Yogic Breathing and Meditation:
When the Thalamus Quiets the Cortex andRouses the Limbic System
Richard P. Brown MD
stimulate the strained breathing pattern. This causes increased
brain perfusion and prevents hyperventilation. Renal sodium
excretion is decreased. Ujjayi induces oscillations of bloodpressure and an exaggeration of the normal respiratory sinus
arrhythmia. It also stimulates vagal nerve afferents to the brain,
ultimately increasing attention and vigilance. In nature, Ujjayi
most often occurs in an animal that has been defeated in battle
by a dominant animal or when it is confronted with a dominantanimal by whom it had previously been defeated. The original
stimulus for the breathing pattern derives from the
hypothalamic vigilance area, which is separate from the
hypothalamic defense area. In other words, the animal, if
unable to escape and use fight or flight reflexes, becomes
extremely vigilant in order to protect itself. Stimulation of thevagal efferent neurons induces a parasympathetic reductionin heart rate and most likely a withdrawal of sympathetic
input to the heart. This restores energy in preparation for
activity. A strong respiratory rhythm in the vagus nerve is set
up, such that enhanced respiratory sinus arrhythmias occur;these have been noted in anxious patients awaiting surgery,in rats during submissive behavior, and in advanced yogis
during meditation4. An increase in the tidal volume during
Ujjayi breathing probably prevents a tendency towardhypoxia/hypercapnia (decreased O2/increased CO2), whichmight otherwise occur during hypoventilation. Further
research would be valuable to investigate concurrent bloodgas changes. Similar breathing in animals is associated witharousal, attentiveness, tension, and submission. Enhanced
respiratory sinus arrhythmias, particularly with low heartrate, occur in rats and humans during perceptual tasks
requiring enhanced attention, especially when an immediate
response is not needed.

Assoc. Clinical Professor of
Psychiatry, Colombia
University College ofPhysians and Surgeons, NewYork City, USA.
&
Patricia L. Gerbarg MD

This paper presents a neurophysiological model for the effectsof yogic breathing techniques, called Pranayama (including
Ujjayi, Bhastrika, and Sudarshan Kriya), chanting, andmeditation as taught in Art of Living (AOL) courses.
Methodologic challenges in future studies of yogic breathing
include choice of control groups, blinding and randomization.
Functional MRI (magnetic resonance imaging) is the best
current modality for studying the brain during Pranayama,
chanting and meditation. Directions for future clinical researchin neuropsychiatric conditions will be discussed.
Sudarshan Kriya yoga has been most studied by Dr.
Janakiramaiah and colleagues at NIMHANS (National
Institute of Mental Health and Neurosciences), particularly
for the treatment of dysthymia and depression.1,2 They describe
three sequential breathing cycles separated by 30 second
periods of normal breathing: Ujjayi - slow breathing 3 cycles
per minute; Bhastrika - rapid exhalation at 20-30 cycles per
minute; and Sudarshan Kriya - rhythmic, cyclical breathingof slow, medium and fast cycles. Between Bhastrika and theSudarshan Kriya there is brief chanting. These variations ofrhythmic breathing are practiced while sitting with eyes closed
and awareness focused on the breath. A state of relaxed
sleepiness comes by the end of the cyclical breathing and theprocess ends with a ten-minute rest in a tranquil supine
position. This can be followed by a 20-minute meditation. The
breathing practice enables meditation to proceed with muchless effort than otherwise. We will correlate data on eachmethod of breathing with related research on hyperventilation,
slow breathing, vagal nerve stimulation, and meditation tofurther understand their effects on the brain.

Strained breathing can be overdone. It may occur as acomponent of cardiovascular disease, obstructive sleep apnea,
and high altitude mountain sickness. Aside from thesepathological conditions, it probably functions to inhibit anactivated physiology and restore energy reserves. This has
survival value in circumstances in which enhanced attention
is required and/or during defensive behavior when prolonged
mental activation cannot immediately lead to physical activity.
It also enhances cerebral perfusion necessary for very active
mental processing.

Ujjayi Breathing
Ujjayi breathing is a strained, somewhat forceful inspirationand expiration against airway resistance using a slow
breathing cycle of 3-4 breaths per minute. Fokkema reviewed
the literature in animals and humans on strained breathing
and its cardiovascular and behavioral affects3. Active behavior
is inhibited in animals during strained breathing. It occurs
naturally under stressful circumstances. Muscle tension andlaryngeal reflexes cause a strong reduction of airflow in theglottis resulting in prolonged expiration/inspiration, and anelevated intrathoracic pressure. The resulting increases inblood pressure and carbon dioxide (CO2) level further

