However, as the quality of these products may vary, we would recommend the use of USP grade supplements. Furthermore, nanoformulation-based combination therapy has emerged as a potent approach for drug delivery systems. (724) A nanodrug co-delivery system incorporating chemotherapeutic agents has demonstrated greater cancer cell sensitivity. Curcumin has been characterized as “generally safe” by the US Food and Drug Administration (FDA). No toxicity is seen for doses of up to 8–10 g/day. 

However, diarrhea can be a frequent side effect, especially if the daily dose exceeds 4 g. Liver injury (hepatitis) is a rare complication and therefore liver function tests should be monitored during long-term use. Curcumin does not appear to have any overt negative effects, but it has been noted that this compound can inhibit several cytochromes P450 subtypes, including CYP2C9 and CYP3A4. Consequently, curcumin has been reported to interact with several different drugs, including antidepressants, antibiotics, and anticoagulants like coumadin and clopidogrel. Curcumin has anticoagulant effects and may prolong bleeding in people using anticoagulants.  

New Curcumin Forms

Convenience and efficiency has driven many of the changes in the forms of curcumin in later years. Because it's a fat-loving or lipophilic molecule, many newer preparations now include some sort of oil or fat, which improves its absorbability and bioavailability. Such preparations typically have seven to eight times higher absorption than the raw, unprocessed 95% concentration of dry powder. There are also newer sustained release preparations.

Turmeric and black pepper each have health benefits, due to the compounds curcumin and piperine. As piperine enhances curcumin absorption in the body by up to 2,000%, combining the spices magnifies their effects. (Healthline)

Click here to buy Bioavailable Curcumin. (Disclosure: Paid link)

3. Magnesium and Molecular Hydrogen

PubMed has indexed more than 5,000 research studies on magnesium and cancer.

Magnesium and Vitamin C

A 2020 study demonstrated that vitamin C treatment with magnesium supplementation provided more effective anticancer therapy than vitamin C treatment alone.

Molecular Hydrogen and Cancer

More than 600 articles related to molecular hydrogen and cancer were retrieved from Cochrane, PubMed and Google Scholar, and 27 articles were included for this systematic review (2023). 

Based on the authors' analysis, "H2 plays a promising therapeutic role as an independent therapy as well as an adjuvant in combination therapy, resulting in an overall improvement in survivability, quality of life, blood parameters, and tumour reduction."

Although H2 has demonstrated significant anti-cancer effects, the underlying mechanisms have not yet been elucidated. Many studies have shown that H2 therapy can reduce oxidative stress. This, however, contradicts radiation therapy and chemotherapy, in which ROS (Reactive Oxygen Species) are required to induce apoptosis and combat cancer. 

A 2020 study in Japan administered hydrogen therapy to 42 patients with stage-four lung cancer. The researchers found that hydrogen therapy could extend the overall survival of the patients. Specifically, patients receiving hydrogen therapy had a median survival time of 28 months, almost triple the survival time of those undergoing immunotherapy.

Related: Best Molecular Hydrogen Tablets

Note: Most Molecular Hydrogen tablets uses pure elemental magnesium as its carrier and provides you with approximately 80 mg of magnesium per tablet. So, you receive also highly bioavailable magnesium for a healthy brain, muscles, cells, kidneys, and heart.

4. Vitamin C

Ascorbic acid, commonly known as vitamin C, is an essential water-soluble vitamin that humans are unable to synthesize endogenously, and must therefore obtain from dietary sources.

PubMed has indexed more than 3,000 research studies on vitamin C and cancer.

Treatment

2023 - A systematic review to evaluate the existing literature on the safety and efficacy of vitamin C, E and selenium supplementation in cancer patients. Twenty-four articles met the inclusion criteria. Of the included studies, nine evaluated selenium, eight evaluated Vitamin C, four evaluated Vitamin E, and three of these studies included a combination of two or more of these agents. Findings were generally favorable among the studies, and adverse effects of supplementation were limited. The review concluded that antioxidant supplements may provide benefits in reducing incidence or severity of treatment-induced side effects with limited risk for adverse effects.

