The researchers found that four of these health conditions were associated with up to a threefold increase in the risk of developing Parkinson\u2019s disease, and 13 others with a higher likelihood of developing Alzheimer\u2019s (see infographic on page 62<\/em>). All of these conditions typically develop years before the first symptoms of either neurodegenerative disease appear. Type 1 and type 2 diabetes, as well as intestinal disorders such as irritable bowel syndrome, were shown to be linked to an increased risk of developing both Alzheimer\u2019s and Parkinson\u2019s.<\/p>\n \u201cIn the case of Alzheimer\u2019s, problems related to fat metabolism, vitamin D deficiency, mineral imbalances, and inflammation of the digestive tract, such as esophagitis, gastritis, and colitis, also stood out,\u201d says Bandr\u00e9s-Ciga, who now works at the biotechnology company Valo Health, in an interview with Pesquisa FAPESP<\/em>. \u201cIssues such as chronic indigestion, pancreatic dysfunction, and B-complex vitamin deficiencies were associated with an increased risk of Parkinson\u2019s disease.\u201d<\/p>\n The researchers emphasize that these findings do not establish a causal relationship\u2014that is, they do not prove that conditions such as diabetes cause Parkinson\u2019s or Alzheimer\u2019s. However, the fact that digestive and metabolic problems tend to appear long before the onset of neurodegenerative diseases suggests that they may contribute to their development.<\/p>\n \u201cThe hypothesis is that these digestive and metabolic disorders may influence the progression of Parkinson\u2019s and Alzheimer\u2019s,\u201d explains Brazilian neurologist Artur Schumacher Schuh, from the Federal University of Rio Grande do Sul (UFRGS), a coauthor of the study. Among the results, he highlights the increased risk linked to type 2 diabetes, which can appear 10 to 15 years before Alzheimer\u2019s. \u201cDiabetes is known to raise cardiovascular risk, and there are indications that it may cause protein glycation [the binding of sugars to proteins, which makes them toxic] and that this process could contribute to the buildup of beta-amyloid plaques characteristic of Alzheimer\u2019s.\u201d<\/p>\n Multiple connections<\/strong> \u201cThe gut and brain communicate in various ways,\u201d explains immunologist L\u00edcio Velloso, from the University of Campinas (UNICAMP), who was not involved in the study. The gastrointestinal system contains neurons and glial cells that interact with the same types of cells found in the central nervous system. One connection pathway is neural, mediated by the vagus nerve, which links the digestive tract to the brain and helps regulate satiety. Another is hormonal, through compounds produced in the stomach and intestines that modulate appetite. A third involves substances synthesized by the gut microbiota (bacteria and other microorganisms living in the intestine) that can enter the bloodstream and influence brain function. \u201cThis set of mechanisms, which has been more clearly described in recent years, shows how deeply interconnected the digestive and nervous systems are,\u201d says Velloso, coordinator of the Center for Research on Obesity and Comorbidities at UNICAMP, one of the Research, Innovation, and Dissemination Centers (RIDCs) funded by FAPESP.<\/p>\n![](\"\/wp-content\/uploads\/2026\/01\/rpf-alzheimer-Contribuicoes_Indesejaveis-ING-DESK.jpg\")
\n <\/picture>Glauco Lara<\/span>\n
\nPrevious studies have suggested that inflammation, imbalances in the gut microbiota, or nutritional deficiencies may trigger signals that impair brain function. \u201cThere is evidence that malformed proteins, such as those associated with Parkinson\u2019s disease, may even originate in the gut and migrate to the central nervous system via the vagus nerve,\u201d notes Bandr\u00e9s-Ciga.<\/p>\n![](\"\/wp-content\/uploads\/2026\/01\/RPD-Parkinson-2025-10_ING-DESK.png\")
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