An Update from the Research Team – February 2024

“The heart and the brraaaainnnn…”


This phrase you hear at events during meditations may be the key to understanding how the mind can change the body and how the heart can influence the mind.

My graduate studies at the Medical College of Wisconsin (from January 1999-May 2022) focused on stress adaptation in the heart. In the mid-1980s it was discovered that small amounts of stress protected the heart from a subsequent stress that was more lethal and toxic [1]. This concept, known as preconditioning, involves activating endogenous systems regulating kinases and protein modulators in the acute phase and altered gene response in a delayed phase. This process is also universal and can be coaxed in virtually all organs.

Training as a pharmacologist, my thesis focused on uncovering a therapeutic approach to induce these same pathways using exogenous drug treatments. The laboratory I worked in was the first to uncover the role of opioid receptors in the induction of this endogenous protection, leading to several novel findings. One finding we also showed (but never published as I could not confirm with additional experiments as I was moving on to San Diego) was that the heart likely releases endogenous opioids to induce this protection. This would suggest that apart from being a pump, the heart also acts as an endocrine organ, releasing many endogenous chemicals (i.e., opioids, oxytocin, dopamine, noradrenaline, and various other peptides), that may be protective to the organism.

As I began my post-doc at UCSD, I shifted focus to membrane microdomains in regulating cell physiology. This was a time of expansive growth in this area of biology, and we made great strides in studying membrane biology in the heart and brain. Papers on this topic by our group can be found at the following link: ( Our studies linked these two systems that seem vastly different but are actually closely related.

The cardiac myocyte (major cell in the heart) and the neuron (major cell in the brain) share many characteristics: they are terminally differentiated, meaning they do not undergo any significant cell division (what you have is what you likely get for the rest of your life), they form critical connections with others of their type (a coherent network), they are highly structured, sensitive to injury, undergo aging, and have high mitochondrial metabolic activity. Both the heart and brain are highly metabolic organs and show appreciable functional decline with age. Age is the most important predictor of mortality in patients with heart disease [2]. Mechanisms underlying age-related deficits are unknown but may involve abnormalities in signaling and mitochondrial function [3; 4; 5; 6]. Similarly, brain aging is associated with declining cognitive abilities such as mental speed, executive function, episodic memory, working memory, short-term recollection, processing new information, and spatial memory [7; 8]. These behavioral deficits are due to losses in synaptic contacts, changes in neuronal morphology, reduced structural plasticity and dendritic branching [9], and reductions in cortical (pre-frontal, parietal, temporal, and entorhinal) and hippocampal volume [8; 10; 11]. Our data thus far suggests that week-long events lead to significant resilience in the young and old brain at the electrical and cognitive levels (as seen in the PAIR Study). Whether this is a direct effect on the brain or an interplay between the heart and the brain is currently unknown but of significant interest to our research group.

After much research and controversy, J. Andrew Armour, MD, PhD, in a series of manuscripts, proposed the concept of the little “heart brain,” a series of heart-localized sensory neurites that make up the intrinsic cardiac nervous system [12; 13; 14]. These cells express chemicals and factors found in the brain and are necessary for communication. Studies by Armour suggest that this “heart brain” is independent of the actual brain and can form memories and adapt to stressors in a learned and maintained fashion. This “heart brain” can communicate with the brain to integrate information. This led to an expansion of a field in cardiology called neurocardiology to understand better how the heart may also be a sensory organ. We ascribe several emotional expressions to the heart: a broken heart, a bleeding heart, follow your heart, heart of stone, pour your heart out, young at heart, and many more. Additionally, several stories in the popular media suggest a transfer of memories and behaviors from donors to recipients who undergo a heart transplant. All this suggests that the relationship between the heart and brain may be more complex and important than originally determined. Linking these two organs in a meditative practice may have profound implications for health and disease.

There appears to be a bi-directional drive regarding cardiovascular and neurologic diseases that further fosters the idea of the connectedness of these two organs. There is growing evidence to suggest that individuals with mental health disorders are more prone to cardiovascular diseases [15], and cardiovascular disease is the leading cause of death in individuals with serious mental illness, including diseases such as bipolar disorder, schizophrenia, or schizoaffective disorder [16]. This could be linked to negative emotions and behavioral choices regarding food, habits, etc., that may be at play. Evidence also suggests that cardiovascular disease may be a primary driver of neurodegeneration in diseases such as Alzheimer’s with peripheral blood vessels as well as brain-specific blood vessels related to this pathology [17]. So, it appears that living, learning systems in the heart and the brain communicate, sense each other’s stresses, and respond to this by creating pathology.

