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Antimicrobial action of Amyloid and Prion Protein (PrP)

By Renata Trister DO
Antimicrobial action of Amyloid and Prion Protein PrP

Many neurological conditions are characterized by the formation of proteins or protein plaques in brain tissue. These proteins include amyloid beta and prion protein (PrP). Amyloid plaques are associated with Alzheimer’s disease. Prion protein has been found in patients with Parkinson’s disease, schizophrenia, bipolar disorder, and in some cases of depression. Prion protein is most famously found in Mad Cow Disease. In Mad Cow Disease and other “prion disorders” PrP protein is believed to fold incorrectly.
It is currently thought by many scientists that both amyloid beta and PrP are the causes of neurological inflammation and disease. In Alzheimer’s, amyloid beta “plaque” is believed to exacerbate symptoms and degeneration.

Recent studies at Mass General Hospital in Boston and Lund University in Sweden have called these ideas into question. These studies showed that both amyloid beta and PrP have another, previously unknown function: they are antimicrobial peptides. These antimicrobial peptides are natural, broad-spectrum antibiotics. They can kill bacteria, enveloped viruses, fungi and even cancer cells.

Therefore, if amyloid beta and PrP are antimicrobial, they likely have a protective function in patients with these neurological conditions. Amyloid and PrP most likely are actually the immune system’s response to infection in patients suffering from these diseases. Amyloid beta protects against fungal and bacterial infections. Mouse brains infected with Salmonella Typhi murium, amyloid beta formed in response to the infection. This data demonstrates that amyloid beta deposition, maybe a mediated response of the innate immune system to a perceived infection.

PrP protein is also an antimicrobial peptide. PrP peptides can destroy Escherichia coli, Pseudomonas aeruginosa, Bacillus subtilis and Staphylococcus aureus.
PrP had an anti-fungal effect against Candida. PrP expression was found to increase in patients with H. Pylori infection, with levels returning to normal as the infection clears.
PrP has been found in skin cells of patients with psoriasis, contact dermatitis, squamous cell carcinomas, and viral warts. These conditions associated with micro biome imbalance of the skin. These findings also point to the possibility that prion protein is actually a response to an infection.

The pathology of these diseases may have an infectious component. The specific infectious agent in these neurological conditions is not yet identified. It is also possible that these proteins fight infection initially, but then with increasing levels cause more problems. Many Alzheimer’s medications are aimed at destroying amyloid deposits. These new findings call this approach into question.


Myrrh.Antimicrobial Properties.

By Renata Trister DO
Health Benefits of Myrrh
Myrrh has antimicrobial, astringent, expectorant, antifungal, anticatarrhal, antiseptic, immune boosting, circulatory, tonic, anti-inflammatory, and antispasmodic properties.
Scientifically called Commiphora Myrrha, myrrh is native to Egypt. The resin was frequently used in incense and perfumery.
In addition to extensive use in aromatherapy, myrrh has medicinal uses too.
Myrrh has antimicrobial properties. It can be used to prevent many problems occurring due to microbial infection. It has no adverse side effects, unlike other antibiotics, such as weakening of liver or digestive malfunction.
Myrrh is an astringent, which means that it strengthens the gums and muscles, intestines, and other internal organs, and smoothens the skin. One more serious aspect of this astringent property is that it stops hemorrhaging in wounds. When this astringency makes the blood vessels contract and checks the flow of blood, it can stop you from losing too much blood when wounded.
Myrrh is useful for a cough and cold. It fights the viral infections that can cause them, as well as relieves congestion, and reduces the deposition of phlegm in the lungs and respiratory tracts. Myrrh is an antifungal. It can be used both internally and externally to fight fungal infections.
Myrrh increases perspiration and removes toxins, extra salt, and excess water from your body. Sweating also cleans the skin pores and helps harmful gases like nitrogen escape.
Small amount of myrrh essential oil on cuts and wounds, can keep the cut from becoming infected.
Myrrh stimulates blood circulation and ensures the proper supply of oxygen to the tissues. This is good for attaining a proper metabolic rate as well as for boosting the immune system. Increasing the blood flow to all the parts of the body helps in staying healthy. This tonic effect helps the organs in the body, serving as a protection from premature aging and infection.
Caution: Despite these benefits myrrh it can have toxic effects if used in excess. Pregnant women should avoid it since it stimulates the uterus.


Fasting for health.Just information.Not a guidance.

Fasting has been used to manage various chronic conditions such as asthma, diabetes, obesity, allergy, autoimmune disorders as well as depression and anxiety.  It is especially useful for chronic conditions, refractory to conventional treatments.

The 5 stages of prolonged water fasting, as used in the practice of Dr. Yuri Nikolayev, the Director of the Fasting Clinic of The Moscow Institute of Psychiatry.

Dr. Yuri Nikolayev treated more than 7,000 patients suffering from various conditions by using therapeutic fasting. The average duration of a fast would be 30 days.

Dr. Yuri Nikolayev (1905 – 1998) was first exposed to the practice of fasting in his early childhood. Whenever he or his brother Lev would get sick, their mother treated them with 2-3 days of fasting.  He was very inspired by Upton Sinclair’s book The Fasting Cure.  The two communicated in letters.  These letters together with Sinclair’s book would have a profound influence on young Yuri’s personal experience with fasting as well as the implementation of therapeutic fasting in his medical practice.

Dr. Nikolayev cautioned that the hunger treatment should be administered only under carefully controlled conditions. The patient and his relatives must approve the procedure and the patient is thoroughly examined before the treatment starts.

Food Deprivation – Eating Cessation – The First 2-3 Days

During this first initial stage, the patient is being given a solution of MgSO4 (magnesium sulfate, otherwise known as Epsom salt) to trigger complete bowel discharge. The bitter after-taste is usually masked with a sip of juice. For this purpose, lemon water is used.

