All posts in For Patients

Gerald J Domingue MD

“Demystifying Pleomorphic Forms in Persistence and Expression of Disease: Are They Bacteria, and Is Peptidoglycan the Solution?”
Review by Jon Trister MD
The interaction of microbes within the host can lead to the enhancement or depression of their individual properties. Clinical expression of their presence in the host depends on the genetic vulnerability of the host, the particular environmental stresses, and the number and location of such consortia. The clinician who faces this tangled scenario must quantitate and define the dynamic that has led to the patient’s illness.
Many bacteria-like elements can be visualized at the ultra-structural level, but cannot be grown in culture. Nucleic acid analyses in vitro can approximate the locations of these bacteria on the phylogenetic tree. Unfortunately, none of these sophisticated laboratory procedures are consistently successful in identifying pleomorphic organisms persisting in tissues, nor are they guides to optimal therapy.
Pleomorphic, cryptic organisms, whether intra- or extracellular, are ubiquitous. A first step would be to demonstrate their presence in tissue samples when laboratories report culture negative findings in patients suspected of having a bacterial infection; or to attempt to grow them in culture. Quantifying and identifying the cells most parasitized are impractical routine clinical approaches. Koch’s postulates cannot be fulfilled, because it is impossible to precisely duplicate all the variables that are involved in disease expression.
Any patient with a history of recurrent infections and persistent disability is sending signals that this phenomenon is occurring. The autoimmune disorders, in which no organisms can be identified by routine techniques, are suspect in this regard. The selection of antimicrobial agents for patients with cryptic infections can be quite frustrating. Even if an organism grows in vitro, it may not represent the primary pathogen. In addition, drug susceptibility testing fails to reveal the action of the agent on the infecting organism’s toxicity and capacity to adhere to cell membranes in vivo.
Although physicians are discouraged from the indiscriminate use of antimicrobial agents without strong cultural, immunologic, or molecular evidence that the therapy is appropriate and that the severity of the illness justifies the risk of side effects, it is, nevertheless, a common clinical practice and undoubtedly contributes to the development of pleomorphic, persisting bacterial forms and mutants in vivo.
Survival of a species requires that a reasonable identity be maintained. Over time, mechanisms to maintain “self” have evolved. Many such relationships have been so successful that both host and invading organism benefit. Such a process, which transiently reduces immune competence, can occur episodically in healthy subjects in association with various stresses .
As one ages, there tends to be an insidious accumulation of intracellular microbial forms. Such quiescent organisms tend to be activated to a more toxic form when homeostatic disturbances threaten their cellular loci. The numbers and locations of cells involved with one or more types of organisms determine the clinical reaction. It can be very difficult to decide whether a new illness is due to a new organism or to an interaction with one or more pleomorphic cryptic organisms. These interactions can be as complex as the well-known increase in toxicity of Corynebacterium diphtheriae when this bacterium is infected by bacteriophage. The distinction between phage genes and bacterial genes is blurred with respect to both function and reality. It is conceivable that much of the heredity of bacteria is of viral origin, because many unknown defective proviruses may exist in nature; on the other hand, phages may be fragments of bacterial DNA that have acquired the capacity for independent reproduction. Indeed, with a history of mutual interaction of viruses and bacteria over the course of evolution, the endeavor of sharply distinguishing their genes must be meaningless. These philosophic concepts are implicit in any discussion of the role of dormant, persistent, difficult-to-culture, and impossible-to-culture bacteria in disease (Domingue and Woody, 1997).
From the evidence available in the literature, it seems that mycoplasmas are a diverse group of wall-less prokaryotes derived from various bacteria. It has been convincingly demonstrated by immunologic methodology that acholeplasmas are descended from streptococci, specifically from groups N and D. It therefore seems logical to conclude from molecular and immunologic data that mycoplasmas are not a true phylogenetic class and that they are not descended from one single common ancestor. A teleologic approach to the evolutionary relationship between mycoplasmas and cell wall-defective/deficient bacteria should consider the survival advantage of an organism with a cell wall in a hostile primordial environment. Only after the appearance of higher life forms was there a protective niche for mutant microorganisms (Domingue and Woody, 1997).
If we are to extend these findings to clinical relevance, it is tempting to speculate that in vivo genetic events may lead to development of bacteria with aberrant cell wall morphology and physiology and may involve complex interactions among a variety of bacteria and host cells. Such interactions might lead to persistence of a dormant bacterial phase in patients with infectious diseases. This may be a continual biologic process in all living hosts, with the host environment serving as the determinant for evolution, persistence, and survival of morphologically altered microbes. Previously described, newly published, provocative, molecular microbiological data lend credence to the hypothesis and corroborate the multiplicity of pleomorphic forms that develop during reproduction of L-forms in vitro. Recent studies on modifications of gene expression and modes of division for stressed bacteria are highly relevant to the hypothesis. It is proposed that in vivo persistence of these bacterial elements escape immune surveillance partially, completely, or may integrate with host cell organelles to create bacteria-host-cell-antigen complexes which could provoke immunopathologic consequences. To speculate further, bacterial persisters in a scenario of molecular mimicry might possess peptide sequence similarities with self peptides sufficient to result in cross-activation of autoreactive T or B cells by pleomorphic form derived peptides.
Might there also be an analogous situation to that of H. pylori growth in the human stomach: Do persistent atypical bacterial forms produce enzymes which neutralize hostile host factors creating a more hospitable tissue environment; and are there microbial factors antagonistic to white blood cells preventing their migration to the infectious site or scene of pleomorphic form persistence? Furthermore, there may be an exchange of genetic material between the persisting prokaryote nucleoid (oncogenic plasmids or unknown nuclear interactions) and host eukaryotic chromosome creating cellular alterations adequate to initiate neoplastic growths.
Scientists skilled in disciplines such as cellular adhesion, transposition of genetic elements, and microbial reassembly as mechanisms for the genesis of unusual organisms should be able to design, execute, and interpret experimentation that will confirm or refute, unambiguously, the proposed hypothesis. If pleomorphic forms in tissues are confirmed as bacteria by sensitive and specific methodology, the clinical and research implications are unlimited; and have the potential for clarifying the mysterious and poorly understood host-pathogen interactions in persistent infections and expression of innumerable idiopathic diseases.


The common pathogenesis of Alzheimer’s disease and diabetes.

