Lifestyle

In contrast, up to 14 percent of Alzheimer’s cases diagnosed worldwide are probably attributable to smoking. Tobacco carries a major stroke risk, and strokes in turn increase dementia risk and also lead directly to an increased amyloid burden in the brain and oxidative stress. The good news is that the risk in former smokers is the same as in nonsmokers. Intervention studies to demonstrate cause and effect are difficult to carry out due to a lack of long-term compliance, both for smoking cessation and for comprehensive dietary changes. However, it can be shown that the cognitive abilities of people who have quit smoking develop significantly better over time than those of people who were unable to do so. Exposure to secondhand smoke is also associated with an increased risk for Alzheimer’s and other forms of dementia.

Dementia and cognitive decline also repeatedly occur with polluted air. Interest in the effects of air pollutants was sparked 20 years ago by the study “Air Pollution and Brain Damage.” For it, the brains of dogs in cities with high air pollution were compared with those from cities with low air pollution, and pathology similar to that seen in Alzheimer’s was found. Magnetite nanoparticles in the human brain suggest that pollutants from traffic exhaust can enter the brain directly through the nose via the olfactory nerves, but they could also indirectly lead to brain damage via systemic inflammation.

Alcohol-related dementia is referred to as a silent epidemic. Excessive alcohol consumption can play a role in up to 24 percent of dementia cases. And low alcohol consumption? The hope that low alcohol consumption might even be beneficial for cognition was disappointed by a Mendelian randomization study finding that alcohol consumption at most leads to an earlier onset of Alzheimer’s. The good news is that even heavy drinkers who stop drinking can regain lost brain volume and cognitive function with prolonged abstinence.

Don’t kiss your memories away

To reduce risk, you also have to be careful who you make out with. Beta-amyloid has been well conserved in evolution. The human variant has existed for at least 400 million years and is now found in most vertebrate species. So it must have some benefit. Historically, survival of the fittest has been less about predator-versus-prey combat than about an irreconcilable “us versus them”—namely, the microbial threats lurking for us. Beta-amyloid may be part of our immune system, an antimicrobial peptide that protects us from brain infections. It has proven antibacterial, antifungal, and antiviral against a range of common pathogens. For example, temporal lobe samples from Alzheimer’s brains show that they can kill Candida yeast fungi, a cause of fungal meningitis, better than the temporal lobes of people who died from other causes.

Beta-amyloid also binds to herpes simplex virus 1 (HSV-1), resulting in a protective viral entrapment. HSV-1 is the virus that normally causes herpes, or cold sores, but it also attacks the brain. Could infection with this widespread virus trigger amyloid deposition because the body is trying to fight it, which then ultimately accidentally results in Alzheimer’s?

I was surprised to find about 100 scientific publications linking HSV-1 infection with Alzheimer’s. In a study with tens of thousands of participants, scientists found that in people with oral (HSV-1) or genital herpes (HSV-2), the likelihood of developing dementia during the 16-year follow-up was more than twice as high. Even more compelling (and good news) is that HSV patients who took antiviral drugs (such as aciclovir) were 90 percent less likely to develop dementia than people with untreated HSV. Unfortunately, there are still no approved vaccines against HSV-1, but you can reduce your risk of infection by avoiding kissing people with an active oral infection or sharing utensils, cups, water bottles, towels, and lip balm with them (although asymptomatic viral shedding can also occur).

A brain wash every night

Sleep is a great mystery. It must be vital if it has withstood the selective pressure in all animal species to eliminate such a vulnerable state. In fact, admittedly shameful experiments have proven that animals kept awake long enough die after 11 to 32 days. One function of sleep is the removal of toxic waste, as a newly discovered drainage system in the brain shows. This could explain why PET scans show a substantial buildup of beta-amyloid in critical brain regions after just a single all-nighter. Learn more about this fluid-transport network, the so-called glymphatic system, in my video see.nf/brainwash.

Unfortunately, this filtering system of the brain appears to decline with age. More about the role sleep position may play can be found at see.nf/glymphatic. (Teaser: Sleeping on the right side can increase brain drainage.)

Can melatonin help?

How about using melatonin to improve sleep quality, in the hope that it will also dispose of the debris? There was an interesting case report about identical twins. Both had Alzheimer’s, but only one received melatonin. This one seemed not only to sleep better, but also to have less memory impairment. In rats with an artificially accelerated aging process, an Alzheimer’s lab model, melatonin improves memory, but what about in humans?

Overall, seven randomized placebo-controlled double-blind studies of melatonin for the treatment of Alzheimer’s have been conducted in hundreds of patients, lasting between 10 days and 24 weeks. Those who received melatonin slept better, but unfortunately, the melatonin did not bring about any improvement in their cognitive abilities.

Growing waist, shrinking brain

People who are overweight have a one-third higher dementia risk, and those who are obese in midlife see the risk rise to about 90 percent. In my video see.nf/obesitydementia, I go into these data and show how excess body fat can impair cognition at any age, which occurs in parallel with structural differences in the brain. As the waist grows, the brain seems to shrink, perhaps due to inflammation and oxidative stress, both of which are part of obesity. According to a meta-analysis of 20 studies, mental performance is significantly improved on many levels even with moderate weight loss. However, there are still no studies on whether losing weight also translates into a normalization of Alzheimer’s risk.

Train your brain

If cognitive abilities improved in weight-loss studies, that could also be due to physical activity. I have summarized all the important intervention studies on this in see.nf/exercisebrain. More exercise tends to improve the cognitive abilities of adults with normal cognition or mild impairment. Based on a meta-analysis of nearly 100 randomized controlled studies, total exercise time—about 52 hours in all—may be more important than the duration of the exercise sessions, weekly frequency, program duration, or intensity for demonstrating a benefit. However, once dementia was present, exercise could no longer slow cognitive decline.