Autoimmunity

To be completed

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

What is the general understanding of autoimmunity?

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

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Autoimmunity describes a situation where the body mounts an immune response against its own healthy cells and tissue. The immune system fails to differentiate between self and non-self, thus attacking the host. Conditions that create this kind of a response are called autoimmune diseases. Examples include celiac disease, type 1 diabetes, Hashimoto’s thyroiditis, Grave’s disease, Addison’s disease, rheumatoid arthritis and multiple sclerosis (MS).

• There are multiple mechanisms thought to cause autoimmunity. They include discordant T and B cell activity, which creates autoreactive B cells, or infections bypassing T cells, creating super-antigens that activate B and T cells. An extrinsic antigen can also have similarities with host antigens, making antibodies attach to some host antigens, exaggerating the immune response. Defective apoptosis in dendritic cells can activate lymphocytes in a dysfunctional way, leading to a decline in self-tolerance. Genetic abnormalities in T cells, immunoglobulins and the MCH complexes are associated with risk factors for developing autoimmunity.
• Women tend to be more susceptible towards certain autoimmune diseases because they mount a much larger inflammatory response upon activation than men. Pregnancy appears to create increased risk of autoimmunity due to the direct exchange of cells between the mother and child.
• There is an inverse relationship between infections and autoimmunity. In some studies, parasite infections are associated with reduced autoimmune diseases, such as type 1 diabetes, autoimmune brain inflammation and multiple sclerosis. Hypothetically, different pathogens can promote the increase of regulatory T cells and anti-inflammatory molecules that will also provide protection to the host. In any case, manic hygiene and elimination of all bacteria and pathogenic agents in your environment will weaken your immune system.
• Many immunodeficiencies have characteristics of autoimmunity. Compromised immunity can promote autoimmunity through chronic immune system activation. An example would be common variable immunodeficiency (CVID), where several autoimmune diseases are manifested, such as inflammatory bowel disease, autoimmune thrombocytopenia and autoimmune thyroid disease.

• Intestinal permeability or leaky gut is associated with autoimmune diseases and the development of several inflammatory diseases. Increased low-grade inflammation makes one more prone to infections. Bone broth, tendons and ligaments have collagen and glycine that promote tissue rejuvenation. Butyrate is also essential as the main source of energy for cells in the large intestine. You can get butyrate mainly from the fermentation of fiber like beans, vegetables and legumes but also ghee and butter. Microbial metabolites through the Nrf2 pathway have shown to enhance gut barrier integrity.
  • Diversity of the gut microbiota is linked to stronger immunity because microbes have an important role in modulating our body’s defense systems. They also help the host adapt to the microbial and pathogenic environment they’re in.
  • Skin integrity is another essential component to immunity through enhanced barrier strength. The skin is constantly exposed to various pathogens and internal reactive oxygen species. Nrf2 plays a crucial role in modulating that oxidative stress.

Immunity and autoimmunity can be manipulated by immunosuppressive and anti-inflammatory drugs. They are used to control inflammation and autoimmune attacks or prevent organ transplant rejection. Unfortunately, some of them, like glucocorticoids, can have negative side-effects that include hyperglycemia, weight gain and osteoporosis. Cytotoxic drugs, like methotrexate and azathioprine, inhibit the immune response by killing activated T cells, which affects other cells and organs as well, creating toxic side-effects. Immunosuppressive drugs, such as cyclosporin, block T cells from responding appropriately.

What Drives Autoimmunity

Although harmful in excess, a small amount of autoimmunity has its benefits and protective effects. It can help to rapidly recognize foreign antibodies during the early stages of an infection when there aren’t many pathogens around and maintain helper T cell responsiveness. However, it can become a problem when this kind of self-vs. non-self-recognition gets out of hand or dysfunctional.

Autoimmunity is believed to be the result of failed regulatory mechanisms in the immune responses, creating an imbalance with effector immune cells. The underlying mechanism of autoimmune reactions is defective elimination of self-reactive lymphocytes, like B cells, T cells and NK cells. There is also evidence that self-antigen abnormalities are also involved, which activates unconventional T cells with pathogenic potential.

Dendritic cells appear to be the ones that keep T cells in balance and hold autoimmunity at bay. They maintain self-tolerance by either deleting T cells or generating regulatory T cells.

Despite the great variation in autoimmune diseases, it is thought they all follow three stages: initiation, propagation and resolution.

Here is an overview of them:

1. Initiation of autoimmunity is the point when disease progression starts. Because the disease itself begins well before any symptoms show up, it is hard to know exactly what is lighting up the flame. There are both environmental and genetic factors that trigger the initiation of autoimmunity.

• a. Genetic factors linked to autoimmune diseases include several genetic polymorphisms related to immunoglobulins, T cell receptors and the major histocompatibility complex (MHC).
  • i. HLA RD2 is an MHC class II cell surface receptor that is positively correlated with systemic lupus, narcolepsy and multiple sclerosis. HLA DR3 is correlated with type-1 diabetes, and Sjögren syndrome. HLA DR4 is correlated with rheumatoid arthritis, type-1 diabetes and pemphigus vulgaris.
  • ii. Another gene, PTPN22 in humans, is associated with type-1 diabetes, rheumatoid arthritis, systemic lupus, Hashimoto’s thyroiditis, Graves’ disease, multiple sclerosis and Addison’s disease.
  • iii. Tumor Necrosis Factor Receptor Superfamily Member 1A (TNFRSF1A) is a membrane receptor that binds tumor necrosis factor-alpha (TNF-alpha), which is a major inflammatory cytokine. TNFRSF1A (identified by TNFR1, rs1800693) is strongly associated with multiple sclerosis.
  • iv. Interleukin-2 (IL-2) receptor α (CD25) is expressed on activated T cells and T regulatory cells. Risk alleles in CD25 (rs2104286) are associated with multiple sclerosis and type-1 diabetes. Interleukin-23 receptor (IL23R) genetic polymorphisms have also been discovered in Crohn’s disease, psoriasis, and ulcerative colitis.
  • v. Women appear to have a bigger risk of developing certain autoimmune diseases because they tend to create larger inflammatory responses than men. The direct exchange of cells between the mother and child during pregnancy can also lead to autoimmunity.
• b. Environmental triggers for autoimmunity include infections, diet, stress, chemicals, UV radiation-induced apoptosis and heavy metal toxicity. The most common foods or food constituents that are associated with increased intestinal permeability and autoimmune diseases include gluten, grains, nightshade, lectins, dairy, sugar and others. Some “cross-reactive” foods, such as milk, coffee, corn, rice and millet, may act similarly like gluten by the body in certain susceptible individuals, creating a similar autoimmune response. In younger children, respiratory infections are temporally associated with type 1 diabetes autoimmunity. This isn’t to say that gluten itself is harmful per se (except for those with celiac disease) if coming from traditional unrefined grains but many people have damage to the intestine and are consuming refined grains and the gluten may not be tolerated.
• c. Molecular mimicry describes how certain pathogens share structural similarities with some host antigens. Any antibody created against that antigen will then bind to host antigens and cause a potential autoimmune response. Molecular mimicry may be involved with the pathogenesis of rheumatic fever and heart disease. There are many viruses and bacteria that employ molecular mimicry, such as Streptococcus pyogenes, H. pylori, Salmonella, Escherichia coli, Cytomegalovirus, Epstein‐Barr virus and Coxsackie virus.