The common pathogenesis of Alzheimer’s disease and diabetes.
By Renata Trister DO

Recent studies show new evidence that Alzheimer’s disease and type 2 diabetes share common features in their pathophysiology. Insulin resistance is a characteristic feature of both diseases. Glucose metabolic disorders, related to Alzheimer’s disease, are type 2 diabetes, and pre-diabetes/metabolic syndrome. Based on the common pathophysiology of these two diseases, Alzheimer’s disease is by some called type 3 diabetes. This is yet another example of chronic illnesses that caused by modern diets and lifestyle habits. Diets high in refined carbohydrates lack of sleep and physical activity all contribute to insulin resistance. In the research on dementias, insulin resistance has much documented harmful effects on cognitive function. Insulin-like growth factor also influences cognitive functions. Insulin resistance causes glycation and oxidative stress on the brain. In Alzheimer’s brains, amyloid deposition, hyper-phosphorylation of tau proteins and neurofibrillary tangles, are characteristic features. Amyloid ß is co-secreted in the ß-cells of the pancreas with insulin. Amyloid ß and hyper-phosphorylated tau protein can be found in the Langerhans islets (in autopsy). Amyloid deposits, found in the pancreas and brain are similar. As a result of hyperglycemia, glycation end products cause the development of amyloid plaques, neurofibrillary tangles; these are all typical in Alzheimer’s disease. Hyperglycemia leads to oxidative stress, which plays significant role in the development of both illnesses. Low-grade inflammation is also a significant pathophysiological factor in both disorders. The sources of this inflammation are inflammatory adipo-cytokines, dysbiosis, and metabolic endotoxemia, caused by lipopolysaccharides. Cerebral glucose metabolism is also impaired in Alzheimer’s disease. A reduced presence of insulin and resulting decrease in cerebral glucose metabolism creates an energy crisis in the brain. Neurons are unable to harvest energy and basically starve. In order to conserve energy, these affected neurons degrade axons and dendrites. The retraction of these projections results in damaged synapses and cell communication loss. Symptomatically, this presents as cognitive impairment. Another possible etiology of this glucose deficit is reactive hypoglycemia. Reactive hypoglycemia is low blood glucose that occurs within four hours after eating, especially high glycemic foods. After eating sugary foods, blood glucose levels spike rapidly and become very high. In response insulin is produced. Reactive hypoglycemia results from having too much insulin produced in response to eating, leading to low blood glucose levels. This happens chronically and can be very damaging. During waking hours the symptoms are quickly ameliorated by having another snack. However, consuming sweets at night, this hypoglycemia goes unnoticed and not corrected. This hypoglycemic state continues until you wake up and eat. Consequently cells in the body have an energy deficit. Alzheimer’s disease is a heterogeneous disorder, and as yet there is no effective therapy. Encouraging results have emerged by using intranasal insulin spray. Insulin sensitizers like metformin, have shown some improvements in cognitive functions, mainly in animal experiments. The real breakthrough comes from prevention of both chronic diseases via a healthier life-style. Reducing refined carbohydrates in diet appears essential.


Vitamin C

In 1928, Albert Szent-Gyorgyi discovered Vitamin C> He won Nobel Prize in 1937 for its discovery.
Man , monkey are unable to synthesize vitamin C which make them dependable on exogenous sources.
Vitamin C is NOT an Ascorbic Acid. Ascorbic acid is a PART of Vitamin C Complex which also, in addition , includes Vitamin P complex ( bioflavonoids).
Through recorded history, Scurvy was the scourge of armies, explorers, and sailors on extended trips without fresh food, until they learned to include an adequate source of vitamin C, such as lime juice, in their diet.
Function of Vitamin C:
1.Collagen synthesis
2.Degradation of protein to amino acids
3.Synthesis of neurotransmitters.
4.Most active reducing agent
Collagen is the most abundant structural protein in the body tissues. Collagen is a foundation of structural integrity of all organs.Collagen ( and vitamin C) is essential for the deposition of the calcium phosphate crystals to form mature bone.Vitamin C provides the collagen needed for elastic vessel wall and required for synthesis of the essential neurotransmitters-epinephrine and serotonin.Vitamin C is important for detoxification, stress response,reduces susceptibility to infections.
Vitamin C is needed for the hydroxylation of the amino acids lysine and proline to proto-collagen molecule.
Initially, scorbutic patients presents with weakness, lassitude, irritability, and vague aching pains in the joints and muscles.They may complain of weight loss. Later, as the disease progresses easy bruising and even hematoma in the skin and muscles develop.
The gums become swollen, red and bleed easily.
Perifollicular hyperkeratotic papule develop.
Deficiency in the USA due to inadequate dietary intake, smoking, alcoholism, intestinal dysfunction and in patients with psychiatric illnesses.
Vitamin C is present in fresh fruits and vegetables, and especially deep green buckwheat juice.This juice contains high quality of Vitamins C, P and Rutin.


Anti-Candida diet

By Renata Trister DO

Most of the anti Candida diets recommend removing sugar, starch, alcohol, and refined foods–candida’s preferred food sources. However, cutting all starchy carbs with a very low carb diet may not be the optimal plan, and studies indicate that yeast may actually feed on the ketones that result from a very low carb diet. So cutting all starches and sources of glucose isn’t a great idea. The best diet will depend mostly on you. We each have a gut microbiome as unique as our fingerprint. If you have leaky gut, intestinal inflammation, or malabsorption issues, you may fare well on the specific carbohydrate diet or low FODMAP diet that limits hard-to-break -down starches (see links below for more information). When a compromised digestive tract can’t fully break down these complex starches (grains, potatoes, certain legumes), they ferment, feed yeast, and cause gas and bloating.

There is a 3-part process used to kill candida overgrowth. It involves starving the candida, killing it and reinoculating the gut with good bacteria. Note that you may need to complete this cleanse more than once to completely get rid of it. Plan on 8 weeks.
Starve it.
Eliminate gluten, dairy, refined white sugar, soy, processed foods, corn, and ideally grains (gluten free grains can be excepted) Focus on organic eggs and animal protein + vegetables and good fats. Note that diet alone will not kill the yeast overgrowth! You have to combine diet with herbal protocol.
• Consume high quality, hormone-free protein at each meal from sustainable, antibiotic-free sources: Wild, cold water fish; free-range chicken & turkey; properly prepared legumes (soaked); cage free eggs; beef/bison; lamb
• Eat plenty of fresh vegetables: lightly cooked, sautéed, steamed, and raw. Focus on leafy greens and cooked cruciferous
• Use good quality fats for cooking: olive oil, coconut oil, and ghee. Avoid vegetable oils!
• Drink filtered water (6 – 8 glasses/day to help flush toxins)
• Drink 2-3 cups of Pau d’arco herbal tea daily, and bone broth. Bone broth heals the gut and Pau d’Arco helps kill yeast.
• Add fermented foods such as raw kraut, kefir or kimchi (recipe video link below).
• Take 1-3 tbsp. of coconut oil daily. It’s a powerful yeast killer and boosts metabolism.
• Take 1 tsp. apple cider vinegar in a little water if needed to help digestion and detox. Avoid all other vinegars! Candida feeds on the sugars produced from this type of fermentation.

