alzheimers
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Want to Remember Your Life Story? 3 Habits to Protect You From “Losing Your Mind” to Alzheimer’s Disease.

Think back to the last time you forgot something. Something you needed for work that got left at home. Something you needed from the grocery store that you forgot while there. It’s frustrating. Perhaps you’ve thought you were “losing your mind”.

Now imagine living like that every day, all day. Alzheimer’s disease is a frustrating and lonely disease, with no cure in sight. And yet there is plenty you can do to prevent or postpone the impact of Alzheimer’s disease. This is life-saving information for you and your aging loved ones. Lean in for simple, practical ways to protect yourself from “losing your mind” from Alzheimer’s disease.

DISCLAIMER: Before I begin any comments about health, I am required by law to make a disclaimer: “The following comments are not meant to diagnose or treat any disease, nor have they been approved by the FDA.” (By the way, any M.D. would have to make a similar disclaimer.)

The Research

Alzheimer’s disease is a global issue, with statistics growing in the wrong direction. 10% of people over the age of 65 are diagnosed with Alzheimer’s disease. That number jumps to nearly 50% of the global population for people over 85. It is not surprising that 71% of cases of Alzheimer’s disease occur within developing countries where life expectancy tends to be higher (Reiman et al., 2004).

In this month’s newsletter, we bring you the latest understanding of what causes Alzheimer’s disease, how it is being treated, and how you can prevent it from destroying your brain and the brain of your loved ones.

What is Alzheimer’s Disease?

Alzheimer’s disease is the leading form of dementia that progressively damages and destroys brain cells. Although it is most common in people over the age of 65, early-onset Alzheimer’s disease is a growing problem. In the brain of Alzheimer’s patients, the outer cortices of the brain shrivel up as the disease attacks areas of the brain involved in thinking, planning, and remembering. The hippocampus, a key region for memory formation, is highly impacted by the disease (Jaroudi et al., 2017).

The most common difference in a brain with Alzheimer’s disease is the loss of connection between brain cells (or ultimately the death of brain cells). In the most simplistic explanation, memories are formed as connections are made in the brain. When connections are lost, so are memories.

What is causing the loss of connection? Two things – plaques and tangles. Plaques are microscopic clumps of a protein fragment called beta-amyloid. Tangles are microscopic twisted strands of the protein tau. The presence of plaques and tangles interfere with brain cells trying to communicate with each other.

Current Approaches for Treating Alzheimer’s Disease

The diagnosis of Alzheimer’s disease is usually retrospective, meaning the disease and symptoms are already present. The predominant treatment plans involve minimizing symptoms, not targeting the source of the disease. Why? Even though it has been over 100 years since the discovery of plaques and tangles, scientists and doctors are still trying to figure out how to get rid of them (Profenno, Porsteinsson, & Faraone, 2010).

Billions of dollars have been spent searching for a drug to target the amyloid protein. 99.6% of clinical trials fail. Meanwhile, Big Pharma companies are bringing in upwards of 10 billion dollars a year in sales off the few drugs approved by the FDA (Cummings, Morstorf, & Zhong, 2014).

There is, however, some encouraging news when you look at Alzheimer’s disease through a different lens.

A New Hope – Reducing Neuroinflammation

Inflammation is the body’s natural “emergency” response from your immune system to fight off adverse events – bacteria, viruses, wounds, accidents, and toxins that can cause illness. Did you know your brain has its own separate immune system? It does!

There is a blood-brain barrier that blocks immune cells in the blood from reaching the brain. Hence, the necessity for the brain to have its own immune system. This system is led by microglial cells who work to remove invading germs and dead nerve cells. Neuroinflammation, then, is the response from the brain’s immune system to fight off unwanted “intruders” – in this case, plaques and tangles. The connection between neuroinflammation and the development of Alzheimer’s disease is providing encouraging hope for preventative treatments and slowing the progression. (Passamonti et al., 2019; Bachiller et al., 2018; Heneka et al., 2015).

Researchers have been studying ways to reduce neuroinflammation. There are many lifestyle habits you can start TODAY to reduce neuroinflammation to prevent and postpone the development of Alzheimer’s disease. Your destiny is not pre-determined by genetics. For 90% of people with Alzheimer’s disease, it is the interplay between environment, genetics, and lifestyle. The power of prevention is in your hands (Windblad et al., 2016).

3 Habits to Protect You From “Losing Your Mind” to Alzheimer’s Disease

1.   Stay Active – Cognitively

Alzheimer’s disease is defined as the loss of connection between brain cells and ultimately death of brain cells. To prevent or postpone this disease, work against that deterioration by building new connections and new brain cells (neurogenesis) through enriching learning experiences. Meaningful cognitive activity can reduce neuroinflammation.

