Rosacea – Hashimoto’s – Helicobacter pylori

A Hashimoto’s patient wrote about her experience with a gastroenterologist seeking antibiotics for an H. pylori infection. She initially sought my assistance with her Rosacea. Her face was like a bad sunburn and she suffered constant burning which would flair up with food or sugar. While at the same time, she was experiencing symptom of hypoglycemia. After eating she would experience extreme nausea and dizziness, feeling like she was going to pass out. She was being treated for Candida and had spent the last eight months following a very strict Candida diet.

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I gave her a Metametrix 2100 Gastrointestinal Function Profile (GIFX) test kit. The results showed a severe oral infection, H. pylori and a severe exposure ingested mold from her home. The GIFX is able to distinguish mold vs. Candida. She did not have Candida but did have Yeast/Fungi: Taxonomy Unavailable – an ingested mold from her home. The H. pylori were killing her stomach linings ability to produce stomach acid that allowed the mold to enter her digestive tract unsterilized. This was her email:

“Hi. Dr. Peterson:

Today was my GI appointment with the Barnes doctor.  It went about the way I expected.

He did not take the GIFX lab test results or me seriously.  He said he did not believe the lab test results and actually said that some of the items on the test were not measureable.  He hinted at quackery.

He said that I was old enough to have had a colonoscopy and have not, so he wanted to schedule one right away.  I was OK with that since it is time to get one.  He said that they could do a stomach biopsy at the same time.  I said NO, that we did not need to do anything so invasive.  He said that we should then do a blood test for the H-pylori.  He said that IF the blood test was positive, then he would treat the infection with antibiotics.  He did not offer a breath test, and I figured that the blood test would be more accurate than the breath test.

Hopefully we should have the results this week yet.  I told him that I understood that the H-pylori bacteria could move to different organs and part of the body.  He said NO that it remains in the lining of the stomach.  I said that it takes on a different name when it leaves the stomach.

He said that absolutely is not true.  I said this is what I have been dealing with for 15 months – Different opinions from different doctors. He said this is not an opinion.

He did not know anything about lectins, nor what being on a Paleo diet meant as far as allowable foods.

He had no concern regarding my weight loss or my Rosacea.  He did not know that there was a link between H. pylori and Acne Rosacea, which was in the lab report.  As long as I get the prescription, I guess it was a successful visit, but I do not plan to ever go back.”

Why did she react to badly to sugar?

In her case she was producing antibodies to insulin. The insulin was being attacked by the immune system making her hypoglycemic. Eating fruit or any other foods stimulates the release of insulin. The insulin antibodies respond to the release of insulin by provoking the mast cells to release histamine. The histamine causes the increased swelling, redness and other symptoms.

Insulin release is impacted by the foods that you eat. Fruits are rich in sugar, but many fruits are digested slowly, which limits their impact on insulin levels.

Histamine is produced by the body & is also present in many foods. The body releases it during times of stress and allergic response. In an allergic response, an allergen stimulates the release of antibodies, which attach themselves to mast cells. Histamine is then released from the mast cells and causes a host of symptoms.

Because histamine is contained in almost all body tissues, especially the lungs, nose, sinuses, skin, intestinal mucosa and certain blood cells (mast cells, basophils), it is able to cause a wide variety of symptoms. In addition because 70% of your immune system is in your gut, if digestion is impaired so is your immune system!

Thus the flair ups (cytokine storms) when she cheated on the Candida diet. She was also eating a healthy amount of raw vegetables high in lectins, which were provoking a histamine and complement cascade immune response which a more aggressive type of cytokine storm, making her face angry and burning. A piece of seedless watermelon caused a particularly severe reaction. Seedless watermelons are genetically-modified (GMO) to not produce seeds.

H pylori shape

Helicobacter pylori and Autoimmune Thyroid Disease

The origins of autoimmune thyroid disease (ATD) have many factors. Helicobacter pylori (Hp) infection has been proposed to be involved in non-gastrointestinal conditions and reported more frequently in ATD and/or Hashimoto’s.[i],[ii] It was recently found that antibodies to H. pylori reacted with follicular cells of the thyroid gland.[iii]

Helicobacter pylori and rosacea.

There has been a long purported anecdotal association between rosacea and gastrointestinal disease. The discovery that Helicobacter pylori causes gastritis and duodenal ulcer disease has led to a new look at the role for this organism in connection with rosacea.[iv],[v],[vi] Studies are reporting a higher occurrence of Helicobacter pylori infection is found in rosacea patients than in healthy people.[vii] It more likely that the survival strategies using by H. pylori of hacking into the NEI Supersystem alters the immune system resulting in rosacea.

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Helicobacter bilis orchestrates immune responses towards good gut flora in inflammatory bowel disease.