2022 - A systematic review on the effect of vitamins C and E on cancer survival showed improvement of survival and progression rates of cancers by vitamins C and E. However, the authors concluded that more high quality trials with large sample sizes are required to confirm.

Vitamin C is known as an antioxidant, but at high concentrations, vitamin C can kill cancer cells through a pro-oxidant property (Transl Oncol. 2020). This study has also demonstrated that vitamin C treatment with magnesium supplementation provided more effective anticancer therapy than vitamin C treatment alone.

High-dose vitamin C cancer therapy was introduced by Linus Pauling and Ewan Cameron [source]. Clinical demonstration results by Pauling and Cameron showed that intravenous injection of 10 g/day of vitamin C extended the survival time of terminal cancer patients by about 4.2 times. However, results from the Mayo Clinic in 1979 showed that the survival time of vitamin C–treated patients was even shorter than that of the placebo group patients [source]. A significant difference between those two research groups was the route of AA administration: intravenous injection and oral administration, respectively. 

When treating cancer, IV needs to be used because you simply cannot take the high dosages required orally. Doses over 10 to 20 grams of ascorbic acid will cause loose stools when taken orally, but IV administration bypasses the limitation of the gut. It also allows the vitamin C to get directly into the blood to the extracellular fluid, into the tumor microenvironment, to penetrate the tumor and saturate the entirety of the tumor.

To understand the mechanism of AA's (ascorbic acid) anticancer activity, many research groups have treated colon, prostate, leukemia, lymphoma, brain, and stomach cancer cells and chemically or genetically transformed cancer cells with AA and showed cancer growth inhibition and even cancer cell death through hydrogen peroxide–mediated reactive oxygen species (ROS) generation [source]. 

In most cases, the pharmacological concentration of vitamin C required for anticancer effects (EC50 value of 1–10 mM) could only be achieved by intravenous administration. Thus, to apply vitamin C as an anticancer therapy, a high intracellular concentration in cancer cells is critically important (source).

According to the Mayo Clinic (2023):

"More recently, vitamin C given through a vein (intravenously) has been found to have different effects than vitamin C taken in pill form. This has prompted renewed interest in the use of vitamin C as a cancer treatment.

There's still no evidence that vitamin C alone can cure cancer, but researchers are studying whether it might boost the effectiveness of other cancer treatments, such as chemotherapy and radiation therapy, or reduce treatment side effects.

There are still no large, controlled clinical trials that have shown a substantial effect of vitamin C on cancer, but some preliminary studies do suggest there may be a benefit to combining standard treatments with high-dose IV vitamin C."

 

According to the concluding remarks from a 2020 article from the National Cancer Institute:

Vitamin C as a cancer therapy has had a controversial past. What has been intriguing are small clinical trials that suggest some responses, but with no clear rationale for why cancers should respond to vitamin C or a path forward for explaining which patients are most likely to respond. Now a growing number of preclinical studies are showing how high-dose vitamin C might benefit cancer patients. Importantly, these preclinical studies provide a clear rationale and potential biomarkers that may help personalize the therapeutic approach and identify patient populations that are likely to respond to high-dose vitamin C therapy. Since the mechanisms of action of vitamin C are becoming better defined, we can propose vitamin C combinations in a more rational, hypothesis-driven manner. In addition, given the current high financial cost of new cancer drugs, it seems rational to improve the effectiveness of current therapies by studying their clinical interactions with vitamin C. In our view, the implementation of this treatment paradigm could provide benefit to many cancer patients.

Ascorbic acid vs whole food vitamin C?

Synthetic Ascorbic acid is NOT the same as whole food or whole fruit vitamin C. 