Bhastrika
A series of studies reported that Pranayama exercises(including Bhastrika, Kapalabhati, Nauli, and Agnisara) led
to central nervous system (CNS) excitation. Roldan andDostalek described three major excitatory patterns on the brain
EEG including a peculiar arc or wicket rhythm of 12 to 17 Hz
with maximal amplitude over the parietocentral region of thenon-dominant hemisphere, a 26 to 33 Hz sinusoidal rhythm,
and a high amplitude paroxysmal activity similar to11

recordings made during orgasm in humans and animals5 6.
The subjective experience is one of stimulation followed
immediately by relaxation. The mechanism probably involves
stimulation of visceral (including vagal) afferents. Kapalabhati
increased the low mid frequency component of heart ratevariability (an indirect measure of sympathetic nervous system
function) while alternate nostril breathing had complex effects,
apparently increasing both sympathetic and parasympathetic
tone (measured by the high and low frequency component ofheart rate variability)7.

suggest that the vasoconstriction observed during mechanicalhyperventilation may reduce cerebral blood flow by about
50% due to a central neurogenic response to hypocapnia at abrain stem level. This depressant effect on the mesencephalicreticular formation is associated with depression of corticalactivity and slow waves.
The most common EEG response to hyperventilation in anormal individual consists of diffuse slowing; in adults this
response is most prominent at the vertex of the brain. Slowing
will disappear within a minute after stopping
hyperventilation. In patients prone to epilepsy, focal slow
wave activity is enhanced, particularly in the temporal region
and 3 Hz spike and wave activity may be detected only duringhyperventilation.

The highly active rhythms observed during Bhastrika andother excitatory forms of pranayama are similar to the gammafrequency band of neuroactivity described in other situations.
The gamma band is hypothesized to reflect synchrony ofneural assemblies involved in integration of perceptions ofvarious features of an object within a sensory modality, acrossmodalities and over time, i.e. a form of accumulated complex
knowledge. For further discussion, see Kwon8.

Balzamo and colleagues, reviewing prior data in addition totheir own research, show that the diffuse slowing response to
hyperventilation can be abolished by lesions of the nonspecific thalamic projection system (NSTPS) and the thalamus
or by destruction of both vagal nerves.10 Peripheral vagal
afferents from the respiratory system play a major role in EEGchanges caused by artificial hyperventilation and they
probably input to the NSTPS.

Summary of Breathing Practices
To review at this point, the practice begins with Ujjayi
breathing. People’s subjective experience is one of being calmed.
The proposed neurophysiology based on the current data
involves a shift to parasympathetic dominance through vagal
stimulation. Although I could find no EEG studies during
this breathing state, we might expect that there would be analpha rhythm and that brain imaging would probably show
a quieting of executive pathways in the frontal cortex,
pathways involved in planning, anticipation, worry, and thecarrying out of plans of action.

Tomita-Gotoh and Hayashida recorded direct shifts inelectrical potential from scalp electrodes when they induced
hypocapnia and hypercapnia in human subjects.
Hyperventilation increased cortical excitability withhypocapnia (decreased CO2)11. Seyal, et al. showed widespreadincreased excitability as measured by motor evoked potentials
with hyperventilation in six human subjects. They also notedthat hyperventilation improved visual function in patientswith multiple sclerosis12. Kukumberg and associates foundincreased cortical excitability in ten human subjects 13.
Hyperventilation also increases the excitability of skin andmotor nerves. In experimental animals, hyperventilation
increases excitability of hippocampal neurons. The
hippocampus is responsible for attention and orientation.
Carbon and associates most recently have shown that fifteen
minutes of hyperventilation increased sensorimotor cortex
excitability
measuredbydirectcurrent
magnetoencephalography14.

Bhastrika seems to be excitatory with activation of temporoparietal cortical areas. The subjective experience is one ofexcitation during the breathing followed by emotional calmingwith mental activation and alertness.

Sudarshan Kriya and Hyperventilation: Potential
Mechanisms Underlying Clinical Effects
Although there are no studies recording EEG effects or brain
imaging during Sudarshan Kriya, there is a large body of dataon voluntary hyperventilation in humans, mechanicalventilation in brain injured patients, animal models ofhyperventilation under anesthesia, and in vitro preparationsof hippocampal slices. Clinically hyperventilation has beenused either to activate the EEG in order to identify epileptic
patients or to reduce pressure in the brain after traumatic brain
injury.

The peripheral physical effects of voluntary hyperventilation
include modest hypocapnia and normal PO2 leading toincreased cardiac output, increased renal blood flow,
increased lithium and sodium excretion, and a minor increase
in renal sympathetic activity.15 Djarova and colleagues showedthat three minutes of hyperventilation produced a brief
increase in cortisol and human growth hormone in 11 men16.