In the initial phase, the patient is very sensitive to any reference to food – visual, olfactory, or even a mere discussion about food. Any perception of food triggers salivary effects and may cause stomach cramps. Sleep is reduced and superficial, patients are irritable and may develop exacerbation of their symptoms. Weight loss is between 800 grams to 1 kg per day, blood pressure remains stable, while the cardiac rhythm may be easily intensified and irregular.

Acidosis Phase  Day 3-5

Between the 3rd and 5th days of fasting, food no longer stimulates the patient. There are occasional headaches, dizziness – especially upon waking or going from sitting to standing.  Nausea and generalized weakness are also reported.

The tongue is usually coated with a white layer. Blood sugar may decrease to 65% of its initial level. The feeling of nausea is due to the increased blood acidity. In reality, as the body adapts to the lack of food intake it starts burning its own fat, and the incomplete oxidation may result in products that increase acidity.

The protocol demands increasing water intake, as well as exercise – 3 hours daily.

This active routine is that helps the body ventilate, and sweat.  This engages organs of elimination to eliminate toxins from the body (skin, kidneys, bowels, liver). Daily colonics are also used for this.  During this stage ketosis has started.  Your body is using fat stores for energy.

Burning fat has several benefits for your health—the first being weight loss. Ketosis is a predictable way to target fat stores that otherwise remain untouched even with a healthy lifestyle. Additionally, getting rid of that extra fat has a detoxifying effect on the body. Your body’s natural defenses use fat stores to store toxic metals and other toxins so they can’t wreak havoc on your system. However, during ketosis, these toxic metals and toxins are safely expelled from your body as fat reserves get used up. This cleansing effect may temporarily alter some people’s complexion or cause other signs of a healing crisis.

Compensation and Balance Day 4-7

During the 4-7 day the body suddenly regains balance and the overall status of the patient is radically altered. With the feeling of gone, the patients feel strong, motivated, with significant improvement in mood. After the tenth day, weight loss stabilizes at 200g/day, the white tongue coating clears and the tongue regains its pinkish color.

During stage three, your body starts to enter into a “healing mode.” This healing process begins as your digestive system takes a rest from daily toxins. Consequently, free radicals are reduced and oxidative stress decreases.

Fasting causes a kind of “mental power stress” that provides health benefits. This is a kind of mild stress that is comparable to the stress caused by the discipline of exercise, which ultimately makes you stronger and your immune system more resilient.

When the cumulative effects of this stage add up, they can be the catalyst for significant health improvements. Limiting free radicals and oxidative stress is the cornerstone of healthy aging.  This healing process seems to improve health for some.

Another tremendous benefit is the accomplishment of personal goals and growth. Getting this far, the benefits becomes personal and extremely empowering. Fasting, especially beyond the first seven days, takes tremendous dedication. What you get out of the fast in these later stages can be a culmination of all the earlier stages plus the accomplishment of a personal challenge.

Breaking the Fast – Reintroducing Foods

Once the patient passes the crises and gains a feeling of euphoria. The symptoms begin to disappear, until the stored energy source is consumed. This occurs after about 30 days. By that time, the patient’s tongue is clean, his skin color is a healthy pink, bad breath disappears.

Food is reintroduced gradually. Diluted fruit juices are used first, then whole juices and grated fruit mixed with yogurt. Cooked vegetables and boiled cereals follow. Near the 40th day, normal eating is resumed. The doctor said the hunger treatment gives the entire nervous system and the brain a rest. The body is cleaned of poisons and the tissues and glands renovated.

Normal Alimentation (eating)

The fourth to the sixth day after breaking the fast the appetite of the patient may be significantly increased. This is when, at his request, he may be provided with more fruits, bread, and plenty of vegetables.

If the fasting cure was successful, the pathologic disorders of the patient will show improvement. Their blood pressure and the glucose levels stabilize at their initial values. The increased appetite and the increased mood usually last for 2-3 weeks after which they resume to normal.

(Dr. Nikolayev was a vegetarian; therefore his recommendations were low meat consumption).  There are many variations of these fasts also.

In conclusion, therapeutic fasting may be a very powerful tool in optimizing wellbeing, it should be implemented with the most caution possible and under medical supervision.  Prior to implementing this or any fast/diet discuss your options with your doctor.


Medicinal Uses of Artemisia Herb

Medicinal Uses of Artemisia Herb
By Renata Trister DO
Artemisia commonly known as Wormwood is a perennial shrub-like plant of the aster family. It is the main ingredient of Absinthe, an alcoholic beverage.
Artemisia is one of the strongest bitters in the plant kingdom.

Artemisia’s biologically active compounds include:

Acetylenes (trans-dehydromatricaria ester, C13 and C14 trans-spiroketalenol ethers, and others)
Ascorbic acid (vitamin C)
Azulenes (chamazulene, dihydrochamazulenes, bisabolene, camphene, cadinene, sabinene, trans-sabinylacetate, phellandrene, pinene and others)
Flavonoids (quercitin 3-glucoside, quercitin 3-rhamnoglucoside, spinacetin 3-glucoside, spinacetin 3-rhamnoglucoside, and others)
Lignins (diayangambin and epiyangambin)
Phenolic acids (p-hydroxyphenylacetic, p-coumaric, chlorogenic, protocatechuic, vanillic, syringic and others)
Thujone and isothujone
sesquiterpene lactones (absinthin, artabsin, anabsinthin, artemetin, artemisinin, arabsin, artabin, artabsinolides, artemolin, matricin, isoabsinthin and others)

It also contains the anti-inflammatory agents artemisin and anabsinthine that gives this plant its bitter taste.

The bitter substances absithin and anabsinthin are thought to improve digestions and stimulate the digestive system. Historically, this herb was used as an herbal remedy for gallbladder, liver and stomach ailments.

It has been used traditionally as a natural treatment for irritable bowel syndrome (IBS), colds, chronic fever, heartburn and to enhance the immune system.

