ElectroSenses – Why a New Journal?

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Julia Ferencz

Editorial

Volume 1 ♦ Issue 1 ♦ March 2026 ♦ Pages 1-3

ElectroSenses – Why a New Journal?

Article Data

• Volume 1 ♦ Issue 1 ♦ March 2026 ♦ Pages 1-3
• DOI: to be assigned 
• Dates:
  • Received:   03.03.2026
  • Revised:     11.03.2026
  • Accepted:  13.03.2026
  • Published: 16.03.2026
• Keywords:
  • Electrons
  • Genetics
  • Mitochondria
  • Microbiom
  • Environment
• Corresponding Author:
  • Julia Ferencz
  • j.ferencz@deep-diagnosis.com
  • ORCID: 0000-0003-2196-571X
• Author:
  • Julia Ferencz^1,2
    • ¹ Deep Diagnosis – Practice for Functional and Environmental Medicine, Ulm, Germany
    • ² Society of Functional and Environmental Medicine, Cluj, Romania
• Citation: Ferencz J. ElectroSenses – Why a New Journal?. ElectroSenses. 2026;1(1):1-3
• Funding: No funding
• Ethical Approval: Not applicable
• Data availability: Not applicable
• AI Usage: AI-assisted tools were used only for language editing.
• Conflict of interest: The author declares no conflict of interest.

Perspective

In recent years, biomedical science has rapidly advanced our understanding of molecular processes. Breakthroughs in genomics, metabolomics, microbiome research, and systems biology have deepened our understanding of the intricacies of biological regulation. Nonetheless, many chronic diseases continue to defy complete mechanistic explanation. Disorders like metabolic syndrome, neurodegeneration, persistent inflammation, and multisystem conditions frequently emerge from disruptions that exceed the scope of single-pathway or organ-based models.

A growing body of research suggests that many of these disorders involve disruptions in cellular energy regulation. Mitochondria, once considered primarily as ATP-producing organelles, are now recognized as central regulators of metabolism, redox signaling, apoptosis, immune responses, and cellular stress adaptation [1,2]. Through the mitochondrial electron transport chain, cells generate electrochemical gradients that drive oxidative phosphorylation and maintain bioenergetic stability across tissues.

Viewed through this lens, living systems are not solely collections of biochemical reactions—they are also orchestrated by the deliberate movement of electrons and energy within molecular frameworks. Life can be seen as the sustained, organized flow of energy across intricate regulatory circuits. Disturbances in this energetic flow may gradually erode a system’s capacity for stable regulation.

Genetic variability plays a crucial role in maintaining the stability of organisms. Polymorphisms in genes involved in regulating oxidative stress, mitochondrial function, and xenobiotic metabolism can influence metabolic resilience. Variants affecting antioxidant defense systems, such as superoxide dismutase (SOD2), redox-sensitive transcriptional regulators, such as NRF2, detoxification enzymes, including the glutathione S-transferase family, or enzymes involved in catecholamine and methylation metabolism, such as COMT, illustrate how genetic background can modify the capacity of biological systems to cope with metabolic and environmental stress.

Environmental exposures further interact with these regulatory networks. Pollutants, toxic metals, nutritional deficiencies, and other environmental stressors can converge on mitochondrial function and redox signaling pathways.

Metals such as mercury, arsenic, cadmium, and aluminum are known to interfere with mitochondrial enzymes, disrupt electron transport chain activity, and impair iron–sulfur cluster–dependent proteins that are essential for oxidative phosphorylation. Such disturbances may reduce ATP generation, increase reactive oxygen species production, and destabilize signaling pathways that regulate metabolic adaptation [3].

Importantly, the relevance of mitochondrial energetics for disease mechanisms has been recognized for several decades. Early work already highlighted the role of mitochondrial dysfunction in aging and complex disease processes [4]. However, technological limitations hindered detailed investigation of these mechanisms, and these concepts remained relatively peripheral to mainstream biomedical research. Only in recent years have advances in metabolomics, imaging technologies, and systems biology enabled the study of cellular energy regulation in a more integrated manner.

Recent studies increasingly support the view that mitochondria act not only as metabolic engines but also as signaling platforms that integrate environmental cues, metabolic stress, and immune responses [2,5]. These findings suggest that disturbances in mitochondrial bioenergetics may represent a fundamental layer underlying many chronic disease processes.

Modern biomedical research has traditionally focused on identifying molecular components—genes, proteins, and metabolites. Yet biological systems operate through dynamic processes such as electron transport, redox flux, membrane potentials, and energy gradients. Understanding these functional dimensions of living systems may therefore be just as important as cataloguing their molecular parts.

In this sense, the next frontier of medicine may lie not only in decoding genes, but in understanding how cells generate, distribute, and regulate energy. Disease may ultimately be understood as a failure of biological energy regulation within complex adaptive systems.

Despite growing recognition of these interactions, research addressing the intersection of mitochondrial bioenergetics, genetic variability, environmental exposures, and bioelectrical regulation remains fragmented across multiple disciplines. Studies of mitochondrial metabolism are typically published in metabolic research journals, investigations of environmental toxicants appear in toxicology literature, and research on genetic susceptibility often remains confined to genomics publications. Opportunities for conceptual integration across these domains remain limited.

ElectroSenses – Journal of Bioelectromagnetics, Environmental & Functional Medicine was established to explore precisely these intersections. The name ElectroSenses reflects the concept that biological systems continuously sense and respond to their environment not only through biochemical pathways but also through electrical gradients, electron transport processes, and bioenergetic signaling mechanisms that regulate cellular physiology.

