Helicobacter Pylori Infection (H. Pylori)

What Is Helicobacter Pylori (H. Pylori) Infection?

[dropcap]H[/dropcap]elicobacter pylori infection is a potentially deadly stomach disease characterized by chronic superficial inflammation and ulcerations in 100% of infected patients.

This infection disrupts normal defense and repair of the stomach lining and is difficult to cure. H. pylori is classified as a class I carcinogen because of its ability to cause cancer.

The causative organism is a gram negative and mobile bacteria. What enables H. Pylori bacteria to be mobile, or able to move about, is a whip-like action of its 4 to 6 flagella (thread-like structures).

Q: How does the bacteria damage the stomach’s mucosal lining?

A: Healthy mucosa protects underlying tissues from hydrochloric acid that is normally present in stomach juice for the purpose of dissolving food. However, invasion by these bacteria inflame and swell the stomach mucosal lining, and this raw damage makes the mucosa susceptible to further injury from hydrochloric acid…like pouring vinegar on a serious sunburn.

H. pylori infection induces oxidative stress, which has been shown to play a very important role in the inflammation of the gastric mucosa and increases the risk of developing gastric cancer.¹

Besides damaging the stomach lining, H. pylori bacteria impair iron sufficiency in the body. These bacteria deplete iron from the body by using it for its own growth. Also, a considerable amount of iron never makes it out of the stomach to enter the duodenum where it should normally be absorbed into the body.

How is this infection diagnosed? The gold standard diagnostic test for H. pylori is by stable isotope breath test.

• During the test, you swallow a special substance that has urea. Urea is a waste product the body produces as it breaks down protein. The urea used in the test has been made harmlessly radioactive.
• If H. pylori are present, the bacteria convert the urea into carbon dioxide, which is detected and recorded in your exhaled breath after 10 minutes.
• This test can identify almost all people who have H. pylori. It can also be used to check that the infection has been fully treated.²

Medical treatment uses two or three antibiotics to kill the bacteria and medications to block acid secretion such as omeprazole (Prilosec® and others). Unfortunately, H. pylori is becoming resistant to antibiotics, resulting in treatment failure.³ Extensive and unreasonable application of antibiotics is the main cause of antibiotic resistance which is a challenging situation for clinicians.³

H. pylori eradication treatment may fail for a number of reasons, including H. pylori strain factors, host factors, environmental factors, and inappropriate treatment.³

Importantly, numerous medicinal plants have been reported for their anti-H. pylori activity.⁴ See more below under “6 Steps To Improve H. Pylori Infection In Celiac Disease and/or Gluten Sensitivity.”

Nontreated H. pylori infection is a major pathogenic factor for the development of gastritis, duodenal ulcer, and gastric cancer.⁵ In fact, 10 to 50 percent of infected individuals develop peptic ulcer disease (PUD), and 1%-3% of PUD patients progress to gastric cancer.⁶

More than 50% of the world population is infected with H. pylori. Of them a high percentage remain asymptomatic, but they are still at risk of developing the diseases associated with H. pylori.⁷

What Is H. Pylori Infection In Celiac Disease and/or Gluten Sensitivity?

• Relationship between H. pylori infection and celiac disease: H. pylori infection is an associated disorder in celiac disease. Micronutrient homeostasis is frequently impaired in H. pylori–infected individuals,⁵and this makes the health worse for those with celiac disease who are infected.  On the other hand, lymphocytic gastritis is strongly associated with celiac disease, with increasing prevalence correlating with more advanced villous atrophy. Chronic active gastritis and chronic inactive gastritis are also significantly associated with celiac disease and this inflammation increases risk of infection by H. pylori bacteria.⁸

• Relationship between H. pylori infection and gluten sensitivity. Gluten inflames the mucosal lining of the stomach, making it susceptible to bacterial invasion.