Many people turn to natural and alternative treatments when it comes to problems with their gastrointestinal health, and for good reason. Studies show that herbal remedies like wormwood are as good or even better at fighting small intestinal bacterial overgrowth or SIBO symptoms.

Today’s typical treatment of SIBO is limited to oral antibiotics with varying rates of effectiveness. A 2014 study had 104 patients who tested positive for newly diagnosed SIBO take either a high dose of rifaximin or an herbal therapy daily for four weeks. The herbal products were specifically chosen because they contained antimicrobial herbs like wormwood, oregano oil, thyme and berberine extracts, which have been shown to provide broad-spectrum coverage against the types of bacteria most commonly involved in SIBO.

Of the patients who received herbal therapy, 46 percent showed no evidence of SIBO on follow-up tests compared to 34 percent of rifaximin users. Adverse effects reported among those taking rifaximin included anaphylaxis, hives, diarrhea and C. difficile colitis, while only one case of diarrhea and no other side effects were reported in the herbal therapy group.

The study concluded that herbal therapies are at least as effective as rifaximin for eradication of SIBO. Additionally, the herbal therapy with wormwood appears to be just as effective as triple antibiotic therapy for individuals who don’t respond to rifaximin. Artemisin also enhances the natural gastric acid and wall barrier.

This herb has anti-infective properties and has been used topically to treat wounds, cuts, and bruises to speed the healing process and prevent infection.

Due to the slight natural anesthetic effect of the herb, it has been used to ease pain associated with arthritis and rheumatism.

An extract made from the plant has been used for centuries as an herbal medicine to rid the body of intestinal worms like round worms and pin worms. This is how the common name wormwood was derived.

Recent experiments have shown that artemisin is effective against the malaria parasite because it reacts with the high levels of iron in the parasite to produce free radicals. The free radicals then destroy the cell walls of the malaria parasite.

Wormwood is thought to have a calming effect and could be helpful to those suffering from epilepsy and muscle spasms and to treat mild forms of depression.

This plant is also also used as an insect repellent.


Medicinal Uses of Thuja

By Renata Trister, DO
Medicinal Uses of Thuja

Thuja occidentalis

Thuja tree has been used traditionally for centuries by the Native Americans to treat a variety of conditions. Homeopathic practitioners have also used it extensively.

Branches and leaves were made into tincture and used to treat a cough, fever, headache, intestinal parasites, cystitis and venereal diseases.

Topically, thuja was used to treat burns, rheumatism, gout, arthritis, warts, and psoriasis.

Thuja is most commonly used against warts. It is also used for acute bronchitis and respiratory conditions. Thuja has expectorant and anti-catarrhal properties.

Additionally, Thuja has been used to treat cystitis.
Extracts of the herb can be applied to painful joints and muscles to increase blood circulation, reducing pain.

For warts thuja is used topically – usually in the form of an essential oil.

The essential oil is only used to burn away warts. When the oil is used in this regard, glycerol is applied to the area surrounding the wart as a protection and then the poisonous essential oil is used on the wart itself.

Thuja has also antibacterial and anti-fungal properties and is used for the treatment of infected wounds, burns and skin infections such as ringworm.

Recently, German scientists demonstrated that Thuja strengthens the immune system by stimulating T lymphocytes and increase interleukin-2 production.

Growing evidence also shows that theses properties of Thuja may be effective for spirochete illnesses such as Lyme. Furthermore, Thuja has promising effects in fighting co-infections that are seen with chronic Lyme. The virus-resistant and immune strengthening properties of the herb can also be used as an adjunct to chemotherapy and radiotherapy.


Medicinal Benefits of Boswellia

Medicinal Benefits of Boswellia
By Renata Trister DO

Frankincense is the common name for the resin extracted from Boswellia trees. Boswellia serrata is a tree native to India. Compounds derived from this tree have been found to have strong anti-inflammatory effects. Boswellia trees have been used to treat inflammatory conditions, such as arthritis, inflammatory bowel disease and heart disease for hundreds of years. This resin is also used in many spiritual and religious practices (Churches etc).

Extracts of the Boswellia tree inhibit certain pro-inflammatory cytokines and mediators that can damage DNA, feed tumor growth and destroy healthy cells. Over the past several decades, research has given us a better understanding of how boswellia and frankincense oils may benefit our health and boost the immune system. Boswellia extracts seem to lower inflammation and support immune function on multiple levels, including:

Interfering with cytokine production that raises inflammation (interferon gamma, interleukin-4 and tumor necrosis factor-alpha)
Delaying reactions to sensitivities
Helping regulate lymphocytes (white blood cells) and T-cells interactions
Regulating production of immunoglobulin G (IgG) antibodies, which protect the body from bacterial and viral infections
Regulating production of immunoglobulin M (IgM) antibodies, which are found mainly in the blood and lymph fluid

Boswellia helps lower inflammation and prevents autoimmune diseases. Inflammation is the response of bodily tissues to any form of irritation, injuries, infections or disorders of the immune system. Whenever you feel pain, redness, swelling and sometimes loss of function, this is inflammation attempting to heal you.

Leukotrienes are small chemicals that contribute to inflammation by promoting free radical damages, autoimmune responses, cell adhesion and migration of the cells to any injured areas.

Terpenes and boswellic acids are anti-inflammatory and protective to healthy cells. These components of Boswellia have been most researched. Terpenes are strong-smelling chemicals found in certain plants, (eucalyptus, basil, peppermint and citrus trees). These plants are also associated with antioxidant activity. Terpenes function to protect the plants from predators and environmental stressors.

Other chemical compounds have been identified in boswellia that naturally reduce the inflammatory response by controlling T-lymphocytes, especially one called AKBA (3-O-acetyl-11-keto-beta-boswellic acid). Although it works similarly to NSAID pain relievers, AKBA’s exact mechanisms of action are very different because they target different inflammatory enzymes. Because they’re better able to preserve the integrity of the stomach and gut lining, boswellia extracts cause less side effects and pose less risk for toxicity compared to NSAIDs.

