Kimberly Eyer

Spouses of rheumatoid arthritis patients shared a gut microbiota pattern intermediate between patients and unrelated healthy controls, suggesting shared living environment, not just genetics, shapes the flora linked to rheumatoid arthritis.

Comparing 14 women with stage 3/4 endometriosis and 14 healthy controls, overall vaginal, cervical, and gut microbiota looked similar, but Atopobium was completely absent from the endometriosis genital tract, and two patients had Shigella/Escherichia-dominant gut microbiomes.

Gut Collinsella and Eggerthella expanded while Faecalibacterium contracted in rheumatoid arthritis, and Collinsella worsened arthritis severity in humanized mice.

Found reduced salivary microbial diversity and altered oral taxa in ACPA-positive high-risk individuals before rheumatoid arthritis onset.

A large American Gut Project cohort shows IBS-D and IBS-U have reduced bacterial diversity and an elevated hydrogen sulfide production pathway, distinguishing them from IBS-C.

In this preliminary study, IBS patients showed abnormal dynamic brain connectivity states linked to specific gut bacterial abundances, pointing to a measurable brain-gut-microbiome disruption.

Periodontally healthy people with rheumatoid arthritis had subgingival microbiomes distinct from healthy controls, driven by periodontal pathogens rather than existing gum disease.

Comparing gut microbiota across Crohn's disease, ulcerative colitis, multiple sclerosis, and rheumatoid arthritis, several taxa including Actinomyces, Eggerthella, and Streptococcus were consistently higher and Gemmiger, Lachnospira, and Sporobacter lower across all diseases, suggesting a shared dysbiosis; a Crohn's classifier reached an AUC of 0.95.

Found reduced gut microbial diversity and Bacteroidetes enrichment, with Collinsella depletion, in female patients with early rheumatoid arthritis.

Women whose chronic pelvic pain came from endometriosis or adenomyosis had a more diverse vaginal microbiome than other pelvic pain patients and healthy women. A two-microbe vaginal signature separated them with 81 percent sensitivity, rising to 89 percent when combined with serum CA125.

In 99 adults, the functional PAV/PAV bitter-taste receptor genotype was over-represented in rheumatoid arthritis, and buccal microbiome composition differed both by disease status and by TAS2R38 genotype, linking taste genetics and oral innate immunity to rheumatoid arthritis.

In 19 people with irritable bowel syndrome, the gut microbiota showed an imbalance of commensal species, with more lactobacilli, bifidobacteria and pathobionts and fewer Bacteroides/Prevotella. A probiotic yogurt eased symptoms but did not correct these compositional shifts.

Rheumatoid arthritis patients carried a higher subgingival bacterial load, a more diverse and pathogen-enriched microbiota, and worse clinical attachment loss than matched controls, with salivary IL-17, TNF, IL-2, and IFN-gamma also elevated. Oral dysbiosis tracked with worse RA activity.

In 52 Graves' disease patients, gut dysbiosis and depleted short-chain-fatty-acid-producing bacteria tracked with elevated LPS, higher pro-inflammatory cytokines, and a skewed B-cell profile. In cultured cells, LPS shifted B cells toward a naive state, while a mix of acetate, propionate, and butyrate curbed cytokine release.

A deep phylogenetic microarray and qPCR analysis of stool from 62 IBS patients versus 46 controls found a two-fold higher Firmicutes-to-Bacteroidetes ratio distinguishing IBS microbiota.

Endometriosis involves ectopic endometrial tissue causing pain and infertility. Validated and Promising Interventions include Hyperbaric Oxygen Therapy (HBOT), Low Nickel Diet, and Metronidazole therapy.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, neurofibrillary tangles, neuroinflammation, and metabolic dysfunction, ultimately leading to cognitive decline and dementia. Emerging research highlights the microbiota-gut-brain axis as a crucial factor in AD pathogenesis, with gut dysbiosis contributing to neuroinflammation, immune dysregulation, and blood-brain barrier permeability. Microbial metabolites, such […]

Hashimoto’s Thyroiditis (HT) is an autoimmune disease that progressively damages the thyroid, often causing hypothyroidism and affecting women disproportionately. Research links HT to gut dysbiosis via the gut–thyroid axis and highlights heavy metals like nickel, arsenic, and lead as contributors to oxidative stress and thyroid dysfunction.

Irritable Bowel Syndrome (IBS) is a common gastrointestinal disorder characterized by symptoms such as abdominal pain, bloating, and altered bowel habits. Recent research has focused on the gut microbiota’s role in IBS, aiming to identify specific microbial signatures associated with the condition.

Parkinson’s disease is increasingly recognized as a systemic disorder involving coordinated disturbances across the gut–brain axis, rather than a condition confined to dopaminergic neurodegeneration alone. Converging evidence implicates gut dysbiosis, altered microbial metabolites, impaired intestinal barrier integrity, and metal dyshomeostasis as upstream drivers of neuroinflammation and alpha-synuclein pathology. These interconnected microbiome, metabolomic, and metallomic signals provide a mechanistic framework for understanding disease initiation, progression, and therapeutic targeting beyond the central nervous system.

This paper proposes that Parkinson’s disease vulnerability is partly a pigment and metal-handling problem. MC1R loss-of-function biases neuromelanin toward pheomelanin-like subunits, weakening iron sequestration and amplifying oxidative stress. We argue that MC1R agonists, including melanotan peptides, could restore eumelanin-like buffering, reduce ferroptosis, and dampen neuroinflammation.

This hypothesis reframes the red hair MC1R–Parkinson’s link as a metal-handling phenotype. Pheomelanin-biased neuromelanin may lose eumelanin casing capacity, saturate with iron earlier, release labile iron, and amplify ROS and ferroptosis in dopaminergic neurons, yielding a modifiable risk target.

This study identifies intrauterine microbial colonization in endometriosis, with enriched Streptococcaceae, Staphylococcaceae, and Enterobacteriaceae. GnRHa therapy exacerbated microbial imbalances, highlighting potential therapeutic targets for managing inflammation and infection in endometriosis. Findings suggest microbial modulation may enhance treatment outcomes.

This study reveals that inflammatory cytokines (IL-6, IL-10, IL-13, and TNF-α) are significantly elevated in the peritoneal fluid of endometriosis patients with infertility. These findings suggest their potential role as diagnostic biomarkers and therapeutic targets for managing reproductive complications in endometriosis.