• Relationship between H. pylori infection and gastritis. In gastritis, lymphocytosis (abnormal increase in white blood cells called lymphocytes) of the stomach lining  is induced by H. pylori infection. However, this increase becomes less obvious on microscopic exam of stomach biopsies from people with celiac disease because profound inflammatory and structural changes by gluten alter the mucosal architecture or appearance. This study also provides further support for a pathogenetic relationship between celiac disease and lymphocytic gastritis.⁹

• Relationship between H. pylori infection and severity of villous atrophy. In a study of 312 patients with H. pylori of whom 72 of them had a diagnosis of celiac disease, there was not a significant difference in terms of the severity of small intestinal villous atrophy in patients with helicobacter pylori infection compared to those without it.¹⁰

• Relationship between H. pylori infection and vitamin C deficiency. Vitamin C deficiency increases the risk and severity of infection by H. Pylori. On the other side, H. pylori induces depletion of vitamin C, with or without gluten sensitivity, by excessive use by the body for its anti-oxidant properties to fight damage by H. pylori. Studies demonstrate the direct inhibitory impact of this vitamin on the growth of H. pylori. Vitamin C is highly concentrated in stomach mucosa and gastric juice and probably lowers the risk of gastric cancer and influences the course of H. pylori infection through a number of mechanisms. It has a positive impact on the stimulation and activity of white blood cells (granulocytes, macrophages, and lymphocytes) and the production of immunoglobulin (antibodies).¹¹ Jarosz et al. showed that four-week treatment of H. pylori infected patients with chronic gastritis with a high dose of vitamin C caused H. pylori eradication in 30% of cases.

• Relationship between H. pylori infection and selenium deficiency. Selenium deficiency increases the risk for H. pylori  invasion and the severity of infection.¹² Treatment with selenium by its powerful anti-oxidant properties reverses inflammation.

• Relationship between H. pylori infection with celiac disease and anemia unresponsive to treatment with iron and gluten-free diet:  H. pylori and celiac disease frequently are found in association with refractory iron-deficiency anemia (unresposive to treatment). It might be entirely appropriate and cost effective to incorporate H. pylori investigations in patients with iron-deficiency anemia and those patients who have a diagnosis of celiac disease with persistent anemia in addition to a gluten free diet.¹³

H. pylori infection is a factor responsible for iron deficiency in celiac disease patients who are predisposed to iron-deficiency anemia by means of the following mechanisms:¹⁴

* Infection causes considerable decrease in the concentration of gastric juice ascorbic acid (vitamin C) that is the best promotor of non-heme iron absorption from food. Non-heme iron comes from plant sources. Heme iron comes from animal sources and is the type of iron in the body.

* Infection may significantly increase iron demand from the body iron stores because iron is an essential bacteria growth factor for H. pylori.

* Bacteria contain a 19.6 kilodalton protein resembling ferritin (iron molecule in the body) with a binding activity for heme iron in erythrocytes (red blood cells). So in this way, H. pylori steals iron from the body.

* Infection probably increases lactoferrin uptake from neutrophils (white blood cells) and significantly increases iron demand.

• Relationship between H. pylori infection and vitamin B12 deficiency. H. pylori predisposes to a vitamin B12 deficiency and related manifestations (macrocytic anemia or neurological manifestations) by severe malabsorption of vitamin B12 from food.¹⁵How? Gastritis caused by the infection leads to dysfunction of the gastric glands in the stomach lining that produce intrinsic factor; these are the same glands that produce hydrochloric acid. Intrinsic factor is absolutely required for vitamin B12 to be absorbed later in the small intestine.  The end result is vitamin B 12 deficiency.

• Relationship between H. pylori infection and anti-oxidants. Foods containing alpha-lipoic acid, a powerful anti-oxidant, are shown to inhibit inflammation of the stomach lining that is caused by H. pylori.¹⁶

• Relationship between H. pylori infection and low stomach acid. H. pylori induces atrophic gastritis which typically produces low stomach acid (hypochlorhydria). Nitrite levels in the gastric juice are increased which probably result from bacteria within the stomach generating nitrite from dietary nitrate. Nitrite compounds damage DNA.¹⁷ Food sources of nitrite and nitrate include preseved meat such as ham and cold cuts.

• Relationship between H. pylori infection and bone loss. H. pylori infection is associated with a significant decrease in mean lumbar bone mineral density but not at the femoral neck and total femur. H. pylori infection causes chronic gastritis by inducing a localized and systematic inflammatory response that may increase the concentrations of tumor necrosis factor-α, interleukin-1, and interleukin-6, which are known to affect bone mineral density.¹⁸

How Prevalent Is H. Pylori Infection In Celiac Disease and/or Gluten Sensitivity?

