Body-Mind Medicine: A Novel Approach to Healing

1 [Implicit learning overview]

2 Reber (1992), The cognitive unconscious: An evolutionary perspective. June 1992 Consciousness and Cognition 1(2):93-133 [Unconscious associations]

3 Nairne et al. (2007), Adaptive memory: Survival processing enhances retention. J Exp Psychol Learn Mem Cogn. 2007 Mar;33(2):263-7 [Squire & Kandel on implicit memory’s link to survival and reproduction]

4 Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008).From inflammation to sickness and depression: when the immune system subjugates the brain. Nature Reviews Neuroscience, 9(1), 46–56. [Immune activation (e.g., infection) signals the brain via cytokines and the vagus nerve, leading to changes in mood, motivation, and cognition—often without conscious awareness.]

5 Critchley, H. D., & Harrison, N. A. (2013). Visceral influences on brain and behavior. Neuron, 77(4), 624–638. [Internal bodily states—including immune activity—are processed through the insula and anterior cingulate cortex, influencing perception and emotion unconsciously.]

6 Harrison, N. A., Brydon, L., Walker, C., Gray, M. A., Steptoe, A., & Critchley, H. D. (2009). Inflammation causes mood changes through alterations in subgenual cingulate activity and mesolimbic connectivity. Biological Psychiatry, 66(5), 407–414.

7 Eisenberger, N. I., Inagaki, T. K., Mashal, N. M., & Irwin, M. R. (2010). Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood. Brain, Behavior, and Immunity, 24(4), 558–563.

8 Stephan, K. E., Manjaly, Z. M., Mathys, C. D., et al. (2016). Allostatic Self-efficacy: A Metacognitive Theory of Dyshomeostasis-Induced Fatigue and Depression. Frontiers in Human Neuroscience, 10, 550. [The brain integrates physiological inputs (including immune status) into predictive models that influence emotion and behavior, supporting an unconscious basis for “gut feelings.”]

9 Mayer, E. A., & Tillisch, K. (2011).The brain-gut axis in abdominal pain syndromes. Annual Review of Medicine, 62, 381–396.

10 Armour, J. A. (1991). Potential clinical relevance of the ‘little brain’ on the mammalian heart. Experimental Physiology, 76(5), 615–625. https://doi.org/10.1113/expphysiol.1991.sp003533[Functional intrinsic cardiac nervous system can process sensory information, make decisions, and modulate output, independent of the brain. The system exhibits plasticity in its reflex responses, a hallmark of primitive learning.]

11 Ardell, J. L., & Armour, J. A. (2016). Neurocardiology: Structure-Based Function. Comprehensive Physiology, 6(4), 1635–1653. [Reviews evidence that cardiac neurons change their output behavior in response to chronic changes in afferent input—demonstrating functional reorganization over time, consistent with neural adaptation and memory formation.]

12 Smith, F. M., & Armour, J. A. (1992). Intrathoracic extracardiac neurons in mammals: a possible site of cardiac memory. Cardiovascular Research, 26(1), 1–7. [Memory-like properties might exist in peripheral autonomic ganglia, particularly cardiac neurons that exhibit lasting alterations in behavior after conditioning.]

13 Gershon, M. D. (1998). The Second Brain: A Groundbreaking New Understanding of Nervous Disorders of the Stomach and Intestine. HarperCollins. [ENS’s independent reflex circuits, long-term modulation, and ability to integrate stimuli and adapt behavior, including evidence of synaptic plasticity in the gut.]

14 Wood, J. D. (2006). Enteric nervous system: reflexes, pattern generators and motility. Current Opinion in Gastroenterology, 22(2), 102–110. https://doi.org/10.1097/01.mog.0000203864.37810.2b[Describes reflex learning in the ENS, with pattern-generating circuits that can be modified by experience—closely analogous to spinal cord learning.]

15 Neunlist, M., Van Landeghem, L., Mahé, M. M., Derkinderen, P. (2013). The digestive neuronal-glial-epithelial unit: a new actor in gut health and disease. Nature Reviews Gastroenterology & Hepatology, 10(2), 90–100. [Describes how gut-immune signals influence emotional and threat-related processing in the brain, often resulting in visceral “feelings” without conscious reasoning.]

16 Patterson, M. M. (1976). Spinal cord long-term memory: learned flexion reflexes in the rat. Science, 194(4261), 891–894. [Spinalized rats (with brains disconnected) can still learn to modify their withdrawal reflex to painful stimuli, showing long-term changes in spinal reflex circuits—i.e., a form of instrumental learning independent of the brain.]

17 Grau, J. W., et al. (2006). Learning in the spinal cord: lessons for the rehabilitation of spinal cord injury. The Neuroscientist, 12(5), 477–488. [Reviews extensive evidence that the spinal cord can learn, adapt, and store memory traces, even after spinal transection. Also discusses metaplasticity—the modulation of future learning by past experience.]

18 Thompson, A. K., Pomerantz, F. R., & Wolpaw, J. R. (2013). Operant conditioning of a spinal reflex can improve locomotion after spinal cord injury in humans. Journal of Neuroscience, 33(6), 2365–2375. [Human clinical study showing that operant conditioning of spinal reflexes improves locomotion after injury—implying experience-dependent plasticity in spinal circuits.]

19 Bergquist, A. J., Clair, J. M., & Collins, D. F. (2011). Motor unit recruitment when neuromuscular electrical stimulation is applied over a nerve trunk in human subjects. Journal of Applied Physiology, 110(6), 1501–1510. https://doi.org/10.1152/japplphysiol.01202.2010[Peripheral nerve stimulation can induce plastic changes in recruitment patterns, suggesting adaptive responses in peripheral motor circuits.]

20 Woolf, C. J., & Salter, M. W. (2000). Neuronal plasticity: increasing the gain in pain. Science, 288(5472), 1765–1769. [Shows that nociceptors in the PNS can exhibit long-term sensitization—a form of memory in which prior painful input enhances future responses. This plasticity underlies phenomena like hyperalgesia and chronic pain.]

21 Coderre, T. J., & Melzack, R. (1992). Central neural mediators of secondary hyperalgesia following heat injury in rats: neuropeptides and excitatory amino acids. Neuroscience Letters, 135(1), 93–96. [In peripheral and spinal systems, excitatory signaling leads to lasting changes in pain sensitivity—indicating memory encoding in nociceptive pathways.]

22 Foster et al. (2007): Epigenetic reprogramming in macrophages after pathogen exposure (Nature Immunology)

23 Sun et al. (2016): Epigenetic memory in wound healing cells (Cell Reports)

24 Egger et al. (2004): Epigenetics in human disease and cellular memory (Nature)

25 [Cells as computers]

26 [Neutrophiul chasing bacterium]

27 [Cell information encoding]

28 [Cellular memory]