Helicobacter. 2015 Feb;20(1):64-8. doi: 10.1111/hel.12154.

Inverse correlation between Helicobacter pylori colonization and obesity in a cohort of inner city children.

Vo HD, Goli S, Gill R, Anderson V, Stefanov DG, Xu J, Kulsum-Mecci N, Schwarz SM, Rabinowitz SS.

Division of Pediatric Gastroenterology, The Children’s Hospital at Downstate, SUNY Downstate College of Medicine, New York, NY, USA.



BACKGROUND: Recently, publications in adults and children have documented a potential role of Helicobacter pylori (H. pylori) in decreasing the likelihood of obesity. The present study compares the prevalence of H. pylori colonization between obese (body mass index [BMI] ≥ 95th percentile) and healthy weight (BMI ≥ 5th to <85th percentiles) children seen at an inner city medical center in the United States.

METHODS: This retrospective study reviewed clinical features, BMI, and gastric histology of consecutive children aged 1-18 years undergoing an esophagogastroduodenoscopy. BMI percentile was calculated for age and gender. Helicobacter pylori colonization was determined by histopathologic identification of the organism. Multiple logistic regression was employed to measure the association between BMI and H. pylori colonization, controlling for baseline age, gender, and presenting symptoms.

RESULTS: Among 340 patients (51.5% female, mean age of 10.5 ± 4.7 years), 98 (29%) were obese and 173 (51%) were healthy weight. The H. pylori colonization rate of the entire cohort was 18.5% (95% CI = 14.7-23.0%). Among obese children, 10% had H. pylori colonization compared to 21% of the healthy weight children (RR = 2.1, 95% CI = 1.1-4.0). Conversely, 39% of noncolonized children, but only 21% of the infected children, were obese (RR = 1.8, 95% CI = 1.1-3.3). Multivariate analysis revealed that being colonized with H. pylori is associated with a 50% reduction in the odds of being obese (adjusted OR = 0.5, 95% CI = 0.2-1.0).

CONCLUSIONS: Our findings in a North American cohort are in agreement with studies from Asia and Europe suggesting that H. pylori infection decreases the prevalence of obesity in children. Further work to characterize the extent and nature of this relationship is warranted.

KEYWORDS: Helicobacter pylori; children; obesity

PMID: 25308209



Helicobacter pylori is the most common bacteria infecting humans with a prevalence of 50% in the developed world by age 50 and nearly 90% by age 18 in the developing world. Gastric infection by this gram negative, microaerophilic pathogen is the primary cause of duodenal ulcer, and a major contributor to gastric cancer. Yet, it is an asymptomatic event for the vast majority of individuals. Epidemiologic data estimate that this bacterium has been colonizing human stomachs for 50,000 years. In most interspecies relationships where there is a clear pathologic consequence for one species (morbidity and mortality secondary to bleeding peptic ulcer and gastric malignancy in humans), there is often a simultaneous more commonly encountered benefit. This benefit permits an uneasy symbiosis to persist despite the negative evolutionary pressures that co-exist. How this may relate to the relationship between Helicobacter pylori and humans remains unanswered.

The gut is the largest endocrine organ in the body, and gastric Helicobacter pylori infection influences hormonal secretions by the host stomach. The specific type of infection that primarily yields peptic ulcer involves colonization of the gastric antrum. This endocrine region of the stomach contains neighboring but distinct populations of hormone secreting G and D cells. G cells secrete gastrin, a peptide hormone that is an important stimulator of both gastric acid synthesis and gastrointestinal tissue proliferation. Antral D cells secrete somatostatin, an apocrine agent that diffuses to neighboring G cells and decreases gastrin release. Antral infection results in decreased release of somatostatin by D cells. Thus, a normal braking mechanism that controls gastrin release is compromised and the result is a hypergastrinemic state. The increase in gastrin leads to over stimulation of gastric parietal cells, the cells responsible for acid secretion. This yields an enhanced secretion of hydrochloric acid which ultimately results in peptic ulceration. If the colonization extends to the body of the stomach, or primarily involves this region, then a compromise in the function of parietal cells is the main sequelae of the infection. Again a hypergastrinemic state evolves. However, without parietal cell acid secretion, the main consequence is ongoing proliferation signaling, potentiating the development of gastric cancer.

