Meditation's Impact on Neurochemicals

Meditation is simple to learn, quiet and still in its presence. But its surface demeanor is deceptive. There’s a lot going on under the hood. Meditation is a complex mind-body process that involves changes in cognition, sensory perception, emotion, brain chemicals and brain circuitry, and autonomic nervous system activity.

The body of research investigating precisely how meditation interacts with neurotransmitter systems and brain mechanisms to promote better health is far from complete. But many clinical researchers looking for practical new ways to treat mental and physical health problems view meditation as one of the most important avenues of research to pursue throughout this decade. So stay tuned.

We can start by saying that the feelings of general well-being and positive emotion during meditation are likely mediated, at least in part, by the release of mood-stabilizing neurohormones and neurotransmitters such as dopamine, serotonin, and melatonin in limbic (emotional) brain regions.

Even early studies found that key neurochemicals such as serotonin, melatonin and dopamine levels are elevated during meditation (Bujatti, M., Riederer P., 1976) and several important neurochemical changes in blood serum concentration have been found to occur during meditation (Newberg, A., Iverson, J., 2003).

Here’s a quick summary of evidence thus far of meditation’s influence on neurochemicals that are critical to maintaining good mental health:

• GABA (gamma-aminobutyricacid) increases
• Dopamine increases
• Serotonin increases
• Acetylcholine increases
• Melatonin increases
• Cortisol decreases
• Arginine vasopressin increases
• b-Endorphins increase and/or undergo rhythm changes
• Glutamate increases
• Norepinephrine decreases
• Epinephrine decreases
• Adrenocorticotropic hormone (ACTH) decreases

For more details on what neurotransmitters and neurohormones are, how they work, and the key characteristics of each, see: Understanding Neurochemicals: The Key Players & Their Impact on Health.

Following is a summary of the key neurotransmitters and neurohormones that meditation research has thus far been found to influence…

Arginine vasopressin (AVP) has been shown to increase dramatically (2.6 to 7.1 times normal plasma levels) during meditation (O’Halloran J. P., et al, 1985). AVP has been found to contribute to arousal, maintaining positive emotion (Pietrowsky R., 1991), self-perceived fatigue, and significantly improving consolidation of new memories and learning (Weingartner H., et al, 1981). Sharp increases in AVP may also help enhance the meditator’s memory of his or her experience, perhaps explaining why meditative experiences are often remembered and described in vivid terms.

During meditation, meditators experience a drop in blood pressure associated with parasympathetic activity. GABA has been found to stimulate the hypothalamus to release AVP, a vasoconstrictor, thereby tightening the arteries and returning blood pressure to its normal level (Renaud L. P., 1996).

A vasopressin-oxytocin neural pathway has been implicated in autism spectrum disorders. AVP has recently been shown to significantly influence social behavior by mediating secretion of the neurohormone oxytocin (Ebstein R.P., et al, 2009). Oxytocin is critical to bonding, trust and socialization skills, and a deficiency of this hormone has been shown to be involved in causing the social deficits of people with autism spectrum disorders (Ebstein R.P., et al, 2009).

Acetylcholine’s involvement with meditative states has not been widely researched, but it’s the primary neurotransmitter found at autonomic (involuntary) nervous system synapses (junctions) and is known to heavily influence parasympathetic nervous system dominance, as is found in states of consciousness such as meditation.

In some studies, increased acetylcholine in the frontal lobes during meditation has been shown to enhance attention, and in the parietal lobes, it tends to enhance orienting ability, without altering sensory input (Newberg, A., Iverson, J., 2003). Acetylcholine (ACh) dominates the parasympathetic nervous system and plays important roles in arousal and regulating states of consciousness. It has important modulatory influences throughout the cerebral cortex, including motivation, learning and perception. ACh is believed to play an important role in storing and consolidating long-term memory.

One widely-cited study found that meditation increased the endogenous (natural, from within) release of the neurotransmitter dopamine during altered consciousness, which decreased the meditators’ desire for action and executive control, heightened their sensory awareness, and increased their ability to detach themselves from the past or future (Kjaer et al., 2002).

Researchers found that meditation decreased binding of a radioactive tracer that competes with endogenous dopamine in the ventral striatum, thus resulting in roughly a 65% increase in dopamine release in limbic or emotional brain regions. This increased dopamine tone coincided with an increase in theta activity that reflected enhanced internalized attention.

