What a wonder of creation—the human brain! A structural and functional masterpiece composed of 86 billion nerve cells making more than 100 trillion connections and 84 billion supportive (glial) cells of different types designed for nerve-cell nurture and support and for the disposal of toxins and debris. Specialized blood vessels and defense systems collaborate to permit or restrict entrance to the brain’s local environment, regulate brain blood flow, and adjust the chemical composition of the soft and liquid brain tissue to keep the nerves functioning at their peak.
This incredible network of brain cells creates consciousness, thoughts, beliefs, memories, emotions, sensations, movements, and the ability to learn. The brain acts as the master control center for the entire human being, interacting with every other organ system as well as the microbes that live in and on the body. It’s an intricate biochemical “machine” designed with regenerative capacity in key areas (neurogenesis) that persist throughout life and with redundancy and adaptability that permit change according to circumstance (neuroplasticity).
Yet with all of the built-in resilience, one new person somewhere in the world experiences “brain failure” (dementia, neurodegeneration, cognitive decline) every three seconds, while only one case in four is diagnosed as such! The global dementia community is estimated to be approximately 50 million people, about the size of the population of Colombia or South Korea. It’s estimated to double every 20 years, thus reaching about 150 million by 2050—the population of Russia or Bangladesh. Alzheimer’s-type dementia (AD), characterized by the accumulation of tangles of protein fragments called tau and plaques of protein called beta-amyloid protein (BA), make up 60 to 80 percent of cases. Interestingly, the rate of new-case occurrence is highest among middle- and low-income countries, even though the number of existing cases is highest in Europe and North America. These alarming statistics have encouraged increasingly greater amounts of research, but a single widely effective drug has yet to be developed. Nonetheless, there is hope on the horizon.
The medical and research communities have begun to embrace what Dr. Alois Alzheimer himself hinted at in his reports of Auguste D in 1906 and Johann F in 1911. Dr. Alzheimer was reluctant to have his name associated with the presenile dementia he described because he doubted the notion of monocausality (one sole cause).
Today, more than 100 years later, it’s known that the majority of community-dwelling patients with dementia have mixed pathology, often including BA plaques and tau tangles alongside a wide range of other defects: small artery blockages, lacunae (tiny holes in the brain), the effects of inadequate oxygenation, and small bleeds.
Additionally, there is overlap in these findings among persons with and without AD. These facts, along with the failure of drugs directed to BA and tau, places in question the “one sole cause” idea, and diminishes the likelihood of finding a “silver bullet” drug to deal with this complex, chronic condition. One recent alternative view is of dementia being a kind of “brain failure,” much like heart or kidney failure, slowly, progressively accumulating the effects of multiple insults that silently begin some 20 years before thinking and memory problems become noticeable. Strange as it may seem, this alternative view presents the world with hope.
Once Alzheimer’s-type dementias (ADs) are placed in a multiple-risk-factor basket similar to other chronic diseases, the comprehensive lifestyle-intervention approach to prevention and treatment as encouraged by Adventists since the late 1800s becomes reasonable to pursue. But, as with other organ-system failures, a deep and broad understanding of risk factors, pathways of abnormal function, and individual variations in what causes AD and how it shows itself become necessary.
With this view it’s easier to accept the idea that plaques and tau-tangles may be a result of or contributors to the processes that lead to a specific kind of brain failure. Rather than initiating AD, plaques and tangles may defend and protect the brain from chemical stress and toxic brain insults, even while their presence worsens nerve-cell nurture and intercell communication.
Embracing multiple potential “causes” and contributors to AD allows consideration of diverse possibilities: invading bacteria from the mouth, abnormalities such as insulin resistance, hormonal deficiencies, excessive blood homocysteine, and zinc deficiency, to name a few. It also provokes examination of how poor air quality, fungal (mold) infestation, dietary inadequacies, herpes virus infection, inability to distinguish between common scents, previous concussion, hyper-caloric diets, inadequate overnight fasting, loneliness, unmanaged hypertension in earlier life (negative), and the development of hypertension in later life (probably protective) modify AD risk. In fact, with this view anything that tips the balance so that nerve-cell death outpaces new nerve-cell birth is a potential contributor and thus a potential therapeutic target. Hope is alive!
Reading, learning to play a musical instrument or a new language, creating artistic works, participating in social events, dancing, playing board games, and other activities that require physical, mental, and social engagement are associated with preserved thinking skills later in life and a reduced risk of AD. Music therapy increases self-expression and decreases agitation and anxiety among AD sufferers. Adequate, restful sleep as well as exercise are essential for new cell birth and growth in the areas of the brain that control learning and memory. Sleep improves BA plaque clearance from the brain tissue; exercise stimulates new brain-cell birth through its effects on chemical growth factors in the brain along with its universal circulatory benefits.
But even though isolated lifestyle interventions have their place, comprehensive, intensive, personalized lifestyle therapy has a growing, positive track record among motivated individuals with early intervention for their chronic diseases. The same appears to be true for AD sufferers. The recently reported cases of more than 100 AD patients treated by different physicians using a standardized, individualizable protocol showed documented improvement in thinking skills, memory and learning ability, and/or improvement in lab and imaging studies.
In another report researchers successfully targeted and reduced the bacterial load of an established brain infection (by an oral bacterium), blocked BA plaque formation, reduced brain inflammation, and rescued damaged nerve cells in the memory areas. A combined approach to mitigating risk factors and treating multiple specific targets simultaneously may be the way to proceed.
The list of risk factors for dementia is long and growing. In addition to those already mentioned, some are potentially modifiable: tobacco smoke, obesity, prior stroke, poor early-life educational attainment, type 2 diabetes, physical inactivity, alcohol use, poor neonatal and infantile diet, less than ideal omega-3 intake, hormonal insufficiency or imbalance, chronic (dis)stress, diets high in processed foods, food sensitivities, poverty, intestinal bacterial imbalance, social isolation, systemic inflammation, gingivitis, and specific genetic-profile carrier status are among them. All may be potential targets to prevent and/or to treat AD.
In London on December 11, 2013, 109 scientists from 36 countries called upon the G8 countries to make prevention of dementia one of their major health aims. They strongly recommended: “Tell people that adopting a healthy lifestyle may help to ward
off dementia as it does for other diseases.” Could we not add in 2019: Prevention is not only better than cure, preventive measures taken together are the “cure” to slow, halt, or even demonstrably reverse various aspects of cognitive decline?
Hope is here—thank God!
Zeno L. Charles-Marcel, M.D., is an associate director of Adventist Health Ministries at the General Conference of Seventh-day Adventists.