An excellent review by Patel and Maulsby found no substantive
evidence to support the theory (which is still quoted in literaturefrom old research) that EEG slowing with hyperventilation is due
to cortical hypoxia secondary to cerebral vasoconstriction and/or
secondary to hypocapnia (decreased level of CO2).9 In fact, theintact thalamus is necessary for the hyperventilation response
and hypocapnia produces decreased activity in themesencephalic reticular formation. They propose that thesetwo phenomena are associated with the slow wave statesfound during EEG activation by hyperventilation, which aresimilar to drowsiness (practitioners of Sudarshan Kriya
commonly experience drowsiness during or at the end of thehyperventilation cycle followed by an “edge of sleep” state orindeed sleep, at least in the beginning of training). They

A major concern in using Sudarshan Kriya in large groups ofpatients with possible medical problems and/or advanced
age derives from a controversy in the treatment of traumaticbrain injury. The issue is about whether the cerebrovascularconstriction and consequent hypoxia might induce significant
ischemia that would be counterproductive in brain injury
patients. However, in a PET scan study, brief moderate
hyperventilation did not decrease cerebral metabolism inpatients with traumatic brain injury17. Hyperventilation usedin this study was more intense than what would be
experienced during Sudarshan Kriya.
12In a rat hippocampal slice model, hyperventilation withhypocapnia led to strong stabilization of gamma oscillationsin the rat hippocampus, probably due to increased
effectiveness of GABA (gamma-amino butyric acid) inhibitory
networks in the cortex18. We have noted gamma rhythms
previously in relationship to Bhastrika and it is possible that
Sudarshan Kriya may produce gamma rhythms after initialactivation and appearance of delta and theta rhythms. Gammarhythms are necessary in sensory integration and higher
cognitive function.

of practice) with twelve healthy controls who had neverpracticed yoga26. Slow yoga breathing decreased chemoreflex(changes in breathing rate in response to changes in thepressure of O2 and CO2 in the blood) responses to hypoxia
and hypercapnia in both groups. Their data also suggest thatlong term practice of yoga breathing independently reduces
chemoreflex sensitivity as opposed to just slow breathing. They
hypothesized adaptation of peripheral/central
chemoreceptors to chronic CO2 retention or adaptation of
pulmonary stretch receptors to a habit of deep slow respiration
which would reduce vagal afferent discharge to bulbopontine
brainstem centers that send projections to the thalamus andlimbic systems. These effects are calming and reduce the riskof cardiovascular disease.

Posse, et al. showed that hyperventilation quieted the frontal
and parietoccipital cortex but not subcortical areas on
functional MRI imaging19. Voluntary hyperventilation did notdecrease cerebral oxygen use in normal subjects20. Although
the form of hyperventilation used in their study was much
more intense than during Sudarshan Kriya, it is relevant.

In healthy elderly people the effects on the baroreflex of yoga
postures (Asanas) and breathing (not clearly specified) werecompared to aerobic exercise training. Six weeks of training of
three hours a week in yoga led to a decreased heart rate,increased vagal tone, and an increase in aerobic capacity of
approximately 11 percent. The yoga improved baroreflex
sensitivity whereas aerobic training did not.27 Khanam
showed that yoga training (Asanas and Pranayama) for one
week decreased sympathetic reactivity in asthma patients andimproved pulmonary ventilation28.

Using electroencephalographic measures of activity fromsomatosensory and auditory cortex, Huttunen and colleagues
showed that voluntary hyperventilation suppressed longlatency evoked responses from the cortex while early shortlatency responses were less reduced. They suggested that theincreased cortical excitability caused by hyperventilationinduced hypocapnia led to spontaneous firing of corticalneurons. They also noted studies showing enhancement of
excitatory glutamate synaptic transmission with concurrent
suppression of GABA receptor-mediated postsynaptic
inhibition.21

Related to this are observations of unusual autonomic control
by yogi adepts. When asked to describe how mastery of
autonomic function was accomplished, one yogic master said
that one must start by developing a slow even breathing at therate of one or two breaths per minute and that regulation of
the respiratory cycle is the most important step in controllingafferent vagal nerve fibers to attain control of the autonomic
nervous system. Even in untrained subjects, slow breathingat eight cycles per minute versus fifteen and thirty per minute
prevents a suppressive effect on parasympathetic input to theheart under the threat of an electric shock4. The consequentenhancement of vagal tone reduces the effects of stress on theheart.

The underlying basis of this cortical excitability, particularlyin the sensori-motor cortex is probably due to thalamic
activation (see figure 1). Using PET scans, Prevett andassociates showed that hyperventilation increased blood flow
to the thalamus in patients with generalized epilepsy in whom
typical absence seizures were induced by voluntary
hyperventilation22.
Marrosu and co-workers showed that SPECT measures of
cerebral blood flow correlated with hyperventilation-enhanced
interictal lateralized discharges in epileptic patients23. Theysuggested that hyperventilation-induced slow activity on EEG
is probably the result of synchronous activity in non-specificthalamocortical projecting systems (see Patel and Maulsby).
However, in epileptics other mechanisms also affect transition
from slow waves to spike-wave discharges.

