Body composition - TOWARDS LIFE-KNOWLEDGE

Modern nutrition science has often reduced food to its macronutrient content and calories, overlooking its role as an ecological signal and symbolic interface between body, mind, and biosphere. This white paper proposes a regenerative reframing of health and disease through the dynamic and recursive relationships between food composition, microbiome composition, and body composition. Drawing upon current research in nutritional biochemistry, gut ecology, fascia science, psychoneuroimmunology, and symbolic systems biology, we explore how food not only nourishes but encodes, how microbes translate meaning into metabolism, and how the human form itself is a reflection of relational coherence or systemic breakdown.

By mapping these interdependent layers, we argue for a transition from symptom-based, reductionist paradigms to coherence-first models of regenerative health — where the healing process begins with recognizing food as a medium of communication, microbiota as ecological interpreters, and the body as a living record of attunement or alienation. We conclude with clinical and policy implications that integrate nutrition, microbial health, social determinants, and symbolic literacy into a unified framework for restoring systemic resilience.

The global nutrition transition, which embraces major changes in how food is produced, distributed and consumed, is associated with rapid increases in the prevalence of obesity, but the implications for diabetes differ between populations. A simple conceptual model treats diabetes risk as the function of two interacting traits: ‘metabolic capacity,’ which promotes glucose homeostasis, and ‘metabolic load’, which challenges glucose homoeostasis. Population variability in diabetes prevalence is consistent with this conceptual model, indicating that the effect of obesity varies by ethnicity. Evolutionary life history theory can help explain why variability in metabolic capacity and metabolic load emerges. At the species level (hominin evolution), across human populations and within individual life courses, phenotypic variability emerges under selective pressure to maximise reproductive fitness rather than metabolic health. Those exposed to adverse environments may express or develop several metabolic traits that are individually beneficial for reproductive fitness, but which cumulatively increase diabetes risk. Public health interventions can help promote metabolic capacity, but there are limits to the benefits that can emerge within a single generation. This means that efforts to curb metabolic load (obesity, unhealthy lifestyles) must remain at the forefront of diabetes prevention. Such efforts should go beyond individuals and target the broader food system and socioeconomic factors, in order to maximise their efficacy.