If you were to compare the two to a car, vitamin C would be the whole car, fully functional, and the engine is an enzyme called tyrosinase, while ascorbic acid is the car frame, with no moving parts. A car with the engine can take you from one place to another but the car frame alone will not be able to do that.

Whole food vitamin C can also boost your copper level, as vitamin C contains an enzyme called tyrosinase, which has 2 atoms of copper in it. Ascorbic acid is prooxidant, while vitamin C complex is actually an antioxidant. Anything that has copper is going to be antioxidant.

Related: Benefits of Vitamin C in Cancer Treatment

5. Melatonin and Cancer

PubMed has indexed more than 3,300 research studies on melatonin and cancer. 

Melatonin is one of the most important antioxidant molecules. In the human body — aside from having direct antioxidant effects — it also stimulates the synthesis of glutathione and other important antioxidants like superoxide dismutase and catalase.

In addition, melatonin increases the expression of the p53 protein, induces its phosphorylation, inhibiting cell proliferation, promotes apoptosis, reduces the levels of the vascular endothelial growth factor and endothelin-1, fundamental for tumor growth and metastasis formation, reduces inflammatory processes and cell migration (Molecules 2018).

Reduction of melatonin production has also been seen in some types of cancer (breast and prostate) (Mogavero 2021).

Melatonin for Cancer Patients

2022 - An umbrella review from 111 different meta-analyses based on randomized controlled trials (Pharmacological Research 2022):

"Survival at one year (P < 0.005) significantly increased with cancer patients."

2020 - A case series of 14 advanced cancer patients (Trends in Oncology 2020), treated with high dose (1,000 mg/day) of melatonin; achieved a disease control of 54% of the patients:

"Moreover, this preliminary study may also suggest that high dose melatonin has no toxicity in cancer patients with poor clinical status, as well as in healthy subjects."

2005 - A systematic review of 10 randomized controlled trials (J Pineal Res 2005):

"All trials included solid tumor cancers. All trials were conducted at the same hospital network, and were unblinded. Melatonin reduced the risk of death at 1 yr (relative risk: 0.66). Effects were consistent across melatonin dose, and type of cancer. No severe adverse events were reported. The substantial reduction in risk of death, low adverse events reported and low costs related to this intervention suggest great potential for melatonin in treating cancer."

Just be careful, though, as using high-dose melatonin long term could be a prescription for disaster. This is because doses of over 5 to 10 mg are likely to draw out heavy metals like mercury and unless you are on a good detoxification program and using sauna regularly these heavy metals could cause biological damage.

Clinical studies 

In addition to case studies, the clinical benefit of melatonin in patients with cancer is supported by the highest level of evidence, namely meta-analyses of RCTs. Seely et al systematically reviewed the effects of melatonin in conjunction with chemotherapy, radiotherapy, supportive care, and palliative care on 1-year survival, complete response, partial response, stable disease, and chemotherapy-associated toxicities. 

This analysis included 21 randomized studies all of which studied solid tumors. The pooled relative risk (RR) for 1-year mortality was 0.63 (95% CI = 0.53-0.74; P < 0.001). Improved effects were found for complete response, partial response, and stable disease. In trials combining melatonin with chemotherapy, adjuvant melatonin decreased 1-year mortality (RR = 0.60; 95% CI = 0.54-0.67). 

In a meta-analysis of RCT’s, Wang reported that melatonin as an adjuvant therapy for cancer led to substantial improvements in tumor remission, 1-year survival, and alleviation of radiochemotherapy-related side effects.  Types of cancers that melatonin may be beneficial for Melatonin may be active in several cancers including cancers of the breast, ovary, pancreas, liver, kidney, mouth, stomach, colon/rectum, brain, lung, prostate, head and neck, and various leukemias and sarcomas.

Dosing and cautions 

The optimal dosing regimen for melatonin is not clear. Most studies have used a dose of 20-40 mg at night. In patients with advanced disease and/or highly malignant disease the night-time dose can be increased to 60 mg with an additional 20 mg dose at midday. 