Benson and colleagues correlated slow breathing observed
during meditation in eight Chi Kung and four Kundalini yoga
meditators with dramatic heart rate oscillations. The amplitudeof oscillations was greater than in the premeditation state. It
was similar to but greater than that found in elite athletes andhealthy adults during sleep. They suggest that this “autonomic
exercise” may benefit the heart. We will return to this point in
the discussion of chanting. 29 Slow breathing improvesbaroreflex sensitivity which tends to become abnormal withaging, cardiac disease, and hypertension.

Acute cognitive effects of hyperventilation have been studied
for many years. Two recent reviews show that hyperventilation
briefly decreases attention and cognitive function24, 25.
Reviewing studies of Pavlovian and operant control of emotion
and cognition through modification of breathing behavior,
Ley describes the complex interrelationship between breathing
and cognition and emotion. Two examples of cognitions andemotions associated with specific breathing patterns are:surrender with Ujjayi breathing and excitement withhyperventilation. However, the process can also work inreverse: specific breathing patterns such as the uniquerhythmic cycles of Sudarshan Kriya can induce particularcognitions and emotions.

Vagal Nerve Stimulation
Unilateral vagal nerve stimulation (VNS) is an effective
treatment in many cases of epilepsy and a promisingexperimental treatment for depression. Data on VNS is relevant
to hyperventilation because both stimulate vagal afferents tothe thalamus, exerting powerful effects on excitability of thecortex as well as producing an edge of sleep state (For a review
of VNS effects in epilepsy see Schachter and Saper).30 Electricalstimulation is only applied to the left vagus nerve because
stimulation of the right vagus nerve would cause undesirable
cardiac effects. Vagus nerve afferents synapse in the nucleus

Slow Breathing and Asanas
Spicuzza and colleagues compared the response of ten
experienced yoga practitioners (with an average of eight years
13tractus solitarius (NTS) (see figure 1). The NTS ascends to theparabrachial nucleus which diverges into two pathways. One
inputs to the hypothalamus, amygdala, stria terminalis, andlimbic cortex, affecting autonomic, endocrine, and emotional
control. The other pathway from the parabrachial nucleus
goes to several thalamic nuclei and thence to the cortex.
Thalamic intralaminar and mid-line nuclei project diffusely
to the cerebral cortex and probably influence corticalsynchronization or desynchronization. In animals slower
stimulation (1 to 17 Hz) causes EEG synchronization whilehigh frequency stimulation (greater than 30 Hz) results in
EEG desynchronization. Two PET studies of VNS on activationof the human brain reported thalamic activation andinconsistent results in areas of the cortex and subcorticalstructures. Rhoden’s studies suggested that VNS raised theseizure threshold by releasing GABA and glycine in wide
spread brain structures5.

consumption. This theta, slow wave pattern was named “postreinforcement synchronization” or PRS. Similar EEG activity
occurs during drinking, grooming, and drowsiness. PRS isalso related to a thalamocortical gating mechanism involving
lateral geniculate, posterior dorsal and other thalamic reticular
nuclei. This can occur prior to sleep onset and during certain
stages of sleep. PRS may also be seen with chemicalinterference with GABA inhibition on thalamic relay neurons
resulting in seizures.
Sterman’s group found that when an animal became satiatedand sat quietly, alternating SMR and PRS frequencies could
be seen in the sensory motor cortex and the ventrobasalthalamus. They hypothesized that the alternation of SMR and
PRS frequencies in mammals reflected excitation-inhibition
sequences in thalamocortical circuits that efficiently code andintegrate information and then reset the system for the nextchallenge. I would further suggest that the SMR patternrepresents vigilance and a search for reward. The PRS sequenceis associated with satiety and pleasure. In humans, PRS was
associated with a dreamy “edge of sleep” state, appearance of
normally suppressed images and emotions, and reduced
cortical excitability. Training humans to produce SMR resulted
in improved sleep patterns, improved memory functions, better
attentional and organizational skills in patients with attention
deficit disorder, and enhanced seizure control in epileptics. It
was also useful in the treatment of substance abuse.

The use of biofeedback to produce what has been called theSMR (sensori-motor rhythm) pattern has been shown todecrease seizure frequency (For a review and discussion of
SMR in treating seizures see Sterman)31. Sterman andcolleagues found an EEG pattern of 12 to 20 cycles per second
localized to the sensory motor cortex which they labeled SMR
for “sensori-motor rhythm.” Behavior associated with SMR
included suppressed physical activity and increased
vigilance. Inhibition of movement was necessary but not
sufficient for production of the SMR rhythm which is precededby a six-second period of muscle decreased tone. SMR was
found to originate in the somatosensory relay nucleus of thethalamus (the ventrobasal nucleus). Furthermore, SMR was
associated with suppression of muscle tone, suppression offurther somatosensory information through the thalamus tothe cortex, and stretch reflex excitability.