This finding of dopamine release in limbic brain regions aligns with a previous PET study, which showed a significant increase in dopamine levels and activation in left frontal and limbic areas while meditators were experiencing a sense of joy (Lou et al., 1999). Dopamine, in other words, was associated with that experience of joy.

Dopamine is involved in regulating attention and is associated with feelings of pleasure and reward and is the primary neurotransmitter involved in motivation and motor activity. Dopamine is also involved in the release of natural feel-good endorphins, which act as natural mood lifters and have a calming effect on us.

Epinephrine is a both a neurotransmitter (acting in the brain) and a stress hormone (acting on other sites, such as the heart or glands). It stimulates our sympathetic nervous systems to produce fight-or-flight responses, such as increased heart rate, increased blood glucose, and increased blood flow to muscles.

Studies have found reduced epinephrine levels during meditation, which reflects, in part, the systemic change in autonomic balance brought about by meditation (Walton, K.G., et al, 1995; Infante, J.R., 2001). During meditation, the hypothalamus may inhibit the adrenaline output of the adrenal medulla, which decreases anxiety. Decreased adrenaline, coupled with the deep relaxation state experienced during meditation, allows the hypothalamus bring about tranquility (Chugh, D., 1987). The hypothalamus links the nervous system to the endocrine system, our hormone-producing system.

Several studies have demonstrated an increase in serum GABA during meditation, which not only enhances your sense of focus by limiting distracting external stimuli in the visual cortex, but also produces a number of important mental health benefits, as well. GABA has a calming, anti-anxiety effect on the brain by modulating or regulating the activity of other neurotransmitters critical to mental health. It’s activity is inhibitory — it helps keep other neurotransmitters such as serotonin, norepinephrine, epinephrine and dopamine in check and balanced. An inability to produce and circulate adequate levels of GABA has been associated with conditions such as, anxiety, tension, insomnia, and epilepsy.

One Yale study found that people with panic disorder had 22% less GABA than those without panic disorder. Addicts, including those addicted to alcohol, drugs, tobacco, caffeine, food, gambling, and even shopping, have all been found to have GABA deficiencies.

The hormonal changes induced by meditation have been found to mimic the calming, inhibiting effects of GABA on the brain. One study of Transcendental Meditation found that meditation produced changes in pituitary hormone secretion by enhancing hypothalamic GABAergic tone, and that the anxiolytic (anti-anxiety) effects resulted from meditation’s ability to increase GABA in specific areas of the brain (Elias, A.N., Wilson, A.F., 2000). This mechanism is similar to the effects of anxiolytic and tranquilizing drugs (e.g., benzodiazepines such as Xanax), which reduce anxiety by binding to GABA-A receptors.

A small study published in the Journal of Alternative and Complementary Medicine compared the effects of a 1-hour yoga session (asana yoga, which involves postures and conscious breathing) to a 1-hour reading session on GABA levels in the brain. GABA levels increased by an average of 27% in the yoga participants, compared to no change in the reading group, suggesting that even a low-key relaxation model of meditation may increase GABA levels (Streeter, C.C., 2007).

The activation of the brain’s prefrontal cortex (PFC) during meditation increases the levels of free glutamate in the brain, which stimulates the hypothalamus to release beta-endorphins. During meditation, there is continued activity in the PFC resulting from the individual’s persistent will to focus attention. As PFC activity increases, it produces ever-increasing levels of glutamate (Harte, et al., 1995).

Glutamate is a workhorse neurotransmitter; in fact, the most commonly found neurotransmitter. It’s an excitatory transmitter that enhances electrical flow among brain cells and is involved in learning, memory and brain plasticity.

Norepinephrine is a stress hormone that causes the heart rate to increase, stored glucose (simple sugar) to be released, and increased blood flow to the muscles. Norepinephrine plays a major part in helping us escape danger, but also in creating or exacerbating anxiety. The effects from prolonged or too-frequent exposure to norepinephrine are very similar to the effects of cortisol. Increased heart rate can cause high blood pressure, and the stored glucose (simple sugar) that’s released can also cause diabetes. Back and body muscle pain can occur due to muscle tension caused by this hormone.

During meditation, activation of the right amygdala results in stimulation of the hypothalamus, with subsequent stimulation of the parasympathetic system, which is associated with a sense of relaxation and profound quiescence.

Respiration and heart rates decrease, which in turn, reduces the activity of areas of the brain that produce norepinephrine. Decreased norepinephrine ultimately decreases stimulation of the hypothalamus, decreasing the stress-related production of ACTH, and cortisol (Newberg, A., Iverson, J., 2003).

