Hypnosis & reward pathway
Hypnosis, dopamine, reward pathway, diabetes,
metabolic syndrome, conditioning
Hypnosis is becoming more and more accepted today as a health care and healing system for many pathologies, which can be treated in less time, with less engagement for the patient, and more efficaciously than with other therapeutic procedures.
As we well know this method plays over natural mental states and takes individuals on journeys through their entire lives in order to establish the rebalancing that leads to wellness.
All this may be traced to the systems that physiologically form our mind, which, when altered, demonstrate involvement in a set of pathological mechanisms with parallel therapeutic implications.
The key elements are:
- an anatomic-functional analysis of the structures involved
- metabolic correlations
- the action of hypnosis on reward pathway
THE REWARD PATHWAY
The reward system is a complex dopaminergic circuitry that in our brain divides itself in two other projecting subsystems that start from the ventral mesencephalon and lead themselves to the nucleus accumbens-tuberculum olfactory system. The webs derived are:
- starting from VTA, the ventral tegmental area, with one medial going to the ventro medial striatum
- from the lateral VTA start projections to the ventrolateral striatum
These two projective circuitries form the dual dopamine striatal system, ventromedial and ventrolateral. Their role is fundamental in regulating arousal, variable complexity concepts, which include mainly attention mechanisms, and also finalized behaviors; they differ in two systems: reward mechanisms versus nocivi (harmful) stimuli.
As neurons, dopaminergic cells are active only phasically. Only in a local excitative condition do neurons gain action potential and determine a flow of dopamine to the nucleus accumbens. This is mostly responsive and ready to conduct the stimulus if there are excitatory stimuli coming directly from the telencefalon, and particularly from structures like the amygdalae and prefrontal orbito-medial cortex. The result, molecularly speaking, is a reduction of gaba at the ventral pallidus level. The inhibition of pallidus leads to a consequent disinhibition of the lymbic system, a link maintained by cortical projections and contemporary connections to and from the VTA.
It is clear that the other systems connected with the reward pathway are those included in the mind’s dopaminergic web, and precisely:
- from the VTA to the other cortex…prefrontal, insular, lymbic, and hyppocampal and vice-versa
- from the VTA to the anteromedial striatum and to the nucleus accumbens
- from the VTA to the amygdalae from which there are hypotalamic projections (lateral) that return to the mesencefalon (medial)
- from the VTA to low-descending brain stem (reticular substance, periaqueductal grey)
Most of these systems vaunt two-directional dopamine circulation ways.
This system determines and forms all the mind functions referred to:
- instinctive mechanisms and automatic or unconscious behaviors
- vegetative reactions
- emotional responses
- regulations of superior hormonal systems and of autonomic nervous system
- dolorific controlled system
The system is also involved in the effects caused by molecules considered “drugs”, whether they are pharmacons, chemicals, natural molecules, or endogenous molecules, given that they are endogenous peripheral products or derive from physiological variations of our mental states whether spontaneous or autonomously and heterogeneously induced.
PATHOLOGICAL AND METABOLIC CORRELATIONS
The reward pathway and more in general the entire dopaminergic system is involved and activated even by variations of metabolic endogenous molecules and by their exogenous analogues.
The increase of postprandial insulin, induced by the increase in glycaemia that determines its exit from the pancreatic beta-cell, leads to a stimulation of the VTA, the ventral tegmental area, thanks to its action on dopaminergic circuitries: experimental data show that insulin determines a rise in dopamine mRNA. The effect is a positive dopamine-induced stimulation in the nucleus accumbens that determines a positive reward pathway, with a further food search, caused by a conscious hungriness sensation.
Insulin is therefore related to a wellness sensation mediated by dopamine.
This system is altered in diabetic people with insulin-resistance because the entire reward pathway system already, hypothetically unbalanced in an insulin-dependent disequilibrium, is altered by the insulin stimulation typical of advanced phases of pathology.
In a similar situation but with some differences are patients affected by metabolic syndrome with criteria of ATP III (central obesity: waist circumference ≥102 cm (m) or ≥
88 cm (f); arterial hypertension ≥ 130/85 mmHg; hyper-trigliceridemia, TG ≥ 150 mg/dL; reduction of cholesterol HDL levels < 40 mg/dL (m) or 50 mg/dL (f); diabetes, or fast glycaemia ≥100 mg/dL). It is known that in these patients there are alterations in the level of leptin, an adipokine normally produced by fat tissue responsible for the sensation of satiety, with a directly proportional relation until medium-elevated levels of pathology are reached over which the adipose tissue dysfunction leads to an altered metabolism of itself manifested through a reduction of leptin and its effects.
