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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.

GERD and HYPOCHLORHYDRIA
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.

Micronutrients

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

Iron
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
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
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.

Magnesium
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
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
Salmonella
Campylobacter
Cholera
Listeria
Giardia

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:

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

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. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2751993/
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.

Asthma

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.

Conclusion

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.

HOW TO TREAT GERD WITHOUT ACID REDUCING MEDICATION

By Renata Trister DO

GERD and reflux symptoms are more likely the result of too little acidity (hypochloridia), bacterial overgrowth and increased intra-abdominal pressure (IAP). The following treatments focus on restoring adequate stomach acid production and eliminating bacterial overgrowth.

This can be accomplished by following the “three Rs”:

1. Reducing the factors that promote bacterial overgrowth and low stomach acid.
2. Replenish stomach acid, enzymes and nutrients that aid digestion.
3. Restore the micro biome of beneficial bacteria to the GI tract and restore a healthy mucosal lining in the gut.

How to reduce bacterial overgrowth and replenish low stomach acid

Carbohydrates

A high carbohydrate diet contributes to bacterial overgrowth. H. pylori can actually suppress stomach acid . A cycle of bacterial overgrowth and low stomach acid reinforce each other creating a progressive decline of digestive function.
As bacteria prefer and thrive on fermentation of carbohydrates for energy, a very low-carb (VLC) diet can be beneficial.

A small study performed by Professor Yancy and colleagues at Duke University. 5 patients with severe GERD that also had a variety of other medical problems, such as diabetes were enrolled. Each of these patients had failed several conventional GERD treatments before being enrolled in the study and for all 5 the symptoms of GERD were completely eliminated within one week of adopting a very low carbohydrate (VLC) diet.

Another small study done by Yancy examined the effects of a VLC diet on eight obese subjects with severe GERD. They measured the esophageal pH of the subjects at baseline before the study began using something called the Johnson-DeMeester score. This is a measurement of how much acid is getting back up into the esophagus, and thus an objective marker of how much reflux is occurring. They also used a self-administered questionnaire called the GSAS-ds to evaluate the frequency and severity of 15 GERD-related symptoms within the previous week. All five of these patients showed a substantial decrease in their Johnson-DeMeester score (meaning less acid in the esophagus). Furthermore, the decreases in Johnson-DeMeester scores were similar to decreases reported by patients taking PPIs. All eight patients reported improvement in symptoms – evidenced through their GSAS-ds scores. The GSAS-ds scores decreased from 1.28 prior to the diet to 0.72 after initiation of the VLC. These results demonstrate both objective (Johnson-DeMeester) and subjective (GSAS-ds) improvement.

Obesity is a risk factor for GERD, because it increases intra-abdominal pressure. This increased pressure overwhelms the lower esophageal sphincter (LES) and causes a dysfunction of the LES. An added benefit of a VLC diet is weight loss.
Another diet that can be used instead of a VLC called a “specific carbohydrate diet” (SCD), or the GAPS diet. On this kind of plan, is not the amount of carbohydrates, but the type of carbohydrate that is important. The theory is that the longer chain carbohydrates (disaccharides and polysaccharides) are the ones that feed bad bacteria in our guts, while short chain carbohydrates (monosaccharide’s) don’t pose a problem. In practice what this means is that all grains, legumes and starchy vegetables should be eliminated, but fruits and certain non-starchy root vegetables (winter squash, rutabaga, turnips, celery root) can be eaten. These are not “low-carb” diets, per se, but there is reason to believe that they may be just as effective in treating heartburn and GERD.

Fructose and artificial sweeteners

Fructose and artificial sweeteners contribute to bacterial overgrowth. Artificial sweeteners simply should be avoided completely, and fructose (in processed form especially) should be reduced.

Fiber

High fiber diets and bacterial overgrowth are a particularly dangerous mix. Almost all of the fiber and approximately 15-20% of the starch we consume escape absorption. Carbohydrates that escape digestion become food for intestinal bacteria.
Therefore adding various fiber supplements is not beneficial and may actually be harmful to GERD sufferers. However, eating green vegetables is not something to avoid.

