Evidence mapPaperPMID 40948987Full record

ArticleThe EPMA journal2025

How to use an extensive Flammer syndrome phenotyping for a holistic protection against health-to-disease transition - facts and practical recommendations.

Olga Golubnitschaja

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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.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

1 author.

Olga GolubnitschajaPredictive, Preventive and Personalised (3P) Medicine, University Hospital Bonn, Rheinische Friedrich-Wilhelms-Universität Bonn, 53127 Bonn, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AIEndothelin-1Flammer syndrome phenotype (FSP)Health policyHealth risk assessmentHealth-to-disease transitionHolistic approachHomocysteineIndividualised protectionIschemia-reperfusionMitochondrial stress and burnoutMitophagyParadigm shiftParasympathetic-sympathetic imbalancePhenotypingPopulation screeningPredictive preventive personalised medicine (PPPM / 3PM)Primary careSmall vessel diseaseSuboptimal healthSympathetic overdriveSympathoexcitationSystemic effectsTear fluid

Identifiers

PMID40948987
PMCPMC12422999

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.