Cancer

To be completed

***

Reminder: Not medical advice, consult doctor before, etc.

What is the general understanding of cancer?

Complications for the person, their family, and the public perception

How to think about recovery, management, and responsibility without distributing blame (the emotionally charged aspect of this topic makes it hard to work on recovery without divisiveness). 

Each condition to address:

•  What is it?
• What may cause it and what are the commonalities between sufferers?
  • Endocrine
  • Anatomy/physiology
  • Environmental
  • Evolution/anthropology
  • Fetal development
  • Maternal/paternal health before conception
  • Genetics/epigenetics
  • Immune system
  • Nervous system
  • Psychology
• What are some potential ways of managing symptoms?
  • Breathwork
  • Sleep and Circadian Rhythm
  • Nutrition
  • Trauma recovery
  • Social/Communal integration
  • Exercise
  • Purpose
  • Environment tailored
  • Tools: eustress

***

Cancer

Cancer creates immunodeficiencies, while immunocompromised states increase vulnerability to malignancies. Immune cells perform a function called immuno-surveillance that helps to detect and eliminate precancerous/cancerous cells. Thus, a reduced immune system can increase the risk of numerous cancers. Cancer weakens immunity by affecting many parts of the body that are involved in producing immune cells.

Viruses themselves can cause or significantly increase the risk of cancer, think hepatitis C with liver cancer, Epstein-Barr virus with lymphoma and human papilloma virus (HPV) with cervical cancer. Thus, anything that increases the virulence of a virus, especially a dysfunctional immune system, may increase the risk of cancer.

What Happens in Cancer

Cancer is a disease of abnormally excessive cell growth, characterized by tumors, lumps, immune disorders and other infections. Cancer is not the same as benign tumors, the latter being non-life-threatening.

The six hallmarks of cancer that are needed to produce a malignant tumor include:

• Cell growth and division in the absence of proper signals
• Continuous growth and division even in the presence of contrary signals
• Evasion of programmed cell death
• Unlimited amount of cell divisions
• Promoting blood vessel formation
• Tissue invasion and formation of metastases

There are over 100 different types of cancer with the most common ones being lung cancer, prostate cancer, breast cancer, cervical cancer, colorectal cancer, leukemia and stomach cancer.

The biggest contributors to cancer are deemed to be smoking, alcohol, obesity, bad diet, lack of exercise and aging. Other factors are environmental pollution, ionizing radiation, stress and certain infections.

Carcinogens are cancer-forming substances that promote carcinogenesis or the development of cancer. Genotoxic carcinogens like N-nitroso-N-methylurea (NMU), UV radiation, ionizing radiation and certain viruses cause irreversible damage or mutations by binding to DNA.

• Known carcinogenic compounds in humans are all radionuclides, UV radiation, x-rays, gamma radiation, chemicals in processed meat, tobacco smoke, nitrites used in food preservatives, chemicals that get created during charring meat, arsenic, benzene, cadmium, nickel, lead, gasoline, alcohol and hundreds of industrial chemicals or heavy metals.
• Probable carcinogens include chemical emissions, androgenic steroids, various plastics and shift work. Electric power transmission, powerlines, radio waves, electromagnetic frequencies and mobile phones are described as possibly carcinogenic by the World Health Organization, but there is not enough evidence to support a consistent link.
• A 2014 meta-analysis found no link between fruit and vegetable consumption and cancer, but it did lower all-cause mortality, especially cardiovascular mortality.
• Cooking meat and protein at high temperatures does create carcinogenic compounds like heterocyclic amines and polycyclic aromatic hydrocarbons (increasing colon cancer risk). Consuming cooked meat with certain spices, coffee and other plant compounds seems to offset these harms.

The vast majority of cancers (90-95%) are the result of environmental factors creating genetic mutations, which are preventable with lifestyle. About 5-10% of cancers originate from inherited genetic defects. People with heritable mutations in BRCA1, BRCA2, mismatch-repair genes and the CDH1 gene have a remarkably high risk (~75%) of developing breast-ovary, colorectum-endometrium or stomach cancer. However, these high-risk mutations are extremely rare (<0.3% of the population) and account to less than 3-10% of annual cancer diagnoses.

• Individuals with one first-degree relative (parent or sibling) who has had colorectal cancer experience a 2-fold higher risk of developing it themselves. Those with two or more relatives, a 4-fold higher risk, independent of age of diagnosis.
• For lung cancer, the corresponding relative risk is 1.5 and 1.9 for prostate cancer.
• The relative risk is 1.8 for breast cancer if the close relative developed the disease after the age of 50 and 3.3 when before 50.
• Taller people also have a higher heritable risk of cancer because they have a greater number of cells that can become malignant.
• Epigenetic alterations in cancer development are just as important, if not more important, than genetic abnormalities. Examples include changes in DNA methylation, histone modification, chromatin and chromosomal mutations.

Internal Factors: Oxidative stress, chronic inflammation, genetics, epigenetics

External factors: Carcinogens, toxins, radiation, pollution

DNA damage is caused by these factors, which lead to: epigenetic alterations/mutations, DNA repair deficiency, and an accumulation of DNA damage and more mutations. Resulting in the development of cancer.

Potential Causes of Cancer:

Metastasis is known as the state in which cancer spreads from its original location to lymph nodes or other distant places in the body via the blood. The majority of cancer deaths are due to metastases.

Nrf2-deficiency has been shown to create lung tumor metastasis by disturbing redox balance in the hematopoietic and immune system. In addition to cancer cells, tumors also create a tumor microenvironment (TME), which includes all the surrounding blood vessels, fibroblasts, immune cells, and signaling molecules that help with the growth of cancerous cells.

Conventional cancer therapies include certain medications, chemotherapy, radiation therapy, laser therapy, hormonal therapy, immunotherapy, palliative care and surgery. Here is a short overview of them:

