Adipose Reduction and Bodyfat Setpoint Efforts to maximize adipose tissue reduction will continue to remain a central concern for both the medical communities (e.g., obesity) as well as—and more central to this article—the elite fitness and athletic communities. A common objective purpose of the elite fitness and athletic communities is, it can be argued, to attain a level of aesthetic definition and sport-specific functional ability which very often includes achieving a minimal level of body adipose reserves with varying degrees of lean body mass (i.e., muscle tissue). The purposive quest to achieve this state, which as a rule creates a voluntarily induced unbalanced metabolic milieu—oftentimes one of a severe and protracted nature—is often fraught with physical and mental discomfort, difficulty, and misunderstanding. This is due in large part to unitary considerations of specific aspects of adipose reduction (e.g., fat loss at the cellular level, anorectic pharmacological aids at the central level) rather than a coherent systems understanding of the dynamics of fat loss and dramatic body recomposition efforts.
In this brief communication, I will present a developmental regulatory-systems view of fat loss and human energetics which has its roots in a multi-disciplinary framework including cell physiology, developmental psychology, neuroscience, and developmental affective neuroscience (Schore, 2002a, b). It is important to note that this article is not a ‘guidebook’ but rather an overarching framework from which to consider relevant aspects of fat loss efforts (e.g., symptomatology) and to promote further understanding into individual differences in body recomposition efforts. I have intentionally eschewed discussions of detail-specific hypothalamic and brainstem microenvironments involved in metabolic energy regulation in order to first present a novel framework from which to reconsider prior discussions of such systems (on the forums).
What is a Developmental Regulatory Perspective?
A developmental regulatory perspective to adipose tissue reduction and bodyfat setpoint is a life-span perspective on the regulatory mechanisms behind adipose tissue growth, maintenance, and degradation. The term “regulatory” is critical because, as Schore (1994) points out, regulation is used as a focal construct in every field of science. Importantly for our discussion, he notes that
In terms of bodyfat reduction and setpoint, readers are most likely well aware of the lengthy discussions concerning the regulatory mechanisms and structures in both the central and peripheral nervous systems that are involved in the homeostatic maintenance of a given bodyfat setpoint (i.e., hypothalamic microenvironment and structure; cellular physiology of lipids; leptin, etc.). However, current discussions on the matter continue to fall short of a full integration of peripheral and central regulatory structures,and have failed notably in considering the role of socioemotional regulation in providing the necessary mental flexibility and balance needed to engage the process of dramatic bodyfat reduction and recomposition. In short, what is needed is a move to the level of multidisciplinary regulatory thinking regarding energetics and body fat and its functional significance. This thinking needs to include the socioemotional domain, as it too is governed by regulatory principles. If we leave this domain out of consideration, as has been previously done, we are committing what Damasio (1994) considered “Descartes Error” or separating the brain/mind from the body.
The Nexus between Energetic Regulation and Emotional Regulation
The idea of a developmental regulatory stance towards bodyfat setpoint and adipose tissue reduction is appealing because it allows for a mind-body connection in that both physiological systems and emotional systems are regulatory. For example, the delicate circuitry that is the leptin-ARC-PVN and leptin-ARC-LH pathways in the periphery and hypothalamus are indeed regulatory1. That is they, along with other peripheral and central subsystems, act to control the regulation of adipose reserves. However, consider also that one’s ability to emotionally regulate, particularly in states of stress and perturbation (e.g., severe hypoenergetic feeding, chronic training), are also governed by similar systems in the forebrain-midbrain-limbic circuit (Schore, 1994) with critical wiring in cites such as the orbitofrontal cortex, hypothalamus, amygdalar nuclei, and medullary nuclei.
As the reader may already be aware, a number of the same midbrain-limbic areas that are integral in controlling adipose regulation are also integral in emotional regulation (e.g., amygdalar-hypothalamic pathway; ventral amygdalofugal pathway; stria terminalis). However, a key cortical brain area for emotional regulation is specifically the right orbitofrontal cortex, which along with other paralimbic neocortical structures, is involved in executing inhibitory control over lower order brain structures which are phylogenetically preserved and primitive in nature. Such primitive structures (e.g., amygdala, hypothalamus) would ensure survival of the organism in times of life-threatening circumstances, such as chronic energy deficit. In dieting and attempting to what may here be referred to as “thriving below setpoint” the individual voluntarily effects a higher order control of primitive brain structures. That is, planning, executive, and inhibitory functions of frontal cortex are used to inhibit lower order putative metabolic centers (e.g., ARC-NPY system; LH-Orexin system) that are activated by their respective chemoreceptors to maintain homeostatic and life-adaptive states. In laymen’s terms, the dieter restricts eating. This hierarchical view of central energetic control is viewed from the Jacksonian (1931) principle of hierarchical, self-organizing brain development.