2. Propagation of autoimmune reactions fans the flames of inflammation and tissue damage. If the products of inflammatory reactions do not get extinguished, they will create an inflammatory environment that begins to spread more inflammation through a vicious loop. Inflammatory mediators most commonly responsible for this phenomenon are tumor necrosis factor alpha (TNF-alpha), NLRP3 inflammasome, nuclear factor kB (NF-kB), interleukin-12, interleukin-17A and interleukin-23. The increased ratio of effector to regulatory immune cells is also a driver of autoimmunity, primarily between killer T cells and regulatory T cells (Tregs).

3. Resolution of autoimmunity puts out the fire, mainly by limiting effector cell activity and promoting regulatory mechanisms. Regulatory T-cells (Tregs) control the immune response to self and foreign particles (antigens) and thus help prevent autoimmune disease. Tregs get produced in the thymus and secondary lymph organs. Thus, any damage to these organs, or to the production or function of Tregs, may initiate autoimmunity. Autoimmune inflammation activates Tregs, which begin to control inflammation and develop immunological memory. Other inhibitory receptors like CTLA-4 and PD-1 also suppress autoimmune reactions. Genetic deletions and mutations in CTLA-4 create immune dysfunction in humans.

Chemicals, leaky gut, stress, genetics, infections -> Initiation of autoimmunity

Bad response -> Chronic inflammation: NLRP3, NF-kB, TNF-a, T cell imbalance -> Propagation of autoimmunity

Good response -> Control of inflammation, helper T cells balanced with killer T cells, immunological memory -> resolution of autoimmunity

In 1989, Strachan proposed the ‘hygiene hypothesis’ that considers increased use of antibiotics, antiseptics, vaccines and sterilized environments a potential reason for the rise in autoimmunity among children. Children who aren’t exposed to bacteria from dirt, animals, grains, and other sources are much more likely to develop autoimmune disorders later in life. C-section newborns are more prone to suffer from all chronic diseases like diabetes, obesity and asthma. Early-life antibiotic use is associated with inflammatory bowel disease. The rise in insulin-dependent (Type 1) diabetes is paralleled with a decline in bacterial infections, which supports the ‘hygiene hypothesis’, i.e., that exposure to bacteria may provide protection against the onset of autoimmunity. Obesity, which is generally a marker of poor diet, is a risk factor for autoimmune diseases.

Treatments for Autoimmunity

• Traditionally, autoimmune diseases have been treated with immunosuppressive, anti-inflammatory and palliative methods. The most critical thing appears to be managing inflammation and curbing the flames of autoimmune reactions. That is why the “western diet”, characterized by high fat, high sugar, processed food, can be a trigger for autoimmunity due to its pro-inflammatory effect. An obese condition impairs cellular immunity to infections and induces a state of chronic low-grade inflammation.
• Ginger supplementation has been shown to improve rheumatoid arthritis by lowering inflammation.
• Naringenin, an anti-inflammatory compound found in citrus fruit, can inhibit defective T cells and supports the restoration of T cell homeostasis. In mice, naringenin attenuates autoimmune encephalomyelitis by modulating autoimmune inflammatory responses.
• The main polyphenol in green tea, EGCG, has been shown to increase regulatory T cells (Tregs), which are critical for maintaining the optimal balance between T cells.
• Curcumin can reduce symptoms of rheumatoid arthritis, multiple sclerosis, psoriasis, and inflammatory bowel disease, by regulating inflammatory cytokines and NF-kB signaling.
• Omega-3 fatty acids can also lower inflammation and inhibit proinflammatory cytokines. Human trials have shown that omega-3s can help with rheumatoid arthritis, inflammatory bowel disease, asthma and psoriasis.
• Another healthy fat with anti-inflammatory effects is extra virgin olive oil, which has been shown to suppress pro-inflammatory genes in patients with metabolic syndrome thanks to its polyphenolic compounds.
• Polyphenolic compounds are found in environmentally challenged dark pigmented vegetables, like broccoli, artichoke, leafy greens, cabbage, berries like raspberries, blackberries, blueberries, chokeberries, fruit like pomegranate, cherries, olives, green tea, black tea, coffee and beans. According to a 2010 study in Nature, the most polyphenols are in cloves, peppermint, star anise, cocoa powder and oregano.
  • Quercetin is another antioxidant or flavonoid found in onions and vegetables shown to strengthen intestinal tight junctions and the gut barrier. Keeping healthy tight junctions and reducing intestinal permeability is paramount for preventing foreign substances from getting into the blood stream, which can initiate an autoimmune response.

There is a direct connection between systemic inflammation throughout the body and the gut microbiome.

The microbiome is a big contributor to innate and adaptive immunity, helping to recognize pathogens and differentiate them from the host. Early-life nutrition and microbiota maturation have been found to shape life-long immunity and reduce the risk of chronic diseases.

Type-1 diabetes (T1D) is associated with low microbiota diversity.

Dysbiosis, or an imbalance in the micro-fauna, controls inflammatory bowel disease. Low amounts of Faecalibacterium prausnitzii have been linked with diseases like Crohn’s. A lower prevalence of bacteria like Akkermansia, Faecalibacterium, and Bifidobacterium may increase the susceptibility to allergies by modulating T cells.

Children with T1D have higher levels of Globicatella sanguinis, Dialister invisus and Bifidobacterium longum and reduced Bifidobacterium pseudocatenulatum and Bifidobacterium adolescentis, unlike healthy controls.

There is a correlation between rheumatoid arthritis and Prevotella copri.

The most known beneficial strains include Enterococcus spp., Lactobacillus spp., Bifidobacterium spp., Bacillus spp. and Streptococcus spp.

• Lactobacillus rhamnosus GG is used to treat pseudomembranous colitis and antibiotic-associated diarrhea. Probiotics like Lactobacillus modulate pro-inflammatory signaling factors like TNF-alpha. Foods with Lactobacillus include sauerkraut, yogurt, tempeh, miso, natto, kimchi, and other fermented foods. These foods have other benefits like antioxidants, vitamins, especially B12, which is important for the nervous system. Consumption of fermented soybeans is associated with reduced osteoporosis in Japanese women.
• Dairy propionic bacteria like Propionibacterium freudenreichii can improve the microbiota by promoting the growth of beneficial strains like Bifidobacteria, while inhibiting pathogens like H. pylori, Salmonella enterica and enteropathogenic Esherichia coli. You can get propionic bacteria from cultured dairy foods like kefir, cheeses, yogurt, etc. Pasteurized milk is devoid of these bacteria because of the high heat manufacturing process. That is why food industries are considering adding supplemental Lactobacillus and Bacillus into their products to obtain their health benefits. Eating raw cheese and kefir, which contain live probiotics, are a great way to support the gut microbiome.
• Bifidobacteria can help to alleviate IBS, according to a 2011 randomized control trial. In newborn infants, a probiotic mix of Bifidobacterium bifidum, Bifidobacterium lactis, and Lactobacillus acidophilus reduced incidence of eczema. Bifidobacterium bifidum PRL2010 modulates the host innate immune response, by regulating the production of interleukins and cytokines.
• Bacillus coagulans is a gram-positive, spore-based bacteria that produces lactic acid. It has been shown to improve symptoms of gut problems, by raising beneficial bacteria and butyrate production. In rheumatoid arthritis, B. coagulans reduces inflammatory markers and pain. Probiotic metabolites of B. coagulans enhance the maturation of antigen-presenting cells in vitro. In healthy adults, B. coagulans promotes TNF-alpha in response to influenza A and adenovirus.