• Chemotherapy involves killing rapidly dividing cells with cytotoxic anti-neoplastic drugs and chemotherapeutic agents. They are divided into different categories like alkylating drugs and antimetabolites. Combination therapies appears to improve survival and reduce disease progression better than using only a single drug. However, this does not seem to lead to better health outcomes considering the accompanied toxicity. There is also targeted chemotherapy, which pinpoints key differences between cancerous and normal cells, such as estrogen receptor molecule inhibition and Bcr-Abl inhibitors. Chemotherapy combined with surgery has proven to be effective in treating many cancers like breast cancer, colorectal cancer, testicular cancer, ovarian cancer, and pancreatic cancer but it is limited by its toxic side effects.
  • Fasting has been shown to improve the effectiveness of chemotherapy in rats as well as humans by protecting against the toxicity and killing off more cancer cells. It already supports the removal of malignant and dysfunctional cells via autophagy.
  • Chemotherapy or chemotherapy drugs when given at night may work better and cause less side effects. During daytime, the body’s own steroid hormones can inhibit the function of epidermal growth factor (EGF) receptors, which are proteins targeted by anti-cancer drugs.
• Radiation therapy involves using ionizing radiation to damage and kill cancerous tissues. The most common radiation treatment for skin cancer is low energy X-rays, whereas internal cancers are treated with high energy X-rays. Radiation beams can also be employed to hit the tumor from precise angles to spare healthy tissue. However, there will inevitably still be some radiation-induced DNA damage that will occur in other cells. Radiation therapy is effective for bone metastasis in about 70% of people.
  • There is quite a lot of pre-clinical and clinical data showing that low dose radiation can help treat cancer patients either alone or as an adjunct to standard therapies. During the early stages of cancer, low dose radiation boosts the immune system, triggering radiation hormesis and increases resilience. Low dose radiation in between standard radiation therapy can also improve primary tumor control and reduce metastasis in patients of non- Hodgkin’s lymphoma.
  • However, exposure to ionizing radiation is a known carcinogen that increases the risk of future cancers, especially leukemia. In high amounts, it causes genomic instability, DNA damage, epigenetic alterations and abnormalities, which promote mutations and vulnerabilities as discussed before. Natural background radiation from radon gas and medical imaging technologies contributes equally in regard to radiation exposure to the average person. Nuclear accidents like Chernobyl or Fukushima are rare but they do contribute to increased incidences of cancer and deaths among the local population. Low-dose radiation exposure, like living near a nuclear power plant, is currently deemed to be safe.
• Laser therapy utilizes high-intensity light to shrink tumors and precancerous cells. It is mostly used to treat surface cancers or those lining internal organs in combination with other therapies. However, lasers are more precise than radiation or surgery, but they are more expensive. The laser-induced hyperthermia diminishes cancers by damaging its cells.
• Surgery is the main method of eliminating isolated, solid cancers. It involves removing either the entire malignant mass or the infected lymph nodes. In some cases, this is enough to eliminate the cancer.
• Immunotherapy is artificially stimulating the immune system with various therapies, which improves its ability to fight cancer. It is categorized into active, passive and hybrid methods. Using modified immunotherapy antibodies, tumor antigens can be marked for destruction. Active therapies involve removing immune cells from the tumor, which includes the use of NK cells, cytotoxic T cells and dendritic cells. Passive antibody therapies involve targeting cell surface receptors, including CD20, CD274 and CD279 antibodies.
• Palliative care is to help the patient alleviate the physical, mental, and emotional challenges that arise during treatment. Its primary goal is to improve quality of life. Palliative care is recommended to people at all stages of cancer.

The Warburg Effect refers to how cancer cells prefer burning glucose via glycolysis even in aerobic conditions. Usually, your body burns fatty acids using the more efficient oxidative phosphorylation pathway and switches over to glycogen at anaerobic intensities but this is not the case with malignancies. When it comes to energy production, aerobic glycolysis is much less efficient than oxidative phosphorylation. However, it produces more by products like lactic acid, which promotes the growth of malignant cells and fermentation.

• Herbert Crabtree concluded that not only do tumor cells show aerobic glycolysis but that there’s also fermentation due to environmental or genetic factors.
• Basically, if you’re burning only sugar, even in aerobic conditions, cancer cells create lactic acidosis, which spreads more cancer and deprives normal cells of oxygen.

Lactic acidosis is a medical condition where you produce high amounts of lactate that accumulates in your body. It’s a form of metabolic acidosis that promotes disease and can cause death. There are two types of lactic acidosis:

• Type A Lactic Acidosis – caused by decreased tissue oxygenation and blood flow
• Type B Lactic Acidosis – caused by metabolic diseases, dysfunctional mitochondria, medication or intoxication

Glycolysis is the process of producing pyruvate from glucose in the Krebs cycle. This is used for energy production primarily at anaerobic conditions, but in the cause of cancer, it also happens during aerobic respiration, thus increasing inflammation, lactic acid and fermentation. High blood glucose has been shown to accelerate cancer proliferation in vitro, while glucose deprivation has the opposite effect. Lower blood glucose in late-stage cancer patients is correlated with better health outcomes.

In 2008, a group of scientists found that a key enzyme found in tumors, called M2-PK, causes the Warburg Effect. Tumor M2-PK gets produced in rapidly dividing cells and is responsible for enabling cancer cells to consume glucose at an accelerated rate. In 2006, to reduce malignant cells’ ability to metabolize pyruvate into lactate, a study knocked out lactate dehydrogenase A (LDH-A) levels, which compromised the ability of tumor cells to proliferate under hypoxia. This suggests that lactate, or lactic acid, increases tumor cell proliferation and that reducing lactate levels may help with cancer.

There are many potential causes of lactic acidosis:

• Genetic Conditions – Deficiencies in metabolizing glucose, fructose, lactate and pyruvate.
• Heart Disease – Atherosclerosis, cardiac arrest and congestive heart failure decrease blood flow and oxygen throughout the body. This is both the cause and result of lactic acidosis.
• Diabetic Ketoacidosis – Having elevated ketones and glucose simultaneously.
• Kidney and Liver Disease – The organs that regulate fluids and pH are vital for controlling the body’s acidity. Damaged kidneys fail at buffering lactate.
• Infections – Sepsis and other infections jeopardize the immune system, reducing oxygenation and causing lactic acidosis. Some bacteria also promote glycolysis and fermentation.
• Cancer and Tumors – Malignant cells are in constant aerobic glycolysis and create lactate. This leads to the accumulation of lactic acid.
• Drinking Alcohol – Getting drunk can cause ketoacidosis and lactic acidosis. Alcohol also damages the liver and kidneys, which are supposed to regulate the body’s pH and acidity.
• Medication and Drugs – Some pharmaceuticals like Tylenol, paracetamol, epinephrine and metformin can cause lactic acidosis. HIV medications can also increase lactic acid levels.
• Overtraining – You produce lactate during intense exercise but most of it should be buffered out. If you’re overtraining and are soar all the time, then that may indicate a buildup of lactic acid.

The most common treatment for lactic acidosis includes IV fluids, oxygen therapy, rehydration, vitamins, and hemodialysis with bicarbonate.

Here’s how to avoid lactic acidosis from developing in the first place:

• Fix Liver Disease – You need to get the visceral fat out of the liver and organs to regain their functioning. Reducing your sugar, fructose, and alcohol consumption. 
• Manage Blood Sugar – Diabetes and insulin resistance keep the body in constant glycolysis, thus creating lactate.
• Improving your biomarkers with a healthy diet is crucial.
• Stop Drinking Alcohol – Alcohol is toxic even in moderation and it promotes lactic acidosis and fermentation. 
• Do Enough Exercise – Insufficient mitochondrial respiration leads to glycolysis and lactic acidosis. Staying fit and healthy prevents mitochondrial function by improving oxygen consumption.
• Stay Hydrated – Dehydration increases acidity in the body and decreases the flux of fluids. This may lead to the accumulation of metabolic waste and lactate.
• Intermittent Fasting – Intermittent fasting accelerates the clearance of lactate from the blood due to conversion into glucose via gluconeogenesis. It also improves blood sugar and organ health.

Symptoms include jaundice (yellow skin and eye whites), breathing troubles, panic attacks, confusion, chronic fatigue, irregular heart beat and nausea. It is measured with a fasting blood test at the doctor’s office.

In the example of M2-PK, it’s even found in healthy cells that need to rapidly divide i.e. wound healing.

Theoretical evolutionary game theory supports the idea that cells with a higher rate, but lower yield, of ATP production may gain a selective advantage when competing for shared and limited energy resources. The amount of ATP required for cell growth and proliferation seems to be much lower than for cell maintenance and survival. That’s why increased glucose metabolism is supportive of anabolism and proliferating cells throughout nature.

When mitochondria become damaged or dysfunctional, they start to promote more lactic acidosis and glycolysis because of lower respiration rates. They can’t produce enough energy and thus spread more inflammation and oxidative stress.