Sterman notes that the “edge of sleep” state is therapeuticallyuseful in allowing suppressed emotional content to emerge.
He suggests that withdrawal of brain stem and normal
thalamocortical regulatory influences leads to relative corticaldisinhibition. This allows suppressed emotion, cognitions,and trauma memories to be evoked while providing a state ofcalmness and relaxation that reduces the risk ofretraumatization.

Figure 1. Vagus Nerve Stimulation______________________________________________________________________________
Hyperventilation
Stimulates¯¯
Vagus ®NTS ® PB ®
Nerve
¯¯

Ventroposterior
Thalamus®®

A pilot study by Bhatia and colleagues compared 19 Art of
Living teachers who regularly practice Sudarshan Kriya with15 control subjects. EEGs of AOL teachers showed increased
beta activity (similar to SMR) in the left parieto-occipital region
indicating cortical activation by the underlying thalamic
generator (set of neurons in the thalamus that sets up a clear
rhythm in a related cortical area). This occurred with increasedalpha activity suggesting increased calm and relaxation
combined with increased vigilance and attention32.

Diffuse Cortical
Areas

Limbic Pathway ®®
Anterior Limbic
MRS
CortexHypothalamus, Amygdala, Stria Terminalis
Endocrine, Autonomic, Emotion
Pituitary Release

For a more complete understanding of the relationship ofcortical EEG activity to underlying subcortical activity,
neurotransmitters and subjective states, see Lubar33. Lubar
discusses three kinds of cortical resonance loops (see figure2). Local resonance occurs between one narrow corticalcolumn and the next and produces high frequency EEG
patterns above 30 Hz such as gamma. Regional resonancesdevelop between macrocolumns (groups of narrow corticalcolumns) that are near each other and produce intermediate
frequencies such as alpha and some beta. Global resonances
can develop between widely separated regions such as thefrontal-parietal or frontal-occipital. These produce resonancesin the delta and theta range. All three types of resonance canoccur spontaneously or be stimulated by thalamic generators.
Coherence is a measure of the degree to which any two areas

Prolactin, Vasopressin, Oxytocin______________________________________________________________________________NTS = nucleus tractus solitarius; PB = parabrachial nucleus;
MRS = mesolimbic reward system
The ventrobasal nuclei relay information not only to the cortex,
but also to related cells in the adjacent thalamic nucleus called
the nucleus reticularis. Oscillations of activity between these
two nuclei set up the SMR recorded on the cortex. Producing
SMR in humans requires a decrease in body and eye
movement. Training mammals, including humans, to produce
this rhythm, resulted in a more focused state, resistance toseizures, and improved memory, vigilance, attention, andsleep. A different EEG pattern (4 to 12 Hz rhythm in the parietal
cortex) was found to be associated with reward and food14

oscillator in the medulla or possibly by the interaction of thebaroreflex sympathetic response and the vagal response torespiratory changes in blood pressure. They showed marked
effects on synchronization and increased variability inrespiratory signals, cardiovascular rhythms, and cerebral
blood flow velocity. This meant that sympathetic andparasympathetic (vagal) outflow were synchronized, also
resulting in rhythmic fluctuations of heart rate and cerebral
blood flow with improved heart rate variability and baroreflex
sensitivity. (Changes in the opposite direction are poor
prognostic factors in heart disease.)in the cortex are functionally connected. Low coherence meansthat two areas are functionally disconnected. High coherence
implies that they are related in function, but not differentiating
the functions adequately. In general, the posterior cortex ismore involved in local functions dealing with visual
processing and image formation.
The left hemisphere is involved in analytical and sequential
processes. The right hemisphere is more involved in intuitive
synthetic processes. EEG activity in the delta/theta sleep
spindle mode is associated with a low frequency burst modethrough the non-specific thalamocortical projection system tolayer 1 of the cortex (see figure 2).

Meditation and Pranayama
Many studies of meditation find that less experienced
practitioners often fall asleep (lose consciousness). However,yogis are able to remain conscious despite the appearance thesleep spindles on EEG that are characteristic of sleep.4 It canbe hypothesized that those who train in meditation can attaintheta- alpha states close to the edge of sleep while maintaining
awakeness and alertness. Alternation or simultaneous
activation of the thalamocortical generators responsible for
the SMR and PRS patterns may be involved.