Low levels of vitamin D are associated with the development of autoimmune diseases. Mutations in the vitamin D3 gene CYP27B1 are correlated with increased risk of type-1 diabetes, Addison’s disease, Hashimoto’s thyroiditis and Graves’ disease. Most cells, including T and B cells, have receptors for vitamin D, which regulate the immune system. It’s important to note however, that these receptors are stimulated by active vitamin D (also known as calcitriol), which requires adequate magnesium in the body. In other words, if you want immune cells to work properly you need to have adequate levels of vitamin D and magnesium. Vitamin D acts on T cells and natural killer cells.

• Low sunlight exposure and living at high latitudes are thought to contribute to multiple sclerosis (MS) risk. Declining UV light due to seasonality has been noted to increase MS activity. Data from over 321 European studies have correlated low UV light exposure with over a 100-fold increased risk of MS. On top of that, occupational and childhood exposure to sunlight is inversely correlated with the risk of MS and mortality.
• Low sunlight exposure is considered a major component to type-1 diabetes (T1D) risk. T1D onset peaks between October and January and reaches its low point during the summer in the northern hemisphere, while the southern hemisphere shows a same reverse pattern. T1D risk appears to be greatly affected by UV irradiation. Regular supplementation with vitamin D3 in children has been correlated with an 88% reduced risk of T1D. In T1D, CD4+ T lymphocytes become pathological and autoreactive, damaging healthy tissue. The same is found in multiple sclerosis.
• Current guidelines for calcium homeostasis show that vitamin D levels below 30 nmol/L causes deficiencies, 30-50 nmol/L is insufficient, and above 50 nmol/L sufficient. Appropriate ranges for autoimmunity are not known, however, 2,000 IU/day of vitamin D that reached 75 nmol/L is associated with maintenance of intestinal permeability, improved quality of life and reduced disease markers in people with Crohn’s disease compared to those who were below 75 nmol/L.

Zinc is another important nutrient needed for optimal immune cell functioning. It plays a key role in over 300 enzymatic reactions and cellular communications. A deficiency in zinc promotes proinflammatory cytokines and weaker immunity. Many studies since the 1970s have noted zinc deficiency is related to different autoimmune diseases such as type-1 diabetes, rheumatoid arthritis, multiple sclerosis, systemic lupus, autoimmune hepatitis, celiac disease and Hashimoto’s thyroiditis.

• A deficiency in zinc creates an imbalance between Th1 and Th2, regulatory and killer T cells and reduced NK cell function. These imbalances can be fixed with increased zinc consumption or supplementation.
• Animal foods are particularly high in zinc, whereas plant foods tend to be lower, suggesting that the diet should include some animal foods.

It is worthwhile to take a look at how you respond to the most common allergenic foods like gluten, nightshade, eggs, fish, shellfish, soy, grains, dairy, etc. Eliminating them for a few weeks may help you gain more insight into what your body does and does not tolerate well. Then re-introducing them one at a time enables you to identify what exactly is causing the issue. You should always consult with your doctor who can help guide you through microbial diversity tests, inflammatory tests (like high sensitivity c-reactive protein) and tests for intestinal permeability (zonulin levels) and put together a potential protocol.

Antinutrients and FODMAPs. Although, complete avoidance may lead to heightened sensitivity. Fix the gut lining first and then reintroduce them. 

Simple sugar therapy for MS: https://www.eurekalert.org/news-releases/483692

IGF-1 fights autoimmune disorders by increasing T-cells and boosts the immune system.

The short chain fatty acids of butter, like butyrate, heal the intestinal lining of your gut that prevents inflammation and autoimmune disorders.

Trauma (Gabor Mate inspired): Repressed anger/rage from receiving no love as a child/not feeling loved, learning that angry children don’t receive attention/love. Repressed identity and emotional resolution expressed as autoimmunity.  

Hypothyroid and Hyperthyroid

Metabolism 101: Your Brain the Furnace

The consumption of energy in the cells of the body for maintenance, growth, and repair. The brain consumes most of your metabolic needs.

Even if you’re very physically active, 75% of calories will go to the brain.

Metabolism isn’t just about losing weight. In general, muscle burns more energy than adipose fat. The metabolism can be increased by adding muscle.

Releasing Hormones from Your Brain, Stimulating Hormones from Your Pituitary

The hypothalamus releases TRH, which tells the pituitary to release TSH, and then thyroid to release TH (T3 and T4).

Thyroid Hormone’s Real Effects: Growth, Repair and Energy Consumption of Tissues

Controls a lot of the features of the eyes and face. The main role of T3 is to promote metabolism. Acting on muscle, liver, cartilage, bone, etc. Takes fats, breaks them down into fatty acids, and turning into ATP. Also, sugars. Liberates fats from fat cells to use for energy.

Iodine, L-Tyrosine & Selenium: The Trio Essential for Thyroid Function

Iodine mostly found in sea salt, kelp, and seaweed. The thyroid needs iodine to produce thyroid hormone. It combines with L-tyrosine (precursor to dopamine) to produce T3 and T4.

Certain areas that are far away from the ocean and mountain regions, people would get goiter. The thyroid would hypertrophy in an attempt to produce enough thyroid hormone and getting a lot of stimulating hormone. Not enough iodine to make it, low levels of TH in blood, the brain has the signal to release more TSH to compensate. Resulting in goiter.

How Much Iodine Do We Need? By Food, Supplement or Ocean Air

People who are hypothyroidal might benefit from added iodine. If you are hyperthyroidal that may be a problem. Living by the coast may be enough to breathe iodine in by the air. Need the iodine, L-tyrosine, and selenium. Need it for growth, repair, and BMI management.

Selenium For Thyroid: Brazil Nuts & Other Valuable Sources

Brazil nuts, fish (tuna), ham, beef, turkey, chicken, etc. Brazil nuts have way more than everything else. A vegan diet is probably going to be deficient. Children requirements are much lower.

Selenium For Pregnancy, Prostate Cancer Risk, Acne

Reduces preeclampsia risk. reduced prostate cancer risk, reduction in acne (probably thyroid hormone pathway related).

“Clean Eating” Downsides: Cruciferous Vegetables, Leeching Iodine

All meat diets probably have low iodine, low meat diets are probably eating veggies that are goitrogens. Also, hard to get enough L-tyrosine with a plant-based diet.

Other Benefits of Iodine: Reducing Inflammation

Reducing levels of CRP and IL-6 (inflammatory response).

Why & How Increased Thyroid Increases Metabolism

Thyroid increase glucose intake by various tissues in muscle and bone. Increasing bone mineral density and recovery from injuries.

Menstruation: Thyroid Carbohydrate & Sugar Craving

During the menstrual cycle thyroid levels may fluctuate. First half (before ovulation) people usually crave carbohydrates more, TH goes up using starchy carbohydrates.

Ketogenic Diet & Its Effects on Thyroid, Rebound Weight Gain

TH decreases with the ketogenic diet. Might explain why when people go back to carbs, they will gain weight very quickly.

Starchy carbs support the healthy production of T3 and T4.

Should You Fast with Low Thyroid?

Low thyroid functioning is most commonly caused by too much stress on the body. If there are too many stress hormones circulating the blood, you’ll lower the thyroid hormones as well as a means of self-defense.

Hypothyroidism is caused by too low amounts of thyroid hormones in the blood and it usually happens in people who’ve had Hashimoto’s disease, thyroiditis or have had their thyroid removed. Thyroid cells absorb iodine found in some foods and combine it with the amino acid tyrosine, which is used to create thyroid hormones: thyroxine (T4) and triiodothyronine (T3). They are then released into the bloodstream to affect your body temperature, your daily caloric needs, your heart rate and what’s your metabolic rate.