Bitters

Bitter herbs stimulate acid production in the stomach. “Bitters” have been used in traditional medicine for thousands of years in an effort to stimulate and improve digestion. Today, studies have actually confirmed the ability of bitters to increase the flow of digestive juices, including HCL, bile, pepsin, gastrin and pancreatic enzymes. Unfortunately, these studies are small as evaluating the therapeutic potential of un-patentable and unprofitable bitters has little incentive.
The following is a list of bitter herbs commonly used in Western and Chinese herbology:

Barberry bark
Caraway
Dandelion
Fennel
Gentian root
Ginger
Globe artichoke
Goldenseal root
Hops
Milk thistle
Peppermint
Wormwood
Yellow dock

Bitters are normally taken in very small doses – just enough to sense a strong taste of bitterness – 5 to 10 drops of a 1:5 tincture of the above herbs taken in 20 mL of water.

Apple cider vinegar, lemon juice, raw (unpasteurized) sauerkraut and pickles are other time-tested, traditional remedies that often relieve the symptoms of heartburn and GERD.

Patients who have been taking acid stopping drugs for several years, it may be necessary to replace the nutrients that are not absorbed without sufficient stomach acid. These include B12, folic acid, calcium, iron and zinc. It’s best to get your levels tested by your doctor, who can then help you replace them through nutritional changes and/or supplementation.

How to restore good bacteria and healthy mucosal lining

Probiotics

Bacterial overgrowth is a major contributor to heartburn and GERD, therefor restoring healthy intestinal bacteria is important. Beneficial bacteria (probiotics) protect against potential pathogens by competing for resources – competitive inhibition. These good bacteria perform several other functions essential to digestive health as well.

Probiotics are effective in reducing bacterial overgrowth and altering fermentation patterns in the small bowel in patients with IBS. Probiotics have also been shown to be effective in treating Crohn’s disease, ulcerative colitis, and other digestive conditions.

Probiotics have also been shown to increase cure rates of treatment for H. pylori when supplemented to an antimicrobial treatment.

It is easy to become confused when facing the vast options of probiotics on the market. As mentioned earlier, it is best to attempt to get the nutrients needed from food. Probiotics are no exception. Fermented foods have been eaten for their digestive benefits for thousands of years. Contrary to popular belief and marketing, foods like yogurt, kimchi and kefir generally have a much higher concentration of beneficial microorganisms than supplements.

For example, even the most potent commercial probiotics claim to contain somewhere between one and five billion microorganisms per serving. In comparison, a glass of homemade kefir (fermented milk) contains as many as 5 trillion beneficial microorganisms!

Fermented milk products like kefir and yogurt also contain minerals, vitamins, protein, amino acids, L-carnitine, fats, CLA, and antimicrobial agents. Studies have even shown that fermented milk products can improve the eradication rates of H. pylori by 5-15%.

The problem with fermented milk products in the treatment of heartburn and GERD, however, is that milk is relatively high in carbohydrates. This may present a problem for people with severe bacterial overgrowth. However, small amounts of kefir and yogurt are therapeutic and may be well tolerated. It’s best to make kefir and yogurt at home, because the microorganism count will be much higher. Dom’s Kefir website has lots of information on this topic.

Non-dairy (and thus lower-carb) options include unpasteurized (raw) sauerkraut and pickles and a fermented tea called kombucha. Raw sauerkraut can easily be made at home, or sometimes found at farmer’s markets. Bubbies brand raw pickles are sold at health food stores, as is kombucha, both can also be easily made at home.

Probiotic supplements are sometimes necessary and can play a crucial role in treatment and recovery. But not all probiotic supplements are the same, and in the case of small intestinal bacterial overgrowth (or SIBO, which is commonly present with GERD), certain probiotics may make things worse. SIBO involves an overgrowth of microorganisms that produce a substance called D-lactic acid. There are a very small number of people who do not respond well to D-lactate—an acid produced by some probiotic bacteria, including lactic acid bacteria like Lactobacillus acidophilus. These patients would do better with a probiotic that contains strains of Bifidobacteria.

Restoring a healthy gut lining

Bone broth and DGL

Restoring the mucosal gut lining to a healthy state is another important aspect of recovering from GERD. Chronic stress, bacterial overgrowth, and certain medications such as steroids, NSAIDs and aspirin damage the mucosal lining of the stomach. The mucosal lining of the stomach that protects it from acid, a damaged stomach lining can cause irritation, pain and ulcers.

Homemade bone broths are effective in restoring a healthy mucosal lining in the stomach. These broths are rich in gelatin and collagen and proline, a non-essential amino acid that is an important precursor for the formation of collagen. Gelatin and collagen have both been beneficial in treatment of ulcers. Bone broth also contains glutamine, important for intestinal cells, glutamine has been shown to benefit the gut lining in animal studies. Please see link at end of this article for more information and recipes for bone broths.

