There is now evidence that mindfulness meditation can alter gene expression. Research carried out jointly by the University of Wisconsin-Madison and the Institute of Biomedical Research of Barcelona, Spain revealed that participating in a day of mindfulness meditation activities reduces levels of pro-inflammatory genes. Perhaps meditation could be used to treat chronic inflammatory conditions.
Steven Cole et al. from UCLA have recently shown that having a deep sense of purpose and meaning in life can lead to positive genetic changes such as lowering the levels of inflammatory gene expression and strengthening the expression of antiviral and antibody genes. Theoretically, this could mean that those with a strong sense of purpose and meaning have a more efficient immune system and are less susceptible to inflammatory diseases.
Parallels can be drawn with Viktor Frankl’s influential book ‘Man’s Search For Meaning‘. In it, he relates his experiences of life in concentration camps during WWII. He believed that finding a meaning to life was crucial to survival in those terrible circumstances. After the war, he continued his work as a psychiatrist with logotherapy (a form of existential analysis) and became convinced that happiness was to be attained by finding meaning and purpose in life.
The team of researchers led by Prof. Laura Stone at McGill University recently found that 6 months after inflicting nerve injuries on mice, the mice still displayed signs of skin hypersensitivity and motor impairment. This was associated with epigenetic changes in the amygdala and prefrontal cortex of the brain. Epigenetics explains how genes can be switched on and off. It’s the study of mechanisms by which the environment controls gene activity. Interestingly, the DNA changes were reversed by placing the mice in a more stimulating environment (three mice per cage, a running wheel mounted on a plastic hut and marbles). Whereas, placing the mice in an impoverished environment (one mouse per cage in the absence of a running wheel, marbles or any other forms of enrichment) didn’t restore normal DNA. DNA changes were found to correlate to hypersensitivity. In other words, placing the mice in a stimulating environment helped decrease their pain.
There’s been a lot of talk in the press (BBC, The Telegraph, Yahoo, Medical News Today, etc.) this week about finding the gene that causes back pain. So now back pain can be added to a host of other inherited conditions such as obesity, depression, cancer and diabetes. Before I give my opinion, I’d like to specify exactly what recent research has found. The study was carried out at King’s College London and was published this month in the Annals of Rheumatic Diseases. They found an association between the PARK2 gene and lumbar disc degeneration (LDD). The PARK2 gene switches off in people with LDD. LDD is the progressive dehydration of lumbar discs leading to disc space narrowing and osteophyte (bony spurs) growth. It is thought to be a common cause of low back pain (LBP).
It’s interesting to note however, that only 5 % of the population is affected by LDD but over 80% of people will have an episode of LBP at some time in their lives. Also, lots of people diagnosed by MRI scan with LDD have not experienced low back pain…strange? The obvious conclusion is that most LBP is not caused by LDD. Now, let’s look more closely at the relationship between the PARK2 gene and LDD. Does having the PARK2 gene automatically lead to disc degeneration? No! The PARK2 gene has to be switched off for that to happen. What switches it off? That there is the million dollar question, and it hasn’t been answered to satisfaction. The researchers have alluded to environmental factors such as lifestyle and diet. This is starting to sound familiar…could this be the old ‘nature vs nurture’ debate again?
Epigenetics explains how genes can be switched on and off. It’s the study of mechanisms by which the environment controls gene activity. “These mechanisms can enable the effects of parents’ experiences to be passed down to subsequent generations eg. paternal grandsons of Swedish men who were exposed during preadolescence to famine in the 19th century were less likely to die of cardiovascular disease, if food was plentiful, then diabetes mortality in the grandchildren increased” (Wikipedia).
Being told that we have a gene for x, y or z disease can lead to a helpless condition where we believe we have no control over what happens to us and so we gloomily go down a predestined path. “I can’t do anything about it, it’s in my genes.” Incidentally, self-fulfilling prophecies can come into play here. On the other hand, epigenetics puts us firmly in the driver’s seat. We can control our environment by controlling what we do, how we think, what we eat, drink, etc. It empowers us to write our own scripts. Gattaca is a beautiful example of this…I know it’s only a film but wasn’t it good!
Coming back to LBP, nothing has changed. Acute back pain is often caused by physical factors such as poor lifting technique, twisting, and prolonged sitting. Whereas with chronic back pain, there is the added contribution of mental, emotional and social factors. The good news is that whether it is acute or chronic, there are lots of things that can be done to prevent, treat and manage low back pain.