Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) in New Zealand affects about 0.4% of the population.
There will be up to 100 affected among our university student population.
It is not surprising then when I mention our ME/CFS research in a lecture, those affected make contact.
When they talk to me they initially seem healthy, bright and interactive (invisible illness
But having been part of an ME/CFS family now for 30 years, I understand they have rested and prepared for the visit, and after relatively short conversation fatigue often sets in.
This phenomenon explains why health practitioners and social agencies without a good knowledge of the illness are perplexed; indeed there are examples of Work and Income-required designated doctor consultations of seven minutes resulting in pronouncement that the ME/CFS patient can work full-time, despite being housebound long-term by the ravages of their “invisible” illness.
For this reason my research group’s focus has been to lift the “veil of invisibility” and find biological explanations for the illness.
We have studied multiple classes of human biomolecules and how they differ between ME/CFS patients and healthy controls.
We have discovered changes in the production of proteins that make up the complexes making energy in our cells, and patient-specific defects in the functioning of these complexes.
Significant changes have been discovered in the expression of genes in the DNA, particularly encoding proteins involving inflammation and the immune system, as well as metabolism and energy production.
The tags on these genes (called the epigenetic code) that regulate this expression show many differences between ME/CFS patients and healthy controls. These results provide an explanation why patients are so debilitated by their illness.
Major research centres, set up in 2019 at Stanford and at Harvard Universities, after a resolution in the US senate acknowledging the seriousness of ME/CFS, give hope of our completely understanding the pathophysiology and finding therapies for the disease.