Foods to Avoid
Aged Cheeses & Dairy Products Conventional dairy contributes to inflammation, and many people are dairy sensitive. Raw dairy is ok occasionally if you’re not sensitive. Fermented dairy (kefir, preferably raw) is ok occasionally if not dairy sensitive, but dairy contributes to dampness in the body.
Additives & Preservatives Anything you can’t pronounce on a food label = trouble.
Conventional Meats & Eggs Use only grass-fed meat products, free-range eggs, and chickens. Non-organic animal proteins contain antibiotics and steroids that contribute to inflammation.
Alcohol Sugar in the alcohol (wine, beer, spirits) is a food source for candida
Over-use of coffee Coffee is acidic, depletes minerals and thins the gut lining. Use green teas and herbal teas.
Fruits The high sugar contents of fruits makes Candida thrive; so stay away from sweet fruits! (Exceptions are berries, lemons, limes low sugar fruits.) You may drink fresh green juice as long as the fruit content is minimal.
Gluten & Grains Avoid anything made from wheat, rye, and barley.
Peanuts Peanuts carry a mold called aflatoxin that contributes to toxins in the body.
Condiments and YEAST in any form Condiments (chutneys, mustards, preserves, ketchup, relishes, vinegar, bottled dressings, etc.) tend to be high in sugars, corn syrup and preservatives. Vinegars feed yeast.

Killing The Candida.
Along with the diet, you’ll need to take herbs to kill off excess candida. You can start the diet and the herbs at the same time. The main antifungal supplements are the following: caprylic acid, pau d’arco, berberine, grapefruit seed extract, zinc, biotin, olive leaf extract and oregano oil. Take the herbs three times daily for at least 6 weeks. If you’ve tried to get rid of candida before unsuccessfully, you may need to rotate between different anti-candida products. Candida builds up a fast resistance to herbs.
Try some stress relief during this phase: meditation, yoga classes, walking, gardening, whatever relaxes and rejuvenates you. You may also use aloe to soothe the gut lining if there is inflammation. A digestive enzyme (Zypan or DiGest from Standard Process are good options) will help you break down food and excess toxins as the candida dies off. Drinking aloe juice is soothing to the gut and helps kill candida.
Warning: some will feel worse before they feel better. People report feeling achy, flu-like symptoms. This could be a reaction to the yeast dying off, which overwhelms detox pathways. This is called a Herxheimer reaction. Liver support tonics and activated charcoal can be used to help rid the body of toxins.
Reinoculate the gut with good bacteria and starve the remaining candida. This is done with a good quality probiotic along with naturally fermented foods.
Books and links on diets Body Ecology, GAPs & FODMAPS:
KIMCHI recipe video link: There is another white kimchi recipe on same site that is very good with easy to find ingredients.


Toxic Skincare and Beauty Products

Toxic Skincare and Beauty Products
Renata Trister DO
The skin absorbs about 60% of what we put on it and what is applied to the skin might be an even greater risk for toxin exposure than what you put in your mouth. When you eat, a vast system of digestion and excretion breaks down what’s ingested and flushes it out of the body. However, chemicals on the skin are absorbed into the bloodstream without such filtering.

The average woman uses 12 different personal care products contain 170 different ingredients everyday. An astounding number of personal skincare ingredients are linked to cancers, allergies, neurological disorders and reproductive issues. Understanding labels and finding alternatives is important. This article will discuss some of the most toxic ingredients to avoid and provide some alternatives.


Triclosan is an antimicrobial agent found in hand sanitizer, but is also added to soap, shampoo, and even tissues! It can be absorbed through the skin, and has been detected in human urine, serum, and breast milk. Triclosan hand sanitizer is probably THE MOST important ingredient to avoid. Hand washing with plain soap is healthier for you and everything around you.

Recent focus on the importance of our micro biome and the growing threat of drug resistant bacteria, the widespread use of unnecessary antibacterial agents has come under question. Studies as early as 2006 have expressed concern over bacterial resistance to triclosan, as well as the greater fear of triclosan-induced resistance to clinically important antimicrobial drugs. Just think of it this way by killing the 99.9% of bacteria (as some bottles claim) the resistant .1% get a greater chance to survive & multiply.

A study was released linking triclosan exposure to liver cancer in mice. In the study, triclosan acted as a cancer promoter, meaning it increased susceptibility to cancer and accelerated tumor formation after long-term exposure.

Triclosan has also been suspected as an endocrine disruptor, although a recent review of the literature concludes that triclosan exposure through the use of personal care products is unlikely to adversely affect endocrine function in humans (although this review was funded by the Colgate-Palmolive Company) and although there’s limited or no evidence that triclosan exposure through personal care products has harmful effects in humans, several studies have shown triclosan to adversely affect thyroid and reproductive function in rats.

Finally, triclosan antibacterial soaps do not provide any benefit over regular soap for preventing the spread of disease! There is no reason to use this and triclosan should be avoided all together.

Phthalates and Parabens

Phthalates and parabens are found in a variety of personal care products, although phthalates are more common in lotions because they act as moisturizers and enhance skin penetration of other compounds. Parabens are absorbed through the skin intact. Both chemicals have been detected in breast milk, urine, and plasma.

Phthalates and parabens increase the risk for breast cancer. An increased concentration of phthalate metabolites in the urine was associated with an increased risk for breast cancer, and intact parabens have been detected in breast cancer tissue. Phthalates have also been implicated in reproductive and endocrine disruption, although like triclosan, the evidence is preliminary.

Sulfates and Fragrances

Sulfates, such as sodium laurel sulfate and sodium laureth sulfate, fragrances, and petroleum by-products are some of the other chemicals commonly used.

Sodium lauryl sulfate, SLS is a detergent and a surfactant (it breaks surface tension and separates molecules in order to allow better interaction between the product and your hair and skin). This in turn creates a lather which makes products such as shampoo and toothpaste more effective cleaners. Sodium Lauryl Sulfate is found in a number of industrial cleaning agents such as engine degreaser. SLS is also widely used as a skin irritant when testing products used to heal skin conditions.

The term “fragrance” is vast, they’re a common cause of contact dermatitis. Fragrances are poorly regulated, and “fragrance” on an ingredient label could mean just about anything. Many dangerous ingredients can be manipulated and categorized as a fragrance. Initially, perfume companies fought the law to list their ingredients so that the secret recipes are not stolen. Thus the term fragrance was born. Now, however dangerous chemical can be classified as a fragrance to avoid getting listed as an ingredient.

Non-toxic alternatives

There are many safe soap options. Just look for soap that only contains oils and other recognizable ingredients.

Oils like coconut, jojoba, and even olive oil are great for your skin and widely available.

