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 (

Additional file 4: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S3. Functional enrichment of DEGs identified in Aβ42, Aβ42/TREM2WT/TYROBP, and Aβ42/TREM2R47H/TYROBP files. (XLSX 23 kb

Additional file 10: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S9 Module membership from weighted gene co-expression network analysis for ROSMAP gene expression data. (XLSX 456 kb

Additional file 8: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S7. Functional enrichment of DEGs identified in Tau/TREM2WT/TYROBP, Tau/TREM2R47H/TYROBP files. (XLSX 23 kb

Additional file 6: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S5. Overlap between MSigDB gene ontology/pathway gene sets and fly-human conserved genes. (XLSX 299 kb

Additional file 7: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S6. Functional enrichment of DEGs identified in TREM2WT/TYROBP, TREM2R47H/TYROBP, and Tau files. (XLSX 18 kb

Additional file 1: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Figure S1. No significant alteration in either the gross morphology of brain structures or the number of neuronal and glial cells was observed in TREM2/TYROBP flies. Figure S2. Molecular pathways affected by neuronal expression of Aβ42 and glial expression of TREM2/TYROBP. Figure S3. Molecular pathways affected by tau do not overlap with those affected by glial TREM2/TYROBP. Figure S4. Gene expression signatures in tau/TREM2/TYROBP flies. Figure S5. Heatmap showing the topological overlapping matrix (TOM) from weighted gene co-expression network analysis. Table S11. Primer sequences for RT-PCR and qRT-PCR. (PDF 4937 kb

Additional file 3: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S2. Functional enrichment of DEGs identified in TREM2WT/TYROBP, TREM2R47H/TYROBP, and Aß42 files. (XLSX 23 kb

DOWN AND DIRTY LOMBROSO’S BORN TO CRIME, THE MORPHOANTHROPOLOGY AND THE IGNORED HUMAN NEUROPHYSIOLOGY: A CRITICAL REVIEW ON A HISTORICAL CONTEXT

Lombroso\u27s theories, in 1800s, gave a strong shock in the international scientific community , regarding the correlation between the human morphology and its tendency to crime. They were followed, especially out of the Europe, and still are being discussed. But, in that century, they were enriched researches on human neurophysiology, which then would be further down to our time and that they denied sharply the Lombroso concepts. In short, the ignored neurophysiology, to the detriment of hypothesis which theorized the tendency to crime as an expression of the physical features of the individual, the whole body, from the face, limbs, ears, the shape of the skull. In this review, are made some critical remarks about Lombroso concepts, on \u27atavism, the people considered inferior on the basis of their physical appearance, in other words what was called morphoanthropology. At the same time, this work emphasizes instead the \u27importance of neurophysiological aspects of\u27 individual tending to crime, that are the basis of abnormal acts against the society \u27and that are related to the dysfunction of certain brain areas, such as the frontal cortex and limbic cortex, under the influence of genotype and environmental factors