Some "Insight" on Meditation

Recently I had the great pleasure of visiting with my friend and colleague Solomon Ben Ezra and speaking on his experiences with meditation as a practitioner and inspiring teacher. Our discussion can be found on the podcast and also on video.


I have discussed many aspects of mind-body health, meditation, and brain health on this blog and on my podcast as this aspect of health is tremendously important.


In a nutshell, unregulated stress can wreak havoc on many organ systems of our body. Let alone, the toll it takes on our mental health. A stress-management practice has become essential much as exercise became essential when we moved to a more sedentary lifestyle at the dawn of the industrial revolution.




We are going to take deep dive in this post on meditation, how it works, and some resources to get people started. I first wrote this article in 2005 and have added some updates and likely will update again. First, a little bit of background.



History of Meditation as a Health Intervention


Meditation has long been associated with eastern spiritual practice, however is now recognized and utilized throughout western society. To understand meditations' emergence, consider that the Shambhala Mountain Center, a meditation retreat center in the Colorado Rockies increased from 1342 visitors in 1998 to a projected 15,000 visitors in 2004.[i] During the past 30 years, meditation has become a scientifically studied intervention to address health concerns ranging from cancer, immune dysfunction, cardiovascular disease, and psychological/behavioral dysfunction.[ii],[iii],[iv],[v] . The National Institute of Health defines meditation as a conscious mental process that induces a set of integrated physiological changes termed the relaxation response [vi] . This term was coined by Harvard professor of Medicine, Dr. Herbert Benson, after researching biophysiological effects of Transcendental Meditators in 1967.

Forms of Meditation:


There many different forms of meditation being practiced; however, the most researched forms are from the schools of Transcendental (concentrative-type) Meditation and Mindfulness technique. Most of the meditation today comes from concentrative (i.e. TM), mindfulness (MBSR), and Movement (i.e. Tai chi). Because these techniques differ it is difficult to make a wide range generalization of the effects of meditation as a whole. Below is a comprehensive list of the different forms of meditation.


.The Anatomical and Physiologic impact of meditation

Because different forms of meditation affect the nervous system in unique ways there has often been conflicting data as it relates to neuroendocrine involvement with meditation. Regardless of the variety in cause-and-effect relationships of variant forms of meditation, advancements of science have allowed us to understand how meditation acts upon the central nervous system and the endocrine system. Much of this data has been determined by measuring blood values of meditation subjects. However, we are now capable of understanding more of the impact of meditation through imaging techniques. In fact, functional magnetic research imaging (fMRI) has been used to identify and characterize the brain regions that are active during meditation. This research suggests that various parts of the brain known to be involved in attention and those concerning autonomic nervous system regulation are activated, providing a neurochemical and anatomical basis for the effects of meditation on various physiological activities.


In the higher centers of the brain, meditation has been shown in one study to produce significant increases in left-sided anterior brain activity, which is associated with positive emotional states.[i] In other studies meditation has shown to generate response in the prefrontal cortex (PFC) of the right hemisphere and cingulate gyrus of the limbic system. The limbic system is related to emotional areas of the brain and includes regions that are called aversion centers or gratification centers of the brain. If an aversion center is stimulated a person will experience fear or sorrow. On the other hand, stimulation of gratification will result in pleasure. There are a number of these centers dispersed throughout the limbic system. [ii],[iii]. The PFC and cingulate gyrus are generally associated with activation during willful or high concentration activities. The prefrontal cortex also has been connected with some of the most distinct human intellectual traits such as judgment, foresight, sense of purpose, sense of responsibility, and sense of social propriety.[iv]This most likely is correlated with forms of meditation that involved sustained concentration on a word or mantra as seen in TM.[v]

We are also aware of meditations' effect on the Thalamic regions of the brain, which generally functions as a gatekeeper of stimulatory and inhibitory data. Most of the thalamic effects that have been observed during meditation has been due to the inhibitory neurotransmitter GABA which appears to be increased during meditation. GABA functions on the sensory or inhibitory effects of the Thalamus. Increased Dopamine levels are also assumed to be involved with this effect on the Thalamus.[vi] In regards to health promoting effects of meditation, this is interesting because the key function of the thalamus is to receive sensory information of many sorts (temperature, pain, vision, and so on) and distribute it to the specific regions in the cerebral cortex to decode it. [vii]

We are also aware of the direct impact of meditation on higher neural regions. For example, the frontal lobe, the most highly evolved part of the brain that is responsible for reasoning, planning, emotions and self-conscious awareness, tends to lower functioning during meditation. In the parietal lobe, the part of the brain whose major function is processing sensory information, slows down during meditation. The Thalamus, which generally functions as a gatekeeper of stimulatory and inhibitory data, reduces the flow of incoming information.Finally, the reticular formation, the brain’s alert enter, has decreased arousal signals during meditation.

