POLYVAGAL THEORY
The researchers at Howard Hughes medical Institute, led by Bruce Lahn have found evidence that the pressure of natural selection has lead to dramatic changes in two genes known to control brain size in humans. Brain size or intelligence is naturally selected for in evolution for obvious survival reasons, and larger brains require more oxygen. Although the brain represents only 2% of the body weight, it receives 15% of the cardiac output, 20% of total body oxygen consumption, and 25% of total body glucose utilization. The larger the brain, the greater the demand of oxygen and hence the more sophisticated the nervous system needed to provide that oxygen… the evolutionary payoff for larger brain size of course being survival. As a natural extension of mammalian evolution we can see that the human neocortex was an inevitable consequence of evolutionary pressure.
{This makes even more sense when one considers the "Aquatic Ape" theory. Taking in lots of oxygen for diving would have been crucial.}
According to the Poly-Vagal Theory during evolution the mammalian nervous system developed two vagal systems. Built onto the relic of amphibians and reptiles is an evolutionary modification unique to mammals. Looking at the history of evolution Poly-Vagal Theory notes the importance of the need for oxygen in evolving the mammalian nervous system.
During evolution as the mammalian nervous system got more complex than its amphibian and reptilian brothers, there was a greater demand for oxygen. Porges says that it was this need for extra oxygen that may have provided the evolutionary pressure leading to the development of the highly adaptive and sophisticated autonomic nervous system found in mammals; and that behaviors such as orienting, attention, emotion and stress are by-products of the evolutionary pressure to optimize oxygen resources.
The Polyvagal Theory addresses the relative roles of the vagus nerve in energy conservation and survival. In Stephen Porges’s Polyvagal Theory he uses the term Polyvagal to distinguish between the two main branches of the vagus nerve:
1: The Vegetative Vagus—originates in the dorsal motor nucleus (DMNX), descends visceral efferent fibers {Conducted or conducting outward or away from something} regulating smooth and cardiac muscle and is associated with passive reflexive regulation of visceral functions: peristalsis of the GI tract, sweating, lungs, diaphragm, stomach. At the heart it is connected to stretch receptors of the aortic arch and chemoreceptors of the aortic bodies and is responsible for heart rate, dilation of blood vessels and blood pressure. The output from the dorsal motor nucleus does not convey a respiratory rhythm.
The most primitive function of the vagal complex is the freeze response, which is dependent on the unmyelinated vagus that is part of the reptilian system.
2: The Smart Vagus—which originates in the medullary source of the nucleus ambiguus (NA), serving efferent fibers regulating the somatic muscles of speech and eating: the larynx, pharynx, and esophagus. The ventral vagal complex (including NA) related to processes associated with attention, motion, emotion and communication. The functional output of the NA-vagus on the heart is part of a common neuronal network producing a cardiorespiratory rhythm. The most evolutionary recent component—the communication system functions through the new-mammalian or myelinated vagus that regulates the heart and the bronchi to promote calm and self-soothing states.
In mammals the two vagal systems are neuroanatomically distinct, have different origins, and are programmed with different response strategies and may respond in a contradictory manner. Thus Porges attributes various medical disorders to competition between DMNX and NA originating fibers. The different vagi may have oppositional outputs to the same target organ. The vagus is a complex of neural pathways originating in several areas of the brainstem. The vagus nerve consists of afferent {Conducting or conducted inward or toward something} and efferent parasympathetic (acetylcholine) fibers that run from the brainstem (medulla oblongata) down to the traverse colon and urinary organs; providing both motor and sensory parasympathetic activation for everything from the neck to the G spot. Efferent fibers originate primarily in two medullary nuclei (NA, DMNX).
The vagus is not solely an efferent or motor pathway, at least 80% of the vagal fibers are afferent; that is they conduct impulses from the periphery of the body to the brainstem.
According to the Polyvagal Theory the growth of the autonomic nervous system evolves through three stages:
1. Freeze—First a primitive unmyelinated visceral vagus that fosters digestion and responds to threat by depressing metabolic activity eg: freeze response.
2. Fight-or-flight—The mobilization or fight-or-flight is dependent on the functioning of the sympathetic nervous system; increasing metabolic output and inhibiting the visceral vagus to foster mobilization behaviors necessary for fight-or-flight.
3. Communication—The third stage, the mammalian myelinated vagus, can rapidly regulate cardiac output to align with the environment and is associated with cranial nerves that regulate sociability via facial expression and vocalization.
