The increased risk of Alzheimer’s disease in football players is certainly a wake up call for the NFL. Yet, the observation may also have profound implications for our society and for the medical establishment at large.
No one was surprised when Muhammad Ali developed Parkinson’s disease after his stellar but traumatic boxing career. No one should be surprised when football players develop Alzheimer’s disease or amyotrophic lateral sclerosis (ALS) or strokes after their careers. Sooner or later, if you knock heads at high speed with tremendous force for a long enough period of time, it’s no surprise that some form of brain injury develops which heals either with or without permanent damage. The fact that is so surprising, and profound in its implications for how we should view our own individual risk for Alzheimer’s, comes from the observation that most NFL athletes do not develop Alzheimer’s (or as it’s termed “chronic traumatic encephalopathy”) despite knocking their brains against their cranium for six months of the year over a period of many years.
Many of us are aware of the genetic predisposition to develop Alzheimer’s disease with the ApoE4 genotype. While the mechanisms responsible for this genetic predisposition are still poorly understood, patients with this allele are at increased risk. Yet, only 40-65% of Alzheimer’s patients have the allele, and many patients at highest risk with two copies of the allele (E4/E4), do not get the disease. So, what does this mean? Does genetic predisposition explain the majority of the risk for Alzheimer’s? No. In some patients, in some complex set of biochemical predispositions and interactions, “cognitive reserve” is eroded more quickly than others. But, what drives our cognitive reserve and what does the obvious association between brain injury leading to Alzheimer’s like illness in NFL players help dispel myths about Alzheimer’s disease—a disease that today has little hope of improvement, and is associated with much despair for affected persons and their families?
The truth about Alzheimer’s that many pathologists and neurologists have understood for decades is that: 1) Alzheimer’s isn’t a single disease but represents a late stage injury pattern to the brain due to many causes; and 2) many patients with classical Alzheimer’s plaques and brain pathology do NOT have clinical dementia. As with many neurodegenerative disorders such as ALS and Parkinson’s, the correlation between the severity of brain lesions and the clinical state of the patient is not linear.
So, if the classical markers of a disease are not well correlated to how the patient is doing, then there must be more to the puzzle than meets the eye. Certainly, the markers aren’t necessarily causing the clinical symptoms since patients with lots of brain pathology may have few or no symptoms. These “outliers” hold important clues to how the brain can repair, regulate and adjust to its environment, even an environment with repeated injury, so that we can enable our own biosystem to optimize this “healing” state on our own.
If you examine the medical histories of known Alzheimer’s patients 20 years prior to the development of their symptoms, you find that they have a higher “burden of nuisance symptoms” and chronic diseases such as diabetes, hypertension, cardiovascular disease, other neurodegenerative diseases and depression. I wrote about this in an earlier blog. The longer the body is exposed to this burden (which represents an early warning system), the more we erode our cognitive reserve to the point that memory and behavioral symptoms emerge.
Our bodies have multiple defense systems such as those that manage immunity, digestion and distribution of nutrients, stress, neural reflexes, and detoxification. Optimize these systems and we can either delay or even prevent Alzheimer’s disease.
Do we know that it is possible to protect our cognitive reserves? When I directed the Ischemia Research and Education Foundation from 1995-2000, the world’s expert institution on the effects of heart surgery and cardiopulmonary bypass on the brain, heart and kidney, we noted that brain injury during heart surgery was much more common than previously recognized,[1] and increased with age (less cognitive reserve). Over a five-year follow-up period, those patients who developed subtle measures of brain injury were more likely to develop clinical symptoms of Alzheimer’s disease. The lesson: if we erode our cognitive reserve as a result of a traumatic event(s), and then count on medications to suppress our chronic symptoms of arthritis, diabetes, high cholesterol and poor dietary choices, our cognitive reserve continues to deteriorate. And, eventually, brain symptoms develop over time.
It therefore behooves us to think about Alzheimer’s as a systemic illness with end-stage damage in the brain. It is an illness that results from longstanding imbalances in our body’s systems that slowly erodes our cognitive reserves, and in some persons more quickly than others. It also emphasizes that a single receptor based classical pharmaceutical approach will not likely lead to a cure. Since characteristic pathology in the brain is not likely a direct marker causing the memory loss and behavioral changes associated with Alzheimer’s, but rather represents a set of more general markers, we don’t yet know what pharmacologic targets to use as potential therapies that cause the symptoms that make us so fearful of Alzheimer’s disease.
The increase in Alzheimer’s in NFL players engages us in a new discussion for an enigmatic disease that still has no standard of care or meaningful therapy. As the disease that is expected to become the most expensive medical condition in the world by 2030, we should take our overall health more seriously and choose a more integrative approach towards wellness than our “one-pill for one-symptom” strategy we still employ today.
[1] Roach, G.W., Kanchuger, M., et al. 1996. Adverse Cerebral Outcomes after Coronary Bypass Surgery. New England Journal of Medicine, 335(25).Retrieved from http://www.nejm.org/doi/full/10.1056/nejm199612193352501.