Shampoo can be a little harder to eliminate. There is an adjustment period. Simple ingredients such as bentonite clay, apple cider vinegar, and honey can clean and condition hair.

A simple 1-time use shampoo can be made with raw honey! (1tablespoon RAW honey with 3 tablespoons water. You may add 2 drops of carrot seed oil and 2 drops of essential oil such as Rosemary or lavender – the oils are optional). Many online resources are available; this is a good example –

Another option would be to forgo soap and shampoo entirely. This might sound extreme research has shown that like our gut, the skin has a micro biome. This micro biome acts as a built-in cleanser, deodorant, anti-inflammatory and immune-booster. The chemicals in skin care can disrupt this micro biome.

In fact, new companies now offer a product that contains Nitrosomonas eutropha, an ammonia-oxidizing bacteria (AOB). AOBs are commonly found in soil and are the reason why animals take “dirt baths” by rolling in the soil. These bacteria were once commonly found on our skin but are easily washed away with soap and shampoo. AOBs, convert the urea and ammonia in sweat—which is abrasive to the skin, causing acne and irritation—into nitrite, which fights most bad bacteria, and nitric oxide, which has anti-inflammatory properties. The idea is that these bacteria will help restore our skin’s natural protective, moisturizing and cleansing abilities, thus reducing or eliminating the need for skin care products.

A growing number of people have chosen to eliminate soaps and shampoos. Although this may be a bit radical for some, check out this article in the New York Times for a good summary and explanations.


Cobalamin (vitamin B12) Deficiency

Cobalamin (vitamin B12) Deficiency
By Renata Trister DO

According to data obtained in the Tufts University Framingham Offspring Study suggests that nearly 40% of people (ages 25-83) have plasma B12 levels in the low normal range. 9% had a significant deficiency and 16% had a near deficiency. Even a mild vitamin B-12 deficiency is associated with a greater risk for accelerated cognitive decline.
B12 deficiency has been estimated to affect about 40% of people over 60 years of age. In these patients, some of the symptoms we attribute to “normal aging” such as cognitive decline and memory loss may in part be caused or exacerbated by B12 deficiency.
Vitamin B12 works together with folate in the synthesis of DNA and red blood cells. It’s also involved in the production of the myelin sheath around the nerves, and the conduction of nerve impulses.
Dietary sources and availability
Microorganisms such as bacteria and algae synthesize and are the source of vitamin B12. The vitamin made by these microorganisms enters the human food chain through incorporation into food of animal origin. In vegetarian/ruminating animals, gastrointestinal fermentation supports the growth of these vitamin B12-synthesising microorganisms. The vitamin is absorbed and incorporated into their tissues. Omnivores and carnivores derive dietary vitamin B12 from animal products (i.e., milk, cheese, eggs, meat).
The absorption of vitamin B12 in humans is complex. Vitamin B12 in food is bound to proteins. The hydrochloric acid present in the stomach cleaves B12 from these proteins. The free form of the vitamin is immediately bound to glycoproteins called R-binders /haptocorrins. This protects B12 from denaturation in the stomach. Intrinsic factor, secreted by parietal cells in the stomach, binds vitamin B12 and enables its active absorption. When the contents of the stomach enter the duodenum, the R-binders become partly digested by the pancreatic proteases, release vitamin B12. The pH in the duodenum is more neutral than that in the stomach, the intrinsic factor has a high binding affinity to vitamin B12, and it quickly binds the vitamin as. The vitamin B12-intrinsic factor complex then proceeds to the lower end of the small intestine, where it is absorbed by phagocytosis by specific ileal receptors.
Over the last 10 years several definitions of Cobalamin deficiency have been published. Cobalamin metabolism is complex and involves a series of processes. A dysfunction in any of these processes can result in a deficiency. The main causes of Cobalamin deficiency are food-cobalamin malabsorption (50%), pernicious anemia (30%), insufficient nutritional vitamin B12 intake (7%) and malabsorption (5%). Dietary causes of the deficiency are found in malnourished elderly people and in strict vegetarians while malabsorption occurs in patients suffering from several gastrointestinal conditions.

Vitamin B12 is an important co-enzyme required for the production of tetra-hydrofolate, which is necessary for proper DNA synthesis. B12 deficiency results in impaired DNA formation and consequent retardation of cell division. This process results in the formation of megaloblastic cells especially in tissues with rapid turnover such as hematopoietic cells and intestinal epithelial cells.
Although measurement of vitamin B12 levels is the gold standard for the diagnosis of B12 deficiency some reports do exist concerning difficulties in its assay. The availability of vitamin B12 depends on its absorption from the ileum and its transport in blood to the liver and bone marrow by a carrier protein called transcobalamin. Circulating vitamin B12 is bound to 2 proteins, haptocorrin and transcobalamin.
Many case reports of normal plasma cobalamin levels in patients with clinical signs of vitamin B12 deficiency and a response to treatment with the vitamin.
B12 deficiency is often missed for two reasons. First, it’s not routinely tested for. Second, the low end of the laboratory reference range may be too low. Many B12 deficient people have so-called “normal” levels of B12.
Severe B12 deficiency – pernicious anemia (an autoimmune condition where the body destroys intrinsic factor, a protein for the absorption of B12). Anemia is the final stage of B12 deficiency. Long before anemia, B12 deficiency causes several other problems, including fatigue, lethargy, weakness, memory loss and neurological and psychiatric problems.
Causes of B12 malabsorption include:
• Intestinal dysbiosis
• Leaky gut and/or gut inflammation
• Atrophic gastritis or hypochlorhydria (low stomach acid)
• Pernicious anemia
• Medications (PPIs and other acid-suppressing drugs)
• Alcohol

In general, the following patients are at risk for B12 deficiency:
• Vegetarians and vegans
• Aged 60 or over
• Regularly use PPIs
• Crohn’s disease, ulcerative colitis, celiac or IBS
B12 is the only vitamin that contains a trace element (cobalt), which is why it’s called coalmine.
Treatment of B12 deficiency

Cyanaocobalamin is the most frequently used form of B12 supplementation in the US. But recent evidence suggests that methylcobalamin is superior to cyanocobalamin especially in neurologic and psychiatric illness. Methylcobalamin is better absorbed because it bypasses several potential problems in the B12 absorption cycle. In conclusion, if the diagnosis of B12 deficiency is suspected on the basis of clinical findings, supplementation treatment should be administered even if the assayed level of the vitamin is not low.