Figure 2. Neocortical Resonance Modes______________________________________________________________________________
EEG: Delta - - Sleep Spindle - - Alpha - - Mu - - Beta - - Gamma
Hypercoupled States - - - Optimal Coupling - - - Hypocoupled States
Low frequency burst

Single action potential mode

Non-specific thalamocortical

Specific thalamocortical

Neocortical layer 1

Neocortical layer 4

There are more studies on the physiology of transcendental
meditation (TM) than any other meditation form, although
there are some studies of yogic, Zen and Chi Kung. A 1992
review of the physiology of meditation by Jevning et al focusing
on TM, found that meditation was associated with increased
central nervous system activity, probably increased cerebral
blood flow and increased cardiac output, yet a generally
hypometabolic state.36 Data suggesting increased plasma
renin and prolactin were noted. Janakiramaiah described
increased prolactin after only one Sudarshan Kriya andPranayama session1. Jevning and colleagues found apparent
cessation of CO2 generation by muscle, decreased meditator
sensitivity to increased PCO2 and a dramatic 5-fold elevationof plasma vasopressin.41 Subjectively deep states of meditation
were accompanied by high amplitude theta and/or fast
frequency beta bursts consistent with the alternation of SMR
with PRS states. Other authors reviewed by them propose arole for the reticular activating system and specific thalamic
nuclei in generating alpha activity in the frontal cortex withthe hypothalamus causing the hypometabolic state observed
during meditation. They postulate that meditation activates
non-specific thalamic nuclei while blocking external sensory
inputs. These authors did not know at that time about thedata on SMR and PRS training. It should be emphasized that
ideally meditation is a state of increased brain alertness.
Relaxation training may increase cardiac parasympathetic
tone 37, but not have other effects associated with meditation.

Brainstem Neurotransmitters
Serotonin
AchGlobal Resonances:

Nor Epinephrine

Dopamine

Local, Regional Resonances:

Visual Imagery

Attention, Orgasm, Bliss

Adapted with permission. Lubar, 1997 33______________________________________________________________________________
These may be conceptualized as hypercoupled states and often
involve acetylcholine, serotonin, and norepinephrine. Fasterfrequencies, such as beta and gamma, operate through specificthalamocortical projections, particularly to layer 4 of the
neocortex. Weak associations (hypocoupled) between different
areas of the cortex having predominantly local resonances
are more reliant upon dopamine.

Chanting
Breathing practices are followed by a brief chanting of “Om.”Our model hypothesizes that the seemingly simple Om chanthas complex effects on the brain. The verbal stimulation andthe vibrational component of the chant probably contribute toactivation of Wernecke’s area and the thalamus. However,other complex physiologic effects are contributory. Telles, etal. studied seven experienced yogic meditators during acontrol period and then while mentally chanting Om. They
showed decreased metabolism, decreased heart rate, andincreased peripheral vascular resistance. These findings wereinterpreted as a sign of increased mental alertness in thecontext of physiological relaxation.34

Two randomized controlled studies found that yogic
meditation enhanced seizure control in epileptics.38 Some theta
frequencies may be associated with a tendency to seizure
activity. Panjwani and colleagues showed that six months
practice of yoga and meditation shifted EEG frequencies inepileptics from the theta range to beta/alpha with decreased
seizure frequency.39 Notably, this is similar to the EEG changes
in the biparietal areas observed with SMR treatment with
biofeedback, and with valproate (anticonvulsant)administration.

Significantly, Bernardi and co-workers showed that a simple
yogic chant (as well as the traditional Latin version of theHail Mary) decreased the breathing rate to approximately six
times per minute, synchronizing it with the inherent six times
per minute natural fluctuation in blood pressure known as
Mayer’s waves.35 In 1876 Mayer described this ten-second
cycle which is thought to be related to both vagal andsympathetic activity generated by a central nervous system15

transcendent experience can be integrated with waking,dreaming, and sleeping with long experience in meditation.45

Travis and colleagues presented data showing that 11
experienced TM practitioners showed greater theta/alphapower during stages three and four sleep compared to nine
short-term practitioners and 11 non-practitioners. They also
had increased rapid eye movement density during REM
periods.40 The subjective experience of “transcending” during
meditation was marked by low breath frequency, higher
respiratory sinus arrhythmia amplitudes, higher EEG alphaamplitude, and alpha coherence.41 A somewhat different
analysis of the data might have also shown increased theta
activity in certain circuits as was found by Aftanas andGolocheikine in 16 long-term and 1 short-term meditators
using the Sahaja yoga meditation.42 Their study, using more
complex spectral analysis of the EEG showed that blissful
states during meditation correlated with left anterior frontal
theta coherence in experienced meditators as well as coherence
between anterior mid-line frontal areas (like the sensory motor
cortex) and posterior association areas. These theta waves
were different from the theta waves observed during normal
sleep. Travis and Wallace proposed a two-phase model of TM,
which is adequate to explain both findings.43 They suggested
that the first phase of meditation involves shutting down
orbital and basal frontal cortex activity, leading to a quietingof mind and body. The second phase maintains the quieter
levels of function while the emergence of thalamocorticalgenerators results in enhanced attention in a state ofconsciousness not associated with processing specificperceptual and cognitive content. In what they called theirattention/intention model, alpha synchrony (I would also say
theta coherence during bliss or transcendence) indicates astate of intention of the mind toward itself (the mind turning
its attention to itself). Travis and Wallace propose that the
prefrontal cortex initially activates the nucleus reticularis of
the thalamus to inhibit specific and non-specific activity inthalamocortical circuits. To maintain and deepen themeditative state, basal ganglia-thalamocortical circuits feed
forward to the globus pallidus and then inhibit themesencephalic reticular formation and the medial dorsal
nuclei of the thalamus. This is relevant to the effect of
Sudarshan Kriya on enhancing the ease of meditation because
hyperventilation shuts off the mesencephalic reticularformation and stimulates thalamocortical circuits, which
enhance meditation and wakefulness.