• H. pylori infection has a 21% prevalence in untreated celiac disease patients of whom 71% had iron deficiency anemia.¹⁹
• The prevalence of helicobacter pylori infection among celiac disease patients was 12.5% compared to 30% in non-celiac patients.
• A pediatric study of 226 children diagnosed with celiac disease found a prevalence for helicobacter infection of 2.7%.²⁰

What Are The Symptoms Of H. Pylori Infection?

H. pylori infection is marked by these symptoms, although most patients remain asymptomatic:²¹

• Belching, probable due to poor digestion.
• Bloating after eating food, probable due to poor digestion.
• Dark, tarry stools, if bleeding is present.
• Dyspepsia or indigestion.
• Gastritis, which may or may not be painful.
• Gnawing pain due to peptic ulcers, if present.
• Heartburn, probable.
• Iron deficiency anemia, causing fatigue, pallor, shortness of breath, irritability, and weakness.
• Muscle wastin (loss).
• Nausea, probable.
• Pain due to gastric ulcerations, possible.
• Vitamin B12 deficiency, causing fatigue, pallor, shortness of breath, irritability, and weakness.
• Vitamin C deficiency.
• Vomiting, possible.

How Does H. Pylori Infection In Celiac Disease and/or Gluten Sensitivity Develop?

• H. pylori infection results from invasion of an inflamed gastric lining by bacteria enabled by lowered resistance to infection, low gastric acidity, and nutrient deficiencies in celiac disease.²²
• Niacin deficiency predisposes to infection because of lowered health of stomach mucosa that develops without adequate niacin.
• A recent meta-analysis of epidemiologic data from 46 studies on vitamins and 10 studies on trace elements identified a significant association of H. pylori infection with lowered concentrations of ascorbic acid and cobalamin (vitamin B12).⁵

Does H. Pylori Infection Respond To Gluten-Free Diet?

Yes. Treatment of celiac disease-related H. pylori infection could be associated with a strict gluten-free diet.²³

A gluten-free diet is equally effective in infected as in uninfected patients.⁹

However, to inhibit H. pylori this diet should be rich in fruit and vegetables including onion, citrus fruits, olives, peas and beans with fish and honey;

and lower in fatty meat such as fast food burgers and sausages, meats preserved with nitrate/nitrites (ham, cold cuts), mayonnaise, soft drinks, and carbohydrate.²⁴

• Polyphenols. Polyphenols are compounds  that actively promote health and prevent disease. They are found in whole, unrefined fruits and fruit drinks, vegetables and vegetable drinks, legumes (peas and beans), and grain. The deeper the color, such as blueberries and cranberries, the richer the polyphenol.

As regards H. Pylori infection, medicinal plant compounds and other natural products provide another choice or opportunity to eradicate H. pylori infection. Plant foods that have documented anti-H. pylori induced gastric inflammatory effects include quercetin (many fruits and vegetables such as red onion, buckwheat, kale, cranberries, plums, and sweet potato), apigenin (many fruits and vegetables such as parsley and celery), carotenoids-rich algae, tea product, garlic extract, apple peel polyphenol, and finger-root extract.⁴,²⁵

2).  As regards peptic ulcer disease that develops from H. Pylori infection, eating a significant amount of dietary polyphenols in the diet or as part of dietary supplementation  along with conventional treatment can result in perfect security and treatment of peptic ulcer.²⁶

• Selenium. Foods containing selenium are important to restore adequate levels to fight inflammation caused by H. pylori. These include Brazil nuts (highest source), cold water fish such as tuna and cod, beef, chicken, shellfish, eggs, garlic, brown rice, nuts and Swiss chard.
• Alpha-lipoic acid. Foods containing alpha-lipoic acid are shown to inhibit inflammation caused by H. pylori. These include beef, some organ meats, spinach, broccoli, and peas.
• Vitamin B12. Foods containing vitamin B12 are necessary to restore normal levels in the body. These foods are animal sources including clams, beef liver, oysters, crab, tuna, halibut, milk, pork, egg, cheese, and yogurt.
• Probiotics. Probiotic administration in the majority of research cases, show an improvement in H. pylori gastritis and a reduction in bacterial colonization. In any case, eradication could be completely attained.²⁷

Note: Studies have found that in patients who have undergone periodontal therapy and an oral cleansing process, the H. pylori eradication rate was significantly higher than that of patients who did not, suggesting that H. pylori may be spread through saliva.³

6 Steps To Improve H. Pylori Infection In Celiac Disease and/or Gluten Sensitivity:

• [dropcap]1[/dropcap]Remove the Trigger. Maintain a Strict, Nutritious Gluten Free Diet:

[box type=”shadow” ]Treatment. In combination with antibiotic therapy, this condition responds to the complete elimination of gluten, which is the required treatment that improves both gastric and gut health in people with gluten sensitivity.

