When two groups of people were assigned different breathing exercises for 40 minutes a day participants ended up with dramatically different levels of amyloid beta, the peptide associated with Alzheimer’s disease. Whether one exercise can stem the rising tide of dementia in society remains to be proven. However, after the failure of more than a dozen drugs that showed promise in pre-clinical trials, anything that looks like working in humans will attract attention.
The trial had 108 participants clip heart monitors to their ears while half spent 20 minutes calming themselves with pleasant music or peaceful thoughts. Their counterparts were instructed to breathe slowly in and out in time to a pacer on a laptop screen that cycled at 0.1 Hertz.
It might sound like the two were similar, both representing a chance to clear the mind of unpleasant thoughts and relax the body. However, a new paper reveals the effects were very different.
The heart rates of those in the calming arm of the trial steadied – indeed they were encouraged to watch the monitor results and keep things as level as possible. Meanwhile, the heart rates of those following the pacer (Osc+ in the trial’s terminology) rose as they inhaled and fell on the outbreath. Increased variability was the goal. Blood samples were taken before the start of the program, and after four weeks of twice daily participation.
The samples were tested for two forms of amyloid beta, which forms plaques in the brains of people with Alzheimer’s, and the Tau protein, whose intracellular tangles are another common feature of Alzheimer’s brains.
By the end of the trial the levels of both amyloid beta types in the blood of the Osc+ group were significantly lower than before they started. Disturbingly, amyloid levels rose in the calming thoughts (Osc-) group by even more than they fell in the Osc+ group. Would imagining walks on the beach or listening to pleasant music have been enough to calm participants down if they knew they’d be raising their dementia risk in the process? Changes to Tau levels were not significant overall, but showed a similar trend to amyloids among the younger participants.
The authors’ theory is that increasing oscillations in heart rate stimulate the parasympathetic nervous system. "We know the sympathetic and parasympathetic systems influence the production and clearance of Alzheimer's related peptides and proteins," said Professor Mara Mather of the University of Southern California in a statement. Parasympathetic activity declines with age, and the authors think this may contribute to age-related diseases such as Alzheimer’s.
The study didn’t test how long the effects lasted, and if they can be sustained through maintaining the exercises for months, not weeks. More importantly, however, it’s unclear how much difference reducing amyloid beta in the blood makes.
Alzheimer’s research has been divided for decades between those who see amyloid plaques as the cause of the disease and those who think they’re a symptom. Most of the researchers who take the latter position consider Tau proteins the true cause, so the lack of significant effects there may undermine the project.
The authors also acknowledge they don’t know whether the reduction in amyloid beta levels in the blood reflects lower production, clearance in the brain, or clearance through the kidneys. In the last case, it's possible levels are not reduced where they need to be, across the blood-brain barrier.
The study is published open access in Scientific Reports.