Although there have been no direct observations of yoga
masters during blissful states of ecstasy, there is one EEG studyof 7 famous Chi Kung masters in China that showed an EEGalpha activity predominantly in the anterior cortical areas
with the peak frequency being slower than the normal restingstate. This was suggested to be a state of increased excitationand is consistent with other findings during yoga meditation
and TM.46 Therefore, I would suggest that continued practicein meditation develops the ability to increase activity in theactivated bands (alpha, beta, gamma) of the EEG and toincrease dopamine stimulation (figure 2) through themesolimbic reward systems (figure 1), which results in theexperience of bliss. The seasoned practitioner can experiencejoy despite any sensory input and in any state ofconsciousness.

Endocrine Changes with Meditation andPranayama
Endocrine changes have been associated with meditation andSudarshan Kriya. A study of three months practice of
Sudarshan Kriya resulted in significant reduction in cortisol(one measure of stress response system activation in the brain)
and correlated significantly with decreased depression scores
over a three-week period.47 Another study of 12 highly trained
yoga meditators (average 6-1/2 years experience) comparedwith 11 elite runners showed an increase in CRH(corticotrophin-releasing hormone) but not endorphins after
meditation. The 11 elite runners showed the same magnitude
CRH release after running as the meditators, but the runners
also released a beta-endorphin not found in the meditators.48
The hypothalamic pituitary adrenal (HPA) axis is essential in
the stress response and survival of mammalian species. It isabnormally overactivated during biological depression andis alternately overactivated and depleted in patients with posttraumatic stress disorder.
There is data suggesting that meditation and probably
hyperventilation cause release of pituitary hormones (figure1),
probably through hypothalamic output mediated throughvagal afferents. The 5-fold increase in vasopressin associatedwith meditation is significant41. There is older evidence thatvasopressin is decreased in depression. 49 Furthermore,
vasopressin and oxytocin receptors are generally foundtogether in the brain. Oxytocin has been described as the“cuddle” hormone. It is very important for affiliative andmonogamous social bonding in voles. It is known that
stimulation of oxytocin in voles will result in increased
bonding to the next vole with which that animal comes incontact with 50. In humans, there is evidence that oxytocin isnecessary for uterine contractions in childbirth, generates milk
production in new mothers, influences bonding and affectionof the mother for her baby 51, and is a primary sexual arousal
hormone. There is some evidence of low oxytocin levels inmajor depression and of SSRIs (selective serotonin reuptake
inhibitors) facilitating oxytocin secretion 52. The antidepressanteffect of SSRIs may be partially mediated by oxytocin. Further
studies of oxytocin release during Sudarshan Kriya in
depressed patients would elucidate the importance of thismechanism. I hypothesize that hyperventilation in Sudarshan

Illuminating the EEG findings is one PET study of meditation
during a relaxation state (Yoga Nidra) versus normal
consciousness in 9 experienced yoga teachers showed an
activation of the hippocampus and a shutting off of cingulate
and frontal cortex normally used in planning, anticipation,and other intellectual activity. This pattern is remarkably
similar to the activation pattern during REM sleep except thatin REM the anterior cingulate and hippocampus are active,
whereas during yoga meditation the anterior cingulate is shut
down. The meditative state was characterized by increased
activity in the hippocampus responsible for orientation andthe posterior sensory and associative cortical areas known tobe activated by imagery whereas normal consciousness
requires activity in the executive attentional system of theforebrain and the cerebellum.44 Travis and Pearson postulatethat the transcendent experience can be seen in the junction
points between waking, dreaming, and sleeping and that this16

Kriya releases oxytocin as well as vasopressin. Thus oxytocin
may turn out to be the “I belong to you” hormone.

techniques. Nevertheless, my clinical impression is that these
aspects are so beneficial that I would not advise depriving
patients of these non-specific factors.