During the initial H. Billis and H pylori infection cause numerous, nagging symptoms:

  • Heartburn
  • Bloating
  • Fatigue
  • Difficulty sleeping
  • Low libido

H. billis and H. pylori are not just throwing a party causing these symptoms. They are busy hacking into your NEI Supersystem trying to access the controls to your immune system. After they take control of your immune system, the symptoms of inflammation calm down. Should a gastroenterologist do a biopsy, it would show demonstrated a mild to moderate inflammatory response (microscopic colitis), one that is not so severe as cause concern.

Then interestingly, an infection with H bilis and H pylori had significantly less gastric inflammation after 6 to 11 months after the infection. After Helicobacter pylori and bilis establish their infestation have the ability to become invisible to the immune system. Thus, the area they colonize looks less inflamed. When the H. pylori and billis become invisible to the immune system, blood test will not show antibodies to these microbes.

These pathogenic bacteria reduce the amount of inflammation they cause by producing more inflammatory cytokines directing the immune response to the normal gastrointestinal microflora and the development of chronic gastrointestinal disease.[viii]

Helicobacter Pylori in Gallbladder & Liver Diseases.

In recent years, attention has been drawn to the possible association of Helicobacter infections not only with stomach diseases but also with several diseases within the abdomen, but outside of the gastrointestinal system, e.g. chronic cardiovascular, liver and gallbladder diseases or colorectal cancer.

Helicobacter bilis (H. bilis) have been isolated from the liver samples … It has been demonstrated that these bacteria are resistant to bile (chenodeoxycholic and deoxycholic acids) in contrast to the Helicobacter pylori (H. pylori) which is disintegrated when exposed to bile. Bacteria resistant to bile convert bile into toxic secondary bile acids. Secondary bile acids are toxic to the lining of the digestive tract, killing off other bacteria, in addition to damaging the ability to absorb Vitamin D. In some cases, secondary bile acids can cause a autoimmune response to Vitamin D.

The standard laboratory culture tests depend on bacteria and other microbes multiplying in a test tube in sufficient quantities for the lab technician to identify them.  The possibility exists that H. pylori and H. bilis may undergo the transformation from their normal form into the spherical pattern in which they are still active metabolically without the ability of multiplying themselves in the standard laboratory culture tests as a survival strategy. However, the microscopic methods of examination looking for a bacteria shaped like H. pylori and culture testing fails to identify H. pylori in the liver and human bile, but are found when microbial DNA testing is done.[ix]

Microbial Biofilm

A biofilm is a community of one or several diverse species of organisms that firmly fix to a surface and grow within a self-produced polymer matrix. Ultimately, the group of organisms begins to function as a unit. The community aspect of biofilm formations offers a number of advantages, including protection from hostile environmental conditions and the opportunity to sequester nutritional resources. In addition, a microbial community offers the possibility for a variety of different organisms (bacteria, fungi, viruses, and single-celled parasites) to live together, exchange genetic information, communicate through chemical signaling, act cooperatively, and, in so doing, enhance their own survival and the survival of the collective.


[i] Larizza D, Calcaterra V, Martinetti M, Negrini R, et. al. Helicobacter pylori infection and autoimmune thyroid disease in young patients: the disadvantage of carrying the human leukocyte antigen-DRB1*0301 allele. J Clin Endocrinol Metab. 2006 Jan;91(1):176-9. Epub 2005 Nov 1.

[ii] de Luis DA, Varela C, de La Calle H, et. al. Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis. J Clin Gastroenterol. 1998 Jun;26(4):259-63.

[iii] Figura N, Di Cairano G, Lorè F, et. al. The infection by Helicobacter pylori strains expressing CagA is highly prevalent in women with autoimmune thyroid disorders. J Physiol Pharmacol. 1999 Dec;50(5):817-26.

[iv] Diaz C, O’Callaghan CJ, Khan A, Ilchyshyn A. Rosacea: a cutaneous marker of Helicobacter pylori infection? Results of a pilot study. Acta Derm Venereol. 2003;83(4):282-6.

[v] Zandi S, Shamsadini S, Zahedi MJ, Hyatbaksh M. Helicobacter pylori and rosacea. East Mediterr Health J. 2003 Jan-Mar;9(1-2):167-71.

[vi] de Luis DA, Varela C, de La Calle H, et. al. Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis. J Clin Gastroenterol. 1998 Jun;26(4):259-63.

[vii] Utaş S, Ozbakir O, Turasan A, Utaş C. Helicobacter pylori eradication treatment reduces the severity of rosacea. J Am Acad Dermatol. 1999 Mar;40(3):433-5.

[viii] J G Fox. Helicobacter bilis: bacterial provocateur orchestrates host immune responses to commensal flora in a model of inflammatory bowel disease. Gut 2007;56:898–900.

[ix] M. GONCIARZ, M. WLOCH, Z. GONCIARZ. HELICOBACTER PYLORI IN LIVER DISEASES. JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 2006, 57, Supp 3, 55 161

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