Leptin has been shown to rise with higher fat mass and inhibit dopaminergic VTA circuits, for a gaba prevalence with negative effect on the nucleus accumbens: in healthy people it inhibits the search of food and reduces the sensation of hungriness.
Both phenomena insulin-resistance and reduced leptin often occur in obese patients. The effect is a reduced dopaminergic stimulation of VTA with a final reduced stimulation of reward, and a parallel reduction of the inhibition of the sensation of hunger due to altered leptin metabolism.
All this helps understand how pathologies derived from peripheral alterations, and particularly specific tissues and organs (in primis pancreas for diabetes and the adipose tissues for metabolic syndrome, even if this is actually related to metabolic compromise considered more systemically) are essentially linked to the with encephalic structure and play important roles, and for such reason could be potential target for care using molecular analogues that act in a similar way, and other therapeutic systems with similar action.
HYPNOSIS AND DOPAMINERGIC SYSTEMS
Hypnosis works on spontaneus physiological and hetero-induced variations of different mental states with balance variably equilibrated between all the structures mentioned above, each one corresponding to a particular mental state.
One starting point is the action mechanism of hypnosis: the reduction of the critical level related with cortical function (with the reduction of the cortical function and the respective raise of dopamine, typical of the subcortex), a reduced control over automatic mechanism, until the achievement of that peculiar action of hypnosis that is the mental review of all that is part of past lived and of unconscious experience re-processed through the hypnotherapist’s help.
The trance state of mind becomes the first step in the revision of the subject’s mental world, which may start from the “knots to solve” with which patient is often – but not always – well aware, a revision that can overcome the automatic proceedings, derived from the people’s experiences, and the same situations that guide the thought of each one of us towards either a pessimistic or positive and optimistic logical direction.
The result is often achieved when after becoming aware of the points behind mental (and neural) proceedings and sometimes the cause of pathologies, the patient is able to unconsciously or subconsciously realize optimized and better systems.
Juxtaposing the hypnosis method alongside the mind structure, it becomes clear that one of the systems most closely involved is the reward system: the gratification that the subject experiences comes from the immediate effect derived from trance status (a mental state with relative augmented dopamine, and a consequent increase in dopaminergic circuits, VTA in primis), and the re-reading in a positive key of new ways to viewing every reality.
This action is partially due to two phenomena that the patient and the therapist develop together:
- initially, a sort of conditioning that is pavlovian more in the essence than in method, that determines a re-interpretation of events lived by highlighting points to solve and elements to emphasize, until they prevail in an almost exclusive way (with multiple action on dopaminergic systems); from which begins a strengthening of the mechanisms most useful to subject that lead to real neural modifications such as those involving the vegetative-insular system, and always the reward pathway
- subsequently, a subconscious systematization of the same methods until they become semi-automatic and prevail over previous ones in order to be immediately realized by the subject who can see positive traits of situations in a more spontaneous way.
Hypnosis is a system that can not only concretely change our way of being but also create and utilize the neural connections, that make us what we are.
The reward pathway is a dopaminergic system responsible of our healthy state and inter-connected with many structures that modify during our lives.
Hypnosis can create an immediate effect by acting on this system, in this way not only treating numerous etiology pathologies, but also determining evident states of wellness in the mind thanks to the establishment of better ways of thinking, being, and living.
- Riccardo Arone di Bertolino (2003) L’ipnosi per un medico, Edizioni Martina Bologna
- John Grindler & Richard Bandler (1981) Trance-formations, Connirae Andras Ed
- Kasper (2005) Harrison’s Principi di Medicina Interna, McGrawHill
- Hilgard’s Introduzione alla psicologia (1999) Piccin
- Figlewicz, Insulin leptin & food reward; Am J Physiol Regul Integr Comp Physiol 296: R9-R19, 2009. First published October 22, 2008
- Joshua, Synchronization of Midbrain Dopaminergic Neurons Is Enhanced by Rewarding Events; Neuron, Volume 62, Issue 5, 695-704, 11 June 2009
- Morton, The action of leptin in the VTA to decrease food intake is dependent on Jak-2 signaling; Am J Physiol Endocrinol Metab 297: E202-E210, 2009. First published May 12, 2009