One very important gene that has been researched in association with Alzheimer’s disease is the APOE gene, which is involved in carrying cholesterol and other fats in your bloodstream.
Late-onset Alzheimer’s disease (after age 60) is thought to be influenced both by genes and by environmental factors, so keep in mind when looking at your genetic risk that your genes are only one part of the equation when it comes to Alzheimer’s (and many other diseases!). But knowing your risk can help you to understand the importance of doing all that you can to prevent AD.
Your APOE type is defined as different alleles (ε2, ε3, or ε4), and you will have one APOE allele from each parent.
From the NIH website:
- “APOE ε2 is relatively rare and may provide some protection against the disease. If Alzheimer’s disease occurs in a person with this allele, it develops later in life than it would in someone with the APOE ε4 gene.
- APOE ε3, the most common allele, is believed to play a neutral role in the disease—neither decreasing nor increasing risk.
- APOE ε4 is present in about 10 to 15 percent of the population and in about 40 percent of all people with late-onset Alzheimer’s. People who develop Alzheimer’s are more likely to have an APOE ε4 allele than people who do not develop the disease.”
|APOE Allele||rs429358||rs7412||Risk of Alzheimer’s|
|ε2/ε2||TT||TT||lower than normal|
|ε2/ε3||TT||CT||lower than normal|
|ε2/ε4||CT||CT||slightly higher than normal|
|ε3/ε4||CT||CC||higher than normal|
Again, your genetic risk isn’t the only factor involved in getting Alzheimer’s Disease. Some people who have the highest risk factors will never get the disease.
Lifehacks for Preventing Alzheimer’s Disease:
If you are at an increased risk of Alzheimer’s, the key is to use this knowledge to do all that you can to decrease your risk. Below are a few studies that I’ve read through on the topic. This is not an exhaustive list by any means, and I highly encourage you to keep up to date with current information on the topic.
Circadian Rhythms, Sleep, and Melatonin:
From what I’ve read on the topic, number one on my list for preventing Alzheimer’s is to block blue light at night with some nerdy-looking orange glasses.
Quite a few studies have found a link between sleep quality and the risk of dementia or Alzheimer’s. Our natural circadian rhythm causes melatonin to rise in the evening and stay elevated until morning. Light in the shorter, blue wavelengths signals through receptors in our eyes to turn off melatonin production in the morning. Our modern reliance on lights at night, especially from TVs and phones, is disrupting the natural circadian rhythms.
Blue-blocking glasses, worn in the evening for several hours before bed, have been shown to increase natural melatonin production by about 50% in just two weeks. More and more research studies are showing a connection between circadian rhythm disruption, melatonin, insulin regulation, and healthy brain aging.[study][study][study] Trials are also evaluating the use of melatonin supplements for Alzheimer’s[study].
There have been several studies showing that both aspirin and non-aspirin NSAID use reduced the risk of Alzheimer’s Disease. Keep in mind that these are population-wide studies that don’t take into account genetic differences; you also need to weigh the risk of liver damage from long-term NSAID usage. Two good studies to read: Nonsteroidal Antiinflammatory Drugs and the Risk of Alzheimer’s Disease, Anti-inflammatory drugs and risk of Alzheimer’s disease: an updated systematic review and meta-analysis
There have been several studies that link cardiovascular health markers to the risk of Alzheimer’s. One study showed that an elevated homocysteine level is associated with higher risk of Alzheimer’s. Homocysteine levels are often genetically related to your MTHFR genes, methylation, and your B6 and B12 levels.
Additionally, staying active, eating well, and keeping your blood pressure low should lower your risk of Alzheimer’s.
A 2014 study found that for older adults who carry the APOE e4 polymorphism, light to moderate drinking increased their risk for cognitive decline. From the study: “Light and moderate alcohol consumption during late life was associated with greater decline in learning and memory among APOE e4 carriers, whereas light and moderate alcohol consumption was associated with an increase in learning and memory among non-APOE e4 carriers. There was not a significant interaction between midlife alcohol consumption status and APOE e4 on the trajectory of learning and memory.[ref]”
There have been lots of studies on antioxidants and Alzheimer’s disease; unfortunately, most are contradictory or inconclusive. Eating a healthy diet is, of course, always a good idea. Luteolin, an antioxidant flavonoid, has been studied recently with interesting potential as far as Alzheimer’s.[ref]
One mineral that has been tied to a reduced risk of Alzheimer’s is lithium. Lithium is naturally found in food sources; most people consume to be between .1 and 1 mg per day from food. High doses of lithium, such as prescription doses for bipolar disorder, come with side-effects and long-term health risks — along with a decreased risk of dementia. But what about low doses of lithium as a mineral supplement? One study showed that low doses of lithium helped AD patients to have no decrease in cognitive impairment over 15 months. You can buy lithium in 5mg doses as a supplement. There are interactions between lithium and several prescription drugs, so always check before starting any supplement. Here is another source that looks at several studies on lithium.
- From the Alzheimer’s Drug Discovery Foundation, an article on APOE4 and prevention ideas that don’t work as well for APOE4 carriers: http://www.alzdiscovery.org/cognitive-vitality/what-apoe-means-for-your-health
- Very interesting article on the discovery of the APOE link to Alzheimer’s and current research: http://www.nature.com/news/alzheimer-s-disease-the-forgetting-gene-1.15342
- SNPedia on APOE: http://www.snpedia.com/index.php/APOE
- Stanford slide show on Alzheimer’s: http://stanford.edu/class/gene210/files/projects/Gen210AlzheimersDisease.pdf