• Gut health is the foundation to restore ALL health. Restored health will enable you to maintain a strict gluten free diet, just as other life tasks will be easier.
• A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.
• Cutting out bread and other obvious sources of gluten is not good enough for recovery. Even 1/8th teaspoon of flour or bread crumb is enough to sustain the inflammation that is damaging your small intestine, causing increased permeability (leaky gut) and allowing undigested gluten to enter your body where it can damage structures and function, and instigate immune inflammatory responses.

Correct Your Individual Nutritional Needs.

• Eat foods that can replenish missing nutrients. Find them under NUTRIENT DEFICIENCIES.
• Take nutritional supplements as needed. Find them under NUTRIENT DEFICIENCIES.

Recovery from H. pylori infection. You should begin to feel better within a week and notice more energy as inflammation subsides and the gastric cells that make up the surface lining of your stomach are better able to function.

Gastric cells lining the stomach are replaced every 3 days. The healing process is like sunburn where the damaged surface layer of skin sloughs off and is replaced with new normal cells.

Recovery from gluten. You should begin to feel better within a week and notice more energy as inflammation subsides and the  absorbing cells that make up the surface lining of your small intestine are better able to function.

• Intestinal lining cells are replaced every 5 days.
• Leaky gut normally resolves in two month after starting a gluten free diet and brings about a big improvement in health. Improvement in intestinal permeability precedes morphometric recovery (cell appearance and structure) of the small intestine in celiac disease.²⁸
• The intestinal lining may take up to a year to heal.[/box]

• [dropcap]2[/dropcap] Reduce Inflammation. Foods to Eat and Foods Not to Eat:

Because gluten is inflammatory, eliminate OTHER inflammatory foods from your diet to reduce an additive effect to gluten. At the same time, try to eat foods that reduce inflammation (anti-inflammatory).

[box type=”shadow” ]Here Are Major Inflammatory Food Types That Reduce Healing:

• Damaging Foods. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk disrupts intestinal permeability causing leaky gut.²⁹
• Allergenic Foods. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.
• Shelf Stable Processed Foods. Includes any that contain additives and preservatives. Look for them on the nutrition label of the box or package. Additives and preservatives also disrupt intestinal permeability causing leaky gut.²⁹
• Fats. Limit deep fried foods, trans-fats, saturated fats (animal fat/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Rancid fats, sodium caprate (a medium chain fat), and sucrose monester fatty acid (a food grade surfactant) induce significant disruption of the intestinal barrier that causes leaky gut.²⁹.
• Excessive Refined White Flours (bran layer removed). Includes products made from them such as cookies, bread, cakes, pies. Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream. Also disrupt intestinal permeability causing leaky gut.²⁹
• Refined Sugars.  Includes white sugar, corn fructose and high fructose corn syrup.
• Certain Spices. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.²⁹
• Alcohol and Caffeine. Disrupt intestinal permeability causing leaky gut.²⁹[/box]

[box type=”shadow” ]Here Are Important Anti-Inflammatory Food Types to Promote Health:

• Foods to eat that specifically inhibit H. pylori and/or reduce stomach inflammation and the damage this bacteria can  cause.

Honey and green/black tea intake reduce prevalence of H. pylori infection and also inflammation and erosion.³⁰

Broccoli and red wine inhibit infection while being consumed but do not eradicate.

Celery preparations have been used extensively for several millennia as natural therapies for acute and chronic painful or inflammatory conditions and are now verified by medical research to specifically inhibit H. pylori.³¹

Pea protein prevents H. pylori from adhering to the stomach wall and as such acts to prevent infection.⁷

Probiotics. These foods supply friendly, necessary microbes needed for colon health and health of the body such as these fermented foods: yogurt, kefir, and unpasteurized apple cider vinegar.

Anti-H. pylori species of Bifidobacterium inhibits adhesion to the stomach mucosa by competition with H. pylori. Several studies have demonstrated a direct relationship between the addition of potential probiotic strains and the inhibition of H. pylori growth. These include Lactobacillus acidophilus, Lactobacillus casei strain Shirota, Bacillus subtilis, and Weissella confusa, among others.