AKBA helps fight pain thanks in part to its ability to inhibit an enzyme called 5-LOX (5-lipoxygenase) and therefore shuts down mechanisms of leukotrienes, which are inflammatory mediators produced by the process of oxidation (specifically of arachidonic acid). AKBA has shown to be effective in helping to fight against a large number of inflammatory diseases, such as arthritis, bronchial asthma, chronic colitis, ulcerative colitis, Crohn’s disease and cancer.

Another active component of boswellia is called incensole acetate, which has similar powers over lowering inflammatory reactions, especially those that target the brain and speed up cognitive decline. Studies show that incensole acetate is protective over neurons, helps fight the formation of tumors and has mood-enhancing benefits, making it a potential natural antidepressant and anti-anxiety compound.
Boswellia serrata extract is so powerful that today it’s considered comparable to NSAID pain relievers.
Boswellia and turmeric have similar actions and some research shows that when used together, these two herbs potentiate each other’s effects.


Medicinal Benefits of Ginger

Renata Trister DO
Medicinal Benefits of Ginger

Ginger has over 40 pharmacological actions.

To summarize these include antibacterial, antioxidant, antifungal and anti-parasitic properties.
Ginger is an anti-inflammatory, and therefore useful for pain relief.
Ginger is also a thermogenic substance with beneficial impacts on metabolism.

The medicinal uses of ginger have been known for at least 2,000 years in cultures all around the world. Although it originated in Asia, ginger is valued in India, the Middle East and Africa.

The most commonly used medicinal portion of the ginger plant is the root-stem, which grows underground.
Ginger (like many natural plant compounds) is anti-inflammatory, which makes it a valuable tool for pain relief. In 2001, research showed that ginger oil helped reduce knee pain in people with osteoarthritis. Therefore ginger may be used instead of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) to decrease joint pain, muscle soreness and menstrual pain.
Along with help for muscle and joint pain, ginger has been found to reduce the severity of migraine headaches as well as the migraine medication Sumatriptan – with fewer side effects.
Ginger’s anti-inflammatory properties make it beneficial for many chronic inflammatory diseases.

Ginger also can benefit in treatment of diabetes. According to one comprehensive review, a clinical trial that was performed found that after consuming three grams of dry ginger powder for 30 days, diabetic participants had a significant reduction in blood glucose, triglyceride, total cholesterol, and LDL cholesterol. It’s thought that ginger has a positive effect on diabetes because it:

Inhibits enzymes in carbohydrate metabolism
Increases insulin release and sensitivity
Improves lipid profiles
Ginger also has also been established to have a protective effect on the diabetic’s liver, kidneys, central nervous system, and eyes.

Ginger is most famously used for treating digestive upsets. It is one of the best natural remedies for motion sickness or nausea.

Taking one gram of ginger daily may help reduce nausea and vomiting in pregnant women, and those suffering from motion sickness.
Ginger is great for indigestion. Ginger relieves pain and is an antispasmodic agent, which may explain its beneficial effects on your intestinal tract.

Finally, ginger is a thermogenic or metabolism boosting substance with beneficial impacts on overall metabolism and fat storage. Research suggests that consuming thermogenic ingredients like ginger may boost your metabolism by up to 5 percent.


Vitamins B. Review

B vitamins
By Renata Trister DO

The B vitamin family has eight B vitamins. Viewed as a group called B complex, this vitamin family works together, however each of the B vitamins has unique function. All B vitamins help the body convert food (carbohydrates) into fuel (glucose), which the body uses to produce energy. These B vitamins, help the body metabolize fats and protein. B-complex vitamins are needed for a healthy liver, skin, hair, eyes and nervous system function. This is a quick guide to each member of these important vitamins.

B1 Thiamin:

Thiamin is needed to produce cellular energy from the food, it also supports normal nervous system function. It is rare to be deficient in thiamine, although alcoholics, people with Cohn’s disease, anorexia, and those undergoing kidney dialysis may be deficient. Symptoms of thiamine deficiency include:

Abdominal discomfort

Thiamine plays a crucial role in metabolic reactions. Your body needs it to form adenosine triphosphate (ATP), which every cell of the body uses for energy. Thiamine deficiency can occur in alcoholics, people with Cohn’s disease, anorexia, and those undergoing kidney dialysis may be deficient. Symptoms of thiamine deficiency are:
Abdominal discomfort
People with thiamine deficiency have trouble digesting carbohydrates. This allows a substance called pyruvic acid to build up in the bloodstream, causing a loss of mental alertness, difficulty breathing, and heart damage, a disease known as beriberi.

The most important use of thiamine is to treat beriberi, which is caused by not getting enough thiamine in your diet. Symptoms include:

Swelling, tingling, or burning sensation in the hands and feet
Trouble breathing because of fluid in the lungs
Uncontrolled eye movements (nystagmus)

Wernicke-Korsakoff syndrome is a brain disorder brought on by thiamine deficiency. Wernicke disease involves damage to nerves in the central and peripheral nervous systems. Malnutrition due to alcoholism is mostly the cause. Thiamin is found in lentils, beans, meats, yeast, nuts, sunflower seeds, peas, milk, cauliflower, spinach.

B2 Riboflavin:

Also known as vitamin B2, riboflavin supports cellular energy production. Riboflavin is found in a variety of foods such as fortified cereals, milk, eggs, salmon, beef, spinach and broccoli.

B3 Niacin:

Niacin is also known as vitamin B3, and supports cellular energy production. Niacin, in the form of nicotinic acid, helps support cardiovascular health. Good sources of niacin include beef, poultry and fish as well as whole wheat bread, peanuts and lentils.

