The Hidden Enemy of the Heart | How Malignant Complexes Hijack the Pankseppian CARE System, a Precise, Neurobiological, Trauma-Informed Guide

Malignant Complexes are trauma-born, autonomic patterns that can distort Panksepp’s CARE system (oxytocin/prolactin biology), producing compulsive caregiving, self-erasure, and enmeshment. This article maps primary neurobiology, prolactin pleiotropy (immune, metabolic, behavioral, homeostatic effects), and exact mechanisms by which hormonal and circuit dysfunctions benefit and maintain Malignant Complexes, with clinical and self-help implications.

The Paradox

At its healthiest, the Pankseppian CARE system (one of the brain’s seven primary emotional-action systems) enables the biology of parental and social nurturing:

• Empathy

• Attunement

• Safe Boundary-Keeping

• Calibrated Self-Sacrifice

When early trauma or chronic relational wounding sculpts hidden, survival-based parts of the mind (what we call Malignant Complexes) that same CARE machinery can be co-opted:

• Empathy becomes compulsive caretaking

• Mirroring becomes enmeshment

• Trust becomes codependent survival strategy

• Self-Sacrifice becomes a martyrdom

Understanding the exact neurobiology (oxytocin, prolactin, receptor sensitivities, endophenotypes, and downstream immune/metabolic effects) self-analysis users concrete levers for reality-testing and instinctual healing.

Panksepp’s CARE System

Jaak Panksepp’s affective-neuroscience model identifies seven conserved subcortical emotional-action systems (RAGE, LUST, FEAR, CARE, PLAY, SEEKING, PANIC/GRIEF). The CARE circuitry is evolutionarily designed to drive parental nurturing, affiliative bonding, and prosocial behaviors, and it’s tightly linked to neuropeptides and neuromodulators (most notably oxytocin, and to a significant degree prolactin and endogenous opioids).

Dysfunction or dysregulation of CARE does not imply a moral deficit, it indicates a circuit that has been adaptively engrained by early relational contexts.

Primary Neurobiology

Oxytocin: Production, Release, and Core Behavioral Roles

• Where it’s made & released: Oxytocin is produced by magnocellular neurons of the hypothalamic supraoptic and paraventricular nuclei and released centrally and peripherally via the posterior pituitary.

• Core functions: social bonding, trust modulation, maternal attachment, sexual behavior, attenuation of social threat signals, and modulation of social salience and memory. Oxytocin’s effects are context-dependent. It can increase in-group trust while sometimes enhancing defensiveness toward perceived out-groups. 

  “Modulation of social salience and memory” means that oxytocin can change what kinds of social cues your brain notices and how strongly you remember them.

Social salience: How much a particular social signal (tone of voice, facial expression, touch, etc.) stands out to you and captures your attention.

Memory: How your brain encodes, stores, and recalls those social experiences later.

Oxytocin doesn’t just make you “nicer,” it can bias your brain toward noticing certain emotional or relational details more than others, and it can strengthen or weaken the memory traces of those interactions.

Prolactin: Production, Receptor Distribution, and Pleiotropy

• Where it’s made: Prolactin (PRL) is primarily produced by lactotroph cells in the anterior pituitary under predominant hypothalamic inhibitory control (dopaminergic tone).

• Pleiotropy: Prolactin is highly pleiotropic: A biology term meaning that one gene, protein, or biological factor influences multiple, seemingly unrelated traits or functions. It acts across reproductive axes, brain circuits, immune cells, adipose and metabolic systems, sleep regulation, neurogenesis, oligodendrocyte proliferation, and stress responsivity. These actions are grouped into categories (reproductive, immune regulation, metabolism, behavior, homeostasis).

Prolactin’s major functional categories

Below is a list representing many overlaps of evidence-based functions organized by category.

Immune regulation

• Prolactin signals like a cytokine, PRL receptors are expressed on T and B lymphocytes, dendritic cells, and macrophages. PRL can promote lymphocyte proliferation, lower activation thresholds of anergic B cells, and modify T-regulatory cell functions; in many contexts it has immune-stimulatory properties and has been implicated in autoimmunity (e.g., lupus, rheumatoid arthritis).

  
  

Metabolism (energy balance, adipose, leptin interactions)

• PRL acts on adipose tissue, pancreas, and the hypothalamus to modulate appetite, leptin expression, insulin sensitivity, and calcium/lipid handling. In lactation models, PRL contributes to hyperphagia and changes in energy partitioning; it can also alter leptin mRNA in adipose tissue and interact with neuropeptide Y pathways.

  
  

  If traumatized and chronically stressed, the combined effects on appetite, adiposity, leptin resistance, and insulin sensitivity can raise diabetes risk.

  
  

  Hyperphagia means excessive eating, specifically, a significantly increased appetite and food intake beyond the body’s energy needs.

Behavior (maternal, sexual, stress modulation, reward)

• PRL promotes maternal caregiving behaviors in animal models (nest-building, pup retrieval, nursing). It modulates sexual motivation and post-orgasmic satiety and alters behavioral responses to stress. PRL’s central receptors influence motivational states and affiliative behavior.