In the majority of research cases, an improvement in H. pylori gastritis and a reduction in bacterial colonisation were associated with probiotics administration, and in any case, eradication could be completely attained.⁷

• Prebiotics/ High Fiber Foods.  Food with fiber keeps our population of probiotics healthy.

• Fruits. Anti-H. pylori fruits include plums, cranberries, apples with skin, and citrus.

In general, all fruits contain ample amounts of vitamins, minerals and phytochemicals which are naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens.

• Non-Starchy Vegetables. Anti-H. pylori vegetables include kale, onion, broccoli, and garlic.

In general, these vegetables support intestinal integrity and provide ample amounts of vitamins, minerals and phytochemicals.

• High Quality Complex Carbohydrates. Anti-H. pylori vegetables include green peas, beans and sweet potatoes.

In general, complex carbohydrate foods provide vitamins, minerals, and fiber while boosting serotonin levels to help you relax and feel calm. These plant sources includes whole grains, legumes, and root vegetables such as carrots, parsnips, turnips, red beets, and others.

• Antioxidants. Specific anti-H. pylori sources include olives, green tea, and black tea.

In general, antioxidant foods protect the body from inflammatory oxidant molecules that continually occur and help us handle stress and reduce irritability. Includes vitamin C-containing foods such as lemon, grapefruit, apricot, Brussels sprouts and strawberries, and others. Also, includes vitamin E-containing foods such as nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.

• Omega-3 Fatty Acids. Balance opposing omega-6 fatty acids and bad fats. Fish sources includes tuna, salmon, cod, and others. Plants sources include flax, chia seeds, canola oil, and others.
• Protective Herbs and Spices.  See below #6 below for examples.[/box]

• [dropcap]3[/dropcap] Information Sheet You Can Take to Your Doctor or Other Health Professional:

Click here.

 

• [dropcap]4[/dropcap] Manage Your Medications Safely: 

[box type=”shadow” ]Certain prescription drugs deplete iron that worsens the iron depletion caused by H. pylori infection. Those that deplete vitamin B12 worsen the depletion caused by H. pylori infection. Those that deplete niacin, vitamin C, and selenium increase the risk of infection. Ask your doctor or pharmacist about this possible adverse effect if you are taking any of the drugs listed below. Do not stop prescribed medications without supervision.

 This is not a complete listing.

ANTACIDS / ULCER MEDICATIONS

• Pepcid®, Tagamet®, Zantac® deplete Iron, among others.
• Prevacid®, Prilosec® commonly used to treat H. Pylori deplete Vitamin B12, among others.
• Magnesium and Aluminum Antacid preparations (Gaviscon®, Maalox®, Mylanta®) deplete Iron, among others.

ANTI-DEPRESSANTS

• Adapin®, Aventyl®, Elavil®, Pamelor®, Paxil®, Zoloft®, and others deplete Vitamin B12 among other.

ANTIBIOTICS disrupt intestinal permeability which complicates celiac disease and / or deplete iron, probiotics, vitamin C.

• Gentomycin, Neomycin, Streptomycin, Cephalosporins, Penicillins deplete Probiotics, Vitamin B12, Vitamin C among others.
•  Tetracyclines deplete Iron, Probiotics.
• Penicillins deplete Vitamin B12, Probiotics among others.³²
• Erythromycin depletes Vitamin B12, Probiotics, among others.³³

ANTI-INFLAMMATORIES disrupt intestinal permeability which complicates celiac disease and depletes nutrients.

• Corticosteroids (Prednisone, Medrol®, Aristocort®, Decadron) deplete Vitamin C, Vitamin B12, Selenium among others.
• Aspirin and Salicylates deplete Vitamin C, Iron among others.

ANTICONVULSANTS disrupt intestinal permeability and depletes nutrients.

• Phenobarbital and Barbituates; and Dilantin®, Tegretol®, Mysoline®, Depakane/Depacon® deplete Vitamin B12, Selenium, among others.

ANTI-INFLAMMATORIES  disrupt intestinal permeability and depletes nutrients.

• Aspirin and Salicylates deplete deplete Iron among others.

ANTIVIRAL AGENTS

• Zidovudine (Retrovir®, AZT and other related drugs) deplete Vitamin B12, among others.

