如何使用广泛的弗拉默综合征表型对健康到疾病过渡的整体保护-事实和实用建议。

IF 5.9 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
The EPMA journal Pub Date : 2025-09-04 eCollection Date: 2025-09-01 DOI:10.1007/s13167-025-00423-6
Olga Golubnitschaja
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引用次数: 0

摘要

由于其表现型相关态度主要以高绩效为导向,因此,FS表现型携带者在相应的专业领域获得了成功的职业生涯。然而,这种优势与重大的健康风险相关。FSP携带者对压力非常敏感。相应的途径是表观遗传调控的,可改变的风险因素与表现型特异性心身模式有关,如对一丝不苟、完美主义的驱动,以及对自己的行为和行动的严格、纪律或彻底的锻炼。FS表型的典型特征是短暂交感神经兴奋的慢性化及其对副交感神经放松的支配。副交感神经-交感神经失衡的慢性化以交感神经过度驱动的形式导致外周血管的慢性缺血事件和与循环缺血-再灌注相关的进行性组织损伤。缺血性损伤可以通过血液中血管收缩素-1 (ET-1)的水平粗略估计。然而,其他风险因素和补偿机制对个体层面的损害程度起决定性作用。例如,长期升高的ET-1,甚至轻度高同型半胱氨酸血症,协同作用可能导致小血管疾病的进展、全身性炎症和线粒体应激的慢性化,可能导致受影响个体的慢性疲劳和线粒体倦怠,并伴有一系列相关病理。这就是为什么利用全面个性化患者资料的预测性诊断对于具有成本效益的针对性预防和个性化治疗算法的创建至关重要。由于算法的高度复杂性,人工智能的应用是必不可少的。FS通常在健康个体的青春期成熟早期形成。因此,FS表型对3pm引导的具有成本效益的初级卫生保健是有帮助的。为了满足这一患者队列的需求,强烈建议应用包括线粒体稳态记录在内的数字健康监测,以保护FS表型携带者免受健康向疾病转变的影响。为此,已经建立了患者友好的非侵入性方法,利用泪液多组学,线粒体作为重要的生物传感器和基于人工智能的多专业数据解释;该方法适用于FS表型携带者。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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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