Many people are scared of death, but often tell me they’re more frightened of dementia. “I can’t face that,” one patient told me, “I can’t do that to my family.”
So how to stop it? One Swedish study shows a way.
It includes a follow up of 44 years. Persistence can pay off.
In 1968, Swedish researchers put 191 mid-life women on a cycle ergometer, testing their peak workload and endurance. Then they waited.
After controlling for the usual variables affecting atherosclerosis like smoking, blood pressure, lipids and drinking, they tracked the participants over four decades. About a third of a “low fitness” group developed dementia. Five percent of the “high fitness” group did. After controlling for all the variables they could, the high fitness folks appeared to experience dementia about 11 years later than those who rarely exercised.
Small numbers, yes. Consistent with many other studies, also yes.
Moving literally makes us more biologically intelligent.
So are there well placed national programs telling people to prevent death and dementia by moving? Explaining that even small bursts of activity make the body healthier, including ones that take seconds to minutes?
No. Instead we’re mired in vastly more expensive approaches that may not turn out at all.
Or make things worse.
The New FDA
Scott Gottlieb has won many plaudits as the new FDA director, trying to create different approaches to drug approval. Big Pharmaceutical companies have remarkably ineffective in the last few decades coming up with drugs materially changing public health. Lack of innovation has made their bottom lines suffer.
But preventing dementia has remained a major focus of research. The commercial prospect is enthralling – drugs that might need to be taken by most or almost the entire population for decades to prevent an illness that terrifies nearly everyone. It is no surprise that tens of billions have been spent in this pursuit, perhaps in excess of $100 billion all told.
The results so far? Interesting research, and a commercial goose egg.
The drugs have not worked.
Mainly they have focused on amyloid, the constant bugbear of Alzheimer’s research. Prevent amyloid buildup and you will prevent Alzheimer’s.
That the story is a lot more complicated has escaped Big Pharma. In the Okinawa Project, people dying past the age of 100 were autopsied and generally found to have “horrible” Alzheimer’s disease on neuropathology.
Except lots of them were not clinically demented. Alzheimer’s changes in their brains, certainly. But their relatively clean arteries appeared to have prevented dementia.
Dementia is not all about amyloid plaques. Alzheimer’s in particular is a different disease in different age groups, with older sufferers showing proportionately far less amyloid filled plaques than those who get the disease young.
But don’t tell that to the drug companies, who are still pushing amyloid as the main dementia cause. Now the FDA’s new policies may make it easier for them to gain commercial acceptance for their products.
For one of the main aims of Gottlieb’s often innovative approaches is to use “biomarkers” as the basis for drug approval, not “hard endpoints” like death and dementia.
Less amyloid in the brain, your drug gets approved.
This is a very tricky thing. Biomarket manipulation was used for many years to justify lipid decreases as the basis for drug approval. Statins’ effects were proclaimed entirely the result of their formidable ability to lower cholesterol. It took years for people to realize that stabilizing endometrial membranes was a very large reason they worked so well.
The next move on heart disease was to take another “biomarker” approach on lipids. People with lots of high density lipoproteins had less heart disease. So increase their number, and you should get less heart attacks, right?
Many billions were spent developing drugs to do just that. The drugs indeed increased HDLs. They also killed people faster.
The biomarker approach led to increased mortality.
People desperately want to prevent dementia. Many researchers feel they must provoke changes years, even decades before clinical endpoints like dementia develop.
Yet the story of dementia is vastly more complicated than amyloid levels. And these approaches could, very expensively, produce the same results as the HDL trials.
Hard endpoints, like death, are hard to fake. To get people to take drugs for decades that may not work is not the way to go. And there are alternatives.
Cycling Through Life
Many have recently been entranced by a study from the University of Birmingham on older bicyclists. A group of 125 cyclists aged 55 to 79 agreed to be followed through their routine jaunts to work and through the countryside.
Cycling seems a perfect way to improve biological intelligence. You travel through different environments, challenging your immune system with exposure to more pollutants, viruses, and pathogens. You get biological clock setting and mood enhancing natural light, not always abundant in England. Your body must deal with errant branches, texting motorists and plaguing potholes, teaching the body how to adapt second by second.
The results? Many of these long haul cyclists, many doing 20 kilometers a day or more, demonstrated the body fat and cholesterol levels of youth. For the men, the testosterone levels of youth. For all the group, the T cell numbers of young people. Another British study showed regular cycling cutting the risk of cancer and heart disease by 45%.
Is it strange to recognize that lesser prospects of dementia are also part of the cycling package?
Magicless But Magic
People may want a pill, but ways to prevent dementia are at hand. They require effort – walking, bicycling, paying attention to food – items that enhance life in many ways, including increasing the measure of delight in one’s life. Biological intelligence can be increased by simple and consistent measures in reach of most of us. It’s time to grab them.