B5 Pantothenic Acid:

Pantothenic acid, also known as vitamin B5, is widely available in plant and animal food sources and helps support cellular energy production in the body. Sources include organ meats (liver, kidney), egg yolks, grains, avocados, cashew nuts, peanuts, lentils, soybeans, brown rice and milk.

Vitamin B6:
Involved in over 100 cellular reactions throughout the body. Vitamin B6, also known as pyridoxine, is needed to metabolize amino acids and glycogen (the body’s storage form of glucose), and is also necessary for normal nervous system function and red blood cell formation. Vitamin B6 is found in foods such as meat, poultry, eggs, bananas, fish and cooked spinach.


Biotin, or vitamin B7, is found in brewer’s yeast, strawberries, organ meat, cheese and soybeans. For those who are biotin deficient, studies show that biotin may help support healthy hair, skin and nails. Biotin also supports carbohydrate, protein and fat metabolism.

Folic Acid:

Also known as vitamin B9, folic acid is most commonly known for its role in fetal health and development as it plays a critical role in the proper development of the nervous system. This important developmental process occurs during the initial weeks of pregnancy, and so adequate folic acid intake is especially important for all women of childbearing age. Good sources are dark green leafy vegetables such as well as brewer’s yeast, liver, beets, dates and avocados.

Vitamin B12:

Vitamin B12, or cobalamin is also needed for DNA synthesis, proper red blood cell formation and for normal nervous system function. B12 is predominantly found in foods of animal origin such as chicken, beef, fish, milk and eggs.


Vitamin B12 Deficiency and Brain Health.

Vitamin B12 Deficiency and Brain Health.
By Renata Trister DO

Vitamin B12 has a role in red blood cell production. Deficiency states may result in pernicious anemia. B12 supports myelin (which allows nerve impulses to conduct) and when this vitamin is deficient, symptoms of dementia, multiple sclerosis, impaired gait, and sensation may appear. Vitamin B12 also has a role in psychiatric symptoms such as depression, anxiety and fatigue.

The one-carbon cycle refers to the body’s use of B vitamins as a “methylator” in DNA synthesis and the management of gene expression. There are three concepts that relate to B12’s role in chronic, neuropsychiatric symptoms:


This process marks genes for expression (like a small tag); it is also critical for detoxification and elimination of chemicals and hormones (estrogen), building and metabolizing neurotransmitters, and producing energy and cell membranes.

Homocysteine cycling

B12 is a primary player in the one-carbon cycle and a co-factor for the methylation of homocysteine by activated folate, to recycle it back to methionine. Subsequently, SAMe is produced, the body’s methyl donor.

Genetic override

Sufficient supply of an activated/bioavailable form of a vitamin (methylfolate vs folic acid) is even more necessary in the setting of gene variants such as transcobalamin II, MTHFR, and MTRR which may function less optimally in certain individuals and result in pathology under stress. An example of the importance of this is a report of death in a B12-deficient patient with genetic variants who underwent anesthesia with nitrous gas. As the B12 blood level was normal, this fatality was attributed to functional deficiency, indicating that having available B vitamins does not guarantee proper utilization. Therefore, supplementing with activated forms of B vitamins can enhance the ability to support cellular processes.

Causes of B12 Deficiency

If it is established that a person has overt deficiency (in blood) and/or they respond to treatment, it is important to also find the cause. These are some considerations:

1. Achlorhydria or low stomach acid, occurs in low thyroid function, chronic stress, aging, and – acid blocking medications.

An example:

A patient is eating foods that they are unable to properly digest and this causes local inflammation. These foods may include processed dairy, foods fried in vegetable oils, and sugars. Inflammation further perpetuates improper digestion and slow food transit. The patient feels the reflux of this immobile, poorly digested food, and this is often seen as a sign of high stomach acid. Patients begin using long-term antacids because they feel better. Long-term use is linked to pathogenic overgrowth of bacteria, fracture, and nutrient deficiency. Stomach acid is critical for triggering digestive enzymes, “intrinsic factor” for B12 absorption and managing local microbial populations.
When this kind of digestive imbalance goes unattended, B12 deficiency can occur, along with symptoms that will suggest a need for an antidepressant and the medications begin to grow.

2. Dietary Restrictions

Animal foods are primary sources of B12, although algae and fermented foods are promising options for some dedicated vegans. Stores deplete over time, and deficiency-related symptoms may present long after dietary restriction.

3. Autoimmune

One of the possible mechanisms of deficient B12 absorption is pernicious anemia, an autoimmune reaction on parietal cells, associated with atrophic gastritis in the stomach.

4. GMO/Gluten

There seems to be a powerful synergy of gluten-containing and genetically modified processed foods. This may have an impact on digestion of many. The innate immune system responds to gluten in these grains, and food fragments may pass directly into the blood stream through gated tight junctions. Direct inflammation and damage to the cells in the small intestine may result.

Genetically modified corn may be playing a part in small intestinal villous changes as demonstrated in a study of mice consuming corn oil. There is also reason to believe that Bt-toxin from Monsanto’s GMO corn plays a role in intestinal permeability as it was found in the blood of 93% of pregnant women and 80% of their fetuses. The herbicide itself also drastically changes the gut flora, killing beneficial bacteria.

5. Medications Metformin is a risk factor for B12 deficiency in some.


Treating B12 deficiency, while the underlying cause is being determined is needed. The use of the activated form of vitamin B12 is effective at improving levels. Cyanocobalamin is a synthetic form of B12 that has been bound to a cyanide molecule while hydroxy, adeno, and methyl are all forms of B12 that are found naturally, in the body. The injectable form may yield a powerful effect over the oral form. Supplements may take time to improve symptoms (30 days or so).


