On Hypnosis and Genetics

The Genetics of Hypnosis

Let’s start with a quick introduction to genes. The cells in our bodies store information about their structure and function in the form of a chain of molecule sequences called deoxyribonucleic acid (DNA). Although we are all human beings, our DNA is not entirely identical. Small differences in our DNA are what make each of us slightly different from one another. When specific changes in DNA appear to repeat frequently enough across people, we call them “polymorphisms.” The long DNA chains are often divided by scientists into “genes,” pieces of the sequence that contain instructions about how to build, adjust, and change specific functions of specific cells. When a gene is being “read” and the cell follows its instructions, we say that the gene is being “expressed.”

Our ability to respond to suggestions in hypnosis (hypnotizability) is related to polymorphisms in several genes. For example, the catechol-O-methyltransferase (COMT) gene is responsible for the COMT enzyme (a protein that converts substances using chemical reactions) that affects neurotransmitters such as dopamine, adrenaline, and noradrenaline. Several studies found that hypnotizability is associated with polymorphisms in the COMT gene 1–3. This finding is often interpreted by linking hypnosis to dopamine-related activity (which can be impacted by the COMT enzyme) in specific areas of the brain (learn more with our article about what happens in the brain during hypnosis).

Hypnotizability is also related to polymorphisms in genes that play a role in how we experience pain. You might have heard about opioids, a family of substances that can relieve pain. Opioids can be created by the body (endogenous) or taken as a drug (exogenous). Opioids work by attaching to a “receptor” – a type of sensor on our neurons (nerve cells) that impacts how they work when opioids are around. The opioid receptor μ1 (OPRM1) gene is the main opioid receptor in pain. High hypnotizability is associated with a polymorphism in the OPRM1 gene that reduces the effectiveness of opioids. Because high hypnotizability is consistently related to stronger effects of hypnosis for pain 4,5, this finding suggests that hypnosis reduces pain by other means than the internal opioid system. Indeed we conducted a study showing that hypnotic analgesia persisted even when a drug, naloxone, was given that blocks and reverses the pain reducing effects of opioids.6  One potential way hypnosis can reduce pain is through the endocannabinoid system. Like the opioid system, the endocannabinoid system impacts pain sensation. One study suggested that hypnotizability is associated with the likelihood of having a polymorphism that weakens a gene responsible for fatty acid amide hydrolase (FAAH), an enzyme that deconstructs anandamide (one of the main neurotransmitters of the endocannabinoid system)7. Therefore, it is possible that the endocannabinoid system contributes more to pain reduction in individuals with high compared to low hypnotizability.

Hypnotizability was also related to polymorphisms in the oxytocin receptor gene (OXTR)8. OXTR is responsible for receptors of oxytocin, a hormone that facilitates social bonding and is often referred to as “the love hormone.” Hypnosis might work better with greater oxytocin levels through reduced social anxiety, increased trust, and enhanced ability to respond to cues9.

Psychological stress is known to contribute to the dysfunction of the inner lining of our blood vessels (endothelium) by weakening its ability to control blood flow. Endothelial dysfunction is a recognized risk factor for cardiovascular disease. Hypnosis can reduce the psychological impact of stressors, thereby decreasing their effects on our vascular system. Greater responsiveness to hypnosis is also associated with polymorphisms of the nitric oxide synthase 3 (NOS3) gene. The NOS3 gene contains instructions for the NOS3 enzyme, which synthesizes nitric oxide (NO) in the inner lining of our blood vessels’ endothelium. NO participates in the ability of the endothelium to constrict and expand to control the flow of blood. This allows highly hypnotizable individuals to have lower stress-related endothelial dysfunctions even outside the context of hypnosis,10,11.

Can hypnosis change gene expression?

Our genes can help us benefit more from hypnosis, but did you know that specific experiences can impact how our genes are expressed without DNA differences? Epigenetics is the science of the different ways genes can be “expressed” without altering the DNA sequence. Epigenetic effects play major roles in our psychology, cognitive functions, and health. Preliminary evidence found that hypnosis was associated with gene expressions related to reduced inflammation and cellular stress and supporting healthy immune responses and stem cell growth 12–414.

Neuroplasticity is the ability of our nervous system to adjust itself structurally (for example, by creating new connections between neurons) and functionally (for example, by changing how existing neurons function) in response to experience. Although more evidence is needed, several recent studies argue that hypnosis results in greater neuroplasticity15,16. Because epigenetic changes are crucial for neuroplasticity, some researchers think that the ability of hypnosis to change gene expression contributes to its ability to spark neuroplasticity17,18. Not only that, but being high in hypnotizability might offer greater neuroplasticity benefits from hypnosis [19].

Bottom Line

Although the science of hypnosis and genetics is still young, several genes have been linked to hypnotizability. However, our genetics affect only a portion of our ability to respond to hypnotic suggestions, among various other factors (read more in our article on hypnotizability). Hypnosis can also change how our genetic information comes into play: undergoing hypnosis sessions has been linked to the activation of genetic programs related to a healthy immune response, stem cell growth, reduced inflammation, and decreased stress.