• • The thyroid gland regulates energy metabolism and cellular homeostasis. Thyroid hormones: thyroxine (T4) and triiodothyronine (T3) are produced by thyroid cells that absorb iodine from food and combine it with the amino acid tyrosine. Once released into the bloodstream they affect body temperature, metabolic rate, breathing and heartbeat. Thyroid functioning can affect immunity by regulating the amount of fat and fat-free mass you have, maintenance of lymphocytes, mediating the inflammatory response, controlling immune cells, and preventing autoimmunity. Importantly, two molecules of sodium are required to drive one molecule of iodide into the thyroid gland. Thus, maintaining appropriate sodium status is needed for optimal thyroid and immune health.
  • Hyperthyroidism appears to decrease the proinflammatory effects of monocytes and macrophages, whereas hypothyroidism increases reactive oxygen species and phagocytosis. Involution of the spleen and lymph node due to hypothyroidism decreases cell-mediated immune responses, which can increase the severity of viral infections and sepsis. Thyroid hormones also modulate natural killer cells and low thyroid function depresses NK cell activity. Increasing T3, which is the active thyroid hormone, seems to reverse this phenomenon.
  • Low thyroid function can also make you more susceptible to other immunocompromised and disordered states like diabetes, obesity, autoimmunity and inflammation. With a lower metabolic rate, it is easier for you to gain weight and harder to conduct other important processes of defense. An abundance of energy production helps to provide enough resources for all immune functions, whereas a depletion in energy lowers immune function. However, hyperthyroidism can also cause problems related to autoimmunity, such as Graves’ disease and an increase of pro-inflammatory cytokines.
  • Thyroid hormones convert cholesterol into steroid hormones like testosterone, vitamin D, DHEA and progesterone. These hormones have many benefits, such as muscle growth, faster metabolic rate, bone density, increased fertility, etc. People with low thyroid tend to have higher cholesterol because they do not have enough thyroid hormones to convert it into other hormones. High thyroid stimulating hormone (TSH) can raise cholesterol, whereas hyperthyroidism lowers cholesterol and cause hormonal imbalances.
  • Stress lowers thyroid functioning through adrenal insufficiency. Inflammatory cytokines like interleukin-6 (IL-6), interleukin-1 beta (IL-1β) and tumor necrosis factor (TNF) alpha reduce the conversion of T4 into T3. IL-6 lowers serum T3 directly. Stress-induced low thyroid can cause stress to the body, suppressing thyroid function even further. At the same time, the state of hypothyroidism itself can initiate this stress-induced cascade.
  • Low thyroid function = spleen size reduction, hormonal dysfunction, lower thymic activity -> reduced adaptive immunity, lower metabolism -> weight gain, metabolic syndrome, decreased NK cell activity, risk of autoimmunity, suppressed immunity accelerated immuno-senescence.

• • T3 and T4 are regulated by the hypothalamus and the pituitary gland inside your brain.

    • When thyroid hormones decrease, the pituitary gland releases thyroid releasing hormone (TRH) to signal the thyroid gland to produce more T3 and T4.
    • With high levels of T3 and T4 in the blood, the pituitary gland releases less TRH so the thyroid gland could slow down.
    • TSH production requires adequate protein, magnesium, and zinc.
    • T4 requires iodine, vitamins C, and B2
    • T3 requires selenium, and is dependent on healthy liver and adrenal gland function
    • Most of the thyroid hormones comprise of T4 – nearly 80%. T3 is the active form of T4 and it’s thought to be more potent in regulating energy metabolism. There are also T0, T1, and T2, which act as hormone precursors and byproducts.

    To prevent low thyroid from fasting you want to make sure you get enough calories during your eating window. A slow metabolism isn’t the result of time restricted feeding per se but more by not giving the body adequate nutrients. If you already suffer from low thyroid and experience the symptoms of hypothyroidism, then it would be a good idea to shorten your fasting window a little bit to allow your body time to recover. Simply have your food a few hours earlier and you’ll speed up your metabolic processes.

    Here’s what you can do to overcome low thyroid without medication:

    • Get More Iodine – The thyroid needs iodine to produce thyroid hormones. Even small doses of 250 micrograms of iodine a day can help the thyroid. You can get iodine only from diet and rich sources for that are sea vegetables, algae, wild caught fish, eggs, seaweed, shellfish, iodized salt, and some dairy.
    • Limit Goitrogenic Foods – Goitrogens are compounds that can affect the thyroid gland if consumed in large amounts. Foods high in goitrogens are things like cruciferous vegetables, broccoli, cabbage, kale, and some fruit. However, the benefits of these foods far outweigh the downside. They’d become a problem only if you eat too many raw vegetables. If you cook or steam them lightly then you’ll lower the number of goitrogens in them.
    • Tyrosine-rich foods that support the thyroid are pumpkin seeds, beef, poultry, almonds, avocados, eggs, and fish. They also have B12 and selenium. You should aim for organic meats because they’re not injected with antibiotics and other harmful hormones.
    • A Healthy Insulin Spike – If you eat some carbohydrates like a sweet potato or rice, then you can boost your metabolic rate.
    • Especially, if you’re eating a low carb diet. Prolonged periods of dieting will slow down your metabolism and doing some carb cycling can be very beneficial.
    • Eat More Calories – Dieting and restricting calories for too long will slow down your metabolism and thyroid functioning. Having a diet-break for a few days where you eat slightly above your maintenance can help you to boost your metabolic rate. However, you don’t want to be eating inflammatory foods like processed carbs, pastries, pizzas, or ice cream. Instead, you’d want to get more of the thyroid supporting foods we’ve talked about here.

    Now for the things you don’t want to be doing if you suffer an under reactive thyroid:

    • Avoid All Gluten – Gluten is a common allergen that activates an autoimmune response on the thyroid. People with Hashimoto’s or hypothyroidism tend to be sensitive to gluten as well. Gluten is found everywhere – not just in bread, pasta, and cookies – it’s in almost all packaged foods, sauces, meats, skin care products, and the particles can even float around in the air. 
    • Don’t Drink Tap Water – Most tap water contains fluorine and chlorine that inhibit iodine absorption and dampen your pineal gland’s functioning.
    • Limit other potential allergens as well such as dairy, nuts, shellfish, eggs, fish, soy, or meat if you are sensitive to these foods.
    • Don’t Fast for Too Long – It’ll lower your thyroid functioning further and can decrease metabolic rate. Definitely, you shouldn’t fast for longer than 24 hours if you have low thyroid. Until you’ve healed your thyroid and metabolism, somewhere between 16-18 hours is fine.
    • Reduce Your Stress – It’s going to make you feel more drained and exhausted. Don’t start exercising harder or get more stressed out about work but try to relax more and allow your adrenals to recover.
    • You should also avoid stimulants like coffee and sugar because they’ll activate the adrenal glands.
    • Avoid Environmental Toxins such as pesticides, mold, BPA found in plastics, isoflavones found in soy, potassium perchlorate, cigarette smoke, and keep your home clean from these toxins. Heat saunas and sweating can help you to eliminate these toxins from your body.

Scleroderma and Rheumatoid

(Gabor – When the body says no)

In scleroderma, the immune system’s suicidal assault results in a stiffening of the skin, esophagus, heart, and tissues in the lungs and elsewhere. Medical textbooks take an exclusively biological view. In a few isolated cases, toxins are mentioned as causative factors, but for the most part a genetic predisposition is assumed to be largely responsible.