A. M. Ercolini and S. D. Miller

A. M. Ercolini and S. D. Miller (review by Jon Trister MD)
There are many identified autoimmune diseases . Multiple factors are thought to contribute to the development of immune response to self, including genetics, age and environment. In particular, viruses, bacteria and other infectious pathogens are the major postulated environmental triggers of autoimmunity.
Multiple arms of the immune system may be involved in autoimmune pathology. Antigens are taken up by antigen- presenting cells (APCs) such as dendritic cells (DCs) and macrophages and processed into peptides which are loaded onto major histocompatibility complex (MHC) molecules for presentation to T cells via clonotypic T cell receptors (TCRs). Cytolytic T cells (Tc, activated by MHC Class I on APC) can directly lyse a target, while T helper cells (Th, activated by MHC class II) release cytokines that can have direct effects or can activate macrophages, monocytes and B cells. B cells themselves have surface receptors that can bind surface antigens. Upon receiving signals from Th cells, the B cell secretes antibodies specific for the antigens. Antibody may bind its specific target alone or may bind to and activate macrophages simultaneously via the Fc receptor.
There are multiple mechanisms by which host infection by a pathogen can lead to autoimmunity.The pathogen may carry elements that are similar enough in amino acid sequence or structure to self-antigen that the pathogen acts as a self-‘mimic’. Termed ‘molecular mimicry’, T or B cells that are activated in response to the pathogen are also cross- reactive to self and lead to direct damage and further activation of other arms of the immune system. The pathogen may also lead to disease via epitope spreading. In this model the immune response to a persisting pathogen, or direct lysis by the persisting pathogen, causes damage to self-tissue. Antigens released from damaged tissue are taken up by APCs, and this initiates a self-specific immune response. ‘Bystander activation’ describes an indirect or non-specific activation of autoimmune cells caused by the inflammatory environment present during infection. A domino effect can occur, where the non-specific activation of one arm of the immune system leads to the activation of other arms. Lastly, infection may lead autoimmunity through the processing and presentation of ‘cryptic antigens’. In contrast to dominant antigenic determinants, subdominant cryptic antigens are normally invisible to the immune system. The inflammatory environment that arises after infection can induce increased protease production and differential processing of released self-epitopes by APCs.
Coxsackievirus B
Coxsackievirus B (CVB) is the most common cause of infectious myocarditis. Infectious virus and viral RNA can be isolated from patients’ hearts.CVB3 can cause myocarditis in mice; in most mouse strains, the virus titre peaks at day 4 post-infection and is undetectable after 14 days. The chronic stage of the disease (day 28 onwards) is characterized by mononuclear cell infiltration into the myocardium and the production of antibodies to cardiac myosin which, because of the absence of virus, argues for autoim- munity as the pathophysiological mechanism at this stage of disease. In vitro, cardiac myocytes can be infected and lysed by the virus and CVB infection causes myocardial destruction.
This damage may lead to autoimmunity via epitope spreading. In mice, virus-specific antibodies arise soon after infection, followed by antibodies to several cardiac proteins such as myosin, tropomyosin and actin.
While these studies show that numerous autoimmune mechanisms can lead to cardiomyopathy in infected mice, it remains uncertain if autoimmunity accounts for the pathology seen in humans.

Streptococcus pyogenes: group A strepcococcus
Infection with S. pyogenes can lead to inflammation of the heart, and the involvement of lymphocytes in cardiac pathology has been suggested for some time.
Studies have shown that bacterial materials and DNA can persist in host tissue for some years after infection, so it is possible that ongoing immunity against the bacteria may lead to bystander damage to the organ. However, it is accepted most predominantly that the autoimmune reaction is caused by molecular mimicry. Myosin has been identified as the dominant autoantigen in the heart, and myosin-reactive mAb derived from patients with acute rheumatic fever were shown be cross-reactive to both M protein (the major virulence factor of group A streptococci) and the streptococcus carbohydrate epitope N-acetylglucosamine.
Although somewhat controversial , infection with S. pyogenes has also been associated with the development of movement and behavioural disorders such as Sydenham chorea, Tourette’s syndrome and obsessive–compulsive disorder . Patients with these disorders often have antibodies to the basal ganglia in the brain, and molecular mimicry between basal ganglia and S. pyogenes-derived proteins remains the major postulated mechanism of disease induction. An early paper demonstrated antibody cross-reactivity between S. pyogenes membrane and neuronal cytoplasm in patients with Sydenham chorea .
Using serum, cerebrospinal fluid (CSF) and mAb derived from Sydenham chorea patients, dual-specific antibodies were found that react with both the immune-dominant carbohydrate epitope on S. pyogenes cell wall (GlcNAc) and with lysoganglioside GM1 on the surface of neurones. The same group demonstrated that GlcNAc-reactive antibodies from the sera of patients with pediatric autoimmune neuropsychiatric disorders associated with streptococci was inhibited by lysoganglioside GM1, and that lysoganglio- side GM1-reactive mAb from Sydenham chorea patients could also react with intracellular brain protein beta-tubulin.