Serotonin, a feel-good neurotransmitter, is the primary neurotransmitter influencing mood. Serotonin also plays a role in sleep cycles, circadian rhythm, appetite, pain, aggression, sexual behavior, information processing and autonomic processes such as blood pressure, body temperature and endocrine system function.

The interaction between serotonin synthesis and mood may be a two-way street. One study found that self-induced changes in mood can influence serotonin synthesis. In other words, serotonin influenced mood and mood influenced serotonin synthesis (Perreau-Linck, et al, 2007).

Serotonin has been found to increase after meditation, and higher overall levels have been measured in long-term meditators (Newberg, A., Iverson, J., 2003; Bujatti, 1976). In fact, several studies have shown that after meditation, the breakdown products of serotonin (5-HT) in urine is significantly increased, suggesting an overall serotonin elevation during meditation (Walton, et al, 1995; Newberg, A., Iverson, J., 2003; Solberg et al., 2000a, 2004b).

Serotonin acts as a neuromodulator in the visual centers of the temporal lobe, where it strongly influences the flow of visual associations and internally generated imagery, and may create extraordinary visual experiences during meditation.

Increased serotonin levels can affect other neurochemical systems, such as the dopaminergic system, suggesting a link between the serotonergic and dopaminergic systems that may enhance the feelings of euphoria frequently experienced during meditative states. Activation of the autonomic nervous system can result in intense stimulation of structures in the lateral hypothalamus and other areas of the brain known to produce both ecstatic and blissful feelings when directly stimulated. Stimulation of the lateral hypothalamus, in turn, is known to stimulate serotonergic activity.

Serotonin, in conjunction with increased glutamate, has also been shown to stimulate the release of acetylcholine, which is believed to help modulate attention during meditation.

Serotonin has been closely linked to melatonin; both play an important role in mood stabilization (including depression), positive affect, stress-prevention and aging (Pacchierotti et al., 2001). Serotonin and melatonin have also been linked to migraine attacks through action of the pineal gland, which is a primary source of central serotonin and melatonin (Toglia, J.U., 2001).

Meditation heavily influences the Hypothalamus-Pituitary-Adrenal (HPA) Axis, a brain-body circuit which plays a critical role in the body’s response to stress. Inhibition of the sympathetic nervous system during meditation has many calming, anti-anxiety affects on the nervous system; for example, inhibiting the hypothalamus, which in turn, inhibits the pituitary gland and thereby the release of ACTH (adrenocorticotropic hormone). ACTH stimulates the production of adrenal hormones. The hypothalamus, an important component of the limbic system, integrates mind-body responses throughout the autonomic and somatic nervous systems. (Common physiological meditation effects, such as decreases in blood pressure, blood lactate and urinary vanillylmandelic acid, result from inhibition of the hypothalamus.)

Many studies have established that long-term practice meditative practice has a lasting influence on adrenocortical activity (steroid hormones produced by the adrenal glands) both during meditation and after. Specifically, cortisol and ACTH (adrenocorticotropic hormone) activity is reduced (Bevan, 1980; Jevning, et al., 1978; Kamei, et al., 2000; Michaels, et al., 1979; Subrahmanyam, et al., 1980; Sudsuang, et al., 1991).

People who meditate regularly have higher levels of endorphins, natural opioids that are produced endogenously (within) the body (primarily the hypothalamus) and used internally as painkillers — modulate the body’s pain pathways. Higher levels of the neurotransmitter glutamate during meditation stimulates the hypothalamus to release beta-endorphins.

One study of men found that Sahaja meditation triggered a 70 percent increase of beta-endorphins, as measured in blood plasma levels (Mishra, R., Barlas, C. & Barone, D., 1993).

Endorphins create an all-encompassing sense of happiness and well-being, known to exercisers as “runner’s high.” Endorphins can help reduce blood pressure, depress respiration, reduce fear, reduce pain, and produce sensations of joy and euphoria.

Prolonged high levels of the stress hormone cortisol in the bloodstream can have such damaging effects as: decreased bone density, elevated blood pressure, suppressed thyroid function, chronic stress, blood sugar imbalances (e.g., hyperglycemia), decrease in muscle tissue, decreased immunity and inflammatory response. High cortisol levels can increase abdominal fat, a condition that has been linked to heart attacks, strokes, the increase of higher levels of “bad” cholesterol (LDL) and lower levels of “good” cholesterol (HDL).