• Mitochondrial damage occurs because of oxidative stress on the body, environmental pollutants, inflammation, high blood glucose, processed food consumption, sedentarism and breathing problems.

The Role of Immunity in Cancer

One of the primary roles of the immune system is to recognize and remove tumors, which is called tumor surveillance or cancer immuno-surveillance. It inhibits carcinogenesis and maintains cellular homeostasis via the activity of natural (NK) cells, type I interferons (IFN-α/β), interferon-γ (IFN-γ), lymphocytes and the Perforin and Fas/FasL system.

Tumor-infiltrating lymphocytes (TILs) are known to eliminate tumor cells, and together with CD8+ T cells in cancer cell nests, they predict better survival in colon cancer, esophageal cancer, ovarian cancer, melanoma and others.

NK cell-mediated interference of malignancies is also positively correlated with survival in gastric cancer, colorectal cancer and squamous cell lung cancer.

Other danger signals that can enhance immune surveillance are uric acid, heat-shock proteins and extracellular matrix (ECM) derivatives. They induce a small amount of pro-inflammatory reactions that activate innate immunity to pathogens.

Sauna use or ingestion of beta-glucans (from yeast or medicinal mushrooms) are two ways that enhance immune surveillance. Sauna increases core body temperature, which mimics a fever activating pathways in the body as if there is an infection and priming the immune system. In the case of beta-glucan, ingesting a foreign substance, such as the cell wall components of yeast, puts the immune system on higher alert.

During early stages of tumor development, M1 macrophages have anti-tumor effects but they gradually become pro-tumorous after a while. The hypoxic tumor environment reduces the anti-tumor response of cytokines and increases their pro-tumor effects. Part of this toxic microenvironment is a decrease in pH, or an increase in acidity, in the tumor microenvironment.

• It has been suggested that taking sodium bicarbonate, which increases pH, reduces tumor microenvironment acidity and neutralizing tumor acidity improves antitumor immunotherapies. Bicarbonate can increase tumor pH and inhibit spontaneous metastases. Sodium bicarbonate nanoparticles may even help with chemotherapy drug uptake into tumors.
• An alkaline diet plus supplementary oral sodium bicarbonate (3-5 grams/day) has been shown to increase urine pH (6.85 vs. 6.39) in patients with advanced pancreatic cancer.

The process from surveillance to tumor progression is called cancer immunoediting, which describes the relationship between tumor cells and the immune system. It has three proposed steps, ranging from the initiation to escape:

1. Elimination of cancer by the immune system is the hallmark of successful immune surveillance that eradicates a developing tumor in its tracks. It includes both innate and adaptive immunity. Inflammatory cytokines generated by the tumor cells activate our immune cells, including NK, NKT and T cells, which then kill them. This process has an additional four steps:

• a. Tumor cell recognition by immune cells, which produce interferon-γ
• b. Maturation and migration of dendritic cells, during which IFN-γ expresses some cytotoxic effects
• c. Production of tumor antigen specific T cells, that exert more cytotoxicity
• d. Returning of tumor antigen specific tumor cells to the tumor site and elimination of tumor cells, which is enhanced by IFN-γ

2. Equilibrium is the stage during which cells resistant to immune effector cells get produced. These cells are more able to survive an immunodeficient host. During this process, many variants of the original tumor are killed but new mutated variants will emerge that are resistant to immune attacks.

3. Escape describes tumors avoiding immune responses, which supports malignant progression. There are many tumor-derived factors that contribute to immunosuppression and evasion, like vascular endothelial growth factor (VEGF), IL-10, transforming growth factor beta (TGF-beta), and prostaglandin E2.

• a. Tumor cells express distinct antigens on top of major histocompatibility complex class I (MHC I) molecules that differ from normal cells, which makes them a recognizable target to T cells and helper T cells. This can prevent further carcinogenesis when spotted during early stages of disease development. However, when tumor cells have fewer MHC I molecules than usual, they can evade detection, which helps them to avoid immuno-surveillance and turn cancerous. Fortunately, when this kind of evasion occurs, NK cells can pick up the task and kill these cells before they become malignant. The complement system is able to destroy tumor cells as well by generating antibodies.

Some cancers can also use immune checkpoints to shield themselves from an immune system attack:

• Immune checkpoints are locations of immune regulators that check up on which cells to be attacked and which ones to preserve. They can either be inhibitory or stimulatory.
• Blocking immune checkpoints can prevent the negative feedback signaling that could lead to tumor resistance.
• Currently approved immune checkpoint inhibitors block cytotoxic T-lymphocyte-associated protein 4 (CTLA4), programmed cell death 1 protein (PD-1 or PDCD-1) and ligand 1 (PD-L1). PD-L1 on cancer cells inhibits interferons and protects against T cell cytotoxicity. Targeting PD-L1 can also restore immune function within the tumor microenvironment. CTLA4 controls the homeostasis of regulatory T cells and maintains their suppressive capacity.
• However, patients treated with checkpoint blockers are at a higher risk of experiencing adverse immune-related and autoimmune reactions, which result from T-cell activation.

Inflammation and Immunodeficiency Caused by Magnesium Deficiency

Chronic inflammation is hypothesized to cause mutations, contributing to survival of cancer cells and development of the tumorigenic microenvironment.

About 20% of cancers are connected to chronic infections, autoimmunity and inflammation at the same tissue. Many of the other cancer risk factors like smoking, diabetes, obesity and environmental pollution cause site-specific, as well as systemic inflammation, promoting carcinogenesis.

Immunodeficiencies and pro-inflammatory destruction of both infectious and healthy cells appears to be primarily caused by killer T cells losing their cytotoxicity.

During viral infections, strategies that improve CD8 T cell cytotoxicity may lead to a healthier immune response. Potential strategies would include magnesium and selenium. During magnesium deficiency, monocytes release more inflammatory cytokines, whereas supplemental magnesium may reduce cytokines released by activated toll-like receptors.

Intracellular free magnesium regulates the cytotoxicity of NK cells and CD8 T cells. Reduced intracellular free magnesium causes dysfunctional expression of the natural killer activating receptor NKG2D in NK and CD8 T cells as well as defective programmed cell death in NK and CD8 T cells.

Type 2 diabetics have been found to have low intracellular free magnesium, which might partially explain why they are more susceptible to RNA viruses. Additionally, magnesium supplementation can inhibit NF-kB, which regulates tissue factor expression. Magnesium deficiency also promotes oxidative stress and depletes intracellular glutathione.

Therefore, intracellular magnesium plays a key role in immune function and magnesium supplementation, especially in those with low magnesium levels in their immune cells, may support a healthy immune response.

Intracellular magnesium deficiency = decreased cytotoxicity of NK cells and CD8 T cells -> Increased viral/cancer replication.

Stressful events like exercising, fasting, high blood sugar, insulin resistance, sleep deprivation or even feeling anxious makes you burn through magnesium at a higher rate. That’s why the more stressed out you are the more magnesium you need. Unfortunately, the less magnesium you have, the quicker you become depleted in it.

There are many factors that contribute to magnesium deficiency, such as:

• Poor diet
• Low stomach acid
• High sugar/fat intake
• High refined carbohydrate intake
• Vitamin B6, selenium or sodium deficiency
• Medications: diuretics and insulin
• Type 2 diabetes, gastrointestinal disorders, and heart failure
• High calcium, vitamin D or phosphorus intake
• Proton pump inhibitors and over the counter antacids
• Albuminuria

Magnesium depletion from food is primarily caused by pesticides and fertilizers that deplete the soil of vitamins and minerals. They kill off beneficial bacteria, earthworms and bugs that create nutrients into the soil. A great example is vitamin B12, which gets created by bacterial metabolism. Fertilizers also reduce the plant’s ability to absorb minerals. There are also processing methods like refining oils and grains that remove even more magnesium. The refinement of oils eliminates all their magnesium content.

