In the early 1970s, a psychologist and an immunologist collaborated to examine the effects of regularly feeding rats with sweet water and an immunosuppressant. Presented together repeatedly, the sweet water and immunosuppressant formed a conditioned response. That is, the rats continued to get sick even when they were fed only sweet water. This landmark research was the first to demonstrate that, through taste, the nervous system can affect immune responses.
Once the study was published in 1975, psychologist Robert Ader coined the term Psychoneuroimmunology (PNI), to describe interactions between these systems.
Today, PNI is a multidisciplinary and clinically important discipline that examines pathways and mechanisms by which our thoughts, emotions and health are intimately linked on cellular and molecular levels.
In fact, the research now goes beyond the molecular level and includes studies in the effects of stress and relaxation at levels of chromosomal activity and genetic expression, particularly in immune cells and inflammatory pathways.
PNI demonstrates that all chronic diseases involve inflammatory processes. Furthermore, PNI offers overwhelming evidence that inflammation and depression are linked. It is understood that poor immune function is a key component in major depression1. This link occurs via cytokines, chemical molecules that regulate inflammation. Pro inflammatory cytokines stimulate the inflammatory response and anti-inflammatory cytokines inhibit it. Cytokines are responsible for what is known as ‘sickness behaviour’.
The fatigue, lethargy and cognitive difficulties experienced during a hefty dose of the flu is directly caused by cytokine activity to encourage rest and recovery.
In times of acute stress, we know that pro-inflammatory cytokines decrease depression to help survival. However, pro-inflammatory cytokines increase depression during long-term, chronic stress.
When there is dysregulation of pro and anti-inflammatory cytokines, chronic inflammation can lead to depressive symptoms. In his book, The Inflamed Mind, to be published in December 2018, Edward Bullmore, a psychiatrist at Cambridge University outlines the growing evidence that inflammation and depression are not just linked but appear to have a causal relationship. This exciting development continues to be researched.
Other immune cells such as T cells and natural killer cells are impaired during depression. In depression, these cells demonstrate a significant loss in their activity, distribution, proliferation and ability to kill pathogens.
Bullmore acknowledged that clinical and medical practice often lags many years behind scientific advances. However, to encourage evidence-based, improved clinical practice, researchers at Cousins Institute of Psychoneuroimmunology at UCLA translate current scientific evidence to better clinical practice.
For example, research in mind-body therapies such as Tai Chi, yoga and meditation2 has examined the impact of these therapies on inflammation. A review of 26 randomized controlled trials described the effects of mind-body therapies (MBTs) on circulating, cellular and genomic markers of inflammation. This qualitative evaluation showed mixed effects of MBTs on circulating inflammatory markers. Interestingly, there were more consistent findings showing decreased expression of inflammation-related genes and reduced signalling in pro-inflammatory markers. Results from research like this support the inclusion of MBTs in healthcare.
Other fascinating research in PNI include studies into the effects of therapeutic interventions such as relaxation therapies on telomeres and telomerase.
Telomeres are to chromosomes what plastic tips are to shoelaces. They protect the chromosomes from fraying, deteriorating and risking damage to the DNA.
Telomerase is the enzyme that protects and nourishes telomeres. Reduced telomerase activity reduces telomere health. Everyone’s telomeres shorten with age, while psychological stress, inflammation and chronic disease increase the rate of telomere shortening and decrease telomerase activity, thereby reducing telomere viability. Therefore, telomere length is a marker of cellular aging and health. Recent studies suggest that some forms of meditation, improved diet, exercise, social support and relaxation may reduce the rate of telomere shortening and increase telomerase activity.
One study3 trained caregivers of a family member with dementia to practice a simple form of meditation for a minimum of 12 minutes per day for 8 weeks. Two subjective outcomes – cognitive functioning and depressive symptoms – and one objective outcome – telomerase activity in immune cells – were measured before and after the 12 weeks. Significant improvements were found in all 3 outcomes. However, the extent of improvement in telomerase activity is worth noting. The carers who meditated a minimum 12 minutes per day for 8 weeks had a 43% increase in telomerase activity compared to the control group. In research terms, this is a particularly large improvement.
Forty years ago, PNI studied links between the nervous and immune systems. Today, sophisticated research supports age-old wisdom that the mind and the body are not separate entities. Neuroscientists, doctors, psychiatrists and researchers increasingly recognise evidence that psychological stress can affect inflammatory processes, chronic disease and specific biological markers of health and ageing. Massage therapists can feel confident that by reducing stress, pain and fatigue, hands-on techniques can in turn decrease inflammation and psychological conditions such as depression.
- Dinan & Cryan, Microbes, Immunity & Behavior: PNI meets the Micobiome. Neuropsychopharmacology, 2017: 42, 178-192
- Bower, J & Irwin, M. 2015. Mind–body therapies and control of inflammatory biology: A descriptive review. Brain, Behavior, and Immunity. 51. 0.1016/j.bbi.2015.06.012.
- Lavretsky H, Epel ES, Siddarth P, Nazarian N, Cyr NS, Khalsa DS, Lin J, Blackburn E, Irwin MR. Int J Geriatric Psychiatry. 2013 Jan;28(1):57-65. doi: 10.1002/gps.3790. A pilot study of yogic meditation for family dementia caregivers with depressive symptoms: effects on mental health, cognition, and telomerase activity.