Regular meditators have significantly lower levels of cortisol, which is an age-accelerating hormone (Sudsuang R., Chentanez V., Veluvan K., 1991; Newberg, A., Iverson, J., 2003). Several studies have found that urine and plasma cortisol levels are decreased during meditation (Livesey J. H., et al, 2000; Walton, K., et al, 1995; Sudsuang, R., 1991; Jevning, R., 1978), which may be explained by the fact that decreased norepinephrine during meditation likely decreases the production of ACTH (which stimulates the adrenal cortex to produce cortisol), ultimately decreasing cortisol levels.

Long-term meditative practice reduces adrenocortical activity (steroid hormones produced by the adrenal glands), including the release of cortisol (Bevan, 1980; Jevning, et al., 1978; Kamei, et al., 2000; Michaels, et al., 1979; Subrahmanyam, et al., 1980; Sudsuang, et al., 1991).

The neurohormone melatonin, sometimes referred to as the “sleep hormone” or “the hormone of darkness,” is produced by the pineal gland in the brain, once dubbed “the seat of the soul” by philosopher Rene Descartes. Melatonin regulates our circadian rhythm (sleeping and waking) patterns — it tells the body when it’s time to sleep. Our sleep-wake cycle is regulated by a circadian clock in a tiny specialized structure of the hypothalamus (the suprachiasmatic nucleus). Our internal biological clock is reset daily by environmental and internal stimuli.

Meditation is believed to increase melatonin levels by slowing hepatic (liver) metabolism or by increasing its synthesis in the pineal gland (Massion et al., 1995). Diurnal (24-hour period) melatonin levels were found to be significantly high in Vipassana meditators (approximately 300 pgml) compared to non-meditating controls (65 pgml). Given melatonin’s major role in sleep maintenance, meditation may enhance sleep quality, at least in part, by enhancing melatonin levels.

One study that measured melatonin levels in experienced meditators found that the meditators had significantly higher plasma melatonin levels in the period immediately following meditation compared with the same period at the same time on a control night (Tooley G., Armstrong S., Norman, T., Sali, A., 2000). It’s believed that this increase may be achieved through decreased hepatic (liver) metabolism of the hormone or via a direct effect on pineal physiology.

Several studies of meditation have found increases in blood plasma levels of melatonin (Harinath et al., 2004; Massion et al., 1995; Solberg et al., 2000a, 2004a, b; Tooley et al., 2000) in long-term meditators, as well as acutely after meditation. Melatonin has been closely linked to serotonin, playing an important role in mood stabilization (including depression), positive affect, stress-prevention and aging (Pacchierotti et al., 2001).

Meditation is known to increase serotonin, and this increase, combined with hypothalamic innervation of the pineal gland during meditation, may cause the pineal gland to increase production of melatonin through a conversion of serotonin. Sahaja meditation techniques direct energy flow through the body’s energy centers or chakras and can selectively activate or suppress various glands associated with these energy centers. The pineal gland corresponds to the Sahasrara chakra located at the crown of the head. In Sahaja meditation, the Sahasrara is associated with achieving the state of thoughtless awareness, integration of energy from all chakras, oneness with the collective consciousness and feelings of joy.

Melatonin has also been found to reduce pain sensitivity, possibly by depressing the central nervous system or simply because sleep deprivation can increase pain perception. Melatonin also acts as an antioxidant and immunomodulator, stimulating the immune system and the antioxydative defense system, thus delaying aging (Brzezinski, 1997; Massion et al., 1995). Melatonin secretion tends to naturally decrease with aging, which may help explain why many seniors have poorer sleep quality.

A few studies have suggested that melatonin may act as an oncostatic agent; i.e., have cancer-fighting properties. One meta-analysis of 10 randomized controlled trials of melatonin in tumor patients showed that melatonin significantly reduced the risk of death at one-year follow-up (Mills et al., 2005). Another study, which found that melatonin significantly inhibited tumor growth, postulated that the mechanism may involve modulation of both the endocrine and immune systems, as well as direct oncostatic action against tumor cells, perhaps made possible by antioxidative action that counters DNA damage during radiation treatment and/or exposure to chemical carcinogens (Pawlikowski M., et al, 2002).

Melatonin, in conjunction with serotonin, has also been linked to migraine attacks through action of the pineal gland, which is a primary source of central serotonin and melatonin (Toglia, J.U., 2001).