Beta-Glucans

Beta-glucans are polysaccharides found in the bran of some grains like oat and barley, in the cell wall of baker’s yeast and in many edible mushrooms and seaweeds.

Their main effect comes from being able to modify biological responses, regulate inflammation and shape the function of innate and adaptive immune cells.

Beta-glucans are known for their anti-inflammatory, anti-allergic, anti-parasitic, anti-obesity and anti-osteoporotic effects. In vitro studies find that beta-glucans from yeast, mushrooms or cereals enhance functionality of human primary immune cells, specifically monocytes, macrophages and dendritic cells. This is accompanied by an increase in pro-inflammatory cytokines. The production of oxidative molecules like reactive oxygen species (ROS) is important for killing fungal pathogens.

Beta-glucans have anticarcinogenic effects that include (1) the controlling of cancer cell growth, (2) modulation of the tumor microenvironment and the immune system (3) and synergistic activity with conventional anticancer therapies. They also appear to reduce the negative side-effects of chemotherapy and radiation. Manipulating the TME can lead to a decrease in tumor metastasis.

Increasing:

• Immune cell cytotoxicity
• Innate immune response
• NK cells
• Neutrophils/monocytes
• Phagocytosis

Decreasing:

• Chemo side effects
• Leukocyte deterioration
• Cancer cell growth
• Tumor microenvironment

Beta-glucans found in mushrooms and baker’s yeast appear to be more effective in boosting immunity and providing antitumor defense whereas those in cereals tend to predominantly lower cholesterol and blood sugar. The ones in cereals are structurally different and are not recognized as PAMPs.

After ingestion, beta-glucans reach the small intestine in an undigested form where intestinal epithelial cells deliver them to immune cell populations.

The side effect of a last-ditch attempt at cellular survival in unfavorable conditions.  

Cellular Senescence and Immunosenescence

An accumulation of dysfunctional cells that can start to release cytokines and create inflammation and tissue damage. It’s also called the Hayflick Limit or replicative senescence, coined by Leonard Hayflick in the 1960s, which describes how cells have a maximum limit to how often they can replicate. Hayflick found that cultured human fibroblasts have about 50 doublings before they become senescent.

Senescent cells are characterized by inflammation, morphological changes, inflammatory cytokines, and SASP – Senescence Associated Secretory Phenotype – which contains certain growth factors. They encourage neighboring cells to also become senescent. It’s thought this phenomenon evolved as a mechanism to protect damaged cells from becoming malignant and cancerous. Cancer results from uncontrolled growth of malignant or infected cells. Cellular senescence is supposed to put a halt to that. Unfortunately, senescent zombie cells contribute to many pathologies and aging.

Senescence-associated T cells promote immuno-senescence and age-related disorders by secreting pro-inflammatory cytokines. T cell aging and chronic low-grade inflammation – a term called inflammaging – are implicated in many age-related diseases. In humans, senescent T cells predict the development of hyperglycemia. Circulating senescent T cells are linked with systemic inflammation and lesion size during human cutaneous leishmaniasis. The accumulation of senescent endothelial cells is a big contributing factor to atherosclerosis and cardiovascular disease. Senescent cells in bone marrow promote immuno-senescence.

Here are some causes of senescent cell formation:

• Obesity and excess body fat drive senescence and inhibit neurogenesis. Fat cells, particularly visceral fat, tend to accumulate macrophages and secrete pro-inflammatory cytokines.
• Impaired immune surveillance accelerates accumulation of senescent cells and aging. This increases inflammation and cytotoxicity.
• T cell dysregulation and T cell aging. Immuno-senescence is associated with reduced CD4+/CD8+ ratio, impaired helper T cell development, reduced cytotoxicity of natural killer cells, excessive CD8+ T cells inhibiting anti-viral defense and hampered response to antigens.
• Inflammation, pro-inflammatory cytokines and senescence. It spreads like wildfire to neighboring cells and shortens telomeres. Telomere erosion leaves you more susceptible to cellular senescence.
• DNA damage sets off cell senescence. This results from oxidative stress and activates a protein called p53. It’s a tumor suppressor that tries to prevent the senescent cells from becoming malignant and cancerous.
• Metabolic dysfunction drives senescence. Hyperglycemia causes cellular senescence and inflammaging, which accelerates senescence. Elevated glucose makes macrophages induces SASP and proinflammatory cytokine release, thus promoting low grade inflammation and senescence.
• High nutrient signaling via insulin/IGF-1 and mTOR accelerate cell replication and senescence. They also prevent the clearance of dead cells by inhibiting autophagy. Overactivation of mTOR contributes to SASP.

Here’s a potential strategy to prevent cellular senescence and remove zombie cells:

• FOXO Protein Activation – FOXO proteins are transcription factors that regulate longevity in response to stress. FOXO4 peptide can selectively target senescent cells.
  • Fasting for 48 hours elevates FOXO1, 3, and 4 by 1.5-fold and refeeding drops it back to baseline. Calorie restriction increases sirtuins as well as FOXO factors.
  • Acute exercise increases FOXO1 phosphorylation, improves insulin sensitivity and promotes mitochondrial biogenesis. However, chronic prolonged/strenuous exercise may decrease this exercise-induced FOXO expression. Working out raises oxidative stress in the short-term, but basal inflammation will be lower afterwards.
  • In response to heat stress, FOXO contributes to increased heat shock protein levels, which will protect DNA damage and maintains cellular resistance. Taking a sauna or other means of increasing core body temperature and exercising can promote FOXO activation.
  • Beta-hydroxybutyrate (BHB) is one of the ketone bodies that increases FOXO3 and lowers oxidative stress. BHB can also delay vascular aging through endothelial cells, perhaps by reducing senescence. You can raise ketones with carbohydrate restriction, fasting and exercise.
• Intermittent Fasting – Not consuming any calories promotes autophagy and mitophagy that eliminate waste material as well as misfolded proteins. It also lowers oxidative stress and inflammation.
• Cardiovascular Exercise – Aerobic training protects against the accumulation of senescent cells. It helps to eliminate them as well via autophagy and AMPK activation.
• Heat and Cold Exposure – Heat shock proteins trigger autophagy and help to clear misfolded proteins. Saunas and ice baths also stimulate the lymph and flush out toxins.
• Vitamin D and magnesium – Activation of the vitamin D receptor can oppose the synthesis of SASP proteins, such as IL-6 and IL-8, via inhibition of p38 MAP kinase. The vitamin D receptor is activated by calcitriol (the active form of vitamin D) and magnesium is required for this to occur. Thus, both magnesium and vitamin D are important for reducing SASP protein synthesis. More importantly, magnesium deficiency increases the risk of oxidative damage to DNA, which is the primary cause of cellular senescence. Hence, ensuring adequate magnesium and vitamin D status is an important strategy for reducing cellular senescence.
• Zinc and Copper – Zinc can antagonize the toxic heavy metal cadmium, an inducer of oxidative stress that plays a role in DNA damage and premature cellular aging. Zinc is important in maintaining DNA integrity and zinc deficiency increases DNA damage. Moreover, a 12-week clinical study in elderly subjects with low serum zinc levels showed that supplemental zinc (20 mg/day of zinc from zinc carnosine) reduced DNA damage and improved the antioxidant profile. Considering that around 2 billion people worldwide do not ingest adequate amounts of zinc, this suggests zinc deficiency as a major contributor of increased cellular senescence. Copper deficiency also increases oxidative damage and should always be added to supplemental zinc, typically in a zinc/copper ratio of 15-20/1 ratio.