Several research directions may prove particularly important in the coming years. These include investigations into mitochondrial bioenergetics in chronic disease development, genetic determinants of detoxification capacity and metabolic resilience, environmental influences on mitochondrial signaling pathways, and new methodologies capable of measuring functional aspects of cellular energy metabolism and redox dynamics.

In this context, bioenergetic biology may be defined as the study of how living systems generate, distribute, and regulate energy across molecular, cellular, and physiological levels.

Another important dimension of systemic regulation involves the gut microbiome, which functions as a dynamic interface between environmental exposures and host physiology. The intestinal microbial ecosystem participates in numerous metabolic and regulatory processes, including nutrient transformation, short-chain fatty acid production, immune modulation, and maintenance of intestinal barrier integrity. Increasing evidence indicates that microbial metabolites can directly influence mitochondrial function, redox signaling, and host energy metabolism. At the same time, disturbances in microbiome composition—often referred to as dysbiosis—have been associated with a wide range of chronic conditions, including metabolic disorders, inflammatory diseases, and neurological syndromes. Because the microbiome responds rapidly to dietary factors, environmental toxicants, medications, and lifestyle influences, it serves as a critical intermediary through which environmental signals can shape host metabolic regulation. Understanding how microbial ecosystems interact with mitochondrial bioenergetics and host genetic variability may therefore become an important component of future systems-based approaches to human health.

Beyond metabolic regulation, the gut microbiome is increasingly recognized as an important component of the gut–brain axis, influencing neuroendocrine signaling, stress responses, and neuroimmune regulation. Microbial metabolites and immune mediators can affect central nervous system function through vagal signaling, circulating metabolites, and inflammatory pathways. Disturbances in microbiome composition have been linked to altered stress responses, neuroinflammation, and dysregulation of hypothalamic–pituitary–adrenal (HPA) axis activity. These interactions suggest that chronic environmental stressors, microbial dysbiosis, and mitochondrial dysfunction may converge to influence neuroinflammatory processes that contribute to a variety of neurological and systemic disorders.

Another dimension concerns the integrity of physiological barrier systems that regulate the interaction between environmental exposures and internal biological processes. The intestinal epithelium, the hepatic detoxification system, and the blood–brain barrier form interconnected regulatory interfaces that protect systemic homeostasis. Disruption of intestinal barrier integrity can permit the translocation of microbial components and inflammatory mediators into the circulation, potentially contributing to persistent immune activation. Because the liver is the primary organ responsible for processing gut-derived metabolites and environmental xenobiotics, increased exposure to these compounds may place additional metabolic demands on hepatic detoxification pathways. At the same time, systemic inflammatory mediators and circulating microbial products have been shown to influence the stability of the blood–brain barrier, creating conditions that may facilitate neuroinflammatory signaling within the central nervous system. These interconnected barrier systems, therefore, represent an important regulatory network linking environmental exposures, immune signaling, and neurophysiological stability [7].

A further challenge lies not only in generating new knowledge but also in communicating it effectively within the medical community. Many clinicians are trained within diagnostic frameworks that prioritize well-established disease categories and standardized biomarkers. As a result, concepts such as genetic variability in detoxification pathways, mitochondrial bioenergetics, or the biological impact of toxic metals are sometimes perceived as speculative rather than mechanistically grounded. Bridging this gap requires approaches that resonate with clinical practice: reproducible biomarkers, clearly defined physiological mechanisms, and well-designed clinical studies that translate complex biological insights into practical diagnostic and therapeutic strategies.

Equally important is the development of educational platforms and collaborative networks that enable clinicians, laboratory scientists, and researchers to examine emerging evidence together. Changing medical paradigms rarely occurs through isolated discoveries; it occurs gradually through transparent data, open scientific dialogue, and the accumulation of reproducible observations that ultimately reshape clinical understanding.

If these mechanisms are to become part of routine medical thinking, they must move from the margins of discussion into the center of scientific investigation. Journals that encourage rigorous research and interdisciplinary dialogue can help accelerate this transition.

Ultimately, the aim is not simply to accumulate additional data, but to deepen our understanding of the fundamental principles that govern biological stability and adaptation. Scientific progress will depend not only on larger datasets, but on conceptual frameworks capable of linking genetics, environmental influences, and mitochondrial energy regulation into coherent models of health and disease.

Understanding how biological systems generate, distribute, and regulate energy may ultimately prove central to explaining many of the complex disease patterns that characterize modern medicine.

ElectroSenses aims to explore the bioenergetic foundations of biology, where genetics, environmental signals, and mitochondrial electron transport converge to shape human physiology and disease.

References

1.Spinelli JB, Haigis MC. The multifaceted contributions of mitochondria to cellular metabolism. Nat Cell Biol. 2018;20:745-754.

2.Suomalainen A, Battersby BJ. Mitochondria at the crossroads of health and disease. Cell. 2024;187(11):2601-2627

3.Meyer JN, Leung MCK, Rooney JP, et al. Mitochondria as a target of environmental toxicants. Toxicol Sci. 2013;134(1):1-17.

4.Wallace DC. Mitochondrial DNA mutations in disease and aging. Environ Mol Mutagen. 2010;51(5):440-450.

5.Picard M, McEwen BS. Psychological stress and mitochondria: a conceptual framework. Psychosom Med. 2018;80(2):126–140

6.Zong Y, Li H, Liu X. Mitochondrial dysfunction: mechanisms and advances in disease research. Signal Transduct Target Ther. 2024;9:124

7.Camilleri M. Leaky gut: mechanisms, measurement and clinical implications in humans. Gut. 2019;68(8):1516-1526

Contributions

JF conceptualized the editorial and wrote the manuscript.