ArticleThe EPMA journal2025
How to use an extensive Flammer syndrome phenotyping for a holistic protection against health-to-disease transition - facts and practical recommendations.
Article in The EPMA journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Article
- AI-enabled predictive, preventive and personalised oral health management: a lightweight patient-centred model for automated assessment of dental plaque and gingival inflammation.The EPMA journal · 2026Article
- Innovative mitochondria-based holistic 3PM approach to female health status: Facts and outlook.The EPMA journal · 2026Article
- Multimodal AI-based modeling of glaucoma progression: a 3PM-guided approach integrating structural, functional, and vascular patterns.The EPMA journal · 2025Article
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Abstract
Due to their phenotype-associated attitude predominantly oriented towards high performance, Flammer syndrome (FS) phenotype carriers are blessed to a successful career in corresponding professional branches. This advantage is however associated with significant health risks. FSP carriers are extremely stress-sensitive. Corresponding pathways are epigenetically regulated, and modifiable risk factors are associated with the phenotype-specific psycho-somatic patterns such as a drive for meticulousness, perfectionism and exercised rigour applying strictness, discipline, or thoroughness to their own behaviour and actions. The FS phenotype is typically characterised by chronication of the transient sympathoexcitation and its dominance over parasympathetic relaxation. Chronification of the parasympathetic-sympathetic imbalance in form of sympathetic overdrive leads to chronic ischemic events in peripheral vessels and progressing tissue damage associated with the cyclic ischemia-reperfusion. Ischemic damage can be roughly estimated by levels of the vasoconstrictor endotelin-1 (ET-1) measured in blood. However, other risk factors on the one hand and compensatory mechanisms on the other hand are decisive for the damage extent at individual level. For example, chronically increased ET-1 and even mild hyperhomocysteinaemia synergistically may cause a progressing disease of small vessels, systemic inflammation and chronification of mitochondrial stress potentially resulting in chronic fatigue and mitochondrial burnout with a spectrum of associated pathologies in affected individuals. That is why predictive diagnostics utilising comprehensive individualised patient profiles are crucial for the cost-effective targeted prevention and creation of personalised treatment algorithms. Due to the high level of algorithms' complexity, an application of AI is essential. FS is usually established early in life during pubertal maturation of otherwise healthy individuals. Therefore, FS phenotyping is instrumental for 3PM-guided cost-effective primary healthcare. To meet the needs of this patient cohort, an application of the digital health monitoring including records of mitochondrial homeostasis is strongly recommended to protect the FS phenotype carriers against health-to-disease transition. To this end, patient friendly non-invasive approach is already established utilising tear fluid multi-omics, mitochondria as vital biosensors and AI-based multi-professional data interpretation; the approach is offered to the FS phenotype carriers.
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