Stomach and Intestines are not in any way, shape or form involved in rosacea symptoms. No leaky gut syndrome, no SIBO, no Candida, nothing.... nada.

Please feel free to take acidophilus supplements and, by all means, take care of your GI system for overall health. But colon cleanses, gut cleanses, candida cleanses, stomach stapeling..... Focus your energy on something that will help.

There are over 60 medical clinical studies that demonstrate there is nothing wrong in the stomach or gut in almost all cases. Scope studies, biopsies, genetic testing, absorption tests, measurement of hormones/dilators, etc after different meals. Nothing.

You take a strong antibiotic SIBO and the symptoms temporarily go away.... no surprise. Anti-inflammatory actions of the antibiotic. Similar to the dismal studies done concluding that stomach H. Pylori causes rosacea (and still touted today). You take three different anti-inflammatory medications and they go away for a while.

There are only three GI Disorders that have been clinically proven to affect rosacea symptoms and triggers:

(1) Ulcertive Colitis - Very painful. You would know there is something wrong

(2) Gluten Intolerance - less than 10% are affected and avoidance of gluten-based foods clear these symptoms

(3) Irritable Bowel Sydrome -- Especially in females. IBS should be tested for in any females experiencing intestinal problems. This is a major problem and causes severe rosacea outbreaks. Luckily, several knew medications can put IBS into remission. This site may be helpful, especially for those who experience stomach pain: http://www.ibsgroup.org/medications. Talk to your physician about:

5-HT3 antagonist Alosetron 1/2-1 mg bid Pain,
urgency, diarrhea in diarrhea-predominant female patients May induce constipation requiring separate management

5-HT4 antagonist Tegaserod 6 mg bid Pain,
constipation in constipation-predominant female patients May initially induce diarrhea

Chloride channel activator Lubiprostone 8 mg bid Pain,
constipation in constipation-
predominant female patients May experience nausea or diarrhea


I spent two years in medical grad. school doing studies on the intestine, gut, and digestive disorders:

Nase, G.P., and M.A. Boegehold. Postjunctional alpha 2-adrenoceptors are not present in proximal arterioles of rat intestine. Am. J. Physiol. 274 (Heart Circ. Physiol.): H202-H208, 1998.


J.M. Lash, G.P. Nase and H.G. Bohlen. Acute hyperglycemia depresses arteriolar nitric oxide formation in skeletal muscle. Am. J. Physiol. 277 (Heart Circ. Physiol.): H1513-H1520, 1999.


H.G. Bohlen, and G.P. Nase. Dependence of intestinal arteriolar regulation on flow mediated nitric oxide formation. Am. J. Physiol. 279 (Heart Circ. Physiol.): H2249-H2258, 2000.


H.G. Bohlen, and G.P. Nase. Arteriolar nitric oxide concentration is decreased during hyperglycemia-induced Beta-II PKC activation. Am. J. Physiol. (Heart Circ. Physiol.) 280(2): H621-H627, 2001.


H.G. Bohlen, and G.P. Nase. Obesity lowers hyperglycemic threshold for impaired in vivo endothelial nitric oxide function. Am. J. Physiol. (Heart Circ. Physiol.) 283(1): H391-H397, 2002.


H.G. Bohlen, G.P. Nase, and J.S. Jin. Invited Review: Multiple mechanisms of early hyperglycemic injury of the rat intestinal microcirculation. Clin. Exp. Pharmacol. Physiol 29(1-2):138-142, 2002.


Nase, G.P., J. Tuttle, and H.G. Bohlen. Reduced Perivascular PO2 increases nitric oxide release from endothelial cells. Am. J. Physiol (Heart Circ. Physiol.): 285: H507-H515, 2003.


H.G. Bohlen, and G.P. Nase. Insulin resistance predisposes arterioles to nitric oxide dysfunction during mild hyperglycemia. Am. J. Physiol. (Heart Circ. Physiol.): 2005 (Submitted).
Book Chapters:

Nase, G.P., and M.A. Boegehold. The influence of sympathetic nerves on microvascular tone is modulated by endothelial-derived nitric oxide. Proceedings of the 6th World Congress for Microcirculation, 1996.


Nase, G.P. Endothelium-derived nitric oxide attenuates sympathetic neurogenic constriction in the intestinal microvasculature. Dissertation, WVU School of Medicine, Dept. of Physiology, 1997.


Scientific Abstracts:

Nase, G.P., and M.A. Boegehold. Nitric oxide modulates arteriolar responses to increased sympathetic nerve activity. Microcirculation 2(1): 80, 1995.


Nase, G.P., and M.A. Boegehold. Endothelial-derived nitric oxide modulates sympathetic constriction in the intestinal microvasculature. Microcirculation 3(1): M127, 1996.


Nase, G.P., and M.A. Boegehold. Modulation of sympathetic constriction does not involve the cyclooxygenase pathway. FASEB J, 1996.


Nase, G.P., and M.A. Boegehold. The influence of sympathetic nerves on microvascular tone is modulated by endothelial-derived nitric oxide. Sixth World Congress for Microcirculation, Munich, Germany, 1996.


Nase, G.P., and M.A. Boegehold. Alpha adrenoceptors do not mediate nitric oxide release during increased sympathetic nerve activity. Microcirculation, 1997.


Boegehold, M.A., and G.P. Nase. Arteriolar sympathetic constriction is limited by endothelial nitric oxide via a mechanism that does not involve shear stress or alpha2-receptors. 33rd International Congress of Physiological Sciences, St. Petersburg, Russia, 1997.


Lash, J.M., G.P. Nase, and H.G. Bohlen. Acute hyperglycemia enhances dilation of rat spinotrapezius arterioles to sodium nitroprusside. Microcirculation, 1998.


Nase, G.P., J.M. Lash, and H.G. Bohlen. Periarteriolar nitric oxide concentration is depressed in rat skeletal muscle during hyperglycemia. FASEB J, 1999.


Bohlen, H.G., and G.P. Nase. In vivo intestinal arteriolar nitric oxide concentration is directly altered by blood flow velocity. Microcirculation, 1999.


H.G. Bohlen, and G.P. Nase. Beta-II protein kinase inhibition prevents and reverses in vivo endothelial nitric oxide suppression during acute hyperglycemia. Microcirculation, 2000.


Nase, G.P., and H.G. Bohlen. Arteriolar and venular nitric oxide concentration are increased during localized hypoxia. Microcirculation, 2000.


Nase, G.P., and H.G. Bohlen. Endothelium-derived nitric oxide production is enhanced during reduced oxygen availability. Microcirculation, 2001.


H.G. Bohlen, and G.P. Nase. Insulin resistance predisposes arterioles to nitric oxide dysfunction during mild hyperglycemia. Microcirculation, 2001.


H.G. Bohlen, and G.P. Nase. Arteriolar nitric oxide concentration is decreased during hyperglycemia-induced Beta-II PKC activation. Microcirculation, 2002.


H.G. Bohlen, and G.P. Nase. Obesity lowers hyperglycemic threshold for impaired in vivo endothelial nitric oxide function. Microcirculation, 2002.

Nase, G.P., and H.G. Bohlen. Local hypoxia increases arteriolar and venular nitric oxide concentration in the intestinal microvasculature. Microcirculation, 2002.


H.G. Bohlen, and G.P. Nase. Insulin resistance predisposes arterioles to nitric oxide dysfunction during mild hyperglycemia. Microcirculation, 2002.

__________________
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Best,
Geoffrey

Dr. Geoffrey Nase
Ph.D: Neuro-Vascular Physiologist

Email: drnase1000@hotmail.com
Bibliography: http://drnase.com

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