Vitamin D

Vitamin D
Dr. Renata Trister DO

History of vitamin D

Vitamin D was categorized as a vitamin when it was discovered in 1922. It is not a true vitamin because an ongoing nutrient source is not required to sustain normal levels in the body. Vitamin D is properly classified as a secosteroid (derived from steroid) hormone precursor. A hormone is a chemical substance produced by one organ and then transported in the bloodstream to a target organ, where it causes a specific biological action.
Vitamin D has several metabolites (forms). This summary is limited to two metabolites: 25-D and 1,25-D.
25-D (also known as calciferol, 25-hydroxycholecalciferol) increases calcium absorption in the gut and at high levels, acts as an antagonist on the Vitamin D Receptor. 25-D is produced in the liver and synthesized in the cells of the skin in reaction to sunlight. 25-D dietary sources (fish, fish oils, eggs), foods that are supplemented with vitamin D (dairy products, cereals.) and vitamin supplements.
25-D is the major circulating form of vitamin D. It is used in the production of (1,25-D) in the kidneys.
1,25-D (also known as calcitriol or 1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin-D3) is a potent secosteroid paracrine mediator and virtually affects all cellular activity.
1,25-D is primarily formed in the kidneys; but may also be formed skin, macrophages and other tissues.
Vitamin D dysregulation

The innate immune system refers to the cells and mechanisms that defend the host from infection by other organisms in a non-specific manner. This means that the cells of the innate system recognize and respond to pathogens in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host. The innate immune system provide immediate defense against infection.

Vitamin D is an important immune-modulator.

1,25-D can activate the innate immune system. Elevated levels can be found in patients with chronic conditions.
25-D can suppress the innate immune system.
Normally, production of 1,25-D is tightly controlled by the kidneys in response to a complex system of hormonal regulation. However, when nucleated cells are infected with bacterial pathogens, 1,25-D is generated by the inflammatory response. This causes the level of 1,25-D to exceed the upper limit normally controlled by the kidneys.

It is essential to measure both 25-D and 1,25-D to evaluate vitamin D levels and dysregulation. The level of 25-D doesn’t directly reflect the level of 1,25-D. Patients with Th1/Th17 inflammation often have a low level of 25-D while the level of 1,25-D is high. T helper 17 cells (Th17) are a subset of T helper cells producing interleukin 17 (IL-17) discovered in 2007. They are considered developmentally distinct from Th1 and Th2 cells and excessive amounts of the cell are thought to play a key role in autoimmune disease such as multiple sclerosis, psoriasis, autoimmune uveitis, juvenile diabetes, rheumatoid arthritis, and Crohn’s disease.


Gastrointestinal health, Thyroid and Immune connection

By Renata Trister DO

“All disease begins in the gut.”
– Hippocrates

The health of your gut and the function of your thyroid are interrelated. Poor gut health can suppress thyroid function, and low thyroid function can lead to an inflamed and leaky gut.

Low Thyroid <—->Inflammation<—->Immune Dysregulation<—->Leaky Gut<—->Low Thyroid

The gut-thyroid-immune connection

About half the lymphocytes of the immune system are in the Mucosa-associated lymphoid tissue (MALT). MALT is situated along the surfaces of all mucosal tissues. The mucosa-associated lymphoid tissue initiates immune responses to specific antigens encountered along all mucosal surfaces. These surfaces protect the body from an enormous quantity and variety of antigens. MALT includes gut-associated lymphoid tissue (GALT), bronchial/tracheal-associated lymphoid tissue (BALT), nose-associated lymphoid tissue (NALT), and vulvovaginal-associated lymphoid tissue (VALT). The nomenclature is based on location. The gut contains a large portion of the body’s immune tissue. This portion of the immune system is referred to as GALT, or gut-associated lymphoid tissue. Gut-associated lymphoid tissue is comprised of Peyer’s patches, inter-digitating lymphocytes, plasma cells and lymphocytes present in the lamina propria, and mesenteric lymph nodes. The role of GALT is to manage the immune response to the massive antigen exposure experienced by the gut while maintaining a potent adaptive immune response to protect the host from mucosal pathogens. The mucosal epithelium of the gastrointestinal tract is inundated by potential pathogens on a continuous basis. Salivary enzymes, gastric acidity and surface mucous production provide protection sufficient against numerous invaders. However, an adaptive immune response is necessary to fully protect organisms against all virulent microbes. In the gut, a network of interdigitating lymphocytes in the epithelium, in addition to lymphocytes and plasma cells that circulate through the lamina propria, play an important role in mounting the proper immune response against pathogens.
Problems occur when either of these protective functions of the gut are compromised. When the intestinal barrier becomes permeable (i.e. “leaky gut syndrome”), large / partially digested food particles escape into the bloodstream. Since these food particles don’t belong outside of the gut, the body mounts an immune response and attacks them. In fact, these food particles become a “pathogen” putting strain on the immune system.

Gastrointestinal manifestations of thyroid dysfunction are numerous and involve all portions of the tract. Thyroid hormone action on motility has been widely studied, but more complex pathophysiologic mechanisms are not fully understood. Both thyroid hormone excess and deficiency can have similar digestive manifestations, such as diarrhea, although the mechanism is different in each situation. The liver is the most affected organ in both hypo- and hyperthyroidism. Specific digestive diseases may be associated with autoimmune thyroid processes, such as Hashimoto’s thyroiditis and Grave’s disease.

Thyroid hormones influence tight junctions in the gut. These tight junctions are closely associated areas of two cells whose membranes join together to form the impermeable barrier of the gut. Thyroid hormones promote actin polymerization. Hypothyroid conditions could affect tight junction functionality as tight junction proteins are directly linked to the actinomyosin cytoskeleton. Conformational changes in the cytoskeleton of epithelial cells may result in alterations in the function of the tight junction, which leads to increased para-cellular permeability. As a result, luminal contents can more penetrate the lamina propria causing an immune and/or inflammatory reaction influence the tight junctions in the small intestine. T3 and T4 have been shown to protect gut mucosal lining from stress induced ulcer formation. Likewise, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) both influence the development of the GALT. T4 prevents over-expression of intestinal intraepithelial lymphocytes (IEL), which in turn causes inflammation in the gut.

Gut bacteria and the thyroid connection

Healthy gut bacteria assists in converting about 20 percent inactive T4 thyroid hormone into the active form of T3 by producing an enzyme called intestinal sulfatase. An imbalance between harmful and beneficial bacteria in the gut, called intestinal dysbiosis, significantly reduces the conversion of precursor thyroid hormones to active T3. This is one reason people with poor gut function may have thyroid symptoms but normal lab results. Inflammation in the gut also reduces T3 by raising cortisol. Furthermore, low stomach acid, increases intestinal permeability, inflammation and infection (see article acid reflux).
Constipation can impair hormone clearance and cause elevations in estrogen, which in turn raises thyroid-binding globulin (TBG) levels and decreases the amount of free thyroid hormones available to the body. On the other hand, low thyroid function slows transit time, causing constipation and increasing inflammation, infections and malabsorption.

Hypothyroidism impairs gallbladder function by reducing bile flow; a sluggish gallbladder interferes with proper liver detoxification.