The Hypothalamic Pituitary Axis:

The main system linking the endocrine and nervous system and that which applies to meditation is the Hypothalamic Pituitary Axis. The interactions that occur along this axis most aptly describe the relationship between the endocrine system and nervous system. In general, the hypothalamus has two main regions that have opposite functions. The caudolateral region when stimulated produces behavior associated with anxiety these include 1) increased sympathetic activity of the visceromotor system 2) increased aggressive behavior, 3) increased hunger, and 4) increased body temperature. In contract the rostromedially hypothalamus typically produces behavioral manifestations that are generally associated with contentment. These include 1) increased activity of the parasympathetic division of the visceromotor system, 2) increased passive behavior 3) increased satiety and 4) decreased body temperature.[i]


The hypothalamus main function on the Hypothalamic Pituitary axis is the regulation of factors of adrenocorticotropic hormone (ACTH) and its counterpart B-lipotropin via Corticotropin Releasing Hormone (CRH). Afferent signals arrive which influence the release of CRH. These include afferent signals coming from;1) The Limbic System which carries emotional “emotional stimuli” to the hypothalamus 2) Reticular Formation: which carries systemic stimuli to the hypothalamus; 3) Hypothalamic and Anterior Pituitary Cells sensitive to Circulating Blood Cortisol Levels and 4) Suprachiasmatic Nuclei (diurnal rhythm sensitivity). In addition, catecholamine (Norepinephrine/Epinephrine) release is coordinated through afferent pathways from the limbic region concerned with emotion[1]. Also, stimulation of caudolateral, especially the lateral areas, produce diffuse sympathetic discharge and increased adrenal medullary secretion like the mass sympathetic discharge seen in animals exposed to stress. There are also additional separate areas for the control of norepinephrine and epinephrine secretion.[2]


A couple additional points about CRH worth mentioning. CRH is potentiated by Antidiuretic Hormone (Also known as Arginine Vasopressin) which can be released into the same hypothalamic region. And, research now shows us that CRH is responsible for more than just ACTH secretion, where CRH receptors have been identified on inflammatory cells. This gives clues that peripherally released CRH may be pro-inflammatory. Finally, CRH secretion has now been identified to be associated in other besides stress including increased ACTH/adrenal activity associated with stress but also certain associated behavioral symptoms such as depression, sleep and appetite disturbances and psychomotor changes.[ii]. This author postulates that this may be a critical link to understanding sustained levels of cortisol that may eventually lead to adrenal failure.


The Pituitary Gland acts in direct response to the hypothalamic function. The hormones produced by the pituitary gland which concern meditative technique is ACTH. The biosynthesis of adrenal hormones is dependent on ACTH, which stimulates the rate limiting enzyme cholesterol desmolase. Without this step the cholesterol precursor will not produce the adrenal hormones. The adrenal hormones resultant of ACTH are adrenal glucocorticoids (i.e., Cortisol), mineralocorticoids (aldosterone), and adrenal androgens (Dehydroepiandrosterone (DHEA) and Androstenedione). Normally there is a negative feedback where free glucocorticoids inhibit ACTH secretion from the pituitary gland and also to some degree inhibiting CRH secretion from the hypothalamus. So, as we have found one of the key afferent factors that affect the hypothalamus and the amount of free corticosteroid are the main factors that regulate ACTH secretion[iii]

Other important pathways must be considered when understanding the link between meditation and neuroendocrine effects. One pathway is concerning Serotonin which may be elevated in mediation and serves as a precursor to melatonin in the pineal gland. Serotonin has apparently been shown to elevate CRH and subsequent levels Apparently a direct synaptic connection between serotonergic terminals and corticotropin-releasing hormone (CRH)-containing neurons in the paraventricular nucleus of the hypothalamus has been described. Precursors of 5-HT (the precursor to serotonin) or drugs that enhance the effect of 5-HT increase CRH in portal blood and ACTH in plasma. In addition to effects at the hypothalamus, 5-HT may have direct effects on the anterior pituitary to stimulate the release of ACTH and at the level of the adrenal cortex to regulate release of corticosterone or cortisol. Actions of serotonin on 5-HT1A, 5-HT2, 5-HT3 and 5-HT4 receptors seem to be involved in these effects on the hypothalamic-pituitary-adrenal axis.[iv]


Hypothalamic-Pituitary-Axis and Disease


It has been known for a long time that vital stress induced hypercortisolism induced by surgery, trauma, or sepsis is associated with augmented release of ACTH, which in turn is presumably driven by corticotropin-releasing hormone (CRH), cytokines and noradrenergic system. Accordingly, circulating aldosterone rises markedly, probably under the control of activated renin-angiotensin system. Hypercortisolism acutely shifts carb, fat, and protein metabolism, so that energy is instantly and selectively available to vital organs such as the brain and so that anabolism is delayed. Also, intravascular fluid retention (see aldosterone) and the enhanced inotropic and vasopressor response to respectively catecholamines and angiotensin II offer hemodynamic advantages in the flight or fight reflex. In addition, the hypercortisolism elicited by acute disease or trauma can be interpreted as an attempt by the organism to dampen down its own inflammatory cascade, thus protecting itself against over responses.


In prolonged illness, serum ACTH was found to be low while cortisol concentrations remained elevated, indicating that cortisol release may in this phase be driven by an alternative pathway possible involving endothelin.


The reason why ACTH are low in prolonged critical illness is unclear; a role for atrial natriuretic peptide or substance P has been suggested.


Also, circulating serum cortisol levels of adrenal androgen, Dehydroepiandrosterone sulphate (DHEA-S) which has

immunostimulatory effects on TH1-helper cells are low during prolonged critical illness.

Despite increased plasma renin activity, paradoxically low reduced levels are found of aldosterone and are found in protracted critical illness. This suggests a shift of pregnenolone metabolism away from both mineralocorticoids and adrenal androgen pathways toward glucocorticoid pathways orchestrated by an unknown peripheral force. Ultimately the compensatory mechanism may fail and lead to adrenal insufficiency. [i]


In wild baboons the chronic stress associated with subordinate social status appears to elevate the cortisol response to acute stressors, and to impair mechanisms of negative feedback.[ii]