Our research at the Advanced Week-long Retreats has focused on the impact of positive emotions on wellness and wholeness, and a key feature of this is the integration of heart and brain health. The meditations that focus on opening the heart and feeling in the brain are grounded in the biological ideas that these two critical organs that define “humanness” in a deep way need each other to survive and thrive in the human condition. We have conducted numerous studies over the years that looked at brain health, from fMRI, qEEG, and cognitive testing to biomarker analysis, and they all point to a positive benefit across health and disease at week-long events. We have less data on the heart, but it is still a massive amount from the Garmin devices worn by thousands of individuals. Preliminary analysis suggests that the heart behaves very differently after a week-long event than with a standard meditation event. Heart rate variability and heart dynamics are shifting in unexpected ways that may reveal much about how the body integrates parasympathetic and sympathetic information. The “heart brain” is driven in a unique unknown path leading to a massive integration of information, which creates changes in biology. We have plans to study the heart in more detail using more sophisticated approaches as events unfold in the coming year and next. The heart and the brraaaainnnn …may be what leads to a better understanding of the potential of a week-long event that empowers us to heal and thrive.


[1] C.E. Murry, R.B. Jennings, and K.A. Reimer, Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 74 (1986) 1124-36.
[2] E. Boersma, K.S. Pieper, E.W. Steyerberg, R.G. Wilcox, W.C. Chang, K.L. Lee, K.M. Akkerhuis, R.A. Harrington, J.W. Deckers, P.W. Armstrong, A.M. Lincoff, R.M. Califf, E.J. Topol, and M.L. Simoons, Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation 101 (2000) 2557-67.
[3] E.J. Lesnefsky, D. He, S. Moghaddas, and C.L. Hoppel, Reversal of mitochondrial defects before ischemia protects the aged heart. FASEB J. 20 (2006) 1543-1545.
[4] J.N. Peart, E.R. Gross, J.P. Headrick, and G.J. Gross, Impaired p38 MAPK/HSP27 signaling underlies aging-related failure in opioid-mediated cardioprotection. J Mol Cell Cardiol 42 (2007) 972-80. PMCID: PMC2497430.
[5] M. Tani, Y. Honma, H. Hasegawa, and K. Tamaki, Direct activation of mitochondrial KATP channels mimics preconditioning but protein kinase C activation is less effective in middle-aged rat hearts. Cardiovasc Res 49 (2001) 56-68.
[6] B. Swynghedauw, S. Besse, P. Assayag, F. Carre, B. Chevalier, D. Charlemagne, C. Delcayre, S. Hardouin, C. Heymes, and J.M. Moalic, Molecular and cellular biology of the senescent hypertrophied and failing heart. Am J Cardiol 76 (1995) 2D-7D.
[7] F. Remy, F. Mirrashed, B. Campbell, and W. Richter, Mental calculation impairment in Alzheimer’s disease: a functional magnetic resonance imaging study. Neuroscience letters 358 (2004) 25-8.
[8] A.M. Fjell, L. McEvoy, D. Holland, A.M. Dale, K.B. Walhovd, and I. Alzheimer’s Disease Neuroimaging, What is normal in normal aging? Effects of aging, amyloid and Alzheimer’s disease on the cerebral cortex and the hippocampus. Progress in neurobiology 117C (2014) 20-40.
[9] J.M. Henley, and K.A. Wilkinson, AMPA receptor trafficking and the mechanisms underlying synaptic plasticity and cognitive aging. Dialogues in clinical neuroscience 15 (2013) 11-27.
[10] A.M. Fjell, K.B. Walhovd, C. Fennema-Notestine, L.K. McEvoy, D.J. Hagler, D. Holland, J.B. Brewer, and A.M. Dale, One-year brain atrophy evident in healthy aging. The Journal of neuroscience : the official journal of the Society for Neuroscience 29 (2009) 15223-31.
[11] A.M. Fjell, L.T. Westlye, H. Grydeland, I. Amlien, T. Espeseth, I. Reinvang, N. Raz, D. Holland, A.M. Dale, K.B. Walhovd, and I. Alzheimer Disease Neuroimaging, Critical ages in the life course of the adult brain: nonlinear subcortical aging. Neurobiology of aging 34 (2013) 2239-47.
[12] J.A. Armour, The little brain on the heart. Cleve Clin J Med 74 Suppl 1 (2007) S48-51.
[13] J.A. Armour, Potential clinical relevance of the ‘little brain’ on the mammalian heart. Exp Physiol 93 (2008) 165-76.
[14] I. Duraes Campos, V. Pinto, N. Sousa, and V.H. Pereira, A brain within the heart: A review on the intracardiac nervous system. J Mol Cell Cardiol 119 (2018) 1-9.
[15] M. De Hert, J. Detraux, and D. Vancampfort, The intriguing relationship between coronary heart disease and mental disorders. Dialogues in clinical neuroscience 20 (2018) 31-40.
[16] R.C. Rossom, S.A. Hooker, P.J. O’Connor, A.L. Crain, and J.M. Sperl-Hillen, Cardiovascular Risk for Patients With and Without Schizophrenia, Schizoaffective Disorder, or Bipolar Disorder. J Am Heart Assoc 11 (2022) e021444.
[17] A. Saeed, O. Lopez, A. Cohen, and S.E. Reis, Cardiovascular Disease and Alzheimer’s Disease: The Heart-Brain Axis. J Am Heart Assoc 12 (2023) e030780.

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