Dear Dr. Roach: Up until recently, the recommended amount of sleep was seven and a half to eight hours per night. Now a study says people who get more than six and a half or less than three hours of sleep a night are headed for dementia. What’s the consensus about sleep?
M.S.
Studies are published all the time (so often that it makes my job a challenge), and those that upend the standard teaching tend to get airplay in the media.
However, I think there is a consensus based on decades of sleep research, and that is that lower amounts of sleep are not good for you, neither for your length of life nor for the likelihood of developing dementia. A very well-done study was just published confirming that persistent short sleep duration (defined as six or fewer hours) during their 50s, 60s and 70s puts people at a roughly 30% increased risk of dementia.
Long sleep duration — that is, greater than eight hours — was associated with a lesser, but still increased, risk of dementia. However, people who sleep much longer than the average may have an underlying condition that puts them at increased risk rather than it being the sleep itself. When the authors of the study adjusted for additional conditions, the effect of long sleep on dementia was no longer significant.
The optimal amount of sleep for overall health still appears to be around seven hours, but every person is different. People who feel well rested with less sleep, and who naturally wake up at a given time (rather than force themselves to get up) are at lower risk for development of complications of poor sleep.
Dear Dr. Roach: I have been advised that I have a deadly disease called myocardial amyloidosis. If this is true, are there successful treatments?
E.J.R.
Amyloidosis is a condition where one of a number of amyloid proteins are deposited in tissues, outside of cells. The deposits can interfere with the proper functioning of the tissues. Deposition of abnormal proteins in the brain is the major cause of many types of dementia. Amyloidosis can also affect the kidneys, lung, skin and other organs.
In the heart (“myocardial” means “heart muscle”), these abnormal proteins interfere with the ability of the heart to function, and eventually lead to heart failure, meaning that the heart can’t pump enough blood to take care of the body’s needs. Amyloid protein can also block the arteries of the heart, leading to heart attack, or may damage the electrical conduction system of the heart, leading to heart block or abnormal rhythms.
Years ago, the expected lifespan upon the diagnosis of cardiac amyloidosis in a person having symptoms was only six months. Newer treatments have extended the prognosis to an average of more than five years. Partly, this depends on the type of protein deposited — the most common are called light chain (“AL”) and transthyretin (“ATTR”).
Light chain amyloid is closely related to multiple myeloma and similar blood abnormalities. ATTR amyloid is caused by a binding protein, which can be either normal (“ATTRwt”) or abnormal (“ATTRv”). As you might guess, the treatment also depends on the type of amyloid protein, with chemotherapy and stem cell transplantation used for AL amyloid. ATTR amyloid is often treated with tafamidis. Liver transplantation is considered for people with ATTRv.
As complicated as that all is, I’ve only scratched the surface of this complicated disease. You can read more and get suggestions on treatment centres at .
Dr. Roach regrets that he is unable to answer individual letters, but will incorporate them in the column whenever possible. Readers may email questions to [email protected]