GOOD:

Reishi or Lingzhi mushroom is a fungus that grows in humid regions. It improves the immune system and red blood cell functioning, which makes the body more capable at fighting disease. In fact, a study of over 4000 breast cancer survivors found that 59% of them were consuming reishi.

Shitake Mushroom – a Dark brown fungus that grows on decaying trees. It contains polysaccharides, terpenoids, and sterols that boost the immune system, lower cholesterol and fight cancer.

Turkey Tail – Looks like a turkey tail. Cancer patients are sometimes given turkey tail extract to recover from chemotherapy and strengthen immunity. It’s another adaptogen that lowers stress and makes the body stronger.

THC helping colon cancer: https://www.forbes.com/sites/benjaminadams/2020/10/06/thc-prevents-colon-cancer-in-mice-findings-suggest/?sh=7344a09c5a3e

Ultrasound destroys 80% of prostate cancer: https://newatlas.com/medical/ultrasound-destroys-prostate-cancers-one-year-study/

Sustained weight loss reduced breast cancer: https://www.eurekalert.org/news-releases/897045#.XfjNVIj9Crg.reddit

Exercise for those starting cancer treatment: https://www.eurekalert.org/news-releases/889367

Coffee use increases survival in metastatic colorectal cancer patients: https://www.sciencedaily.com/releases/2020/09/200917181251.htm

Thomas Seyfried (Cancer as a Metabolic Disease) says that the optimal glucose ketone index range for cancer treatment and prevention is between 0.7-2.0, preferably around 1.0.

Medium-chain, as well as short-chain fatty acids, have strong anti-tumor properties.

What Inhibits mTOR?

• Dietary protein restriction lowers mTOR. Amino acid deficiency, in particular, regulates mTOR.
• Calorie restriction lowers mTOR and promotes autophagy.
• Ghrelin the hunger hormone activates AMPK in the hypothalamus and inhibits mTOR.
• Fasting lowers glucose, insulin, and suppresses mTOR while raising AMPK. This is the most effective method of inhibiting mTOR. It also raises autophagy and promotes ketosis.
• Ketogenic Diets are moderate in protein and low glucose, which lowers mTOR activity. Glucagon, which is a hormone that raises in the presence of low glucose and insulin, activates AMPK and represses mTOR.
• Exercise inhibits mTORC1 in liver and fat cells. This is great because you’ll be preventing fat gain while promoting longevity and muscle growth. The post-exercise time window, however, facilitates muscle protein synthesis in muscle cells because of the mechano-overload. That’s another mechanism by which resistance training is great for increasing lifespan – more mTOR in muscles and less mTOR in fat cells.
• Glucocorticoids and cortisol get elevated during physiological stress. Cortisol helps to mobilize glycogen and fatty acids. This shifts the body into a more catabolic state.
• Metformin is a potent anti-diabetic drug that lowers blood sugar and insulin, thus lowering mTOR. Berberine is a medicinal compound that has similar effects.
• Rapamycin is an immunosuppressing drug that lowers mTOR. It’s been used to fight cancers and tumors in humans.
• Resveratrol is a compound found in certain fruit and red wine that has a longevity-boosting effect. Part of it has to do with sirtuins and autophagy.
• Curcumin inhibits mTOR signaling in cancer cells. Reishi fights tumors as well by blocking mTOR. Rhodiola Rosea and astragalus too.
• Anthocyanins found in blueberries and grape seed extract promote AMPK and block mTOR. Pomegranate as well.
• Alcohol activates AMPK and regulates the mTOR complex. It doesn’t go to say that drinking is going to boost your longevity. Remember that mTOR inhibition is just a single piece of the puzzle.
• Oleanolic acid contributes to anti-tumor activity. Main food sources of oleanolic acid are apples, pomegranates, bilberries, lemons, grapes, bilberries, and olives.
• Carnosine inhibits the proliferation of human gastric carcinoma cancer cells by retarding mTOR signaling. Carnosine is an amino acid with anti-aging and antioxidant benefits that fights free radicals as well. Interestingly, it’s found the most in animal foods and meat.

How to Inhibit IGF-1

• Caloric restriction and intermittent fasting can help to reduce cancer development, protect against cognitive decline, reverse diabetes and slow down aging.
• Intense walking affects serum IGF-1 and IGFBP3. This is probably because physical movement helps to lower insulin and blood glucose, thus lowering IGF-1 as well.
• Curcumin lowers IGF-1 by activating AMPK and autophagy.
• Luteolin inhibits proliferation of breast cancer cells induced by IGF-1. It’s a polyphenol and flavonoid that stimulates AMPK.
• EGCG from green tea inhibits IGF-1 stimulated lung cancer. Another polyphenol in action.

BAD:

Antibiotic use and colon cancer: https://www.sciencedaily.com/releases/2021/09/210901090057.htm

High fructose and colorectal cancer: https://www.cancer.gov/news-events/cancer-currents-blog/2021/fructose-promotes-obesity-colorectal-cancer?cid=eb_govdel

Aspirin and cancer: https://www.theladders.com/career-advice/this-common-over-the-counter-drug-now-linked-to-cancer-in-older-adults

Men taking over 100 mg/day of zinc experience a 2.9-fold increase in the risk for metastatic prostate cancer, which is likely due to copper deficiency.

Gabor Mate – When the Body Says No

Smoking no more causes lung cancer than being thrown into deep water causes drowning. Smoking vastly increases the risk of cancer, not only of the lung but also of the bladder, the throat and other organs. But logic alone tells that us it cannot, by itself, cause any of these malignancies. If A causes B, then every time A is present, B should follow. If B does not follow A consistently, then A cannot, by itself, be the cause of B—even if, in most cases, it might be a major and perhaps necessary contributing factor. If smoking caused lung cancer, every smoker would develop the disease.

Kissen supported his clinical impressions that people with lung cancer “have poor and restricted outlets for the expression of emotion, as compared with non-malignancy lung patients and normal controls.” The risk of lung cancer, Kissen found, was five times higher in men who lacked the ability to express emotion effectively.

• Those lung cancer patients who smoked but did not inhale exhibited even greater repression of emotion than those who did. Kissen’s observations implied that emotional repression works synergistically with smoking in the causation of lung cancer. The more severe the repression, the less the smoke damage required to result in cancer.

While smoking is a huge risk factor, for lung cancer to occur, tobacco alone is not enough: emotional repression must somehow potentiate the effects of smoke damage on the body.

The immune centers—previously thought of as acted on only by hormones—are extensively supplied with nerves. The so-called primary immune organs are the bone marrow and the thymus gland, located in the upper chest in front of the heart. Immune cells maturing in the bone marrow or in the thymus travel to the secondary lymph organs, including the spleen and the lymph glands. Fibers issuing from the central nervous system supply both primary and secondary lymph organs, allowing instant communication from the brain to the immune system. The hormone-producing endocrine glands are also directly wired to the central nervous system. Thus, the brain can “talk” directly to the thyroid and adrenal glands, or to the testes and ovaries and other organs.