Ghrelin, a 28 amino acid peptide hormone also secreted by the stomach, yields orexigenic (appetite stimulating) behavior through multiple mechanisms (1). Locally, it influences gastric physiology by contracting the fundus and stimulating gastric emptying. Centrally, it binds to specific receptors mediating satiety and hunger in the hypothalamic paraventricular and arcuate nuclei. Recently, it was reported that Helicobacter pylori infection decreases the secretion of ghrelin by decreasing the number of gastric ghrelin producing cells (2). Eradication of the infection is accompanied by a subsequent increase in serum ghrelin concentration. In the future, these preliminary observations will need to be validated as the in vitro measurements of ghrelin are not straightforward (3). However, the above referenced report describing a cohort of Italian children, noted that the severity of their Helicobacter pylori gastritis was inversely proportional to the decrease noted in their serum ghrelin levels (2).

Two previously published Pediatric studies have suggested an inverse relationship between the prevalence of Helicobacter pylori infection and the presence of obesity (2, 4). The Italian cohort with the decreased ghrelin gained a significant amount of weight after eradication of the bacteria (2). The same relationship was also reported in a Chinese cohort, with the most striking impact being noted in a group of school aged children (4). This study identified Helicobacter pylori infection based on serology, which is known to not be reliable in children. Our recently published manuscript represents methodological advances from the previous epidemiologic reports. A group of obese children were compared to a contemporary non-obese cohort from the same geographic area, where “obesity” was defined employing the American Academy of Pediatrics criteria of BMI > 95% for age. In addition, the diagnosis of Helicobacter pylori infection was made by the gold standard, direct visualization of the bacteria in inflamed gastric tissue followed by confirmatory immunostaining.

The primary result of our retrospective study was that only 10% of obese children had Helicobacter pylori infection as opposed to 21% of the healthy weight children (BMI >5% to < 85%). This difference was statistically significant. Conversely, the healthy weight children were 2.2 times more likely to be infected than the obese children. Thus, our study performed in a cohort of primarily Afro-American and Caribbean American children validates and re-enforces the epidemiologic connection previously observed in Chinese and European cohorts. Future prospective studies that reliably measure serum ghrelin and BMI (a) before Helicobacter infection, (b) once colonization has occurred, and (c) after eradication, will be required to definitively establish this intriguing relationship. A comprehensive review of the mechanisms by which the infection may prevent obesity is included in the article and summarized in Figure 1.




Figure 1. Hypothetical mechanisms explaining an inverse relationship between H. pylori infection and obesity


Theoretically, if Helicobacter pylori colonization of the human antrum yields a decreased level of ghrelin, a centrally mediating orexigenic hormone, an infected host would have an easier adaptation to extended periods of famine. This benefit may explain the establishment of a symbiotic relationship between a host and a “commensal” pathogen that has existed for 50 millenia, despite the risk of life threatening consequences to the host. This novel type of interaction would expand our understanding of how the microbiome may influence host phenotype. It also establishes that the non-colonic flora can make a significant contribution to the total impact of the human microbiome. Finally, further characterization of this evolutionary interaction may ultimately suggest the potential for anti-ghrelin pharmacology as the elusive anti-obesity therapy.



  1. Camilleri M. Peripheral Mechanisms in Appetite regulation. Gastroenterology (2015); 148:1219-1233.
  2. Pacifico L, Anania C, Osborn JF, Ferrara E, Schiavo K, Bonamico M, et al. Long term effects of Helicobacter pylori eradication on circulating ghrelin and leptin concentrations and body composition in prepubertal European Journal of Endocrinology (2008); 158 (3):232-32.
  3. Jeffrey PL, McGuckin MA, Linden SK. Endocrine impact of Helicobacter pylori: Focus on ghrelin and ghrelin o-acyltransferase. World Journal of Gastroenterology (2011); 17(10):1249-60.
  4. Wu MS, Lee WJ, Wang HH, Huang SP, Lin JT. A case control study of association of Helicobacter pylori infection with morbid obesity in Taiwan. Arch Intern Med (2005); 165(13):1552-5.




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