Stephen Porges points out the phylogentic hierarchy of response to challenge: “The hierarchy emphasizes that the newer “circuits” inhibit the older ones. We use the newest circuit to promote calm states, to self-soothe and engage. When this doesn’t work, we use the sympathetic-adrenal system to mobilize for flight and flight behaviors. And when that doesn’t work, we use a very old vagal system, the freeze or shutdown system.”
Stephen Porges suggests that the true freeze response is dangerous to mammals. For example, high tone in the dorsal motor nucleus vagal system maybe lethal in mammals through an overdose of the immobility response . Whereas high tone from the NA-vagal system maybe beneficial in adaptive significance of mammalian affective processes including courting, sexual arousal, copulation, and the establishment of enduring social bonds. In the development of enduring pairbounds the mammalian vagus communicates safety and trust, via oxytocin and vasopressin, between the hypothalamus and the medullary source nuclei of the viscera vagus.
Porges suggests that we use our higher cognitive processes to calm the stress response and establish effective connections with others by using our facial muscles, making eye contact, modulating our voice and listening to others. In this way we increase the influence of the myelinated vagus, which calms us and turns off the stress response and makes us more metabolically efficient. He says the social neural circuit supports our health through its calming influences on the heart and lungs and its reduction of HPA axis activation.
The vagus is asymmetrical with the left and right sides performing different tasks, with the right vagus most active in the regulation of the heart.
Primary emotions are related to autonomic functioning since they are often survival related, they must be integrated into the regulation of the heart and lungs. Emotions have a right limbic bias, as does the brainstem medullary structures controlling visceral function. Only when the environment is perceived as “safe” is there cortical regulation of the visceral pathways, because while under threat, cortical control of brainstem structures would compromise the individual’s ability to mobilize. Therefore when stressed or in danger, cortical control of brainstem is “inhibited” and the brainstem structures are “disinhibited” to allow the sympathetic nervous system to efficiently increase metabolic output.
Stimulation of the ascending fibers of the vagus releases norepinephrine into the amygdala strengthening memory storage in regions of the brain that regulate arousal, memory and feeling responses to emotionally laden stimuli. These ascending fibers is how the peripheral epinephrine from the adrenals released into the blood during the fight-or-flight response activates the release of norepinephrine in the limbic system sharpening memory of the events.
Since the adrenal hormone epinephrine cannot cross the blood brain barrier it activates the vagus nerve, which in turn stimulates neurons in the brainstem known as the “Nucleus of the Solitary Tract (NTS). This third medullary nucleus, located near DMNX, is the terminus of many of the afferent pathways traveling through the vagus from peripheral organs.
Vagus afferent sensory fibers carrying information to the brain from the head, neck, thorax, and abdomen relay information to the NTS. These NTS neurons release norepinephrine into the memory processing areas such as the amygdala and hippocampus to activate long term memory storage of emotionally laden events. This explains why vagus nerve stimulation was found to improve memory consolidation of recent events. Researchers found that by microinjecting the NTS with either GABA agonists or glutamate antagonists, they thereby increased GABA or decreased glutamate in the NTS and this blocked seizures.
Stephen W. Porges, Ph.D. found that he could improve autism by stimulating the newer structures and prompting the social engagement system with the use of acoustic sessions using frequencies associated with the human voice. Check out Stephen Porges’s fabulous papers on the web.
VIVA LA VAGUS
Vagus Nerve Stimulation (VNS) is now being used for depression, seizures and eating disorders. Although the precise mode of action of VNS is not known, researchers suggest that VNS increases seizure threshold by causing widespread release of GABA and Glycine in the brain. Reported changes in blood flow in the cerebellum, thalamus and cortex might activate inhibitory structures in the brain reducing seizure kindling. One VNS study showed mean seizure frequency to decrease by 25%. Altered synaptic activities at sites of persisting VNS-induced cerebral blood flow changes may reflect antiseizure actions.
Depression affects some 340 million people worldwide and there is a correlation between depression and the likelihood of developing seizures. VNS increases cognitive skills reflecting a reduction in depression. Areas of the brain that are affected by Vagus Nerve Stimulation include the medulla, cerebellum, parabrachial nucleus, locus ceruleus, hypothalamus, thalamus, amygdala, hippocampus and cingulated gyrus. Noradrenergic and/or serotonergic deficits, may contribute to predisposition to some epilepsies and depressions. Evidence suggests that vagus nerve stimulation exerts at least some of its anticonvulsant and antidepressant effects through its capacity to increase noradrenaline and serotonin transmission. The vagus is responsible for keeping the larynx open for breathing and also feeds the lungs and diaphragm. Deep breathing stimulates the vagus nerve bringing balance between the parasympathetic and sympathetic nervous systems.