However, the inhibition of the primitive energetic systems is maladaptive when maintained over time (i.e., anorexia, training-related pathologies, body dysmorphic disorder, HPA irregularities, and immunosuppression). After a period of time, a process of “decompensation” (Wang, Wilson, and Mason, 1996, as cited in Schore, 2003) occurs in which the central system begins to rapidly disorganize. This idea of decompensation of the system applies to regulatory functions of the human both in terms of emotion-related phenomena as well as other regulatory-governed behaviors and systems such as the energetics system. In terms of Jacksonian (1931) principles, the resultant pathology (i.e., emotional and physiological disturbance) involves a “dissolution”—a loss of inhibitory capacities of the most recently evolved layers of the nervous system that support higher functions (negative symptoms; i.e., absence of eating/bingeing), in addition to the release of lower, more automatic and primitive functions (positive symptoms; i.e., hyperphagia, emotional dysregulation, physical symptomatology) (Schore, 2002a, b). In reverse developmental order, post-dieting sequalae may be understood, in part, by losses in orbitofrontal control, anterior cingulate function deterioration, and finally by the emergence of primitive drives which are no longer inhibited by higher-order structures (e.g., primitive neuroendocrine functions).
Because we are conceptualizing both the energetics and stress-regulatory (HPA) systems as well as the emotional-psychological system as regulatory systems in this framework it is not surprising that we see individual differences in the commorbidity of both dieting ‘chaos’ (cf. Herman & Polivy, 1987; see also ‘boundary model of regulated eating’, same article) and eating dysregulation as well as emotional (psychological) dysregulation and concomitant maladaptation (endocrine and psychological; e.g., the neurotic triad noted in starvation: depression, hypochondriasis, and hysteria; Keys et al., 1950).
The conceptualization outlined here also is in agreement with the notion of ‘processive’ and ‘systemic’ stress pathways (Herman and Cullinan, 1997). In short, the systemic stress pathway is activated in immediate, life-threatening physiologic events, such as hypoxia, and directly activates PVN neurons by way of efferent projections from the locus coeruleus, A1, A2, A5 & A7 cell groups, and serotonergic projections from the reticular formation. In contrast, processive stress pathways do not project directly to the PVN because they do not require life sustaining immediate responses. They require assembly and processing of signals from multiple sensory modalities prior to initiation of a stress response. Such stressors would include emotional stressors. These stressors activate the PVN through the pathways outlined earlier via the amygdalar and related pathways (i.e., the stria terminals and ventral amygdalofugal pathways). Processive pathways are ‘limbic sensitive’ and systemic pathways are ‘limbic insensitive’ (Herman and Cullinan, 1997). Under the constant amplificatory stress of protracted dieting, training, and/or general hypoenergetic climates, processive stress activation has the potential to facilitate dieting chaos and the inability to maintain altered lower bodyfat setpoints. Herman and Cullinan (1997) note the potential for hypothalamic modulation of processive (e.g., emotional; interpersonal) stressors,
In this introductory piece, I have applied a developmental regulatory perspective to bodyfat setpoint and adipose tissue regulation which links both psychology and physiology in the context of developmental affective neuroscience (Schore, 2002a, b). Furthermore, I have argued that in dieting or trying to alter the setpoint of a given adipose system, one can not separate the mind or emotion from the body. Since the systems are integrated at the neurobiological level, it becomes necessary to adopt an interdisciplinary stance to understanding the dynamics of adipose regulation and associated metabolic conditions. In subsequent offerings, I will provide more specific descriptions of the integration of the mind-body systems and microenvironments and explain using a developmental pathways approach: (a) why some individuals are able to maintain functional adaptation at reduced adipose states with greater ease than others; and (b) how to incorporate this regulatory model into either a short or long-term plan (including nutrition and specific behavioral strategies) to remain at reduced adipostatic states for greater periods of time while minimizing both physical pathophysiology and socioemotional maladaptation.
Damasio, A. R. (1994). Descartes’ error. New York: Grosset/Putnam.
Herman , J. P. & Cullinan, W. E. (1997). Neurociruitry of stress: Central control of the hypothalamic-pituitary-adrenocortical axis. Trends in Neuroscience, 20, 78-84.
Herman & Polivy (1987). Diagnosis and treatment of normal eating. Journal of Consulting and Clinical Psychology, 55, 635-644.
Jackson, J. H. (1931). Selected writings of J. H. Jackson: Vol I. London: Hodder and Soughton.
Keys, A., Brozek, J., Henschel, A, Mickelson, O., & Taylor, H. L. (1950). The biology of human starvation: 2 volumes. Minneapolis: University of Minnesota Press.
Schore, A. N. (1994). Affect regulation and the origin of the self: The neurobiology of emotional development. Hillsdale, NJ: Lawrence Earlbaum Associates.
Schore, A. N. (2003a). Affect dysregulation and disorders of the self. New York: W. W. Norton and Company.
Schore, A. N. (2003b). Affect regulation and the repair of the self. New York: W. W. Norton and Company
Wang, S., Wilson, J. P., & Mason, J. W. (1996). Stages of decomposition in combat-related posttraumatic stress disorder: A new conceptual model. Integrative Physiological and Behavioral Science, 31, 237-253.
1 For purposes of brevity, pathways mentioned have been done so in a simplistic broad fashion ignoring intrapathway signaling systems and additional microanatomical features.