Although it is best to obtain nutrients from food whenever possible, supplements are sometimes necessary – especially for short periods. Deglycyrrhizinated licorice (DGL) has been shown to be effective in treating gastric and duodenal ulcers, and works as well in this regard as Tagamet or Zantac, with far fewer side effects and no undesirable acid suppression. In animal studies, DGL has even been shown to protect the stomach lining against damage caused by aspirin and other NSAIDs.

DGL works by increasing the concentration of compounds called prostaglandins, which promote mucous secretion, stabilize cell membranes, and stimulate new cell growth – all of which contributes to a healthy gut lining. Both chronic stress and use of NSAIDs suppress prostaglandin production, so it is vital for anyone dealing with any type of digestive problem (including GERD) to find ways to manage their stress and avoid the use of NSAIDs. Important note, licorice products that contain glycyrrhizin and whole licorice (in contrast to DGL- Deglycyrrhizinated licorice) may increase the effects of corticosteroids, cause sodium and water retention and increase blood pressure, increase the effect of digitalis preparations, alter the effect of estrogens/progesterone, and decrease the effect of anti-hypertensive medications. Avoid whole or licorice root if you have high blood pressure, kidney or liver disease, diabetes or heart disease, are pregnant or are breastfeeding.

There are no known side effects for DGL products and it is a safer alternative to whole licorice supplements.

Conclusion

The general medical approach to treating heartburn and GERD involves taking acid stopping drugs for as long as these problems occur. Although these drugs work incredibly well to relieve symptom quickly. This temporarily relief is analogous to “sweeping dirt under the rug”. These medications do not address the actual pathology of behind the symptoms. In many cases they make the condition worse, while masking the symptoms. This means that many patients initiating treatment with antacid drugs end up taking them for the rest of their lives.

A serious problem arises as acid stopping drugs promote bacterial overgrowth, weaken our resistance to infection, reduce absorption of essential nutrients, and increase the likelihood of developing IBS, other digestive disorders, and cancer. The manufacturers of these drugs have always been aware of these problems. When acid-stopping drugs were first introduced, it was recommended that they not be taken for more than six weeks. Unfortunately, this recommendation has been largely discarded. There are many patients who have been on these drugs for decades – not weeks.

What is especially disturbing about this is that heartburn and GERD are easily prevented and cured by making simple dietary and lifestyle changes. The vast marketing of pharmaceuticals overshadows this crucial information. Drug companies make more than $7 billion a year selling acid suppressing medications. Teaching doctors and their patients to learn how to treat heartburn and GERD without these drugs would cut into these profits. Furthermore, any treatment protocol with out “data” to support its effectiveness is generally seen as unacceptable in our medical system. Although gathering evidence for safety and efficacy is very important, roughly 2/3 of all medical research is sponsored by drug companies – meaning that most of the research is focused on showing how well a product works. Large studies on the effects of a low-carb diet on acid reflux and GERD are unlikely. In this environment it is important to remember just because a treatment used for thousands of years has little published research, does not mean it is to be discarded.

Recommended Resources

Why Stomach Acid is Good For You, by Jonathan Wright, M.D. and Lane Lenard, Ph.D. The title says it all. Great book.
Heartburn Cured – The Low-Carb Miracle, by Norm Robillard, Ph.D. Good information on the connection between bacterial overgrowth and GERD.
The GAPS Diet Book and The GAPS Diet Guide. Excellent resources for a specific-carbohydrate diet that reduces bacterial overgrowth and repairs the gut lining.
The 30-day Heartburn Solution, by Craig Fear NTP. A 30day plan that uses real food to heal your body. Book contains practical information and a simple meal planning methods.
Brodo: A Bone Broth Cookbook, by Marco Canora. New York City chef Marco Canora has been credited for the recent explosion of interest in medicinal broths after improving his own health by integrating bone broth into his diet.
Link to information and recipes for bone broths

Cooking with Bones

Important links for physicians:

1. Overutilization of proton-pump inhibitors: what the clinician needs to know.
Joel J. Heidelbaugh, Andrea H. Kim, Robert Chang, and Paul C. Walker http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388523/

