On page 2, the authors assert that aging is shaped by social habits, listing “dietary choices, physical activity, social engagement, and stress management… as well as infidelity and righteousness.” While the first four are well-established in the aging literature with clear mechanistic pathways, the latter two are introduced without a convincing scientific rationale.
Lack of Mechanistic and Epidemiological Foundation
The paper does not establish, nor cite robust evidence for, a direct biological pathway through which infidelity or righteousness influences cellular aging, telomere length, or inflammaging. The sole reference for this inclusion (Bożek et al., 2020) discusses spirituality and well-being, not infidelity. This raises critical questions:
What biologically-plausible model links moral behavior to senescence?
Was a systematic review conducted to justify these constructs alongside diet and exercise?
How are these terms operationally defined in a way that is measurable and generalizable across cultures?
Introducing value-laden, culturally subjective constructs into a biogerontology review risks conflating moral or social judgments with scientific causality. It inadvertently frames aging as a moral outcome rather than a biological process influenced by modifiable risk factors.
Entire subsections (5.6 and 5.7) are devoted to these topics, relying largely on psychosocial and relational studies without integrating them into the preceding biological framework. This creates a disjointed narrative and weakens the paper’s interdisciplinary credibility.
We appreciate ScienceGuardians’ detailed evaluation of our review article, “Deciphering the mechanisms, biochemistry, physiology, and social habits in the process of aging” (Archives of Gerontology and Geriatrics Plus, 2024), and welcome the opportunity to clarify our scientific intent, conceptual framing, and scope. We regard this engagement as a constructive contribution toward strengthening rigor and transparency in interdisciplinary aging research.
1. Clarification of Authorial Intent
Our review was conceived and executed as an integrative synthesis of aging, explicitly positioned at the intersection of biological mechanisms, physiological and biochemical processes, and social-behavioural influences. The manuscript was not intended to redefine aging as a moral phenomenon, nor to suggest that moral attributes exert direct causal effects on cellular senescence, telomere dynamics, or inflammaging.
Rather, the inclusion of selected social behaviours, including relational instability and value-aligned conduct, was intended to illustrate how persistent psychosocial environments and behavioural contexts may indirectly influence aging trajectories through established stress-responsive, neuroendocrine, and behavioural pathways. At no point does the manuscript assert that aging outcomes represent moral judgements or ethical consequences.
2. Scientific Framing and Rationale
Contemporary aging research increasingly recognises aging as a biopsychosocial process, wherein chronic psychosocial stressors, social cohesion, behavioural consistency, and psychological well-being influence healthspan and disease susceptibility through interconnected neuroendocrine, inflammatory, and behavioural mechanisms.
Within this framework:
Infidelity was discussed as a behavioural context associated with chronic interpersonal stress, emotional dysregulation, social instability, and maladaptive coping behaviours. These factors are known to influence hypothalamic–pituitary–adrenal (HPA) axis activity, inflammatory tone, and health-risk behaviours, which are recognised modifiers of aging-related outcomes.
Righteousness, as used in the manuscript, was not intended as a theological or moral absolutist construct, but rather as a descriptor of enduring value-aligned behaviours associated with psychological coherence, social trust, purpose in life, and prosocial engagement. These dimensions overlap with well-established constructs such as meaning in life, ethical congruence, and social integration, which have documented associations with mental health, stress regulation, and longevity-related outcomes.
Importantly, these constructs were presented as psychosocial correlates and behavioural milieus, not as independent biological variables. Their relevance lies in indirect modulation of aging-relevant pathways, rather than in direct molecular causation.
3. Acknowledgement of Limitations and Need for Clarification
We acknowledge the need for additional clarity, particularly for readers approaching the manuscript from a strictly biological or mechanistic perspective. Specifically:
The terms “infidelity” and “righteousness” are culturally contingent and value-laden and are not standardised exposures within biogerontology or epidemiological aging research.
These constructs do not currently possess well-defined, direct mechanistic pathways comparable to those established for diet, physical activity, or metabolic regulation.
The literature informing these sections is primarily psychosocial and relational, and the manuscript could have more explicitly articulated their indirect biological relevance via stress physiology, behavioural mediation, and neuroendocrine regulation.
Sections 5.6 and 5.7 would have benefited from clearer integration into the preceding biological framework or more explicit positioning as exploratory components within an interdisciplinary narrative.
These limitations are not indicative of conceptual error but rather highlight areas where terminological precision and mechanistic articulation can be strengthened in future interdisciplinary syntheses. We view this as a reflection of the evolving nature of aging research rather than a deficiency in scientific intent.
4. Reaffirmation of Interdisciplinary Value
Despite these acknowledged limitations, we maintain that the central contribution of the review remains scientifically sound and intact. Aging research increasingly underscores the necessity of moving beyond disciplinary silos, recognising that biological aging unfolds within behavioural, social, and psychological contexts that shape exposure to stress, resilience, health behaviours, and social support.
Excluding psychosocial dimensions entirely risks biological reductionism, whereas carefully framed inclusion promotes a more comprehensive understanding of aging as both a biological and lived process. Our review aimed to stimulate integrative thinking and foster dialogue among molecular gerontology, physiology, behavioural science, and social health research.
We welcome the critique as an opportunity to clarify scope and interpretation and believe it ultimately strengthens scholarly discourse surrounding holistic and personalised approaches to healthy aging.
Conclusion
In summary, we respectfully submit that:
The article does not conflate morality with biological causality.
The contested constructs were intended as contextual psychosocial modifiers, not biological determinants.
The need for additional clarity has been acknowledged and is instructive.
The interdisciplinary premise and overall scientific integrity of the review remain robust.
We appreciate ScienceGuardians’ engagement and regard this exchange as a constructive contribution to advancing clarity, rigor, and interdisciplinarity in aging research.