Trypanosoma cruzi
Chagas disease is caused by infection with the protozoan parasite T. cruzi. 10–30% of infected individuals develop the disease, which occurs in two major clinical phases, acute and chronic. The acute phase is characterized by parasitaemia, preferentially in heart muscle cells, and inflammatory infiltration of infected tissue. This is followed by an asymptomatic indeterminant phase, which can last up to 30 years. Patients who progress to the chronic phase of the disease are affected mainly by irreversible cardiomyopathy.Although it has been suggested that parasite persistence can contribute to chronic Chagas disease cardiomyopathy (CCC), T. cruzi antigens and DNA can also be detected in infected people who remain asymptomatic. This suggests that the tissue destruction that characterizes this phase may be largely autoimmune. CCC is characterized histopathologically by mononuclear cell infiltrates, with CD8+ T cells outnumbering CD4+ T cells 2:1. Local production of interferon (IFN)-g, TNF-a, IL-4 and IL-6 has been reported. In addition, real-time polymerase chain reaction (PCR) analysis showed selective up-regulation of IFN-g-inducible chemokines and chemokine receptors in CCC heart tissue. Collectively, these data suggest that bystander tissue destruction mediated by inflammatory cytokines (especially IFN-g) may play a role in CCC pathology. Although the chronic phase usually affects the heart, a subset of patients develop motor dysfunction of the gastrointestinal tract, essentially through the destruction of neurones of the enteric nervous system. It was discovered that antibodies raised in rabbit against a flagellum- associated surface protein on T. cruzi (FL-160) are cross- reactive with a 48-kDa protein found exclusively in nervous tissue [79]. It was then found that antibodies raised against the amino terminus of FL-160 react to a different epitope on mammalian sciatic nerve than antibodies raised against the carboxyl terminus. The medical relevance of this apparent mimicry is uncertain, as the ability of human sera to react to FL-160 did not correlate with clinical disease. Other studies have also shown molecular similarity between T. cruzi antigens and antigens from mammalian nervous tissue.
Borrelia burgdorfeii
In the United States, Lyme disease is caused by the tick-borne spirochete Borrelia burgdorfeii (Bb). Sixty per cent of untreated patients develop arthritis that can last for several years, mainly in large joints such as the knee. These patients have high titres of Bb-specific antibodies, and Bb DNA can be detected in the joint fluid by PCR. Treat- ment of these patients with antibiotics usually ameliorates the arthritis, which indicates that bystander inflammatory response to the spirochete is responsible for early Lyme arthritis. A subset of patients will progress from acute to chronic arthritis despite treatment with antibiotics and lack of detectable Bb DNA in synovial fluid. Antibiotic- resistant Lyme arthritis is associated with the MHC class II alleles human leucocyte antigen (HLA)-DRB1*0401, *0101 and *0404, indicating that its mechanism is T cell-mediated and distinct from acute Lyme arthritis. Cellular and humoral responses to outer surface protein A (OspA) of Bb develop in around 70% of patients with antibiotic-resistant Lyme arthritis, often at the beginning of prolonged arthritic episodes. T cell and humoral responses to OspA, but not to other spirochete antigens, were found to correlate with the presence or severity of arthritis. Synovial fluid mono- nuclear cells from patients with antibiotic-resistant arthritis produced IFN-g in response to both OspA and LFA1a, suggesting that mimicry between these two proteins may cause the inflammation associated with arthritis. LFA-1a has also been identified in the synovia of patients with antibiotic-resistant Lyme arthritis.
Neurological complications, including myelitis and peripheral neuropathy, can occur in 10–12% of untreated patients infected with Bb and can arise even after antibiotic treatment. Patients with chronic neuroborreliosis have been reported to have antibodies reactive to nerve axons in their serum, as well as antibodies and T cells specific for myelin basic protein (MBP) in spinal fluid. Patient serum that was reactive to axons and neuroblastoma cells was also cross-reactive with Bb flagellin.
Next, it was discovered that a mAb for flagellin was cross-reactive with human heat shock protein 60 and with neuroblastoma cell lines and slowed neurite outgrowth in culture. Antibody cross- reactivity has also been described between human central nervous system (CNS) proteins and Bb OspA.