2. Common gastrointestinal symptoms: risks of long-term proton pump inhibitor therapy. Fashner J, Gitu AC. Discusses risks of long term ppi use and includes step down regimens to prevent or minimize the discomfort that can occur with abrupt ppi discontinuation. http://www.ncbi.nlm.nih.gov/pubmed/24124705

3. Disruption of the gastroesophageal junction by central obesity and waist belt: role of raised intra-abdominal pressure. Lee YY, McColl KE. http://www.ncbi.nlm.nih.gov/pubmed/24575877

GERD (Gasto-Esophageal Reflux Disease)
By Renata Trister DO

When asking the average person on the street what causes heartburn, he/she will most likely answer “too much stomach acid.” Most of the ads on TV and in magazines seem to suggest the same.
However, there is a big problem with this explanation: the incidence of heartburn and GERD increases with age, while stomach acid levels generally decline as we get older.

Many studies have shown that stomach acid secretion declines with age. One study showed that over 30 percent of men and women past the age of 60 suffer from atrophic gastritis. Patients with condition produce little or no acid.
Another well established fact in scientific literature is that the risk of GERD increases with age.

Consequently if heartburn were caused by too much stomach acid, we should see teens requesting antacid medications, but of course the opposite is true.

In fact, when stomach acid of heartburn and GERD suffers is measured, it is almost always low, not high. Excess stomach acid is only found in a few rare conditions like Zollinger-Ellison syndrome), and GERD is hardly ever associated with too much stomach acid.

Moreover, many clinicians have found that giving hydrochloric acid supplements to patients with heartburn and GERD can relieve their symptoms. When nutritional changes are made and supplemented with hydrochloric acid and pepsin capsules
Symptoms and digestion are improved even further.

Symptom vs Cause

When people first hear that GERD is caused by a lack stomach acid, rather than excess, they are skeptical. After all, if this were true then why would antacid drugs provide relief?

The painful symptoms of heartburn and GERD are caused by stomach acid refluxing into the esophagus. Reducing or eliminating this “refluxed” stomach acid with medications will relieve symptoms.

It is crucial to understand is that ANY amount of acid in the esophagus is going to cause painful symptoms. The esophagus has a delicate lining that isn’t protected against acid like the stomach lining is.

We often focus on suppressing symptoms without paying attention to what is causing the problem. Symptoms are designed to alert one that there is a problem. Simply masking the symptom can lead to damage and exacerbation.
Furthermore, Americans spend more than $13 billion on acid reducing medications each year. If antacids were actually curing heartburn and GERD, this kind of expense would be justified. However, not only do these drugs fail to cure GERD, they make the underlying condition (low stomach acidity) worse. Subsequently creating a chronic, lifelong need for these medications.

GERD is caused by increased intra-abdominal pressure

GERD is caused by an increase in intra-abdominal pressure (IAP). Acid reflux occurs when increased intra-abdominal pressure, either secondary to gastric distention (bloating) or pressure changes outside the stomach, pushes acidic stomach contents through the LES (Lower Esophageal Sphincter) into the esophagus. Factors contributing to this are obesity, postprandial positional changes (bending over, lying down). Several studies have shown an association between obesity and GERD, and a paper in Gastroenterology concluded that increased intra-abdominal pressure was the causative mechanism.

The two primary causes of increased intra-abdominal pressure

In the book, Heartburn Cured, Dr. Norm Robillard argues that carbohydrate malabsorption causes bacterial overgrowth, resulting in IAP producing reflux. Dr. Robillard makes a strong argument that carbohydrate malabsorption plays a significant role in IAP. But what is causing the carbohydrate malabsorption? Are there other reasons for bacterial overgrowth? It seems that low stomach acid is key. Low stomach acid can contribute to both bacterial overgrowth (independently of carbohydrate intake) and can cause carbohydrate malabsorption.

Low stomach acid causes bacterial overgrowth

Stomach acid plays an important role in killing pathogens. At a normal pH of 3 or less, most bacteria will die in 15 minutes. However, if the acidity is insufficient this protective process is impaired. At pH of 5 + bacteria begin to thrive. This process is seen in the gastrin knockout mouse. These mice do not produce stomach acid and as a result suffer from bacterial overgrowth, severe inflammation, damage and precancerous polyps in its intestines. Likewise, use of strong/IV acid-suppressing medications in hospital patients can cause bacterial overgrowth. Long-term use of Prilosec, one of the most potent acid suppressing drugs, reduces the secretion of hydrochloric acid (HCL) in the stomach to near zero. In a trial of 30 people with GERD treated with a high dose of Prilosec (40g/day) for at least 3 months; 11 of the 30 Prilosec-treated people developed significant bacterial overgrowth.