Homeostasis (stress responsivity, neurogenesis, sleep, oligodendrogenesis)

• PRL is secreted during many stressors and interacts with the HPA axis; it has been implicated in stimulating adult neurogenesis (e.g., hippocampal progenitors), promoting oligodendrocyte proliferation, and influencing sleep architecture (changes in REM/NREM patterns). These effects make PRL a genuine homeostatic/neuroplastic regulator.

If prolactin alters sleep architecture, especially the emotional-processing role of REM, it can reinforce trauma-linked memories and emotional responses, making it easier for the complex to “replay” its old scripts. Inconsistent or shallow NREM can also keep the body in a low-recovery state, feeding fatigue and vulnerability cues that the complex can exploit.

How oxytocin & prolactin dysfunctions can benefit a Malignant Complex

Below the word “benefit” is used clinically: how dysregulation produces states, signals, or behaviors that the hidden, trauma-survival-based Malignant Complex uses to persist and gain control. Each mechanism link is phrased as a plausible, psychogenic pathway (not a universal causal law).

Oxytocin dysregulation: Mechanisms that sustain a Malignant Complex's Hypo-oxytocinergic patterns (low central oxytocin or reduced receptor sensitivity)

• Increased social threat sensitivity, reduced secure attachment responses, higher interpersonal mistrust and isolation.

• A Malignant Complex that depends on threat vigilance gains fuel: mistrust and withdrawal justify self-protective, controlling behaviors and keep the person in defensive modes that block corrective relational experiences.

  
  

• Intensely selective affiliative responses (over-bonding/enmeshment with certain caregivers) and increased social salience of attachment cues.

• Over-bonding converts care into compulsion: the part that once secured safety by clinging now enforces caretaking rituals (people-pleasing, boundary dissolving), sustaining the Malignant Complex’s program.

Clinical note: oxytocin’s valent effects are not straightforwardly “good” or “bad.” Its directionality depends on receptor distribution, context, history, and interacting systems (dopamine, opioids), which is why a trauma-informed map matters.

Prolactin (PRL): How immune, metabolic, behavioral, and homeostatic dysregulation help a Malignant Complex

Immune regulation: PRL as a chronic interoceptive signal

• PRL’s immune-stimulatory actions increase cytokine signaling, alter T/B cell thresholds, and are associated with autoimmune flares and systemic low-grade inflammation.

• Chronic low-grade inflammation creates persistent somatic cues (fatigue, malaise, pain, affective blunting) and strengthens bodily narratives of fragility/need. Those interoceptive cues are raw material for a complex that says, “you are vulnerable; you must use X survival strategy (people-pleasing, hiding) to be safe.” In short: inflammation is embodied distress, which repeat protective behaviors that the complex rewards.

Metabolism: Energy states, leptin signaling, and caregiving economy

• Prolactin alters adipose signaling (including leptin mRNA), drives lactation-style hyperphagia in mammalian models, and modulates hypothalamic appetite circuits (e.g., neuropeptide Y).

• Metabolic dysregulation produces chronic energy imbalances called Drive States (fatigue, hunger, reward shifts) that can be read by the psyche as helplessness or dependence. A complex that depends on eliciting care gains leverage: hunger/fatigue justify seeking care, remove bandwidth for boundary setting, and create a perpetual “I need you” physiological script.

Behavior: Maternal programming repurposed

• PRL’s central actions promote caregiving sequences (nesting, retrieval) and modulate sexual and stress-related behaviors.

• Early life PRL-sensitive caregiving circuits that were adaptive become re-used by the Malignant Complex to generate compulsive caregiving patterns (over-responsibility, caretaking at self-cost), or conversely to weaponize care (using caretaking to control relationships). The net effect is that the person is biologically primed to do the very behaviors that keep the complex alive.

Homeostasis & neuroplasticity: Stress, sleep, and consolidation of maladaptive patterns

• PRL is secreted by many stressors, interacts with the HPA axis, influences sleep architecture, and can modulate neurogenesis and oligodendrocyte proliferation, all key processes for memory consolidation and emotional learning.

• When stress-related PRL release and altered sleep converge, traumatic or survival-scripts can be re-encoded more strongly. Poorly consolidated restorative sleep, representing exhaustion stress promotes a neuroplastic environment where the Malignant Complex’s procedural programs (automatic shame, protective caretaking, hypervigilance) are preferentially rehearsed and hardened.

When CARE’s ancient circuitry is hijacked by a Malignant Complex, what was meant for safe connection becomes a survival straightjacket, neurochemically reinforced and biologically rehearsed until compassion feels like compulsion. This is not a failure of character. It’s a predictable outcome of how oxytocin and prolactin interact with memory, stress, and social threat systems under trauma.

But because the CARE system is state-dependent and inherently relational, it can be re-scripted. In Dream Circles, we work directly with the Instinctual Consciousness that speaks through dreams, restoring CARE to its original purpose:

Compassion with boundaries

Love without depletion

Connection without self-loss

In the presence of others walking the same path, the very instinct that was exploited becomes the instinct that heals.

This content is educational, not medical advice.