A higher dosage has been suggested in patients with severe disease; namely 20-30 mg at 10 am and 4 pm with 60 mg at nighttime (personal communication Dr Russel Reiter). Considering the impressive safety profile of melatonin (see below) a therapeutic trial of the higher dose should be explored. A proportion of patients are intolerant of higher doses of melatonin due to REM sleep induced nightmares (slow metabolizers with reduced first pass effect). 

Consequently, providers should advise patients to begin with 1 -5 mg at night; a slow-release/extended release preparation at nighttime may minimize REM sleep-induced nightmares (best taken an hour before retiring). The dose should be increased up to 20-30 mg, as tolerated. Melatonin is probably the safest medical compound available, with a LD50 of infinity (it is impossible to kill an animal with industrial doses of melatonin). The only side effects reported are early morning drowsiness and “bad dreams” (when the dose is increased too rapidly).

Related: What You Need to Know About Melatonin

6. Omega-3 Fatty Acids

The term omega-3 polyunsaturated fatty acids (omega-3 FAs) refers to a group of polyunsaturated fatty acids (PUFA) that contain a double carbon bond at the third carbon atom (n-3 position) from the methyl end of the carbon chain. Alpha-linolenic acid (ALA, 18-carbon PUFA obtained from plant sources), eicosapentaenoic acid (EPA, 20-carbon PUFA form fish) and docosahexaenoic acid (DHA, 22-carbon PUFA obtained from marine source) are the most common omega-3 FAs.

Clinical studies 

In a prospective RCT, the intake of omega-3 FAs and vitamin D was associated with a dramatic reduction in the risk of developing cancer. In the VITAL cohort study conducted in postmenopausal women, the current use of fish oil was associated with reduced risk of breast cancer (HR 0.68, 95% CI: 0.50-0.92).

A meta-analysis of 16 prospective cohort studies examining marine omega-3 FAs intake suggests a reduction in breast cancer risk when individuals with highest intakes are compared with those with lowest intakes of marine PUFA. 

Two large observational studies have demonstrated significant inverse relationships between omega-3 FAs intake and the risk of colorectal neoplasia. 

A recent meta-analysis of six prospective case–control studies and five cohort studies evaluated the omega-3:omega-6 intake ratio and/or omega-3:omega-6 ratio in serum phospholipids in relation to the risk of developing breast cancer. The authors concluded that each 1/10 increment in the dietary n-3:n-6 ratio was associated with a 6% reduction in breast cancer risk, and each 1/10 increment in the serum n-3:n-6 phospholipid ratio was associated with a 27% reduction in breast cancer risk. Patients with familial adenomatous polyposis who had previously undergone colectomy and ileorectal anastomosis were randomized to 2g EPA/day or placebo. In this RCT there was a 22.4% reduction in polyp number in the EPA group (p=0.01).

A phase II study evaluated addition of 1.8 g DHA daily to an anthracycline based chemotherapy regimen for metastatic breast cancer. The DHA group had a significantly longer time to disease progression and overall survival (median 34 months vs 18 months). 

In a small RCT, supplementation with fish oil increased first line chemotherapy efficacy in patients with advanced non-small cell lung cancer.(804) Higher intakes of EPA and DHA from dietary sources were reported to be associated with a 25% reduction in breast cancer recurrence and improved overall mortality in a large cohort of over 3,000 women with early-stage breast cancer followed for a median of 7 years. 

Cohort studies assessing the risk of prostate cancer mortality and fish omega-3 FAs intake suggest an association between higher intake of fish and decreased risk of prostate cancer–related death.

In a small RCT, patients with leukemia or lymphoma concurrently receiving chemotherapy were randomized to receive 2g /day of fish oil or placebo for 9 weeks. (807) Overall long-term survival was greater in the fish oil group (p < 0.05). 

In a meta-analysis that included 12 RCT and 1184 patients with cancer cachexia, the use of omega-3 FAs was associated with a significant improvement in quality of life and duration of survival (median survival ratio, 1.10; 95% CI, 1.02-1.19; P = .014). 