Cytokines, secreted by immune cells, can induce the feelings of fever, loss of appetite, fatigue and increased need for sleep. Distressing as they are, such rapid adaptations are designed to conserve energy, helping us to overcome illness. Inappropriate secretion of the same substances, however, would interfere with normal functioning—for example, by causing excessive fatigue or chronic fatigue.

Lymph cells and other white blood cells are capable of manufacturing nearly all the hormones and messenger substances produced in the brain and nervous system. Even endorphins, the body’s intrinsic morphine-like mood-altering chemicals and painkillers, can be secreted by lymphocytes. And these immune cells also have receptors for the hormones and other molecules originating in the brain.

It is through the activation of the HPA axis that both psychological and physical stimuli set in motion the body’s responses to threat. Psychological stimuli are first evaluated in the emotional centers known as the limbic system, which includes parts of the cerebral cortex and also deeper brain structures. If the brain interprets the incoming information as threatening, the hypothalamus will induce the pituitary to secrete an adrenocorticotropic hormone. ACTH, in turn, causes the cortex of the adrenal gland to secrete cortisol.

Simultaneously with this hormonal cascade, the hypothalamus sends messages via the sympathetic nervous system to the medulla. The adrenal medulla manufactures and secretes adrenalin, which immediately stimulates the cardiovascular and nervous systems.

“Psychological factors such as uncertainty, conflict, lack of control, and lack of information are considered the most stressful stimuli and strongly activate the HPA axis. Sense of control and consummatory behavior result in immediate suppression of HPA activity.”

• Consummatory behavior is behavior that removes the danger or relieves the tension caused by it. We recall that stress-inducing stimuli are not always objective external threats like predators or potential physical disasters but also include internal perceptions that something we consider essential is lacking. This is why lack of control, lack of information—and, as we will see, unsatisfied emotional needs (e.g., lack of love), trigger the HPA axis. Consummation of such needs abolishes the stress response.

The mechanistic view holds that cancer results from damage to the DNA of a cell by some noxious substance—for example, tobacco breakdown products. This perspective is valid but cannot explain why some smokers develop cancers while others do not, even if the amount and type of tobacco they inhale are exactly the same.

• Why are the cells of some individuals more susceptible than those of others? Why does DNA repair occur in some people but not in others? Why do the immune system and other defenses keep cancer at bay in some people but not in others? What accounts for vast differences in cure or disease progression from one person to the next, even when the identical cancer is diagnosed at exactly the same stage and even when all other factors – age, gender, income, general health – are exactly matched.

Tobacco smoke has a directly damaging effect on the genetic material of lung cells. It is estimated that for the initiation of cancer, the lung cells must acquire as many as 10 separate lesions or points of damage to their DNA. However, most lesions are transient and eliminated by DNA repair or cell death.

Ohio State University College of Medicine wrote: “Faulty DNA repair is associated with an increased incidence of cancer. Stress may alter these DNA repair mechanisms; for example, in one study, lymphocytes from psychiatric inpatients with higher depressive symptoms demonstrated impairment in their ability to repair cellular DNA damaged by exposure to X-irradiation.”

• Apoptosis ensures normal tissue turnover, culling older cells with weakened genetic material, leaving room for their healthy and vigorous offspring. “Dysregulated apoptosis contributes to many pathologies, including tumor production, autoimmune and immunodeficiency diseases, and neurodegenerative disorders.”

Perpetually abnormal steroid hormone levels can interfere with normal programmed cell death. Also participating in cell death are NK cells. Depression—a mental state in which repression of anger dominates emotional functioning—interacts with cigarette smoking to lower the activity of NK cells.

In short, for cancer causation it is not enough that DNA damage occur: also necessary are failure of DNA repair and/or an impairment of regulated cell death. Stress and the repression of emotion can negatively affect both of these processes.

Hormone-dependent cancer cells bear on their membranes receptors for various hormones capable of promoting cell growth. It is generally understood that many breast cancers are estrogen dependent, this being the rationale for the use of the estrogen-blocking drug tamoxifen. Less well known is that some breast cancers have receptors for a broad array of other “information substances,” including androgens (male sex hormones), progestins, prolactin, insulin, vitamin D and several more—all of them secreted by the HPA axis or regulated by it.

Cancers of the female gynecological organs such as the ovaries and the uterus are also hormone related. Ovarian malignancy is only the seventh most common cancer in women, but it is the fourth leading cause of cancer deaths. Of all cancers, it carries the highest tumor-to-death ratio.

• Since infertility is one of the known risk indicators for ovarian cancer, hormonal factors are obviously important. Unfortunately, the picture is confusing. Early menses and late menopause increase the risk of developing ovarian cancer, while pregnancies and the birth control pill decrease it. This pattern would suggest that the more women ovulate, the more susceptible they become to the disease. On the other hand, infertility—when no ovulation takes place—also adds to the risk. U-shaped curve like all stress responses.

Eating patterns are directly connected with emotional issues arising both from childhood and from current stresses. The patterns of how we eat or don’t eat, and how much we eat, are strongly related to the levels of stress we experience and to the coping responses we have developed in face of life’s vicissitudes. In turn, dietary habits intimately affect the functioning of the hormones that influence the female reproductive tract. Anorexics, for example, will often stop menstruating.

Malignancies of the hematological (blood-cell producing) system such as leukemia and lymphoma are also hormone dependent, being profoundly affected by cortisol produced in the adrenal gland. Adrenal corticoid hormones inhibit the division and spread of leukemia and lymphoma cells. Thus, hematological malignancies may, in part, result when blood and lymph cells escape from normal inhibition owing to a chronically unbalanced HPA system.

• A fifteen-year study of people who developed lymphoma or leukemia reportedly found that these malignancies were “apt to occur in a setting of emotional loss or separation which in turn brought about feelings of anxiety, sadness, anger or hopelessness.”
• The amount of cortisol-like hormone needed to block the replication of leukemic cells is only a little higher than what should normally be functionally available in the body. In the case of leukemia, episodes of acute stress in which the cortisol levels temporarily rise are sometimes enough to induce a remission.

It is customary to conceive of cancer as an invader against whom the body must wage war. Such a view, while perhaps comforting in its simplicity, is a distortion of reality.

• First, even when there is an external carcinogen like tobacco, the cancer itself is partially an outcome of internal processes gone wrong. And, of course, for most cancers there is no such identified carcinogen.
• Second, it is the internal environment, locally and throughout the entire organism, that plays the major role in deciding whether the malignancy will flourish or be eliminated.
• The malignant transformation of normal cells, in other words, is a process determined by many factors that have at least as much to do with the biopsychosocial state of the organism as with the type of cancer itself.

Once a cancer reaches the stage where its cell surfaces display molecules different from the normal body proteins, it should be destroyed by the immune system. T-cells should attack it with noxious chemicals; antibodies should be formed against it; specialized blood cells should chew it up. Under conditions of chronic stress, the immune system may become too confused to recognize mutated cell clones that form cancer or too debilitated to mount an attack.

The cancer cell itself may even secrete growth factors, inhibitory substances, and messenger molecules to promote tumor growth.

For a tumor to become clinically noticeable, even on an easily accessible body tissue like the skin or the breast, it has to become about half a gram in size, comprising about five hundred million cells. A single cell with a malignant mutation would have to double about thirty times to reach such dimensions.