CHOLESTEROL DRUGS

• Colestid® and Questran® deplete Iron, Vitamin B12 among others.

DIABETIC DRUGS 

• Metformin® depletes Vitamin B12, among others.

DIURETICS

• Loop Diuretics (Lasix®, Bumex®, Edecrin®) deplete Vitamin C, among others.

FEMALE HORMONES disrupt intestinal permeability and deplete nutrients.

• Oral Contraceptives (Norinyl®, Ortho-Novum®, Triphasil®, and others) deplete Niacin, Vitamin B12, Vitamin C, Selenium,among others.

 

[/box]

• [dropcap]5[/dropcap]Nutritional Supplements To Help Correct Deficiencies:

[box type=”shadow” ]

The type and quantity of nutritional supplements that may be needed depend on which nutrients are deficient. Please search individual nutrients at right for more information.

• Multivitamin/mineral combination that provides 100% once a day is useful to improve overall nutrient levels. This is a safe dose, but always check with your doctor to avoid interactions with medications.
• Ferrous fumarate or gluconate by mouth as prescribed following blood test for iron status necessary for follow-up.
• Niacinamide by mouth is the preferred form of vitamin B3 supplementation to restore niacin status. Other B vitamins should also be taken at the same time because these vitamins work together.
• Vitamin B12 in tablet or as part of multi-vitamin supplement to restore normal level as prescribed following blood test for status necessary for follow-up.
• Selenium by mouth to restore normal levels if deficient.
• Resveratrol treatment exerts significant effects against oxidative stress and inflammation in H. pylori-infected mucosa.³⁴
• Glutamine supplementation by mouth may be beneficial for preventing gastric inflammation as well as oxidant-mediated carcinogenesis (start of a cancer).³⁵
• Alpha-Lipoic Acid by mouth to inhibit stomach inflammation.
• Vitamin C (ascorbic acid) by mouth to reduce gastric inflammation.

Storage Note for Supplements: Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet  – not in the bathroom or on the kitchen table.[/box]

• [dropcap]6[/dropcap]Manage Natural Remedies:

[box type=”shadow” ]Hydration:

• Eight glasses of water are recommended per day unless there is a contraindication such as kidney or heart disease. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water, from all beverages and foods, each day for women and 3.7 liters (125 ounces) daily of total water for men.
• If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.
• Hydration Test: Urine should be pale yellow. Fingertips should be plump, without pruning but this may not be reliable when fingers are swollen with edema. Lips should be plump, without puckering. The feeling of thirst can be unreliable.
• What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.[/box]

[box type=”shadow” ]Carminatives are plant sources that tone muscle and improve peristalsis, and thus aid in the expulsion of gas from the stomach and intestine to relieve digestive colic and gastric discomfort. Puree any foods that cannot be thoroughly chewed. Cook meats well or make them into soups and stews for ease of digestion.

Carminative Food Remedies:

• Raspberry.
• Carrot is also a cleansing digestive tonic.
• Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.
• Redbeets stimulate and improve digestion and are easily digested.
• Cabbage stimulates and improves digestion and is also a liver decongestant.
• Lettuce stimulates and improves digestion and is also an alterative, meaning it improves the function of organs involved with the digestion and excretion of waste products to bring about a gradual change.
• Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.

Carminative Herb Remedies:

• Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa. Drink as tea or use in cooking.
• Chamomile (as a tea) also promotes healing and helps relieve nervous tension. Drink as a tea.
• Parsley relieves colic, gas and indigestion.
• Rosemary as a tea and in cooking also is a nervous system tonic for stress and fatigue, bile stimulant, and can relieve headaches and indigestion.
• Thyme is a soothing remedy useful for stimulating digestion of rich, fatty foods.
• Plantain is a common garden weed that has soothing, wound healing properties for the stomach. Drink 3 cups of tea a day. Steep a tablespoon of fresh leaves in hot water for 10 minutes.³⁶

Carminative Spice Remedies:

• Cloves are also antispasmodic.
• Nutmeg is also useful for abdominal bloating, indigestion and colic.
• Ginger also supresses inflammation.[/box]

[box type=”shadow” ]Exercise Helps:

Exercise improves circulation and rids the body of toxins.

• Walking is aerobic exercise that reconditions the whole body to improve stamina. Read more about Exercise and Fitness.
• Weight training builds muscle. Read more about Exercise and Fitness.
• Stretching improves flexibilty. Read more about Exercise and Fitness.