• A patient of his started out with Raynaud’s, which resulted in the scleroderma. In this situation, he realized that she had emotional trauma and never felt worthy of attention. She also compulsively took the responsibility for the needs of others.
• It’s almost as if her inability to say no was forcing her body to revolt and say it for her.

The more specialized doctors become, the more they know about a body part or organ and the less they tend to understand the human being in whom that part or organ resides.

We can’t deny the benefits of the application of scientific methods. But not all essential information can be confirmed in the laboratory or by statistical analysis. Not all aspects of illness can be reduced to facts verified by double-blind studies and by the strictest scientific techniques. “Medicine tells us as much about the meaningful performance of healing, suffering and dying as chemical analysis tells us about the aesthetic value of pottery,” Ivan Ilyich wrote.

Psychoneuroimmunology: the science of the interactions of mind and body, the indissoluble unity of emotions and physiology in human development and throughout life in health and illness.

Our immune system does not exist in isolation from daily experience. For example, the immune defences that normally function in healthy young people have been shown to be suppressed in medical students under the pressure of final examinations. Also, the loneliest students suffered the greatest hit to their immune system.

Stress is a complicated cascade of physical and biochemical responses to powerful emotional stimuli. Physiologically, emotions are themselves electrical, chemical and hormonal discharges of the human nervous system. Emotions influence—and are influenced by—the functioning of our major organs, the integrity of our immune defences and the workings of the many circulating biological substances that help govern the body’s physical states. When emotions are repressed, this inhibition disarms the body’s defences against illness. Repression—dissociating emotions from awareness and relegating them to the unconscious realm—disorganizes and confuses our physiological defences so that in some people these defences go awry, becoming the destroyers of health rather than its protectors (inflammation and autoimmune disorders I assume).

He observed the same patterns in people treated for multiple sclerosis, ALS, inflammatory ailments of the bowel such as ulcerative colitis and Crohn’s disease, chronic fatigue syndrome, autoimmune disorders, fibromyalgia, migraine, skin disorders, endometriosis and many other conditions. In important areas of their lives, almost none of his patients with serious disease had ever learned to say no.

While all of us dread being blamed, we all would wish to be more responsible—that is, to have the ability to respond with awareness to the circumstances of our lives rather than just reacting. We want to be the authoritative person in our own lives: in charge, able to make the authentic decisions that affect us. There is no true responsibility without awareness.

One of the weaknesses of the Western medical approach is that we have made the physician the only authority, with the patient too often a mere recipient of the treatment or cure.

In healthy mother-infant interactions, the mother is able to nourish without the infant’s having in any way to work for what he receives.

The rheumatic diseases include rheumatoid arthritis, scleroderma, ankylosing spondylitis and systemic lupus erythematosus (SLE). In these disorders, a disturbed immune system reacts against the body’s own tissues, particularly against connective tissues like cartilage, tendon sheaths, the lining of joints and the walls of blood vessels. These illnesses are characterized by various patterns of inflammation that strikes the joints of the limbs or the spine; or surface tissues like skin or the lining of the eyes; or internal organs such as the heart or the lungs or—in the case of SLE—even the brain.

Characteristic of many persons with rheumatoid diseases is a stoicism carried to an extreme degree, a deeply ingrained reticence about seeking help. People often put up silently with agonizing discomfort, or will not voice their complaints loudly enough to be heard, or will resist the idea of taking symptom-relieving medications.

• The non-complaining stoicism exhibited by rheumatoid patients is a coping style acquired early in life. Sometimes developing anxiety for the health of others, despite being abused themselves. The sufferer feels like they can somehow manage and rationalize issues so that they can minimize the felt pain.
• An intensive medical-psychiatric study of people with rheumatoid arthritis conducted for the Maryland Chapter of the Arthritis and Rheumatism Foundation in 1969 concluded that “despite the diversity in the group, the patients’ psychological characteristics, vulnerabilities and life conflicts were remarkably similar.” One common characteristic was a pseudo-independence, described by the authors as a compensating hyper-independence.
• A child may lie to themselves in survive dire situations, about not requiring assistance.

In 1969 the British psychiatric researcher John Bowlby published Attachment, the first volume of his classic trilogy exploring the influence of parent-child relationships on personality development. “The reversal of roles between child, or adolescent, and parent, unless very temporary, is almost always not only a sign of pathology in the parent,” he wrote, “but a cause of it in the child.” Role reversal with a parent skews the child’s relationship with the whole world. It is a potent source of later psychological and physical illness because it predisposes to stress.

Other traits identified in the psychological investigations of people with rheumatoid disease include perfectionism, a fear of one’s own angry impulses, denial of hostility and strong feelings of inadequacy. As we have seen, similar traits are said to be associated with the “cancer personality” or with personalities at risk for MS, ALS, or any other chronic condition. None of these traits represent innate features of a person, nor are they irremediably fixed in the individual.

Another finding was the loss of one or both parents being a contributing factor. Effectively emotional deprivation.

Like compensatory hyper-independence, the repression of anger is a form of dissociation, a psychological process originating in childhood. The young person unconsciously banishes from awareness feelings or information that, if consciously experienced, would create unsolvable problems. Bowlby calls this phenomenon “defensive exclusion.” “The information likely to be defensively excluded is of a kind that, when accepted for processing in the past, has led the person concerned to suffer more or less severely.”

• In other words, the angry child got into trouble and experienced rejection. The anger and the rejection had to be deflected inside, against the self, in order to preserve the attachment relationship with the parent. That, in turn, leads to the “strong feelings of inadequacy and a poor self-concept” researchers have recognized in people with rheumatoid disease. “Not infrequently anger is redirected away from an attachment figure who aroused it and aimed instead at the self,” Bowlby explains. “Inappropriate self-criticism results.

Emotions safeguard the organism from external threat; like the nervous system and the hormones, they assure the satisfaction of indispensable appetites and needs; and, like all these systems together, they help maintain and repair the internal milieu.

An animal experiences anger when some essential need is either threatened or frustrated. Although animals lack conscious knowledge of emotional phenomena, they do feel emotion and experience the physiological changes of Emotion I. And, of course, they manifest the behavioral displays classified as Emotion II. The specific purpose of Emotion I biological changes is to prepare the creature for fight or flight responses. But since fight or flight both demand great expenditures of energy and impose risks of injury or death, the Emotion II displays serve a crucial intermediary function: they often settle the conflict without any of the participants having to get hurt.

• When two creatures approach each other (over territory or some sort of resource), instead of immediately fighting, they have the option of displaying threatening signs of anger to give the other creature a chance to avoid harm and so the angry creature can reduce its own potential harm.
• Anger represents both a recognition of the foreign and dangerous and a response to it.

The first essential task of the immune system is distinguishing self from non-self. Thus, immunity also begins with recognition. Recognition is a sensory function, performed in the nervous system by the sensory organs. Any failure of the immune system in its responsibility of recognition would expose us to as much danger as we would face if our capacities to see, hear, feel or taste were impaired. Another function of the nervous system is memory. The immune system must also have memory: it needs to recall what in the external world is benign and nourishing, what is neutral and what is potentially toxic.