Types of cancers that omega-3 fatty acids may be beneficial

Omega-3 FAs may be beneficial for breast cancer, colorectal cancer, leukemia, gastric cancer, pancreatic cancer, esophageal cancer, prostate cancer, lung cancer, and head and neck cancer.

Dosing and cautions 

We suggest a dose of 2-4 g omega-3 FAs daily. Omega-3 fatty acids may increase the risk of bleeding and should be used cautiously in patients on anticoagulants.

7. Green Tea (EGCG) and Cancer

PubMed has indexed more than 2,000 research studies on EGCG and cancer.

Green tea also contains chemicals called polyphenols that have antioxidant, anti-inflammatory properties and anti-angiogenic properties, and the catechins in green tea polyphenols show very strong anti-angiogenic properties.

Green tea is a significant source of a type of flavonoid called catechin, which includes epigallocatechin gallate (EGCG), epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC). The most abundant individual catechin in fresh tea leaves is EGCG, which is more than 40% of the total content of catechins. (242) Green tea catechins (GTCs) have been proven to be effective in inhibiting cancer growth in several experimental models. 

Epigallocatechin 3-gallate (EGCG), the active compound in green tea, is synthesized from epicatechin and gallic acid, has garnered considerable attention in the scientific community due to its multifaceted biological and pharmacological properties. These include its anti-oxidant, anti-inflammatory, anti-angiogenic, anti-proliferative, pro-apoptotic, and anti-metastatic functions. 

According to a 2018 review, EGCG and green tea extracts may help prevent or delay cancer onset, cancer recurrence, and secondary growths from cancer.

However, the National Center for Complementary and Integrative Health (NCCIH) state that studies of green tea and cancer in humans have so far produced inconsistent results.

Several epidemiological studies (2011) have reported that the consumption of green tea may decrease cancer risk. Studies have also confirmed numerous health benefits of green tea including prevention of cancer (R, R) and cardiovascular disease, as well as anti-inflammatory, antioxidant, antiarthritic, antibacterial, and antiviral effects. (R, R, R, R).

Given these promising insights, a phase I clinical trial (NCT00516243) has been initiated that targets women with hormone receptor-negative stages I-III breast cancer and aims to explore the safety and effectiveness of EGCG. Concurrently, several clinical trials for CRC (NCT02321969 and NCT01360320) are also in progress. However, while these studies are promising, the potential therapeutic application of EGCG in cancer treatment is still restricted by its limited bioavailability.

If you have cancer, consider drinking up to 3 cups of green tea per day to experience the benefits. Green tea pills are also available, but may be too concentrated. Some studies show health benefits in people who drink as little as one cup per day, while other studies deem five or more cups per day to be optimal (Source, Source).

Numerous experimental models have explored the mechanistic anticancer effects of GTCs (Green Tea Catechins); this data is supported by epidemiologic data, a case series of patients with B cell malignancies, several case reports and a RCT. A meta-analysis including 18 prospective cohorts and 25 case-control studies showed a significant inverse association between intake of tea catechins and risk of various cancers, with a relative risk (RR) being 0.935 (95% CI = 0.891- 0.981). 

Similarly an umbrella review and meta-analysis by Kim et al, which included 64 observational studies (case-control or cohort) demonstrated that GTC significantly reduced the risk of gastrointestinal cancer (oral, gastric, colorectal, biliary tract, and liver), breast cancer, and gynecological cancer (endometrial and ovarian cancer) as well as leukemia, lung cancer, and thyroid cancer. 

In a phase I dose finding study in patients with Chronic Lymphocytic Leukemia, EGCG was well tolerated and a decline in the absolute lymphocyte count and/or lymphadenopathy was observed in the majority of patients.