Low stomach acid impairs carbohydrate digestion

Stomach acid (HCL) supports the digestion and absorption of carbohydrates by stimulating the release of pancreatic enzymes into the small intestine. If the pH of the stomach is too high, the pancreatic enzymes will not be secreted and the carbohydrates will not be broken down properly.

Bacterial overgrowth + maldigested carbohydrates = Increased Abdominal Pressure (IAP)

Although microbes are able to metabolize proteins and even fats, they prefer carbohydrates as an energy source. The fermentation of carbohydrates that haven’t been digested properly produces gas. The resulting gas increases intra-abdominal pressure, which is the driving force behind acid reflux and GERD. In the book Hearburn Cured, Dr. Robillard noted a study:

According to Suarez and Levitt, 30 g of carbohydrate that escapes absorption in a day could produce more than 10,000 mL (ten liters) of hydrogen gas!

If stomach acidity is sufficient, carbohydrates are properly broken down into glucose and rapidly absorbed in the small intestine before microbial fermentation can take place. Provided that carbs are eaten in moderation. However, if stomach acid is insufficient and/or carbohydrates are consumed in excess, some of the carbs will escape absorption and become available for intestinal microbes to ferment.

It follows that gas produced by microbial fermentation of carbohydrates causes distention, and increased IAP. This pressure pushes acidic gastric contents into the esophagus causing reflux. Thus, reflux can be treated by 1) reducing bacterial overgrowth or 2) reducing carbohydrate intake. A study showing that administration of erythromycin significantly decreased esophageal reflux supports this. Only a couple small trials have been performed to test the effects of carbohydrate restriction on GERD. Both had positive results. Many case reports show an almost immediate resolution of GERD symptoms in obese individuals who are put on a very low-carb diet.

In summary, low stomach acid contributes to bacterial overgrowth in the bowel which in turn can lead to carbohydrate mal-absorption. This may be so in most cases, but there are patients on a very low carbohydrate diet that still experience heartburn, which improves when stomach acidity is increased. In part 2 of this article we will look at important roles of stomach acid and the significant damage of long term hypochlorhydria.

By Renata Trister DO
ADAPTOGENS

The American Academy of Family Physicians estimates that approximately two-thirds of all office visits are due to stress-related complaints. Although stress itself is not an illness, its impact on the physiology of our bodies is immense. Impatience, anxiety, irritability are just a few of its more obvious consequences. Patients are often not sure what is wrong with them as a stressed mind has difficulty interpreting signals from the body. Under stress, people forget to eat (or overeat), are unable to sleep well, consume alcohol, become very tense and can make poor choices. The stressors have changed over time, but human physiology has remained the same and reducing the impacts of stress on the body and mind is very important.

Humans developed a powerful stress reaction living with a risk of being attacked by wild animals or hostile people. The body responds to threats by producing powerful hormones hormones that change our physiology, enhancing our ability to flee or defend ourselves. Termed “fight or flight,” this stress response causes an intense stimulation of the sympathetic nervous system and the adrenal glands resulting in faster respiration rates, increased heart rate and contraction force, higher blood pressure. There is also decrease in digestive secretions. These mechanisms are designed to divert all available resources to protect oneself from danger. In acute stress, the situation is often resolved quickly, returning to normal state. However if stress is chronic, this response can become detrimental.

The body expends a great amount of energy keeping itself in a heightened state of readiness. Prolonged stress weakens the body in a multitude of ways. Furthermore, lack of sleep, poor diet, chemical toxins in the environment compromise the body’s ability to maintain homeostasis, resulting in illness. Adaptogenic herbs have traditionally helped prevent the imbalances that can result from stress.

An adaptogen is a substance that demonstrates a nonspecific enhancement of the body’s ability to resist a stressor. The term was first introduced in 1947 by Russian scientist N.V. Lazarev. He was first to describe the unique action of a material claimed to increase nonspecific resistance of an organism to an adverse event. In 1958, I.I. Brekhman, a Russian holistic medical doctor, and his colleague I.V. Dardymov, established the following definition of an adaptogen: It “must be innocuous and cause minimal disorders in the physiological functions of an organism, it must have a nonspecific action, and it usually has a normalizing action irrespective of the direction of the pathological state.”