• Under the watchful eyes of the parent, the infant and toddler explore the environment, learning what is edible and what is not, what is comfortable or a source of pain, what is hazardous or safe. The acquired information is stored in the developing brain’s memory banks. Immunity is also a matter of learning. Memory is stored by the immune system in cells programmed to recall instantaneously any threat previously encountered. And just as the nervous system must retain its potential for learning throughout the lifetime, so the immune system has the capacity to develop new “memories” by forming clones of immune cells trained specifically to recognize any new threat.

When our psychological capacity to distinguish the self from non-self is disabled, the impairment is bound to extend to our physiology as well. Repressed anger will lead to disordered immunity. The inability to process and express feelings effectively, and the tendency serve the needs of others before considering one’s own, are common patterns in those who develop chronic illness. Representing a blurring of boundaries, confusion of self and non-self on the psychological level. This extends to the cells, tissues, and organs. The immune system becomes unable to distinguish self from other or is too disabled to defend against danger.

One of the laboratory hallmarks of rheumatoid arthritis is the finding of an antibody directed against the self by the confused immune system. It is called rheumatoid factor, or RF. Found in over 70% of patients with rheumatoid arthritis, RF may also be present in people without the condition.

• The RF-positive group scored significantly higher on psychological scales reflecting the inhibition of anger and concern about the social acceptability of behaviors. They also scored higher on a scale that indicated traits such as “compliance, shyness, conscientiousness, religiosity and moralism.”
• The presence of the antibody in these subjects suggests that emotional repression had already initiated immune reactivity against the self, although not to the point of clinical disease. One might expect that should additional stressful events occur in the lives of these women, they could further incite the immune mutiny, activate inflammation and trigger frank disease. “Emotional disturbances in conjunction with rheumatoid factor may lead to rheumatoid disease,” the researchers concluded. It is also possible to develop rheumatoid arthritis without the anti-self-antibody RF.

In women with rheumatoid arthritis, the immune system has shown increased disturbance during periods of stress, but those who enjoyed better marriage relationships were spared exacerbations of disease activity like inflammation and pain. Another study found that increases in relationship stresses were associated with increases in joint inflammation.

There are several potential pathways by which overwhelming psychological pressures could become manifested as inflammation in joints, connective tissues and body organs.

• Discharges originating in the brain can stimulate faraway nerve endings to release powerful pro-inflammatory molecules capable of inducing joint damage through hyperactivity of the immune cells. Some nerve-derived chemicals are also potent irritating agents for inducing pain. In autoimmune diseases, elevated levels of some of these substances are found in the fluid of inflamed joints as well as in the circulation.

Normal cortisol secretion by the adrenals regulates the immune system and dampens the inflammatory reactions triggered by the products of immune cells. In rheumatoid arthritis, there are lower than normal cortisol responses to stress: we can see why, then, there would be disordered immune activity and excess inflammation. On the one hand, the immune system escapes from normal control and attacks the body to cause inflammation, and on the other, the required anti-inflammatory responses are weakened and ineffective.

Multiple Sclerosis

(Gabor – When the body says no)

Multiple sclerosis is the most common of the demyelinating diseases that impair the functioning of cells in the central nervous system. Its symptoms depend on where the inflammation and scarring occur. The main areas attacked are usually the spinal cord, the brain stem and the optic nerve, which is the bundle of nerve fibres carrying visual information to the brain. If the site of damage is somewhere in the spinal cord, the symptoms will be numbness, pain or other unpleasant sensations in the limbs or trunk. There may also be involuntary tightening of the muscles or weakness. In the lower part of the brain, the loss of myelin can induce double vision or problems with speech or balance. Patients with optic neuritis—inflammation of the optic nerve—suffer temporary visual loss. Fatigue is a common symptom, a sense of overwhelming exhaustion far beyond ordinary tiredness.

Patients burdened by qualitatively extreme stresses, such as major relationship difficulties or financial insecurity, were almost four times as likely to suffer exacerbations.

The French neurologist Jean-Martin Charcot was first to give a full clinical description of multiple sclerosis. Patients, he reported in a lecture in 1868, connect “long continued grief or vexation” with the onset of symptoms. Five years later a British physician described a case also associated with stress: “Aetiologically it is important to mention another statement the poor creature made when giving a more confidential account to the nurse—that the cause of her disease was having caught her husband in bed with another woman.”

Excessive emotional involvement with a parent, a lack of psychological independence, an overwhelming need for love and affection, and the inability to feel or express anger have long been identified as possible factors in the development of the disease. A study in 1958 found that in nearly 90% of cases, patients experienced traumatic life events that “threatened their security system.”

“The common characteristic is the gradual realization of the inability to cope with a difficult situation… provoking feelings of inadequacy or failure,” said the authors of a 1969 study.

The blurring of psychological boundaries during childhood becomes a significant source of future physiological stress in the adult. There are ongoing negative effects on the body’s hormonal and immune systems, since people with indistinct personal boundaries live with stress; it’s a permanent part of their daily experience to be encroached upon by others.

Even people who have all the necessary genes for MS require environmental factors to trigger it.

The fundamental problem is not the external stress, but an environmentally conditioned helplessness that permits neither of the normal responses of fight or flight. The resulting internal stress becomes repressed and therefore invisible. Eventually, having unmet needs or having to meet the needs of others is no longer experienced as stressful. It feels normal. One is disarmed.

Artistic expression by itself is only a form of acting out emotions, not a way of working them through.

Crohn’s Disease

(Gabor – When the Body Says No)

Crohn’s is one of the two major forms of inflammatory bowel disease (IBD). Ulcerative colitis is the other. Both are characterized by inflammation of the bowel but in different patterns. In ulcerative colitis the inflammation begins in the rectum and spreads upward. The entire colon may become involved. The inflammation is continuous but confines itself to the mucosa.

In Crohn’s disease, the inflammation extends through the entire bowel wall. Most often the ileum, which is the third and final part of the small intestine, and the colon are affected, but Crohn’s may appear in any part of the tract. It will skip areas of the alimentary canal so that normal tissue alternates with diseased segments. IBD may be associated with inflammation in the joints, eyes, and skin.

The symptoms of IBD depend on the site of involvement. Diarrhea is common in both diseases, along with abdominal pain. Patients may need to defecate many times during the day or even find themselves incontinent. When the colon is affected, there will be bloody stools or hemorrhaging. Patients may experience fever and weight loss. Sometimes fistulas created by inflammation.

IBD is usually a disease of young people. Although it may occur at any age, most commonly onset happens between the years from fifteen to thirty-five.

Medical science considers IBD to be “idiopathic,” of unknown causation. Heredity plays a role, but not a major one. About 10 to 15 per cent of patients have a family history of IBD. The risk is estimated to be from 2 to 10 per cent if a first-degree relative has been diagnosed. Research shows that “most people with inflammatory bowel disease believe that stress is a major contributor to illness.”

A 1955 survey of ulcerative colitis patients found that “colitis patients’ mothers were controlling and had a propensity to assume the role of martyr.” No one sets out consciously to be a martyr to her children or to be controlling. A less judgmental way to put this would be that the child perceived himself to be responsible for his mother’s emotional suffering.

• The 1955 study, which looked at over seven hundred people with ulcerative colitis, concluded that a high proportion of these patients “had obsessive-compulsive character traits, which included neatness, punctuality, and conscientiousness. Along with these character traits, guarding of affectivity (emotional expression), over-intellectualization, rigid attitudes toward morality and standards of behavior.

Inflammation is an ingenious process invoked by the body to isolate and destroy hostile organisms or noxious particles. It does so by tissue swelling and the influx of a host of immune cells and antibodies. To facilitate its defensive function, the lining, or mucosa, of the bowel is in a “state of perpetually controlled or orchestrated inflammation.”