Healing the intestine-thyroid axis
These connections make it clear that you can’t have a healthy gut without a healthy thyroid, and you can’t have a healthy thyroid without a healthy gut. To restore proper function of the gut, both must be addressed simultaneously.

The influence of thyroid hormones on the gut is immense. Low thyroid hormones make it difficult to heal the gut, while an inflamed and leaky gut contributes to many illnesses, including hypothyroidism.


Infection, autoimmunity

Jon Trister MD

Humans and microorganisms have lived in reasonable harmony for many millennia.
Coevolution for so long has resulted in mutual benefit.
Humans accommodate vast numbers of microorganisms.
Evolution produced a wide variety of microorganisms well adapted to live harmoniously with their human partners. Microorganisms exist on all exposed body surfaces:skin,mucosal lining, gastrointestinal tract.
These microbes learned to avoid and suppress immune response of the host.
Humans have adapted mechanism to evade the harmful activities of the microorganisms.
This delicate coevolution produced stable microbial population-microbiota-which actually exceeds by 10-fold the numbers of cells that compromise human body.
This coexistence results in a homeostatic equilibrium advantageous for both.Members of the Microbiome have found a congenial environmental niche.
In turn, it benefit the human host by performing valuable physiologic reactions and generating needed nutrients.
The resident microbial population itself retards infection or overgrowth by potentially harmful microorganisms.
At times, the symbiotic relationship established between the microbial population and its human counterpart become unbalanced because both parties are constantly subject to change.
Aggressive microorganisms with overwhelming disease-induced properties may gain within microbiome.
Alternatively, the ability of human immune system to cope with microbial population may falter because of age, hormonal status, nutrition and lifestyle. This dysfunction interrelationship is a promotion of autoimmune disease as a consequence of infection.(N.Rose, 2015)

One of the classic example of dysregulated immune response is Rheumatic Fever-when particular infection ( Streptococcus pyogenes ) can induce autoimmune disease in human. Madeleine Cunningham showed that antibodies and T lymphocytes specific for epitopes on the streptococcal M protein cross-react with cardiac myosin of the myocardium and N-acetyl-beta-D glucosamine residues on the cardiac valve endothelium.(M.Cunningham , 2012).
Another example is a Guillain-Barre syndrome where antigen (GM1) from Campylobacter jejuni cross-reacts with similar antigen in human peripheral nerve axones causing acute motor axonal injury.(S. Kuwabara , 2013)
These are two examples where defined microbial antigen mimicking its counterpart in the human host and inducing immune response in human.

Mechanisms of autoimmunity:

-Molecular or epitope mimicry between a microorganism and a host constituent induces pathogenic autoimmunity following resolution of the infectious process. Molecular mimicry is a compelling theory to explain the association of infections with autoimmune disease.Sometimes the microorganisms involved have little or no clinical or epidemiologic association with the particular human disease but capable to induce autoimmune process. ( N.Rose,2000).

-Charles Gauntt suggests that when damaging cells, the invading microorganism may cause the expression of otherwise unavailable autoantigens , providing both a trigger and a vulnerable target for a pathogenic autoimmune response. Cell damage or “spillage” inflicted by the microorganism overcome “immunologic ignorance” of previously ignored antigen.(C.Gauntt, 1979). {examples: DM type 1, post-viral myocarditis ( Coxsackievirus B3), CMV}.

-Host antigen sometimes incorporated into an infecting virion and can induce an autoimmune response in the manner recalling classic hapten-carrier relationship.( N.Rose, 1990)

-Infecting microorganism may alter a host protein to the point where it is perceived by the host immune system as foreign


GERD part 3

By Renata Trister DO
The stomach is meant to produce acid. It is an important component of the digestive process. Acid is found in the digestive processes of all vertebrates. We will discuss the roles of stomach acid and the effects of having low acidity – hypochlorhydria.

The vital role stomach acid play in our bodies is often underestimated. The common view is that stomach acid is not needed and is actually the cause of illness is a misconception. Somewhat proliferated by drug companies. Subsequently, millions of people use antacids on a chronic, everyday basis. Although painful symptoms are managed, the underlying condition is not.

The primary consequences of hypochlorhydria are:

Impaired ability to resist infection
Increased bacterial overgrowth
Impaired nutrient absorption
Increased risk of illnesses including cancer

Bacterial Overgrowth
Low gastric acidity causes bacterial overgrowth in the stomach and other parts of the intestine. This is a result of impaired carbohydrate digestion and decreased ability to fight off ingested bacteria – both consequences of hypochlorhydria. Bacterial digestion of carbohydrates through fermentation produces gas. This gas increases the intra-abdominal pressure, which overpowers the lower esophageal sphincter (LES). The dysfunctional opening of the LES allows acidic stomach contents to enter the esophagus, producing the painful symptoms GERD. Although the stomach contents are deficient in acid to function properly, they are still acidic enough to damage the delicate lining of the esophagus.

Bacterial overgrowth has several cascading effects as well. Mainly – reduced nutrient absorption leads to increasing and chronic inflammation, which increases the risk of developing stomach cancer. Studies have confirmed that proton-pump inhibitors (PPIs) significantly change the bacterial population of the GI tract by suppressing stomach acid. One study found that 50% of patients using PPIs had small bowel bacterial overgrowth (SIBO), in comparison only 6% of control subjects not taking PPIs.

Impaired Nutrient Absorption

Gastric acidity plays an important role in digestion. Proper breakdown of nutrients occurs within a narrow range of acidity. Hypochloridia impairs the normal reactions required to properly assimilate nutrients. This can eventually lead to osteoporosis, anemia, depression, cardio-vascular disease and other issues.

Breakdown of Macronutrients

The proper digestion of macronutrients (fats, carbohydrates and proteins) needs acidity. The secretion of acid (HCL) in the stomach induces the production of pepsin. Pepsin is the enzyme required to digest protein. If not enough HCL is present pepsin levels will also be low. Proteins will not be broken down properly into their component amino acids and peptides. A deficiency of essential amino acids can subsequently develop and may lead to depression and anxiety.

Proteins that escape digestion by pepsin may end up in the bloodstream. Since this is not supposed to happen, the body treats these proteins as foreign pathogens, causing allergic and autoimmune responses.


Years of research confirm that low stomach acid reduces absorption of several key nutrients. These include iron, B12, folate, calcium, magnesium and zinc.

Iron deficiency causes chronic anemia. In one study of 40 patients with chronic anemia 35 were found to also have acid secretion. Iron-deficiency anemia is an established side effect of surgeries that remove portions of the stomach where acid is made. Inhibition of acid production by Tagamet, in another study, resulted in a significant reduction of iron. Furthermore, giving acid to patients with achlorhydria, improved iron absorption.