There are many herbs that have these properties. In keeping with the definition, an adaptogenic herbs are plants with properties that have a normalizing effect on the body. They do not stimulate nor inhibit normal body function.

The adaptogen’s main action is the ability to help the body cope more effectively with stress. Adaptogens recharge the adrenal glands, which are the key endocrine organ, responding to stress and emotional change. The adrenals, which cover the upper surface of each kidney, synthesize and store dopamine, norepinephrine and epinephrine. These compounds are responsible for the changes that occur during the fight-or-flight reaction. An adaptogen, is used to reduce stress, both mental and physical. To put it simply: Adaptogens help you adapt.

The list of plants with adaptogenic qualities as the definition of the term is broad. considered the “gold standard” of adaptogens is red ginseng from Asia (called either Chinese, Korean, or Japanese ginseng). Other commonly accepted adaptogenic herbs include the white American ginseng, Siberian ginseng, ashwaganda, astragalus, licorice, schisandra, and Rhodiola rosea. The mushrooms reishi, shiitake and maitake are also considered as adaptogens.

Asian ginseng (Panax ginseng) is considered a chi tonic–more specifically a tonic for the yang chi–in traditional Chinese medicine. It is considered an adaptogen, providing non-specific protection against various mental, physical and environmental forms of stress. This ginseng is usually given to people who display yang deficiency–weakness in muscles, voice and constitution, for example–and is generally best avoided by those who are well muscled and large with a tendency to bursts of anger. Numerous studies support Asian ginseng’s effectiveness at improving a person’s ability to withstand stress, improve work performance and quality, and enhance mental function. It has also been shown to increase the release of adrenocorticotropic hormone (ACTH), which stimulates an increase in adrenal hormone secretion. It also can counteract the shrinkage of the adrenal gland caused by corticosteroid drugs.

Researchers from Okayama University Medical School in Japan found that Asian ginseng extract inhibited hydroxyl radical formation. The authors postulate that this antioxidant effect may be responsible for ginseng’s wide range of pharmacological applications. In a double-blind controlled study, 36 noninsulin-dependent diabetic patients were treated with Asian ginseng for eight weeks. Patients were given either 100 mg or 200 mg of Asian ginseng or placebo. The ginseng elevated participants’ moods, improved physical activity and performance, improved glycosylated hemoglobin, and reduced fasting blood sugars and body weight.
(ref. Sotaniemi, E., et al. “Ginseng therapy in non-insulin-dependent diabetic patients,” Diabetes Care, 18(10): 1373-75, October 1995.)

Asian ginseng has been shown to increase RNA and protein content in the muscle and liver tissue of laboratory animals. That same process may be the biochemical mechanism that makes ginseng such a highly regarded tonic. Asian ginseng is said to tone the chi and the lungs while strengthening the spleen and stomach and calming the spirit. Studies show this ginseng to be antidepressant, antidiabetic and antihypertensive.

Evaluating the effect of Asian ginseng in various forms–cooked, dried and fresh root–in 1,987 cancer cases, researchers found that the risk of developing certain cancers in a population that used ginseng for at least one year was less than the risk for the general population. In the study, ginseng was found to protect against cancers of the mouth, esophagus, lung, stomach, colorectum, and pancreas. The authors conclude that ginseng has a protective effect. (ref. Yun, T.K. & Choi, S.Y. “Preventative effect of ginseng intake against various human cancers: A case-control study on 1,987 pairs,”
Cancer Epid, Biomarkers and Prev, 24(3): 221-29, June 1995.)

American ginseng (Panax quinquefolius), is in the same genus as Asian ginseng, is considered a yin tonic rather than a yang tonic. As such, American ginseng is indicated for a hotter, more aggressive constitution. It contains many of the same properties as its Asian counterpart and has similar effects on the body.

Siberian ginseng (Eleutherococcus senticosus), as can be seen by its Latin name, is not actually a ginseng, but it has been called one because of its similar properties. Legislation passed in the US now prohibits Wucha, or “Elethero” from being labeled Siberian ginseng. It is found in Russia, Asia, northern China, Japan and Korea and, in fact, Russian researchers consider it to be even more effective than Asian ginseng. Studies of Wucha’s effects on human performance conducted in both Russia and China show that Wucha increases human tolerance to a broad range of stress factors, including heat, noise and increased exercise. Wucha, taken on a regular basis, for several months, increases work output, endurance, athletic performance and mental alertness. Wucha also shows remarkable protective benefits under conditions of serious oxygen deprivation. Wucha is popular among factory workers, miners, soldiers, deep sea divers and others who engage in physically and mentally demanding occupations.