Note: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal. [/box]

What Do Medical Research Studies Tell About H. Pylori Infection In Celiac Disease and/or Gluten Sensitivity?

RESEARCH STUDY SUMMARIES

“Helicobacter pylori prevalence in patients with celiac disease: results from a cross-sectional study.” This study investigating the prevalence of Helicobacter pylori infection in celiac subjects found prevalence of helicobacter pylori infection among celiac disease patients was 12.5%, compared to 30% in non-celiac patients.Among those celiac subjects with concomitant helicobacter pylori infection, histological damage degree and presence of endoscopic markers suggesting villous atrophy seem to be similar to those without helicobacter pylori infection.

Between January 2013 and June 2014, patients over 18 years old undergoing upper endoscopy who required both gastric and duodenal biopsies were included for analysis. Enrolled subjects were divided in two groups: those with a diagnosis of celiac disease and those without a celiac disease diagnosis. Helicobacter pylori infection prevalence was compared between groups. Among celiac patients, endoscopic markers of villous atrophy as well as histological damage severity were compared between those with and without helicobacter pylori infection.

Overall, 312 patients were enrolled. Seventy two of them had a diagnosis of celiac disease. There was not a significant difference in terms of the severity of villous atrophy in patients with helicobacter pylori infection compared to those without it. There was a slight increase in the prevalence of endoscopic markers in those helicobacter pylori-negative celiac subjects.³⁷

“Dietary Intervention of Artemisia and Green Tea Extracts to Rejuvenate Helicobacter pylori-Associated Chronic Atrophic Gastritis and to Prevent Tumorigenesis.” This study evaluating the efficacy of long-term dietary administration of artemisia and/or green tea extracts on H. pylori-initiated, high-salt-promoted chronic atrophic gastritis (inflammation of stomach lining) and gastric tumor development in mice found that long-term dietary intake of artemisia and/or green tea can be an effective strategy either to rejuvenate H. pylori atrophic gastritis or to suppress tumor development.

Helicobacter pylori-infected and high-salt-diet-administered mice were administered with artemisia extracts (MP group) and/or green tea extracts (GT group) for 36 weeks in addition to the control group (ES group, gastroprotective drug, ecabet sodium 30 mg/kg, diet pellet). Gross and pathological gastric lesions were evaluated after 24 and 36 weeks, respectively, and their underlying molecular changes were measured. Detailed mechanisms were further evaluated in in vitro cell models.

The inflammatory and nodular changes and mucosal ulcerative and erosive lesions were noted in the control group at 24 weeks. MP, GT, MPGT, and ES groups all showed significantly improved pathologic lesion compared to the control group.

After the 36 weeks, scattered nodular masses with some central ulcers and thin gastric surface were noted in the control stomach, whereas no tumor and milder atrophic changes were observed in all MP, GT, and MPGT groups except ES group. On molecular analysis, increased expressions of COX-2, TNF-α, IL-6, lipid peroxide, and activated STAT3 relevant to H. pylori infection were significantly decreased with MPGT administration, whereas protective HSP70 (mucin) was significantly increased. Core tumor suppressors involved in cancer development, were significantly decreased with H. pylori infection, but significantly increased in MPGT group.

Increased mucosal apoptotic (cell death) index that was noted in the control group was significantly decreased with MP and/or GT along with significantly preserved stomach gastroprotective mediators such as mucins. H. pylori-induced TNF-α and NF-κB activations in blood were significantly decreased with MPGT administration.³⁸

“Endoscopic and histopathological findings of the upper gastrointestinal tract in patients with functional and organic dyspepsia.” This retrospective study investigating the frequency and type of the macroscopic and histopathological changes in the upper GI endoscopy in patients with symptoms of dyspepsia found that the most common endoscopic lesion was gastritis (inflammation of the stomach), mostly erythematous-exudative and less often atrophic. The presence of H. pylori infection was varied in the different types of inflammation. H. pylori infection occurred most frequently in the case of erosive and follicular gastropathy.

Regardless of the severity of lesions of the upper GI endoscopy, it is advisable to take biopsy from the gastric and duodenal mucosa, which allows for an individualized management of these patients. Celiac disease was found in 3.3% of these patients, and should be considered in the diagnosis of the causes of dyspepsia.