Herpes simplex virus
Herpetic stromal keratitis (HSK) is caused by corneal infection by herpes simplex virus (HSV) and can lead to blindness. Whereas progression from epithelial infection to stromal keratitis is not prevented by antiviral drugs, the symptoms of HSK can be alleviated with immunosuppressive drugs such as corticosteroids, indicating that HSK is an autoimmune disease. Because of the difficulties associated with studying the disease in humans, much of the characterization of HSK has utilized murine infection with HSV-1. Within 72 h of infection proinflammatory cytokines IL-1 and IL-6 are produced, which leads to influx of neutrophils into the corneal stroma. In humans, T cells may cause pathology via bystander destruction.
Uveitis is a group of intra-ocular inflammatory diseases that are potentially blinding.
It is believed that many sub- groups of this disease are autoimmune-mediated, in part because of the strong association with certain HLA alleles. Humoral and cellular responses to the retinal antigens interphotoreceptor retinoid binding protein and S-antigen are well characterized in humans and animal models in rodents and primates (experimental autoimmune uveitis, EAU) are based on injecting these proteins in complete Freund’s adjuvant. Singh et al. identified a CD4+ T cell epitope in human S-antigen and several virus and Escherichia coli-derived peptides with sequence similarity rotavirus and bovine milk casein . In the same study, patients with uveitis were found to have an increased T cell and antibody response to S-antigen and the two identified mimics compared with healthy donors. Aside for a report of an outbreak of uveitis in children after echovirus infection, no pathogen has yet to be associated epidemiologically with uveitis.
Type I diabetes (T1D) results from autoimmune destruction of pancreatic cells by autoreactive T cells and/or inflammatory cytokines. Although there is a definite genetic component to T1D, the concordance rate in monozygotic twins is only approximately 40%, and epidemiological evidence suggests that pathogens play a role in development. Many different viruses have been associated with T1D development. Studies showed a higher incidence of T1D in people with congenital rubella and antibodies to pancreatic islet cells in rubella- infected patients. Similarly, Cytomegalovirus (CMV) was isolated from T1D patients and antibodies to pancreatic islet cells detected in CMV-infected patients. It was also noted that mumps infection often preceded the onset of T1D in children. A convincing study showed that Coxsackievirus (CVB4) isolated from the pancreas of acute-onset patients could induce diabetes upon transfer into susceptible mice. CVB4-specific IgM antibodies could be detected in children newly diagnosed with T1D. There is some evidence that CVB4 may cause T1D via molecular mimicry. T cells isolated from T1D patients reacted with both glutamic acid decarboxylase (GAD-65) (an identified autoantigen in T1D) and protein 2C in CVB4. However, another study did not observe similar T cell cross-reactivity, and yet another showed that cross-reactivity was observed in both diseased patients and healthy controls. As the virus has also been shown to replicate in exocrine pancreas, it is possible that cytokine release and HLA up-regulation following mumps virus infection may lead to autoimmunity.
Guillain–Barré syndrome
Guillain–Barré syndrome (GBS) is a paralytic illness affecting both myelin and axons of the peripheral nervous system. Several studies have demonstrated anti-glycolipid antibodies in the serum of a proportion of patients .There are different clinical variants of the disease, which can correlate with the specific type of glycolipid targeted by the antibodies. Glycolipids found most commonly in neural tissues include the Gangliosides and Cerebrosides. Onset of GBS occurs days or weeks following an infection or immu- nization. Although several microorganisms have been associated with GBS development, Campylobacter jejuni is the most extensively studied pathogen as it is a common antecedent to GBS. In addition, there is mounting evidence suggesting that lipopolysaccharide (LPS) on the outer core of the bacteria can mimic host gangliosides. LPS from C. jejuni serotypes associated with GBS were shown to resemble human Several studies have shown that C. jejuni serotypes associated with GBS are more likely to contain ganglioside-like epitopes compared with serotypes isolated from C. jejuni-infected patients with gastroenteritis but no neurological symptoms, with one study linking ganglioside mimicry to specific GBS clinical subtypes.Patients infected with Mycoplasma pneumoniae prior to the development of GBS often have antibodies to galactocerebroside. These antibodies can cross-react with glycolipids on M. pneumoniae Associated antibodies to GM1 have also been reported. Similar to what occurs following C. jejuni infection, patients infected with Haemophilus influenzae can develop antibodies to bacterial LPS that are cross-reactive with ganglioside. The presence of a ganglioside-like structure on the surface of H. influenzae suggests that molecular mimicry may explain its association with GBS induction.
Multiple sclerosis
Multiple sclerosis (MS) is characterized by a loss of the myelin sheath surrounding axons in the CNS. Demyelination is associated with elevated levels of CD4+ T cells specific for major myelin proteins, and the disease is generally thought to be autoimmune. Although it is not known precisely what triggers the development of MS, it is well established that relapses or disease flares in patients diagnosed with the relapsing–remitting form of MS are often associated with exogenous infections, particular upper respiratory infections. In total, more than 24 viral agents have been linked to MS. Most of the associations have been circumstantial, but some studies have found evidence of specific pathogens in human tissue. Antigens from herpesvirus type 6 were found in MS plaques but not from tissues from other neurological disorders. Similarly, compared with CSF from patients with other neurological diseases, CSF from MS patients was shown to have higher levels of the bacteria Chlamydia pneumoniae. In vitro studies have also provided evidence linking MS and infectious agents. Despite the difficulty in linking MS to any one pathogen, the amount of epidemiological evidence reported over the years shows that environmental factors play a strong role in disease development, and suggests that a cumulative lifetime exposure to certain microorganisms can influence disease development. In addition, a recent study showed that the degree of concordance for monozygotic twins (generally reported at 40% or less) was influenced by environmental factors.
The immune system has evolved checks and balances to prevent the destruction of host tissue. It is perhaps not surprising that a strong immune response to an invading pathogen could disrupt this regulation and lead to autoimmunity. There is significant evidence suggesting that different classes of pathogens (bacteria, viruses and parasites) are involved in triggering or propagating self- reactive immune responses. However, the evidence for a definitive link for infection-induced autoimmunity is stronger for certain diseases than for others.
The argument for infection-induced pathology is much stronger for diseases associated with one or two specific pathogens than for diseases with multiple causal associations. For example, the fact that infection with C. jejuni is a common antecedent to GBS makes a strong argument that this disease is infection-triggered. In contrast, for diseases such as TID and MS that have been associated with dozens of pathogens, but none in particular, much more needs to be done to make a convincing case. The most compelling proof
would be the disappearance of symptoms with the clearance of the infection. This is the case in Lyme disease, where treatment with antibiotics alleviates acute arthritis. There are many ways a pathogen can cause disease even after the infection has been cleared. In these cases, epidemiological studies showing that people infected with a particular agent have an increased incidence of these diseases compared with people never infected, while not wholly definitive, would certainly strengthen the infection-induced autoimmunity argument.
In human autoimmune diseases, where direct evidence for a role for a particular pathogen is still uncertain, it is all the more important to have supporting animal models. The strongest support comes from animal models in which infection with the agent thought to induce disease in humans causes similar symptoms in animals, as exemplified by induction of heart disease in mice infected with T. cruzi and CVB and arthritis in mice infected with Bb. In other animal models, disease can be shown to be induced by priming with a pathogen-derived antigen, thus strengthening the argument for the involvement of that pathogen in the human disease. The ability to induce heart disease in rats primed with Streptococcal M protein is strong evidence that S. pyogenes causes heart disease in humans via molecular mimicry. Although the link between S. pyogenes infection and neurological disorders in humans is uncertain, at best, the fact that movement and behaviour disorders can be induced in mice primed with S. pyogenes homogenate also lends credibility to that theory. In cases where it is uncertain whether a disease pathology is actually autoimmune (such as uveitis and myocarditis following CVB infection), animal models have played a crucial role in elucidating the potential mechanisms of disease induction.
The heterogeneity of the human population, rather than the weakness of the data, may be in play in instances where the evidence linking infection and autoimmunity is tenuous or even conflicting. It is not difficult to imagine that some people may be more susceptible to developing autoimmune disease following a particular infection than others, or that mimic peptides derived from different infectious agents may be able to trigger a particular autoimmune disease depending on the ability of the infected individual to present various epitopes in the context of their various HLA molecules. Defining the genetic markers that predispose patients to different autoimmune diseases with a suspected infectious trigger would be an important contribution to defining the underlying disease pathogenesis.