A diminished capacity by the gut to mount an inflammatory response would invite life-threatening infections. On the other hand, an inability to dampen inflammation exposes the gut tissue to self-injury. The central abnormality in inflammatory bowel disease would appear to be just such an imbalance of what one journal article calls the “pro-inflammatory and anti-inflammatory” molecules in the bowel lining. Emotional influences acting through the nerve and immune pathways of the PNI super-system could tip the balance in favor of inflammation.

Substance P is a powerful stimulator of inflammation because it induces certain immune cells to release inflammatory chemicals such as histamine and prostaglandins, among many others.

Although induced by thought or emotion, the placebo effect is entirely physiological. It is the activation of neurological and chemical processes in the body that serve to reduce symptoms or to promote healing.

As Dr. Hershfield implies, not the latest technology or miracle drug but encouraging the patient’s capacity to heal may provide the ultimate answer to inflammatory bowel disease. The 55 per cent solution.

IBS

(When the Body Says No)

Medical terminology calls IBS a functional disorder. Functional refers to a condition in which the symptoms are not explainable by any anatomical, pathological or biochemical abnormality or by infection. Doctors are accustomed to rolling their eyes when faced with a patient who has functional symptoms, since functional is medical code for “all in the head.”

Although abdominal pain is a prominent feature of irritable bowel syndrome, by the current definition of the disorder, pain itself is not sufficient for the diagnosis. A person is considered to have IBS if, in the absence of other pathology, she experiences abdominal pains along with disturbances of bowel function, such as diarrhea or constipation. The symptoms may vary from person to person, or even for the same individual from time to time.

It is not unusual for IBS patients to describe stool that is lumpy or small and pellet-like or, on the other hand, loose and watery. They may find themselves having to strain and feeling they have not completely evacuated their bowels. They frequently describe passing mucus with their stool. A sensation of bloating or abdominal distension is also common.

Irritable bowel syndrome is said to affect 17% of the population in the industrialized world and is the most frequent reason for which patients are referred to a gastroenterologist.

In such cases, the complainant finds her symptoms dismissed by doctors. Worse, she may be accused of drug-seeking behavior, of being neurotic, manipulative, of “just looking for attention.” IBS patients, as well as people with chronic fatigue syndrome and fibromyalgia, often find themselves in that situation.

With rectal distension, or even the anticipation of rectal distension, IBS patients activated the prefrontal cortex, an area not activated in normal people. The prefrontal cortex is where the brain stores emotional memories. It interprets present stimuli, whether physical or psychological, in light of past experiences, which can date as far back as infancy. Activation in this part of the brain means that some event of emotional significance is occurring. In people who have experienced chronic stress, the prefrontal cortex and related structures remain in a state of hypervigilance, on the lookout for danger. Prefrontal activation is not a conscious decision by the individual; rather, it is the result of the automatic triggering of nerve pathways programmed long ago.

There is a high incidence of abuse in the histories of patients with intestinal diseases and especially in those patients with IBS and other functional disorders.

• In a more recent investigation at the same center, two-thirds of the women interviewed had experienced abuse of a physical or sexual nature, or both. Again, abused patients were more likely to undergo various surgeries, such as gallbladder operations, hysterectomies, and laparotomies. They also had “more pain, non-gastrointestinal somatic symptoms, bed disability days, psychological distress, and functional disability compared to those without sexual abuse.”

The brain relays to the gut data from sensory organs such as the eyes, the skin or the ears—or more correctly, relayed to the gut is the interpretation of such data by the brain’s emotional centers. The resulting physiological events in the gut then reinforce that emotional interpretation. The signals sent back to the brain give rise to gut feelings that we can apprehend consciously. If we lose touch with gut feelings, the world becomes less safe.

When there are too many “gut-wrenching” experiences, the neurological apparatus can become over-sensitized. Thus, in the spinal cord the conduction of pain from gut to brain is adjusted as a result of psychological trauma. The nerves involved are set off by weaker stimuli. The greater the trauma, the lower the sensory threshold becomes. Normal amounts of gas in the lumen and normal tension in the intestinal wall will trigger pain.

• At the same time, the prefrontal areas of the cortex will be in a heightened state of vigilance, responding with distress to normal physiological processes. Along with increased pain, IBS patients report higher levels of anxiety, arousal and fatigue during rectal distension than do healthy people. During emotional stress, activity of the cortical regions amplifies the perception of distress.

Dr. Lin Chang: “Both external and internal stressors contribute to the development of IBS. External stressors include abuse during childhood and other pathological stresses, which alter stress responsiveness and make a predisposed individual more vulnerable to developing IBS. Later in life, infections, surgery, antibiotics and psychosocial stressors can all contribute to IBS onset and exacerbation.”

The medical name for the distressing chronic experience of stomach acid flowing upward into the esophagus is gastroesophageal reflux disease (GERD).

• While the perception of reflux-associated heartburn by these patients was markedly increased during the stressful stimuli, the objective measures of acid levels were unchanged from one stimulus to another. Stress, in other words, lowered the pain threshold.
• The decreased efficiency of the sphincter muscles permitted more episodes of reflux.

The activity of the vagus is influenced by the hypothalamus. The hypothalamus, as we have seen, receives input from the emotional centers in the cortex that are susceptible to stress. Thus, in GERD, a lower pain threshold is combined with excessive relaxation of the sphincter—both phenomena that can be related to stress.

The downward calibration of the nervous system’s pain “thermostat” does not require abuse; chronic emotional stress is sufficient to diminish the pain threshold and to induce hypervigilance in the brain. While abuse would be a major source of such stress, there are other potential stresses on the developing child that are subtle, less visible, but harmful nonetheless. Such strains are present in many families, with parents who love their children and would be horrified by any thought of hurting them.

Gut feelings are an important part of the body’s sensory apparatus, helping us to evaluate the environment and assess whether a situation is safe. Gut feelings magnify perceptions that the emotional centers of the brain find important and relay through the hypothalamus. Pain in the gut is one signal the body uses to send messages that are difficult for us to ignore. Thus, pain is also a mode of perception. Physiologically, the pain pathways channel information that we have blocked from reaching us by more direct routes. Pain is a powerful secondary mode of perception to alert us when our primary modes have shut down. It provides us with data that we ignore at our peril.

The source of trauma does not necessarily have to be caused by something extraordinary. Some people may have a lack of self-worth or unacceptability due to not receiving the care they needed as a child. A sense of not belonging. These people may begin to care for others to their own detriment and also repress their own anger and pain. Often displayed as IBS, esophageal reflux, migraines, etc.

There is encouraging research evidence that even minimal psychological intervention can be of benefit: “In one controlled study of cognitive-behavioral treatment for patients with irritable bowel syndrome, eight 2-hour group treatment sessions over a 3-month period led to an increase in the number of effective cognitive and behavioral strategies and concurrent reduction in abdominal complaints.”

Asthma, Eczema, Hayfever, etc

Children and infant animals have virtually no capacity for biological self-regulation; their internal biological states—heart rates, hormone levels, nervous system activity—depend completely on their relationships with caregiving grown-ups. Emotions such as love, fear or anger serve the needs of protecting the self while maintaining essential relationships with parents and other caregivers. Psychological stress is whatever threatens the young creature’s perception of a safe relationship with the adults, because any disruption in the relationship will cause turbulence in the internal milieu.