Lemanne et al reported on a patient who demonstrated a complete and durable remission of chronic lymphocytic leukemia (CLL) following high dose EGCG. In a randomized, double-blind, placebo-controlled study, treatment with 600 mg/day of green tea catechins reduced the risk of prostate cancer from 30% to 3% in men with high-grade prostate intraepithelial neoplasia. Types of cancers that green tea may be beneficial for Green tea catechins may be effective against a range of tumors including cancers of the prostate, breast, uterus, ovary, colorectal, lung, liver and gallbladder as well as glioblastoma and melanoma. GTCs appear to be particularly beneficial for prostate cancer as well as breast cancer. 

Related: EGCG for Chronic Lymphocytic Leukemia - Glenn Sabin

Stress Reduction and Sleep 

A substantial body of research has investigated the associations between stress-related psychosocial factors and cancer outcomes. (403) This data demonstrates that psychosocial stress is associated with a higher incidence of cancer and poorer survival in patients with diagnosed cancer. It is critically important that patients engage in activities that reduce stress (meditation, yoga, mindfulness exercises, etc.) and get at least 8 hours of high-quality sleep (ensure adequate sleep hygiene).

Healthy sleep is essential for neural development, learning, memory, cardiovascular, and metabolic regulation. Sufficient sleep is needed to provide recovery after preceding waking activities and to ensure optimal functioning during subsequent wakefulness. 

As recommended by the National Sleep Foundation, in a healthy individual, the recommended sleep duration for younger adults is seven to nine hours, and for older adults it is seven to eight hours. Other than adequate duration, healthy sleep is good quality sleep. 

A study of 23,620 Europeans found that those who slept for less than 6 hours per day were 41% more likely to experience strokes and 44-78% more likely to experience heart attacks. The National Sleep Foundation endorses the following sleep quality indicators: 1) sleep latency of 15 minutes and less, 2) a maximum of one awakening of more than five minutes per night, 3) wake time after sleep onset of 20 minutes and less, and 4) sleep efficiency of 85% or more.

Insomnia is defined by the complaints of difficulty initiating sleep, difficulty maintaining sleep, or early morning awakenings and is associated with one or more daytime symptoms such as fatigue, cognitive impairment, or mood disturbance (depression). 

A systematic review demonstrated that short sleep duration, defined as less than 6 hours of sleep per 24 hours, is associated with a significant mortality increase. Numerous studies have found an association between sleep deprivation and cancer. 

An English study of 10,036 people over 50 found that poor sleep resulted in a 33-62% increased risk of cancer.(417) A study of 23,620 Europeans found that those who slept for less than 6 hours per day were 43-46% more likely to develop cancer. 

When healthy young men slept for four hours, compared to nights where they slept eight hours, there was a 72% decrease in their circulating NK cells. This finding is particularly important in the context of cancer immune surveillance. Furthermore, data shows that sleeping pills (which disrupt normal sleep) are associated with a large increase in one’s risk of cancer.  

Most sleeping pills are sedatives, not sleep aids. What this means is the person taking them is longer conscious, but since this is done through sedating the brain, its ability to initiate restorative sleep functions is greatly impaired. As a result, people who take sleeping pills effectively have greatly reduced sleep, and in turn, are tired throughout the day (because they did not have a restorative night of sleep) and are at high risk of developing a wide range of health issues associated with poor sleep. 

For example, one study found people who used sleeping pills were twice as likely to die as those who did not (and three times more likely if they were daily users. Another study that compared 10,529 sleeping pill users to 23,676 controls, found that over the course of 2.5 years, the sleeping pill users were 3.6-5.4 times more likely to die.

Source: https://covid19criticalcare.com/wp-content/uploads/2023/06/Cancer-Care-FLCCC-Dr-Paul-Marik-v2.pdf

Repurposed Drugs in Oncology

Overview of Repurposed Drugs

As background, some repurposed drugs are better at prevention and others are better when added to treatment.