Vitamin B12
Taking proton pump inhibitors (PPIs – such as Prilosec, Nexium and Prevacid) for more than two years was linked to a 65 percent increase in the risk of vitamin B-12 deficiency.
Researchers also found that using acid-suppressing drugs called histamine-2 receptor antagonists (H2 blockers – such as Tagamet, Pepcid and Zantac) for two years was associated with a 25 percent increase in the risk of B-12 deficiency. Vitamin B12 is critical to proper nerve and brain function. Sufficient HCl (and pepsin) is essential, independent of intrinsic factor secretion, for separating B12 from carrier proteins in food. This is thought to be a major cause of deficiency in the elderly, who generally suffer from low stomach acid. If B12 is not separated from its carrier proteins it will not be absorbed. In patients with atrophic gastritis (chronic inflammation of the stomach mucosa causing mucosal atrophy), more than 50 percent have low vitamin B12 levels. This is of course a consequence of the damage to the parietal cells. Parietal cells produce HCL and intrinsic factor. Intrinsic factor is a glycoprotein that binds B12 & facilitates B12 absorption in the small intestine. lack of intrinsic factor as well as low acidity subsequent to
Various approaches have examined the negative effect of PPI therapy on B12 absorption. Even in healthy subjects treated with daily doses of Prilosec for two weeks, B12 absorption was reduced by as much as 50%. The consequences of B12 deficiency are vast and will be discussed in a future article.

Folate (folic acid) is essential for a healthy cardiovascular system and for proper fetal development. Hypochloridia impairs folate absorption by raising the pH in the small intestine. Folate given to achlorydric patients together with an HCL supplement, absorption of the vitamin can be increased by roughly 50 percent.

In a study, Tagamet reduced folate absorption. The overall reduction of folate absorption was a modest 15 percent. Although this reduction is probably not severe enough to cause harm a healthy person who gets enough folate through diet, it may cause further issues in those with a folate deficiency.

Calcium has a vast number of important functions functions in our body. The absorption of dietary calcium is thought to be mediated by gastric acid release of ionized calcium from insoluble calcium salts. Hence, there have been concerns that hypochlorhydric states, in particular those induced by PPIs, may impair calcium absorption. The effect low acidity has on calcium absorption was first discovered in the 1960s, one group of researchers found that some ulcer patients were barely absorbing any calcium at all (> 2 percent). It was found that these patients had a high gastric pH (6.5) and very little stomach acid. However, when these patients were given HCL supplements, lowering the pH to 1, calcium absorption increased five-fold. In 2010 the FDA even issued a product label warning for all PPIs because of clinical reports inferring increased risk for bone fractures. The FDA revised this warning in March of 2011 to release over-the-counter PPIs, which are intended for short-term use. This revision was said to have come due to conflicting data regarding the risk of fractures and that even the risk is the short-term use would not cause an increase. How releasing over the counter PPIs prevents long term use is still not clear… A 2011 meta-analysis study in The Annals of Family Medicine reported that high doses or long-term usage of proton pump inhibitors (PPIs) have been linked to an increased risk of osteoporosis-related fractures of any type, including wrist, spine, and hip.

There have been several cases of hypomagnesemia that were associated with long-term PPI use. The patients generally presented with profound hypomagnesemia that required hospitalization. In approximately 25% of these cases, the patients had persistent hypomagnesemia despite magnesium supplementation and prompt resolution of magnesium levels following discontinuation of the PPIs. Furthermore, in a few cases patients who were restarted on a PPI, the hypomagnesemia recurred. Clearly this demonstrated a PPI-related effect. The exact mechanism for this magnesium depletion is not well understood, but health care providers need to aware of this side effect.

Zinc is needed in several metabolic processes that are involved in maintaining and stabilizing cell membranes, form new bone, immune defense, night vision, and tissue growth. In one controlled trial, Tagamet and Pepcid, which can raise gastric pH to over 5 reduces zinc absorption by about 50 percent.

The Immune Function

The mouth, the esophagus and the intestines house approximately 400-1,000 species of bacteria. Healthy stomach contents however, are almost completely sterile. This is because acid kills bacteria. The acid of the stomach actually creates a two-way barrier. Stomach acid kills harmful bacteria present in the air, food and drink we take in from entering the intestine. At the same time, stomach acid also prevents normal gut flora in the intestines to move into the stomach and esophagus. Although harmless in the intestine gut flora can cause problems if it spreads beyond the intestine into stomach, esophagus or respiratory tract. The acidic stomach contents are one of the major non-specific immune mechanisms. When the pH of the stomach is 3 or lower, the normal between-meal “resting” level, bacteria are killed in fifteen minutes. As gastric pH rises above 5, many bacteria thrive. Tagamet and Zantac significantly raise the pH of the stomach from about 1 to 2 before treatment to 5.5 to 6.5 after, respectively. Prilosec is even worse as it can reduce stomach acidity to near zero. High pH promotes bacterial overgrowth and makes patients are more vulnerable to infection.
A recent systematic review of gastric acid-suppressive drugs suggested that there is an increase susceptibility to some infections:

C. Difficile
Community Acquired and Hospital Acquired Pneumonia

Acid suppressing drugs weaken our immune system. In vitro studies have shown that PPIs impair neutrophil function, and inhibit neutrophil phagocytosis. When you decrease acid secretion in the stomach, you boost the risk of infection. Without adequate stomach acid present, large amounts of undigested food pass into the intestines, contributing to the growth of opportunistic organisms, an increase in toxins, and an imbalance in intestinal flora. Studies published in the Journal of the American Medical Association revealed that when taking a proton pump inhibitor drug, the risk of developing pneumonia increases up to 89%, and the risk of developing a potentially deadly chronic infection from the intestinal bacterium Clostridium difficile increases also. A randomized, double-blind, controlled trial published in Gastroenterology shows that withdrawal from acid blockers can lead to rebound acid hyper secretion, which then forces the patient to immediately go back to the acid blocker drug. This becomes a vicious cycle. As we mentioned in an earlier article, acid secretion declines with age. In 1996, a British physician noted that age-related stomach acid decline is due to a loss of parietal cells that produce the HCL. Chronic inflammation of gastric mucosa leads to atrophy of parietal cells and eventually mucosa is replaced with fibrous tissue. This condition is called atrophic gastritis. A host of illnesses is associated with atrophic gastritis. This includes the following:

Depression, anxiety, mood disorders
Pernicious anemia
Skin diseases, including forms of acne, dermatitis and eczema
Autoimmune diseases, such as Rheumatoid arthritis and Graves disease
Irritable bowel syndrome (IBS), Crohn’s disease (CD), Ulcerative colitis (UC)
Stomach cancer

Stomach Cancer

Atrophic gastritis is a major risk factor for stomach cancer. H. Pylori is the leading cause of atrophic gastritis. Moreover, long-term use of proton pump inhibitors by people with H. pylori may reduce acid secretion enough to cause atrophic gastritis (chronic inflammation of the stomach). Atrophic gastritis is a well-established risk factor for stomach cancer. To compound concerns, long-term use of PPIs may mask symptoms of stomach cancer and thus delay diagnosis.