• In breast cancer, doubling time has been calculated to range from a few days to one and one-half years, with an average of about four months. “If a tumour cell were to grow constantly at the last rate, it would take about eight years to become clinically evident, and some sources suggest an even longer doubling time with a time span of about 15–20 years to become clinically evident.”
• There are broad fluctuations in growth rate depending on what is happening in the life of the host.
• Microscopic spread of malignant cells seems to happen in many cases of breast cancer without ever causing clinical problems. In other cases, the metastatic deposit may lie dormant in distant tissues for years and then, unexpectedly, declare itself in the form of symptoms. The same dynamic operates with prostate cancer, which is why spread has already occurred in 40 per cent of prostate malignancies by the time the diagnosis is made.

In numerous studies of cancer, the most consistently identified risk factor is the inability to express emotion, particularly the feelings associated with anger. The repression of anger is not an abstract emotional trait that mysteriously leads to disease. It is a major risk factor because it increases physiological stress on the organism. It does not act alone but in conjunction with other risk factors that are likely to accompany it, such as hopelessness and lack of social support. The person who does not feel or express “negative” emotion will be isolated even if surrounded by friends, because his real self is not seen. The sense of hopelessness follows from the chronic inability to be true to oneself on the deepest level. And hopelessness leads to helplessness, since nothing one can do is perceived as making any difference.

The three major types of treatment currently offered for prostate cancer: surgery, radiation, or chemotherapy. Some get through without harm, others suffer unpleasant consequences such as urinary incontinence and impotence.

The loud public campaigns urging men to undergo screening tests for prostate cancer by means of the rectal digital exam or the prostate specific antigen (PSA) blood tests have no proven scientific basis.

• In places where screening is widely practiced, the incidence of diagnosed prostate cancer goes up, and the number of men being treated increases, but the death rate from prostatic malignancy remains unchanged. If anything, prostate cancer mortality rates were slightly higher in the intensely screened areas.
• Also disturbing are findings published in The Journal of the National Cancer Institute, that men aggressively treated for prostate cancer had a higher chance of dying of other cancers than men who did not receive any medical intervention.

Few doctors are willing to let nature take its course in the face of potential disease, even if the value of intervention is questionable. And men, even if well informed, may choose to “do something” rather than tolerate the anxiety of inaction. But patients always deserve to be told what is known about prostate cancer—and, just as important, all that remains unknown.

Orchidectomy, the surgical removal of the testicles, remains part of the treatment arsenal, as does the administration of powerful medications blocking the effects of the male hormones.

By their thirties, many men will have some cancerous cells in their prostate, and by their eighties, the majority are found to have them. By the age of fifty, a man has a 42 per cent chance of developing prostate cancer. Yet relatively few men at any age will progress to the point of overt clinical disease. In other words, the presence of cancerous prostate cells is not unusual even in younger men, and it becomes the norm as men get older. Only in a minority does it progress to the formation of a tumor that causes symptoms or threatens life.

As with estrogen receptors in breast cancer, it appears the sensitivity of tumor cells to normal concentrations of testosterone must have been altered.

Gonadal function is affected by psychological states in both men and women. In depressed men, the secretion of testosterone and other hormones connected with sexual function were significantly diminished. As were those who were fans of a losing football match vs the rising testosterone in the fans of the winning team.

A holistic approach that places the person at the center, rather than the blood test or the pathology report, takes into account an individual life history. It encourages people to examine carefully each of the stresses they face, both those in their environment and those generated internally. In this scenario the diagnosis of prostate cancer could serve as a wake-up call rather than simply a threat. In addition to whatever treatment they may or may not choose to receive, men who are encouraged to respond reflectively, taking into account every aspect of their lives, probably increase their chances of survival.

Lance Armstrong first noticed a slight swelling of his testicle in the winter of 1996 and began to feel uncharacteristically short of breath next spring. His nipples felt sore, and he had to drop out of the 1997 Tour de France owing to a cough and low-back pain. “Athletes, especially cyclists, are in the business of denial,” Armstrong writes. It wasn’t until September, when he coughed blood and his testicle became painfully enlarged, that he finally sought medical attention. By then the cancer had spread to his lungs and brain.

• Long before his cancer, Armstrong had developed a pattern of emotional repression. One of his close friends described him as “kind of like an iceberg. There’s a peak, but there is so much more below the surface.”
• The child of an unhappy mother will try to take care of her by suppressing his distress so as not to burden her further. His role is to be self-sufficient and not “needy.”

Malignant Melanoma

Malignant melanoma, is a life-endangering tumor of melanocytes, the pigmented cells in the skin. A deadly disease with a ready tendency to spread to other organs, melanoma often strikes people in the prime of life.

The exposure of fair-skinned individuals to ultraviolet radiation is the major physical risk factor for malignant melanoma. People of Celtic origin appear to be especially vulnerable, particularly if they have light-colored hair, freckles and blue or grey eyes. Dark-skinned ethnic groups are at little risk for skin cancer—in Hawaii, skin cancer is forty-five times less common among non- Caucasians than in Caucasians.

Patients with malignant melanoma displayed coping reactions and tendencies that could be described as indicating ‘repressiveness.’ These reactions were significantly different from patients with CVD, who could be said manifest the opposite pattern of coping.

Type A individuals are seen as “angry, tense, fast, aggressive, in control”—and more prone to heart disease. Type B represents the balanced, moderate human being who can feel and express emotion without being driven and without losing himself in uncontrolled emotional outbreaks. Type C personalities have been described as “extremely cooperative, patient, passive, lacking assertiveness and accepting…. The Type C individual may resemble Type B, since both may appear easygoing and pleasant, but … while the Type B easily expresses anger, fear, sadness and other emotions, the Type C individual, in our view, suppresses or represses ‘negative’ emotions, particularly anger, while struggling to maintain a strong and happy facade.”

“When people are diagnosed with a disease—whether cancer or cardiovascular—they do not precipitously change their usual ways of coping with stress or suddenly develop new patterns…. Under stress, people usually mobilize their existing resources and defences.”

Hormonal factors likely account for the fact that the number of melanoma tumors is increasing in bodily sites not exposed to sunlight. Researchers have suggested that hormones may be overstimulating the pigment-producing cells.

Cancer patients, to a statistically significant degree, were more likely to demonstrate the following traits: “the elements of denial and repression of anger and of other negative emotions… the external appearance of a ‘nice’ or ‘good’ person, a suppression of reactions which may offend others, and the avoidance of conflict. The colorectal cancer findings were independent of the other risk factors they found (diet, beer intake, and family history). Self-reported childhood or adult unhappiness was also more common among the bowel cancer cases. We have already noted similar traits among patients with breast cancer, melanoma, prostate cancer, leukemias and lymphomas, and lung cancer.

Fair skin alone cannot be the cause of this cancer, since not everyone with fair skin will develop melanoma. Ultraviolet damage to the skin by itself cannot be sufficient, since only a minority of light-complexioned persons who suffer sunburns will end up with skin cancer. Emotional repression is not sufficient either. The combination, however, is deadly.

Repression, the inability to say no and a lack of awareness of one’s anger make it much more likely that a person will find herself in situations where her emotions are not expressed, her needs are ignored and her gentleness is exploited.

It is stress—not personality per se—that undermines a body’s physiological balance and immune defenses, predisposing to disease or reducing the resistance to it. Physiological stress, then, is the link between personality traits and disease. Certain traits—otherwise known as coping styles—magnify the risk for illness by increasing the likelihood of chronic stress. Common to them all is a diminished capacity for emotional communication.