Typically, when one adds repurposed drugs to standard cancer treatment, they improve their outcome, meaning that the tumor shrinks faster or their cancer biomarkers, such as PSA, Ca 125, or CEA, drop.

When this occurs in Stage 1, 2, or 3 cancers, it is sometimes difficult to tell whether it was the standard treatment, that is the surgery, chemotherapy or radiation that produced the benefit.

However, when the cancer has progressed to Stage 4, and particularly when it involves one of the often-incurable cancers such as the types in the below table under the “Palliation Only (Metastatic)” category where standard chemotherapy is largely ineffective, it becomes obvious that the repurposed drug made the difference.

Table Courtesy of Dr. Marik and Cancer Care

Drug repurposing involves using existing medications, originally developed for other conditions, in new therapeutic contexts. Given the lengthy and expensive process of novel drug development, repurposing approved drugs offers a cost-effective and expedited approach to cancer treatment. These agents are categorized based on the strength of evidence supporting their efficacy:

• Tier One: Strong evidence supports their use in cancer therapy (e.g., Vitamin D, propranolol, metformin, melatonin, curcumin, ivermectin and fenbendazole).

• Tier Two: Moderate evidence suggests a potential benefit (e.g., doxycycline, resveratrol, low-dose naltrexone).

• Tier Three: Limited evidence exists, warranting further investigation.

• Tier Four: Evidence suggests a lack of efficacy or potential harm, leading to a recommendation against their use.

Notable Repurposed Drugs

• Metformin: Originally used for type 2 diabetes, metformin has shown promise in reducing cancer cell proliferation by inhibiting the mTOR pathway and improving insulin sensitivity.

• Propranolol: A beta-blocker commonly used for hypertension, propranolol has been found to reduce metastatic potential in various cancers by inhibiting stress-induced catecholamine signaling.

• Ivermectin: Traditionally an anti-parasitic, ivermectin has demonstrated anticancer properties through its impact on cell cycle regulation and mitochondrial function.

Read More: 

Top Repurposed Drugs and Metabolic Interventions for Cancer Treatment: Evidence Based

Ivermectin, Fenbendazole and Mebendazole Peer-Reviewed Protocol in Cancer

Integrative Oncology: A Holistic Approach to Cancer Care

Integrative oncology bridges conventional cancer treatment with complementary therapies, emphasizing personalized patient care. The primary objectives of integrative oncology include:

• Symptom Management: Addressing pain, fatigue, and treatment side effects using acupuncture, mindfulness-based stress reduction (MBSR), and herbal medicine.

• Lifestyle Modifications: Encouraging exercise, stress reduction techniques, and optimized nutrition to support overall well-being.

• Patient-Centered Care: Engaging patients in shared decision-making and tailoring treatment plans to individual needs and values.

Countries such as Germany, Switzerland, and Israel have adopted integrative oncology models where oncologists are trained in both conventional and complementary medicine, improving patient outcomes and satisfaction.

Key Takeaways

The best way to fight cancer is to utilise a menu of strategies by maintaining good health, like from eating a nutritious whole-food diet with lots of fruits and vegetables, avoid ultra processed foods and a healthy lifestyle. 

Everyone’s situation is different, however, it is important to arm yourself with medical knowledge that cancer doctors (Oncologists) may simply not give you.

Whether you’re living with cancer, a survivor, or just concerned for your health, talk to your doctor to determine the best treatment for you. 

• For more information on treatment, causes and prevention, screening, and the latest research, check out this comprehensive resource page (by cancer type) from National Cancer Institute: https://www.cancer.gov/types.

Disclaimer

• Although this is a comprehensive guide, please do not consider this guide as personal medical advice, but as a recommendation for use with professional providers. Consult with your doctor and discuss with her/him.
• Our aim here isn't to replace your doctors' advice. It is intended as a sharing of knowledge and information. Do take note that most strategies are not 100% protective against cancer. It's a continuous struggle between the immune system and the cancer cells. 

Read More: This article is part of the Winning the War on Cancer series.

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