References

  1. Szekely, A. et al. Association Between Hypnotizability and the Catechol-O-Methyltransferase (COMT) Polymorphism. Int. J. Clin. Exp. Hypn. 58, 301–315 (2010).

  2. Rominger, C. et al. Carriers of the COMT Met/Met Allele Have Higher Degrees of Hypnotizability, Provided That They Have Good Attentional Control: A Case of Gene–Trait Interaction. Int. J. Clin. Exp. Hypn. 62, 455–482 (2014).

  3. Katonai, E. R. et al. Dopaminergic and Serotonergic Genotypes and the Subjective Experiences of Hypnosis. Int. J. Clin. Exp. Hypn. 65, 379–397 (2017).

  4. Milling, L. S., Valentine, K. E., LoStimolo, L. M., Nett, A. M. & McCarley, H. S. Hypnosis and the Alleviation of Clinical Pain: A Comprehensive Meta-Analysis. Int. J. Clin. Exp. Hypn. 0, 1–26 (2021).

  5. Thompson, T. et al. The effectiveness of hypnosis for pain relief: A systematic review and meta-analysis of 85 controlled experimental trials. Neurosci. Biobehav. Rev. 99, 298–310 (2019).

  6. Spiegel, D. & Albert, L. Naloxone fails to reverse hypnotic alleviation of chronic pain. Psychopharmacology 81, 140-143 (1983).

  7. Presciuttini, S., Carli, G. & Santarcangelo, E. L. Hypnotizability-Related FAAH C385A Polymorphism: Possible Endocannabinoid Contribution to Suggestion-Induced Analgesia. Int. J. Clin. Exp. Hypn. 68, 29–37 (2020).

  8. Bryant, R. A., Hung, L., Dobson-Stone, C. & Schofield, P. R. The association between the oxytocin receptor gene (OXTR) and hypnotizability. Psychoneuroendocrinology 38, 1979–1984 (2013).

  9. Bryant, R. A. & Hung, L. Oxytocin Enhances Social Persuasion during Hypnosis. PLOS ONE 8, e60711 (2013).

  10. Presciuttini, S. et al. Promoter polymorphisms of the NOS3 gene are associated with hypnotizability-dependent vascular response to nociceptive stimulation. Neurosci. Lett. 467, 252–255 (2009).

  11. Jambrik, Z. et al. Modulation of pain-induced endothelial dysfunction by hypnotisability. Pain 116, 181–186 (2005).

  12. Rossi, E. et al. A Pilot Study of Positive Expectations and Focused Attention via a New Protocol for Optimizing Therapeutic Hypnosis and Psychotherapy Assessed with DNA Microarrays: The Creative Psychosocial Genomic Healing Experience. 7 (2008).

  13. Cozzolino, M. et al. A Monthly Double-Blind Peer Reviewed Refereed Open Access International e-Journal -Included in the International Serial Directories the mind-body healing experience (mhe) is associated with gene expression in human leukocytes A Monthly Double-Blind Peer Reviewed Refereed Open Access International e-Journal -Included in the International Serial Directories. Int. J. Phys. Soc. Sci. 2249-5894 5, (2015).

  14. Cozzolino, M. et al. A Psychosocial Genomics Pilot Study in Oncology for Verifying Clinical, Inflammatory and Psychological Effects of Mind-Body Transformations-Therapy (MBT-T) in Breast Cancer Patients: Preliminary Results. J. Clin. Med. 10, 136 (2021).

  15. Marinella, C. et al. Hypnosis and learning: Pilot study on a group of students. J. Complement. Integr. Med. 17, (2020).

  16. Halsband, U. & Gerhard Wolf, T. Functional Changes in Brain Activity After Hypnosis: Neurobiological Mechanisms and Application to Patients with a Specific Phobia—Limitations and Future Directions. Int. J. Clin. Exp. Hypn. 67, 449–474 (2019).

  17. Rossi, E. L. & Rossi, K. L. The Neuroscience of Observing Consciousness & Mirror Neurons in Therapeutic Hypnosis. Am. J. Clin. Hypn. 48, 263–278 (2006).

  18. Császár, N., Scholkmann, F. & Bókkon, I. Implications on hypnotherapy: Neuroplasticity, epigenetics and pain. Neurosci. Biobehav. Rev. 131, 755–764 (2021).

  19. Spina, V., Chisari, C. & Santarcangelo, E. L. High Motor Cortex Excitability in Highly Hypnotizable Individuals: A Favourable Factor for Neuroplasticity? Neuroscience 430, 125–130 (2020).

About the author:

Afik Faerman, Ph.D. is a postdoctoral scholar at Stanford University. He completed his doctoral training in clinical psychology with an emphasis in neuropsychology, and his clinical training at the University of California, San Francisco (UCSF) and Baylor College of Medicine in Houston, TX. Afik’s research centers on identifying key neurocognitive mechanisms in clinical change, focusing on hypnosis, pain, and sleep. His research was supported and acknowledged by the American Psychological Association, the Society for Clinical and Experimental Hypnosis, and the American Society for Clinical Hypnosis.