The emotional contexts of childhood interact with inborn temperament to give rise to personality traits. Much of what we call personality is not a fixed set of traits, only coping mechanisms a person acquired in childhood. There is an important distinction between an inherent characteristic, rooted in an individual without regard to his environment, and a response to the environment, a pattern of behaviors developed to ensure survival.

What we see as indelible traits may be no more than habitual defensive techniques, unconsciously adopted. People often identify with these habituated patterns, believing them to be an indispensable part of the self. They may even harbor self-loathing for certain traits—for example, when a person describes herself as “a control freak.” In reality, there is no innate human inclination to be controlling. What there is in a “controlling” personality is deep anxiety. The infant and child who perceives that his needs are unmet may develop an obsessive coping style, anxious about each detail. When such a person fears that he is unable to control events, he experiences great stress. Unconsciously he believes that only by controlling every aspect of his life and environment will he be able to ensure the satisfaction of his needs. As he grows older, others will resent him and he will come to dislike himself for what was originally a desperate response to emotional deprivation. The drive to control is not an innate trait but a coping style.

Emotional repression is also a coping style rather than a personality trait set in stone. Gabor has never had a patient with cancer or any chronic illness say they were able to talk to somebody about their negative emotions.

• Many children are conditioned in this manner not because of any intended harm or abuse, but because the parents themselves are too threatened by the anxiety, anger or sadness they sense in their child—or are simply too busy or too harassed themselves to pay attention.

Breast Cancer

(Gabor – When the Body Says No)

Breast cancer patients often report that their doctors do not express an active interest in them as individuals or in the social and emotional context in which they live. The assumption is that these factors have no significant role in either the origins or the treatment of disease. That attitude is reinforced by narrowly conceived psychological research.

Only a small minority of women are at high genetic risk for breast cancer and only a small minority of women with breast cancer—about 7 per cent—acquire the disease for genetic reasons.

One of the chief ways that emotions act biologically in cancer causation is through the effect of hormones. Some hormones, such as estrogen, encourage tumor growth. Others enhance development by reducing the immune system’s capacity to destroy malignant cells. Hormone production is intimately affected by psychological stress.

Natural killer (NK) cells are more active in breast cancer patients who are able to express anger, to adopt a fighting stance and who have more social support. NK cells mount an attack on malignant cells and are able to destroy them. These women had significantly less spread of their breast cancer, compared with those who exhibited a less assertive attitude or who had fewer nurturing social connections. The researchers found that emotional factors and social involvement were more important to survival than the degree of disease itself.

In most cases of breast cancer, the stresses are hidden and chronic. They stem from childhood experiences, early emotional programming and unconscious psychological coping styles. They accumulate over a lifetime to make someone susceptible to disease.

Research has suggested for decades that women are more prone to develop breast cancer if their childhoods were characterized by emotional disconnection from their parents or other disturbances in their upbringing; if they tend to repress emotions, particularly anger; if they lack nurturing social relationships in adulthood; and if they are the altruistic, compulsively caregiving types.

• Researchers were able to predict the presence of cancer in up to 94 per cent of cases judging by such psychological factors alone. In a similar German study, forty women with breast cancer were matched with forty controls similar in age, general health history and lifestyle considerations. Again, on psychological grounds the researchers were 96 per cent successful in identifying who was and who was not diagnosed with breast cancer.

About 1 per cent of breast cancer patients are males. Their emotional histories parallel those of the women with the same disease. David Yeandle, a Toronto policeman, has had four separate cancers: in one of his kidneys, his breast and twice in his bladder. His upbringing was also characterized by a lack of warmth.

• “Dad was never there to talk to, and I certainly wouldn’t discuss it with my mother, because her favourite expression was ‘Oh, you’re being silly.’ I never showed anger with my parents. It was something you just didn’t do. I hold a lot of anger inside me.”
• “Our principal finding was a significant association between the diagnosis of breast cancer and a behaviour pattern, persisting throughout adult life, of abnormal release of emotions. This abnormality was, in most cases, extreme suppression of anger and, in patients over 40, extreme suppression of other feelings.”
• A 1952 psychoanalytic evaluation of women with breast cancer had come to similar conclusions. These patients were said to demonstrate “an inability to discharge or deal appropriately with anger, aggressiveness, or hostility (which, in turn, was masked by a facade of pleasantness).” The researchers felt that patients’ unresolved conflicts were “manifested through denial and unrealistic self-sacrificing behaviours.”

Repression of anger increases the risk for cancer for the very practical reason that it magnifies exposure to physiological stress. If people are not able to recognize intrusion, or are unable to assert themselves even when they do see a violation, they are likely to experience repeatedly the damage brought on by stress. Stress is a physiological response to a perceived threat, physical or emotional, whether or not the individual is immediately aware of the perception.

Even in the small minority of cases where it is a major predisposing factor, heredity cannot by itself explain who gets breast cancer and who does not.

The straightforward connection between childhood experience and adult stress has been missed by so many researchers over so many years that one almost begins to wonder if the oversight is deliberate. Adults with a history of troubled childhoods may not encounter more serious losses than others do, but their ability to cope will have been impaired by their upbringing.

The emotional repression, the harsh self-judgment and the perfectionism Betty Ford acquired as a child, through no fault of her own, are more than a “good recipe for alcoholism.” They are also a “good recipe” for cancer of the breast.

In the example in this chapter, the mother grew up feeling like she got second hand love because her mother said she seemed emotionally independent, she jumped between relationships, her child was sensitive and often sick, and her daughter also got addicted to narcotics up to her breast cancer diagnosis. Very little stability in either of their lives, despite them both being intelligent.

Their relationship seemed to involve the daughter frequently getting angry at her mother but repressing it out of defeat and frustration. The daughter appeared disappointed in the mother and may have been abused and her mother wasn’t there. Their personalities clashed too. The daughter was quiet and holistic and the mother seen as judgmental and rash.

The nature of stress is not always external stress of war, financial trouble, or somebody dying. It is actually the internal stress of having to adjust oneself to somebody else. Cancer, ALS, MS, and rheumatoid arthritis appear to happen to people who have a poor sense of themselves as independent persons. They can be accomplished in the arts or intellectually and yet still suffer from the poor sense of self. They live in reaction to others without ever sensing who they are.

Some children who have an emotionally deprived upbringing develop intelligence and “adultlike” maturity to survive. Her child was, good, precocious, and intellectually mature. She became her mother’s sounding board upon reaching the age of abstract thought. The mother’s needs become more important so any trauma suffered by the child is hidden to protect the mother. When the reality is, the child’s role is not to keep peace.

The parent needs to address their own pain before they are able to see their child’s. Sometimes a person may feel unloved because they emotionally detach from pain. The mother in this story repressed her own pain to become emotionally independent when she realized she wasn’t getting enough love from her own mother. Her family was big and it seemed the other siblings needed more attention. She also couldn’t confront her mother about her hatred for her father. Didn’t want to rock the boat. Creating a sense of abandonment without realizing it.

When a woman marries an immature man, they spend their openness and energy on mothering the husband and have nothing left for the children.

Nightmares in children are potentially an expression of not feeling protected or connected enough. They are our deepest anxieties.

All these generations of people going through emotional pain can result in the culmination of disease in future offspring.

Sweetened beverages: https://pubmed.ncbi.nlm.nih.gov/33945630/

Prostate Cancer

Ketogenesis: https://www.biorxiv.org/content/10.1101/2021.12.29.474437v1