Based on our new findings in asymptomatic volunteers, waist belt and central obesity cause partial hiatus herniation and short-segment acid reflux. This provides a plausible explanation for the high incidence of inflammation and metaplasia and occurrence of neoplasia at the GOJ in subjects without a history of reflux symptoms.

For more detailed proposed mechanism see:

Waist belt and central obesity cause partial hiatus hernia and short-segment acid reflux in asymptomatic volunteers.

Yeong Yeh Lee, Angela A Wirz, James G H Whiting, Elaine V Robertson, Donald Smith, Alexander Weir, Andrew W Kelman, Mohammad H Derakhshan, Kenneth E L McColl.Gut 09/2013; ·

It has long been hypothesized that visceral adiposity, expressed by an increased abdominal waist circumference, could be associated with increased intra-abdominal pressure which promotes carditis by increasing intragastric pressure. Furthermore obesity might determinate increased intra-abdominal pressure that results in extrinsic gastric compression by visceral fat with a subsequent increase in intragastric pressure and gastroesophageal pressure gradient as well as an increased risk for developing a hiatal hernia. In obese patients other factors that play a role are esophageal peristaltic abnormalities, such as incompetence of the lower esophageal sphincter, nutcracker esophagus and non-specific motility disorders

Carditis may be due to H. pylori infection of cardias. A relationship between Helicobacter pylori and obesity has been recently raised by epidemiological data as well as by the reduction of ghrelin levels induced by the bacterium.

Thank you very for very thoughtful comments.

would you provide me a copy of paper (s) showing any significant positive association between obesity and H.pylori infection please.

Here you will find two attached papers concerning the relationship between H. pylori and ghrelin. The association of bacterial presence and obesity has beenreported in a recent International meeting (Bridging Meeting, Berlin 15-16 November 2013) in a study involving more than 1000 patients.

You will find attched the supplemental paper.

Dear Mohammad Derakhshan, a possible association between obesity/related illness and H. pylori infection is suggested even in the Guidelines Maastricht 2012: statement 13, evidence level 2b, grade of recommendation B.

Happy new year Ierardi

Many thanks for your comments and interest on the topic. I reviewed your forwarded literature and like to emphasize on the original question here, which addresses the mechanism of association between obesity and histological carditis.

In our study published in Gastroenterology (Robetston et al 2013), we showed that the association is due to significant acid exposure of the most distal squamous mucosa of oesophagus which is located just above cardia mucosa. We suggested the expanded cardiac mucosa and its inflammation is due to acid damages on the mucosa, which is naturally defective against acid. In this concept, no need classic GORD to start the damage.

In same study, we showed all patients were H.pylori negative that means if there are some forms of carditis due to H.pylori, that group have been studied here.

There is no doubt carditis can be associated with H.pylori infection, but this association is not related to obesity. You kindly have posted some articles as evidence of association between obesity and H.pylori infection, but none of them claimed a positive association.

The fact here is long-term infection with H.pylori leads to chronic atrophic gastritis in most patients, and this will be associated with the gradual loss of glandular components of oxyntic mucosa. This fact has been documented very well during last 2-3 decades. Even recently we showed that serum ghrelin is decreased in patients with atrophic gastritis (Sadjadi et al, PLOS ONE 2013), and this event was associated with simultaneous decrease in serum pepsinogen I/II ratio as well as another evidence of universal destruction or downgrade of secretory cells of oxyntic mucosa.

Therefore, carditis is a histological evidence of a challenge happening in the unstable junctional mucosa and could be due to exposure to gastric acid (with or without bile) or H.pylori infection. The association between carditis and the former can be exaggerated by obesity, but I do not aware of any study showing the association between the H.pylori-induced carditis with obesity.