Since a VNS device and its surgical implantation will run at nearly $30,000 it’s an expensive treatment for seizure, compulsiveness and depression…breathing however does a similar job of activating the vagus nerve and it’s free. The sense of contraction and pain in the core of ones torso and neck during the heating phase prior to popping is obviously the vagus nerve making a valiant effort to counter the revving up of the pituitary-adrenal-axis, and the sympathetic nervous system. The vagus is trying to keep the emotional-memory arousal faculties of the body repressed; hence we feel this conflict as a persistent tension in our core for up to 2 years prior to awakening.
Besides breathing it is also possible to stimulate the vagus into relaxing the body-core by turning the minds eye into ones center and actively warming and purposefully letting the area go. All thoughts, emotions and phenomena are drawn into ones core as though one is an atomic karmic disposal unit. We could call this practice Melting In The Core—turning the minds eye into actively stimulating the vagus nerve into relaxing the viscera. This alleviates depression, increases coherency, lucidity, makes for a more vibrant personality and improves health and well-being.
Scientists are investigating the existence of non-genital orgasms suggesting a more pervasive orgasmic process and its role in neuroendocrine and psychological health. There are vaginocervical sensory pathways to the brain that can produce the absence of pain without loss of consciousness (analgesia), release oxytocin, and bypass the spinal cord via the vagus nerve. That is a paraplegic woman can still have cervical and G spot orgasms because the vagina is fed by the vagus nerve while the clitoris by nerves that come out of the spine. This gives weight to the necessity of sexual intercourse for maintaining healthy balance of the nervous system. Also there might be something to the validity of having sex during an awakening to help the parasympathetic nervous system to maintain its own. Orgasm has been described as a mini-seizure of the limbic system and tends to release or lessen deep limbic activity. Dr Amen noticed that depression, sadness, feelings of hopelessness, and automatic negative thoughts correlate with a hyperactive limbic area. The supplements that seem to help limbic hyperactivity best are DL-phenylalanine (DLPA), L-tyrosine, and S-Adenosyl-Methionine (SAMe).
I find it fascinating that the parasympathetic off-switch vagus turns on activating neurotransmitters in the emotional memory systems...obviously this is a big factor in the reward/punishment building of our response system. One of the contributors to the tenacity of PTSD as well no doubt, and you know they give norepinephrine blockers to trauma victims to block the vividness of their memory. Because stimulation of the vagus nerve activates the memory centers in the brain it is apparent that sex would be good for improving memory ability. Since memory is primary to our sense of meaning and to cognition in general, it is apparent that sex has the potential of improving intelligence and quality of life through improved brain function and freedom from depression. The counter argument to this is that the endorphins produced during sex would reduce mental alertness.
Retraining the Vagus—Lie flat on your stomach with your head to one side. Progressively relax your jaw by imagining it dropping down toward your feet. Feel the sense of your tongue dropping into your belly. You will notice that this stimulates breathing, for you get the sense of oxygen hunger. Obviously a tight jaw is tied into the neural circuits for the suspension of breath and shallow breathing. Repeating this exercise and making this more jaw-contraction more conscious will help to retrain the medulla and vagus toward deeper breathing and change the set point of the nervous system toward greater relaxation.
Mechanism of the Freeze—Animal hypnosis, catalepsy, tonic immobility or the freeze response, is an inborn defensive behavior characterized by a temporary quiescencent state of profound and reversible motor inhibition elicited by danger. Cholinergic stimulation of the dorsal periaqueductal gray matter (PAG) decreases the duration of the Tonic Immobility episodes, while stimulation of the ventrolateral region increases it - lesions of the ventrolateral PAG can greatly reduce conditioned freezing. PAG is the midbrain grey matter that is located around the cerebral aqueduct within the midbrain. It plays a role in the descending modulation of pain, in the ascending pain and temperature fibers. Neurons of the PAG are excited by endorphins (endogenous opioid neurotransmitters) to produce analgesia. Stimulation of the periaqueductal gray matter of the midbrain activates enkephalin releasing neurons that project to the raphe nuclei in the brainstem. Some animal studies indicate that alterations in the levels of cerebral serotonin modulate the analgesic effect of the dorsal periaqueductal gray matter (PAG) stimulation. The EEG activity in animal studies of tonic immobility was characterized by low voltage fast activity. Tonic immobility was always preceded by long bursts of both cortical and amygdaloid alpha range EEG activity which characterized an “awake-alertfixation” state of behavior. This alpha activity may be a necessary but not sufficient condition for the onset of tonic immobility.