Dr. Julie Parsonnet, M.D. of Stanford University Medical School wrote an editorial on this subject stating:

In principle, current [acid suppressing drug] therapies might be advancing the
cancer clock by converting relatively benign gastric inflammation into a more destructive, premalignant process.

PPIs increase the risk of cancer is by inducing above-normal secretion of the hormone gastrin. PPI induced hypochlorhydria results in an elevated gastrin level in an attempt to compensate for increased pH in the stomach. A daily 20 mg dose of Prilosec typically results in up to a three-to-fourfold increase in gastrin levels. Increased expression of gastrin is also seen in Helicobacter infections. Chronic infection of the gastric mucosa with Helicobacter pylori has long been recognized as a significant risk factor for gastric cancer (specifically adenocarcinoma). Recent studies have expanded the role for gastrin and related peptides in inflammation and inflammation-associated cancers, suggesting that their expression in immune cells contributes to the initiation and progression of GI cancers. H. Pylori induces the systemic elevation of serum gastrin through several mechanisms:
H. Pylori infection suppresses gastric acid secretion by parietal cells, causing a loss of feedback inhibition by acid and a compensatory increase in gastrin production by the G cells in the antrum.

Chronic infection and inflammation results in loss of parietal cells (atrophic gastritis). Loss of parietal cell results in reduced acid production, which also triggers the G cells to overexpress gastrin.

A smaller percent of patients (~15%) with chronic gastritis also have decreased somatostatin, also resulting in increased gastrin production by removing the normal feedback inhibition of G cells.

H. Pylori-induced inflammatory cytokines stimulate also G cells to release gastrin.

The combination of hypochlorhydria and hypergastrinemia results in gastric bacterial overgrowth, lack of parietal cell differentiation, development of gastric metaplasia, and eventual progression to gastric carcinoma.

Another mechanism for carcinogenesis involves elevated concentration of nitrites in the gastric contents. Normally, vitamin C removes nitrite from gastric contents by converting it to nitric oxide. This process is dependent upon the pH of the stomach being less than 4. As mentioned previously, acid-reducing medications can increase PH well above that.

These are two distinct mechanisms through which medication induced hypochlorhydria can increase risk of cancer.

Irritable bowel Disorders (IBD)

Adenosine is an important modulator of GI tract inflammation and its anti-inflammatory effects have been well established in humans and in animal models. High levels of extracellular adenosine suppress and resolve chronic inflammation in IBD including Crohn’s disease and Ulcerative Colitis. Increased extracellular adenosine levels activate reduce cytokines responsible for chronic inflammation (by activating A2a receptor). More information is available in this article Adenosine: An immune modulator of inflammatory bowel diseases Jeff Huaqing Ye and Vazhaikkurichi M Rajendran. World J Gastroenterology. 2009 Sep 28; 15(36): 4491–4498.
Chronic use of PPIs has been shown to decrease extracellular concentration of adenosine, resulting in an increase in inflammation in the digestive tract. More information on this topic can be found in this article: Possible mechanism for the inhibition of gastric (H+ + K+)-adenosine triphosphatase by the proton pump inhibitor AG-1749. H Nagaya, H Satoh, K Kubo and Y Maki Journal of Pharmacology and Experimental Therapeutics.

As discussed in previous articles acid suppressors contribute to bacterial overgrowth. Likewise the connection between irritable bowel syndrome (IBS) and small bowel bacterial overgrowth (SIBO) has been established. There is a striking similarity between the symptoms of IBS and SIBO. It has been theorized that SIBO may be responsible for the symptoms of at least some patients with irritable bowel syndrome. The estimates run as high as 50% of patients with irritable bowel syndrome. Support for the SIBO theory of IBS comes from the observation that many patients with IBS are found to have an abnormal hydrogen breath test, and some patients with irritable bowel syndrome have improvement of their symptoms after treatment with antibiotics, the primary treatment for SIBO. Therefore, it is plausible that chronic use of acid suppressing drugs could contribute to the development of IBS healthy patients, and could certainly exacerbate the condition in those already suffering with IBS.

Mood Disorders, Depression and Anxiety

Specific research connecting antacids to mood disorders is lacking. However, as discussed above, some connections are clear. Stomach acid secretion triggers the release of pepsin. Pepsin is an enzyme that cleaves protein into component essential amino acids and peptides. With out pepsin the proteins we eat are not broken down into peptide components. Essential amino acids, such as phenylalanine and tryptophan, play a crucial role in mental health. In addition low stomach acid may predispose people towards developing deficiency in vitamin B12. The combination of these factors can lead to depression, anxiety and insomnia.

Autoimmune diseases

Low stomach acid and consequent bacterial overgrowth cause the intestine to become permeable, allowing undigested proteins to find their way into the bloodstream. This process is known as “leaky gut syndrome”. Both trans-cellular and Para-cellular intestinal permeability is substantially increased in patients with atrophic gastritis.

Undigested proteins that enter the bloodstream, they are treated as pathogens by the immune system. This results in chronic low-level immune response activation. As a result there is constant strain on the immune system. This immune response against proteins we eat contributes to food allergies. A similar mechanism that is not fully understood predisposes people with a leaky gut to develop more serious autoimmune disorders such as lupus, rheumatoid arthritis, Graves disease, and inflammatory bowel disorders. The connection between rheumatoid arthritis (RA) and hypochloridia has been established. A study found that people with RA have decreased stomach acidity and an extremely high rate of atrophic gastritis associated with low stomach acid when compared with normal individuals.


Recently, the connection between asthma and acid reflux has been extensively studied. In addition to wheezing, gastro-esophageal reflux is one of the most common features seen in asthma suffers. It is estimated that between up to 80 percent of people with asthma also have GERD. Compared with healthy people, those with asthma also have significantly more reflux episodes and more acid-induced irritation of their esophageal lining.

When acid gets into the respiratory tract, the lungs ability to breathe air in and out is reduced. This association caused physician to prescribe acid more and more stopping drugs to asthma patients suffering from GERD.


GERD is most often caused by diminished – rather than excessive – stomach acid. In addition to GERD, hypochloridia is associated with bacterial overgrowth, decreased resistance to infection and impaired absorption of nutrients. Hypochlorhydria is also linked to an increased risk of stomach cancer, ulcers, IBS, depression, autoimmune disease, and asthma. Chronic use of acid stopping medications dramatically reduces stomach acid, thus increasing the risk of the above conditions.