Long-term impact of the low-FODMAP diet on gastrointestinal symptoms, dietary intake, patient acceptability, and healthcare utilization in irritable bowel syndrome

Background: The low-FODMAP diet is a frequently used treatment for irritable bowel syndrome (IBS). Most research has focused on short-term FODMAP restriction; however, guidelines recommend that high-FODMAP foods are reintroduced to individual tolerance. This study aimed to assess the long-term effectiveness of the low-FODMAP diet following FODMAP reintroduction in IBS patients. Methods: Patients with IBS were prospectively recruited to a questionnaire study following completion of dietitian-led low-FODMAP education. At baseline and following FODMAP restriction (short term) only, gastrointestinal symptoms were measured as part of routine clinical care. Following FODMAP reintroduction, (long term), symptoms, dietary intake, acceptability, food-related quality of life (QOL), and healthcare utilization were assessed. Data were reported for patients who continued long-term FODMAP restriction (adapted FODMAP) and/or returned to a habitual diet (habitual). Key Results: Of 103 patients, satisfactory relief of symptoms was reported in 12% at baseline, 61% at short-term follow-up, and 57% at long-term follow-up. At long-term follow-up, 84 (82%) patients continued an ‘adapted FODMAP’ diet (total FODMAP intake mean 20.6, SD 14.9\ua0g/d) compared with 19 (18%) of patients following a ‘habitual’ diet (29.4, SD 22.9\ua0g/d, P=.039). Nutritional adequacy was not compromised for either group. The ‘adapted FODMAP’ group reported the diet cost significantly more than the ‘habitual’ group (

Genes Dysregulated to Different Extent or Oppositely in Estrogen Receptor-Positive and Estrogen Receptor-Negative Breast Cancers

<div><p>Background</p><p>Directly comparing gene expression profiles of estrogen receptor-positive (ER+) and estrogen receptor-negative (ER−) breast cancers cannot determine whether differentially expressed genes between these two subtypes result from dysregulated expression in ER+ cancer or ER− cancer versus normal controls, and thus would miss critical information for elucidating the transcriptomic difference between the two subtypes.</p><p>Principal Findings</p><p>Using microarray datasets from TCGA, we classified the genes dysregulated in both ER+ and ER− cancers versus normal controls into two classes: (i) genes dysregulated in the same direction but to a different extent, and (ii) genes dysregulated to opposite directions, and then validated the two classes in RNA-sequencing datasets of independent cohorts. We showed that the genes dysregulated to a larger extent in ER+ cancers than in ER− cancers enriched in glycerophospholipid and polysaccharide metabolic processes, while the genes dysregulated to a larger extent in ER− cancers than in ER+ cancers enriched in cell proliferation. Phosphorylase kinase and enzymes of glycosylphosphatidylinositol (GPI) anchor biosynthesis were upregulated to a larger extent in ER+ cancers than in ER− cancers, whereas glycogen synthase and phospholipase A2 were downregulated to a larger extent in ER+ cancers than in ER− cancers. We also found that the genes oppositely dysregulated in the two subtypes significantly enriched with known cancer genes and tended to closely collaborate with the cancer genes. Furthermore, we showed the possibility that these oppositely dysregulated genes could contribute to carcinogenesis of ER+ and ER− cancers through rewiring different subpathways.</p><p>Conclusions</p><p>GPI-anchor biosynthesis and glycogenolysis were elevated and hydrolysis of phospholipids was depleted to a larger extent in ER+ cancers than in ER− cancers. Our findings indicate that the genes oppositely dysregulated in the two subtypes are potential cancer genes which could contribute to carcinogenesis of both ER+ and ER− cancers through rewiring different subpathways.</p></div

Schematic diagram of a gene dysregulated to a larger extent in ER+ (or ER−) cancer.

<p>Black line indicates average expression level of normal controls. Dysregulated directions are denoted in red arrow for upregulation and in green arrow for downregulation. The length of the arrow lines indicates dysregulated extent. (A) A gene dysregulated to a larger extent in ER+ cancer than in ER− cancer. (B) A gene dysregulated to a larger extent in ER− cancer than in ER+ cancer.</p

Downregulation of PFKP and upregulation of FBP1 contribute to ER+ breast cancers.

<p>ER+ DE genes in the pentose phosphate pathway are denoted in red for upregulation and in green for downregulation. The red frame indicates the elevated oxidative subpathway of the pentose phosphate pathway in ER+ cancers. The figure is created based on KEGG pathway hsa00030. Only a part of the pathway is shown for clarity.</p

Clinical characteristics of the samples at diagnosis.

*<p><i>p</i> denotes results of significant test for the comparison between ER+ versus ER− breast cancer by chi-square test.</p><p>RNA-seq, RNA-sequencing; PR, Progesterone Receptor; NA, Not Available; HER2, Human Epidermal Growth Factor Receptor 2.</p

The biological processes enriched with genes dysregulated to a larger extent in ER+ cancer.

<p>The biological processes enriched with genes dysregulated to a larger extent in ER+ cancer.</p

The biological processes enriched with genes dysregulated to a larger extent in ER- cancer.

<p>The biological processes enriched with genes dysregulated to a larger extent in ER- cancer.</p

Upregulation of PFKP and downregulation of FBP1 contribute to ER− breast cancers.

<p>ER− DE genes in the glycolysis/gluconeogenesis pathway are denoted in red for upregulation and in green downregulation. The red frame indicates the elevated anaerobic glycolysis subpathway in ER− cancers. The figure is created based on KEGG pathway hsa00010. Only a part of the pathway is shown for clarity.</p

Le Courrier

23 novembre 18311831/11/23 (N327)