Sudarshan Kriya and Depression
How might Sudarshan Kriya yoga treat depression? A
considerable body of data suggests that biological depression
is associated with excessive stress response system activation.
Almost all effective antidepressants calm this system down.
Preliminary evidence suggests that Sudarshan Kriya also
quiets the stress response system. Furthermore, there is someevidence that the relationships between the two cerebral
hemispheres, between the anterior and posterior parts of thebrain, and between the top of the cortex and the subcorticalregions are disturbed in depression. (For a review, see
Kinsbourne.53) Pranayama practices probably help balance
the activity between the cortical and subcortical regions.
Sudarshan Kriya may work like electronic vagal nerve
stimulation, which has been shown to be effective fordepression. What role the increased parasympathetic andsympathetic activity induced by various Pranayama have in
improving the function of the stress response remains
speculative but is likely to be extremely important. Activationof forebrain reward systems may also play a role. Changes inacid base balance in the brain are less likely to be a significant
part of the effects of the breathing.9 Another unexploredphenomenon is that intense breathing (or indeed regularbreathing) causes the expiration of oxidant chemicals frombody metabolism called TBARS (thiobarbituric reactive acidsubstances). Whether detoxification of oxidants by exhalation
through the lungs is beneficial for disorders involving excess
oxidation damage (such cardiovascular andneurodegenerative disease) and whether this would enhancethe effect of antioxidants in delaying aging, is purely
hypothetical. Also hyperventilation increases renal output;
whether this enhances excretion of other harmful substances
is unknown.

Even if Pranayama induces a short-term remission ofdepression, what is the long-term compliance rate? Are thesepractices too complicated and time consuming for mostpatients? That does not appear to be the case from studies inIndia by Janakiramaiah in which 80% of the subjects do
continue to practice and benefit. A cross-cultural multi-center
study would address the question of differences in compliance
rates between India and America. In numerous studies ofantidepressant medication the three-month dropout rate isaround 50%.
Perhaps the biggest challenge is to design an adequate placebo
or control for breathing. Should there be a chemical, inert
placebo? Should there be a sham method of breathing such as
the relaxed slow abdominal breathing often used in relaxation
courses? Another significant variable in the effects of thesepractices on the brain involves comparison of very experienced
practitioners such as instructors with those recently practicing
and those who have never practiced the techniques using
brain imaging and other measures.

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Methodological Problems
What methodological problems face us in designing studies
of Pranayama? The same criticisms applied to the study ofyoga and epilepsy also confound the study of Pranayama indepression. 38 In most studies the number of subjects is small.
The design is often an open series without adequate controls,
without randomization or adequate double blinding. Some
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trained yoga instructors must monitor patients in the learningand practice phases. However, outside raters could come inand evaluate patients blindly, i.e. without knowledge of theircondition. Studies of imaging during Pranayama would
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At the current time, Functional MRI is better than PET scanningbecause of its increased resolution and the possibility ofobtaining multiple serial measures.19

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Healing Experience

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Myself, Swadesh Kumar, working as a Forest Officer.
I was suffering from high blood pressure and cold
and taking medicines for it regularly. I did basic
course of Art of Living in October 2001. I am doing
Sudarshan Kriya daily. Now my blood pressure isnormal and I am not taking any medicine.

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Swadesh Kumar Dhiman,
D.F.O. Nahan,Dist Sirmour, Himachal Pradesh.
Tel : O-01702-222240

47. Gangadhar BN, Janakiramaiah N, Sudarshan B, Shety
KT. Stress-Related Biochemical Effects of Sudarshan Kriya
Yoga in Depressed Patients Study #6. Presented at. The
Conference on Biological Psychiatry, UN NGO Mental
Health Committee. 2000.

I was a patient of Chronic Allergic Bronchitis, thisdisease always keeps me depressed. The term
“Chronic” indicated that I had to suffer all my life.
Of course apart from this, my worried parents werealways miserable seeing me in misery. I was on
steroid inhalers and faced 100s of problems. I joined
the Art of Living course because my friend asked
me to do so as it was a good course and I just joined
the basic course.
There was a total change in me. I have not touchedinhalers. I am grateful to my lord Poojya Sri Sri Ravi
Shankar Ji (Guruji)
As Guruji says world is beautiful I happen to see it
now the world is really beautiful.

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Psychol 1995; 40(3):251-65.
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23(8):779-818.
51. Nelson EE, Panksepp J. Brain substrates of infant-motherattachment: contributions of opioids, oxytocin, andnorepinephrine. Neurosci Biobehav Rev 1998; 22(3):43752.

Jai Gurudev,

52. Uvnas-Moberg K, Bjokstrand E, Hillegaart V, Ahlenius S.
Oxytocin as a possible mediator of SSRI-induced
antidepressant effects. Psychopharmacology (Berl) 1999;
142(1):95-101.

Nandini A.N.
250/K 2nd C Main
2nd B Cross,
V.B.N.C., Girinagar 110085.
Tel : 080-26720536

53. Kinsbourne M Editor. Cerebral hemisphere function in
depression. Spiegel D Editor. The Progress in Psychiatry
Series. Washington, DC: American Psychiatric Press. Inc.,
1988.
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