Ashwaganda (Withania somnifera) also called Indian ginseng. It is seemingly grouped with the ginsengs because of its similar actions. Though unrelated to other ginsengs, it appears to share their many properties and actions. Considered a tonic, an alterative, an astringent and a sedative, ashwaganda has been used in Ayurvedic medicine for more than 2,500 years. Of all the medicinal plants used in India’s several millennia old tradition of Ayurveda, Ashwagandha, Withania somnifera, is the most highly prized. Recent studies show ashwaganda to be immuno-modulating and to aid in cases of anxiety and other psychological complaints.

Astragalus (Astragalus spp) is one of the more famous tonic herbs from China. In traditional Chinese medicine it is said to tonify the blood and spleen and aid the defensive chi. Astragalus is often added to formulations used to treat weak patients. It is also used in combination with other herbs to enhance recovery following an illness or prolonged stress and to boost vitality. Astragalus is said to protect and enhance the functioning of distressed organs. Numerous studies show the herb enhances immune function by increasing natural killer cell activity, increasing T cell activity, and enhancing macrophage activity [20] in immune-compromised patients.

(ref. Yang, Y.Z., et al. “Effect of Astragalus membranaceus on natural killer cell activity and induction with Coxsackie B viral myocarditis,” Chin Med J, 103(4): 304-7, 1990.

Zhos, K.S., et al.
“Enhancement of the immune response in mice by Astragalus membranaceus extracts,”
Immunopharmacol, 20(3): 225-33)

Licorice root (Glycyrrhiza glabra and G. uralensis), used in Chinese medicine, is said to tonify the spleen and strengthen chi. Licorice is perhaps the only herb claimed to benefit all 12 meridians in Chinese medicine. Rich in both saponins and flavonoids, it is anti-inflammatory because the saponins have a structure similar to that of corticosteroids. Licorice root also promotes or enhances immune system functioning and has a stimulating effect on the adrenal cortex.

Components of licorice exhibit numerous pharmacological actions, including aldosterone like action. Licorice root has also been used to treat addison’s disease and following steroid use. Today the primary uses of licorice root are as an expectorant for coughs and bronchial catarrh (inflammation of a mucus membrane with a free discharge), and for treating gastritis and ulcers. Glycyrrhizin, a constituent of licorice root demonstrated antiviral, antimicrobial, anti-inflammatory, hepatoprotective, and blood pressure-increasing effects in vitro and in vivo.
Caution: Because of its aldosterone like effect, licorice root may cause sodium retention and thus contribute to high blood pressure in some people.

Schisandra (Schisandra chinensis, also called wuweizi by the Chinese) can be used as an adaptogenic tonic to counter the effects of stress and fatigue. The berry of Schisandra chinensis owes its name Wu Wei Zi (five flavored berry) to the fact that it is sweet, sour, salty, bitter and pungent. Scientific studies show it has normalizing effects in cases of insomnia and improves mental coordination and physical endurance. Research suggests schisandra may actually influence electrical discharges in the brain.

Rhodiola Rosea is well studied adaptogen, Rhodiola defends the body overall, and protects general health and well-being. Its anti-stress and fatigue-fighting properties make it one of the most popular botanicals in all of Siberia. A 2014 study published in Journal of Phytomedicine, concluded that “Rhodiola exhibits a multi-targeted effect on transcription to regulate the cellular response, affecting the various signaling pathways and molecular networks associated with beneficial effects on emotional behavior, particularly aggressive behavior, and with psychological, neurological, cardiovascular, metabolic, endocrine, and gastrointestinal disorders. Each of the purified compounds has its own pharmacological profile, which is both similar to and different from that of the total Rhodiola extract. In general, several compounds contribute to the specific cellular or/and physiological function of the extract in various diseases”.
(ref: Phytomedicine. 2014 Sep 25;21(11):1325-48. doi: 10.1016/j.phymed.2014.07.008. Epub 2014 Aug 7.
Mechanism of action of Rhodiola, salidroside, tyrosol and triandrin in isolated neuroglial cells: an interactive pathway analysis of the downstream effects using RNA microarray data.
Panossian A1, Hamm R2, Wikman G3, Efferth T2.)