There are a lot of diseases that I would like to prevent, but one that I find particularly concerning is dementia. When my grandfather died many years ago, he was clearly losing his short-term memory and suffering from dementia and confusion. He was transferred from the assisted living portion of the facility he lived in, to a locked-down wing for wandering Alzheimer’s patients. It was tough to see him lose his independence.
That was in 2000, and Alzheimer’s awareness wasn’t as strong as it now is. Currently, one in eight seniors has Alzheimer’s Disease (AD), now affecting over four million people in the U.S. That number is expected to triple by 2050. Since 2010, the mortality rate from AD has increased by over 68% (Alzheimer’s Association, alz.org), and is now the sixth-leading cause of death in the U.S. It is increasingly becoming a financial strain on the healthcare system and a significant source of stress on families, especially those who feel obliged to keep the AD family member in their own home for as long as possible.
Accurate and early diagnosis is critical. The diagnostic hallmarks of AD are the presence of beta amyloid plaques and neurofibrillary tangles in the brain, which may be identified on a MRI or PET, however these imaging tests are not refined enough to be entirely precise at this time. As researchers search for a cure for this looming epidemic, their first task is to identify the cause. On the list to date are genetics, inflammation, environmental toxins, free radical damage, and nutrient deficiencies.1
None of the causes on the list are definitive, but it seems that the presence of more than one increases the likelihood of AD development. Inflammation is one of the top potential causes. It can easily be tested for by using markers such as C-Reactive Protein and immune-related cytokines, but none are specific to diagnosing AD. Inflammation can also manifest in many different ways depending on the individual, such as joint pain or cardiovascular disease, so its presence does not necessarily lead to AD.
Researchers have speculated that the use of NSAIDS may help ward off AD by taming inflammation. Interestingly, several epidemiological studies supported this theory when they found that people with arthritis, who took NSAIDS as therapy, had lower rates of AD.2 Unfortunately, NSAIDS have significant side effects, and thus far, clinical trials that targeted NSAIDS as a treatment for AD have not been fruitful.3
As an alternative to NSAIDs, several studies have indicated that curcumin, derived from the Indian spice turmeric, may be effective in halting or slowing the progression of AD. Possible real-life evidence may be that in India, where curry consumption is significant, there are much lower rates of AD than in the US. Research studies also support this treatment. One small study experimented with treating immune cells (macrophages) with curcumin, and it was shown that the treated cells were more effective in uptake and ingestion of beta amyloid plaques than were untreated cells.4 Curcumin is a known anti-inflammatory with minimal side effects which acts on key inflammatory substances, such as COX-2 and inflammatory cytokines. It has a significant antioxidant effect and can also bind to heavy metals, which are also implicated as a cause. Curcumin has been shown to cross the blood-brain barrier and in mice studies, it was shown that low doses of curcumin lowered plaque levels by 43%. It protects nerve cells from beta amyloid destruction, and may someday be proven to help prevent or possibly reverse AD.5 Because curcumin is poorly absorbed, be sure to try a formula that contains bioperine or Meriva for exponentially-improved bioavailability.
Free radical damage is also implicated in the progression of AD since amyloid plaque causes oxidative stress and neuronal damage.6 Some of the causes of increased oxidation may be due to excess levels of iron, copper, and zinc in brain tissue and mitochondrial abnormalities. Antioxidants remain a hopeful yet unproven treatment, due to an abundance of conflicting information found in the scientific literature.
Fortunately, scientists are looking at how nutrition can protect our brains. One large, French study shows that low dietary intake of B vitamins, dietary fiber, and omega-3 fatty acids is associated with higher levels of both cognitive and functional decline.7 Other studies show that Mediterranean diets–those rich in plants and healthy fats–are related to lower rates of AD. A large study showed increased survival time in AD patients who took vitamin E, with or without medication8 Some research found that higher consumption of omega-3 fats was linked to lower rates of AD.9
Supplementation with antioxidants has yet to prove unequivocally beneficial, as many studies failed to see them make a significant impact.10 But if you have ever watched a loved one progress with AD, you might agree with my personal plan for prevention. Consume an abundance of organic fruits and vegetables, throw in some curcumin,
fish oil, and antioxidants every day, and don’t just wait for the scientists to work out an agreement on this one.
1 Nat Rev Neurol. 2011 March ; 7(3): 137–152
2 Neurobiology of Aging, vol. 22, no. 6, pp. 811–817, 2001
3 The Lancet Neurology, vol.1, no. 5, pp. 279–284, 2002
4 J Alzheimers Dis. 2006;10:1–7
5 J Nat Prod. 2002;65:1227–31
6 J Biomed Biotechnol. 2002; 2(3): 120–123
7 Br J Nutr. 2009 August; 102(3): 419–427.
8 American Academy of Neurology (2008, April 17
9 Neurology. 2012 Jun 5;78(23):1832-40
10 Ann Pharmacother. 2005 Dec;39(12):2073-80