Included in this study were 212 patients with dyspepsia, at the age of 18-84 years, including 60 patients to 45 years of age (group I) and 152 patients older than 45 (group II) who underwent gastroscopy. Biopsy specimens were taken from the gastric and duodenum for microscopic examination. The presence of H. pylori infection has been established on the basis of histopathological examination and positive rapid urease test. Normal gastric and duodenal mucosa was revealed in 30% of patients in group I and 9.2% in group II.

In all patients, in whom biopsy specimens were taken from normal duodenal mucosa (14% of patients), histopathological examination revealed the presence of non-specific inflammation, regardless of the coexistence of H. pylori infection.³⁹.

“Endoscopic and histological gastric lesions in children with celiac disease: mucosal involvement is not only confined to the duodenum.” This retrospective study investigating gastric mucosa involvement in celiac children and control subjects found that gastritis is a common finding in children with celiac disease and adolescents in whom 2.7% had helicobacter pylori infection.

In 226 patients with celiac disease (median age: 5.7 years) at diagnosis and 154 controls (median age: 7.4 years), the evaluation of gastric and duodenal mucosa was performed. Celiac disease was diagnosed according to the North America Society for Pediatric Gastroenterology, Hepatology, and Nutrition criteria. Gastric lesions were classified according to Updated Sydney System. Anti-gastric parietal cell antibodies were assayed by enzyme-linked immunosorbent assay.

A total of 21.2% and 7% of patients with celiac disease showed chronic superficial gastritis and lymphocytic gastritis, respectively. Helicobacter pylori infection was found in 6 (2.7%) children with celiac disease. Chronic superficial gastritis was present in 21.4% of controls. No control subject showed lymphocytic gastritis. Among patients with chronic superficial gastritis, helicobacter pylori infection was more frequent in controls than in celiac children. Ten of 90 patients with celiac disease and 1 of 29 controls were positive for anti-gastric parietal cell antibodies.

“Our data suggest the hypothesis that lymphocytic gastritis may be related to a longer exposure to gluten. The presence of anti-gastric parietal cell antibodies may suggest the presence of an underlying autoimmune process.⁴⁰

“Helicobacter pylori infection in patients with celiac disease.” This study which retrospectively evaluated the clinicopathological features of 80 duodenal and gastric biopsies from patients with celiac disease found that the clinical features of celiac disease patients are unrelated to H. pylori gastritis, and a gluten-free diet is equally effective in infected as in uninfected patients.

At baseline, 30 patients had H. pylori infection and 50 did not; at follow-up five new infections were detected. Fifteen patients (3 H. pylori-positive and 12 negative) had lymphocytic gastritis. At baseline, a greater proportion of H. pylori-negative patients had severe villous atrophy, but milder forms were more prevalent in H. pylori-positive patients. After a gluten-free diet, significant improvement occurred in all duodenal features, irrespective of H. pylori status; gastric variables did not change, except for lymphocytic, which resolved in 2 infected and 10 noninfected patients.

Biopsies were obtained from 80 adults with histologically and serologically confirmed celiac disease before and after 12-18 months of a gluten-free diet. Gastritis was classified and scored according to the Updated Sydney System; duodenal biopsies were classified using both the Marsh-Oberhuber and a simplified classification proposed by our group.

The higher prevalence of milder duodenal lesions in celiac disease patients with H. pylori infection suggests that lymphocytosis induced by H. pylori gastric infection becomes less obvious as profound inflammatory and structural changes by gluten alter the mucosal architecture. This study also provides further support for a pathogenetic relationship between celiac disease and lymphocytic gastritis.⁹

“Link between helicobacter pylori infection and iron-deficiency anaemia in patients with coeliac disease.” This study investigating the potential relationship between H. pylori and iron deficiency anemia in 362 patients with celiac disease demonstrated a significant association between H. pylori and iron deficiency anemia.

Bacteria impair iron absorption by means of several mechanisms: 1) considerable decrease in the concentration of gastric juice ascorbic acid that is the best promotor of non-heme iron absorption, 2) may significantly increase iron demand because iron is an essential bacteria growth factor, 3) contain a 19.6 kilodalton protein resembling ferritin with a binding activity for heme iron in erythrocytes, and 4) the gastric colonization by H. pylori probably increases lactoferrin uptake from neutrophils and significantly increases iron demand. Screening for H. pylori proposed because the infection may worsen the alterations of iron metabolism in patients with celiac disease.⁴¹

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