Human beings did not evolve as solitary creatures but as social animals whose survival was contingent on powerful emotional connections with family and tribe. Social and emotional connections are an integral part of our neurological and chemical makeup. From such a biopsychosocial perspective, individual biology, psychological functioning and interpersonal and social relationships work together, each influencing the other.

In asthma, from the Greek root “breathe hard,” there is a reversible narrowing of the bronchioles, the small airways in the lungs, because the muscle fibers that encircle them begin to tighten. At the same time, the lining of the bronchioles becomes swollen and inflamed. All the various components of the PNI apparatus are involved in asthma: emotions, nerves, immune cells and hormones. Nervous discharges can narrow the airways in response to many stimuli, including emotions. The immune system is responsible for inflammation of the bronchiolar lining, the other characteristic feature of asthma. Swelling of the airway lining and the accumulation of inflammatory debris in the bronchioles are the final consequences.

• It is not inhalation but the outflow of air from the narrowed bronchioles that is impaired in asthma. The asthmatic has difficulty exhaling and feels his chest begin to tighten. The lungs attempt to clear the clogged airways by activating the cough reflex. In acute episodes, the labored exhalations produce the well-known wheezing noise from the narrowed bronchioles, as from lips puckered for whistling. In milder cases, the only symptom may be an irritating cough. For some people asthma is chronic, while others experience it only intermittently.
• Depending on individual predisposition, asthmatic attacks may be set off by allergens, exercise, cold temperatures, medications like Aspirin, crying, laughing, viral respiratory infections, and emotional arousal.
• Emotions can play a major role in making a person susceptible, no matter what the immediate trigger may be—Aspirin or cold air or anxiety. Chronic emotional stresses sensitize the immune system, so that it becomes overly reactive to any number of triggers.

Children known to suffer from atopic dermatitis (eczema, itchy allergic rashes) or from asthma have a diminished production of cortisol in response to stress.

Researchers who looked at the interactions between parents and asthmatic children have identified characteristic patterns of insecure attachments. Separation anxiety has been observed in children with asthma to a greater degree, not only in comparison with healthy controls but also when matched with children suffering from cystic fibrosis. Suggesting that the severity was not the cause of the anxiety.

“Regardless of the tone of the voice, asthmatic children showed more abnormal respiratory patterns when listening to their mother’s voice than when listening to that of a strange woman. This interesting result suggested a specific emotional effect on breathing that was contrary to what one would have predicted if the child had seen the mother as being reassuring.

On objective measures, when asthmatic children felt frustrated or criticized, the flow of air from their lungs diminished, indicating airway narrowing. Decreased airflow has also been documented when children with asthma were asked to recall incidents of intense anger or fear.

“Women experiencing a stressor objectively rated as highly threatening and who were without intimate emotional social support had a ninefold increase in risk of developing breast carcinoma.”

A seventeen-year follow-up study of residents of Alameda County, California, looked at the possible links between people’s social connectedness or sense of isolation and the onset of cancer. In this prospective study, none of the adults enrolled at the start had cancer. “The risk factor of major interest for women appeared to be social isolation, not only being isolated, but also of feeling isolated…”

A fundamental concept in family systems theory is differentiation, defined as “the ability to be in emotional contact with others yet still autonomous in one’s emotional functioning.” The poorly differentiated person “lacks an emotional boundary between himself and others and lacks a ‘boundary’ that prevents his thinking process from being overwhelmed by his emotional feeling process. He automatically absorbs anxiety from others and generates considerable anxiety within himself.”

• The well-differentiated person can respond from an open acceptance of their own emotions, which are not tailored to match or resist another’s expectations. Emotions are neither suppressed or acted out impulsively.

Functional differentiation: a person’s ability to function based on their relationship with others. They may only be able to do their work well when others put up with their bad temper, unreliable habits, lack of emotional engagement or abusive behavior.

On the other hand, if my ability to function is independent of other people’s having to do my emotional work for me—that is, if I can remain engaged with others while staying emotionally open to them and to myself—then I would be said to have basic differentiation. The less basic differentiation one has attained, the more prone they are to experience emotional stress and physical illness.

In a study with military cadets, those most susceptible to contract Epstein Barr Virus or to develop clinical disease had the following in common:

• They had high ambitions for themselves
• They were struggling academically
• They had fathers who were high achievers.

We can see here the relationship between the stress and the perceived need to live up to parental expectation—that is, between the internal biological milieu and the child’s continuing need to gain acceptance.

Poorer marital quality was “strongly and positively” related to poorer immune response.

• In the divorced or separated group, the two psychological factors most closely associated with diminished immune functioning were the time elapsed since the breakup (the more recent the marriage failure, the greater the immune suppression) and the woman’s degree of attachment to the former spouse (the greater the emotional attachment, the worse the immune function).
• Women who were more self-regulated, less emotionally dependent on a relationship that failed to work for them, had stronger immune systems. Greater differentiation means better health.

The less powerful partner in any relationship will absorb a disproportionate amount of the shared anxiety—which is the reason that so many more women than men are treated for, say, anxiety or depression. (The issue here is not strength but power: that is, who is serving whose needs?) It is not that these women are more psychologically unbalanced than their husbands, even though the latter may seem to function at higher levels. What is unbalanced is the relationship, so that the women are absorbing their husband’s stresses and anxieties while also having to contain their own.

• The partner who must suppress more of his or her own needs for the sake of the relationship is more likely to develop physical illness as well—hence the greater incidence, for example, of autoimmune disease and of non-smoking-related cancers among women.
• Dr. Kerr writes. “As is the case with the emotional dysfunctions, the one prone to develop symptoms is the spouse who adapts most to maintain harmony in the relationship system.”

Development is a process of moving from complete external regulation to self-regulation, as far as our genetic programming allows. Well self-regulated people are the most capable of interacting fruitfully with others in a community and of nurturing children who will also grow into self-regulated adults. Anything that interferes with that natural agenda threatens the organism’s chances for long-term survival.

With an increased capacity for self-regulation in adulthood comes a heightened need for autonomy—for the freedom to make genuine choices. Whatever undermines autonomy will be experienced as a source of stress. Stress is magnified whenever the power to respond effectively to the social or physical environment is lacking or the person feels helpless, without meaningful choices (when autonomy is undermined).

• The less the emotional capacity for self-regulation develops during infancy and childhood, the more the adult depends on relationships to maintain homeostasis. The greater the dependence, the greater the threat when those relationships are lost or become insecure. Thus, the vulnerability to subjective and physiological stress will be proportionate to the degree of emotional dependence.
• To minimize the stress from threatened relationships, a person may give up some part of his autonomy. However, this is not a formula for health, since the loss of autonomy is itself a cause of stress. The surrender of autonomy raises the stress level, even if on the surface it appears to be necessary for the sake of “security” in a relationship, and even if we subjectively feel relief when we gain “security” in this manner.

The other way of protecting oneself from the stress of threatened relationships is emotional shutdown. To feel safe, the vulnerable person withdraws from others and closes against intimacy. This coping style may avoid anxiety and block the subjective experience of stress but not the physiology of it. Emotional intimacy is a psychological and biological necessity. Those who build walls against intimacy are not self-regulated, just emotionally frozen. Their stress from having unmet needs will be high.

“Social ties and support,” a group of researchers concluded, “… remain powerful predictors of morbidity and mortality in their own right, independent of any associations with other risk factors.” For the adult, biological stress regulation depends on a delicate balance between social and relationship security on the one hand, and genuine autonomy on the other. Whatever upsets that balance, whether or not the individual is consciously aware of it, is a source of stress.