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

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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Publication Details

Journal
The EPMA Journal
Published
2025-09-04
DOI
https://doi.org/10.1007/s13167-025-00423-6
Citations
4
Primary Topic
Birth, Development, and Health
Type
article
Field-Weighted Citation Impact
13.98

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article

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

Olga Golubnitschaja
4 citations
The EPMA Journal
Birth, Development, and Health
13.98
article

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

Olga Golubnitschaja
article en
4 citations

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.

The EPMA JournalVol. 16(3)
University of Bonn (DE), University Hospital Bonn (DE)
Rheinische Friedrich-Wilhelms-Universität Bonn
Openalex Percentile: Top 1%
Birth, Development, and Health
13.98
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