Set goals for yourself (or elderly loved ones) of new things you want to learn each month/year, and then map out a plan of how you’ll boost your learning. It will take more than just asking Alexa to share an interesting fact. Take 10 minutes to dive deeper into the topic before moving on with your day. Read more non-fiction books, attend webinars, listen to stimulating podcasts, etc. If you (or your loved one) are retired, become a pseudo-expert on a topic and then volunteer to be a guest speaker at schools, churches, or community events.

2. Stay Active – Physically

Exercise can both prevent and slow the progression of Alzheimer’s disease (Paillard, Rolland, & Barreto, 2015). How? In short, exercise increases the levels of anti-inflammatory molecules in the brain and reduces pro-inflammatory molecules (Seo, Heo, Ko, & Kwak, 2019).

The great news is it doesn’t matter what you do to stay active. What matters is that you move your body. Aim for at least 5 days a week, ideally for 20+ minutes. Go for a brisk walk, bike ride, or swim. Borrow your neighbor’s exercise DVDs that they aren’t using and press play. If your go-to way to spend time with friends is to grab a drink or a meal, consider instead meeting up for a walk around a neighborhood or park. Or at least tack on a walk to the end of your meal. Your options are endless. The goal is the same – get moving.

3. Diet and Supplements

Let’s start with what to avoid. It is well established that a high-sugar, high-carb (that turns into sugar) diet increases your blood sugar levels (glucose). This can put you at risk of Type 2 Diabetes, cause inflammation, and add stress to your immune system. Patients with low metabolic rates for glucose is a common trait among Alzheimer’s patients (Gudala, Bansal, Schifano, & Bhansali, 2013; Matos, Macedo, & Rauter, 2017).

The key takeaway is this: stop putting so much demand on your body’s glucose metabolic system. For many people, it can’t keep up. And it’s leading to a laundry list of diseases – Alzheimer’s being one of them. How do you do that? Reduce the amount of sugar and carbs you are consuming. Consider where your diet is sugar-heavy: sugar beverages, white bread, candy, or alcohol. Aim to minimize at least one of these. I know they taste good. A daily soda or nighttime scoop of ice cream can be replaced with a cup of tea and a bowl of berries. I know it’s not quite the same, but your grandparenting years won’t be quite the same if you can’t remember them.

Instead, aim to fuel your brain with foods that reduce inflammation and improve your cognitive function. Foods high in antioxidants (berries, dark chocolate, nuts, and olive oil) are powerful anti-inflammatory tools. Complex carbs (brown rice, oatmeal, and sweet potatoes) help fuel your body and brain. Seek out more omega-3s from fatty fish (salmon, mackerel, sardines, and cod).

In addition to a brain-saving diet, many supplements have been shown to prevent or postpone the effects of Alzheimer’s disease. As always, do your own research and consult with a medical professional about the right supplement and dosage for you. Most can be picked up at your local health store or found online. Here are 10 well-researched supplements to consider:

Acetyl-L-carnitine: Studies report that this compound may reverse the memory loss symptoms of Alzheimer’s disease, as well as problems with focus (Ferreira & McKenna, 2017).

CoQ10: Coenzyme Q10 acts as an antioxidant and has been shown to prevent and treat symptoms of Alzheimer’s disease (Yang et al., 2015).

Curcumin: The yellow pigment in turmeric is called curcumin and holds all the power for its medicinal properties. Curcumin is a very powerful antioxidant and has anti-inflammatory properties. It is best absorbed when combined with a bit of black pepper (Zhang et al., 2018).

DHA (Docosahexaenoic acid): People with Alzheimer’s disease have lower than average levels of DHA. According to clinical trials, patients who took this supplement experienced almost immediate memory improvement (Patrick, 2019).

Galantamine: The FDA has approved the use of cholinesterase inhibitors (ChEls) to treat Alzheimer’s disease. Studies show they improve cognition, global function, behavior, and activities of daily living. Galantamine, one of several cholinesterase inhibitors, can be obtained from Life Enhancement on Amazon in its most natural form (Matsunaga, Kishi, & Iwata, 2014).

Gingko Biloba: This supplement has strong anti-neuroinflammatory properties that can prevent or prolong the symptoms of Alzheimer’s disease (Gargouri et al., 2018). Again, readily available on Amazon.

Magnesium: A specific form of this mineral, magnesium-L-threonate (MgT) rebuilds ruptured synapse, and restores damaged neural connections prevalent in Alzheimer’s patients (Wang et al., 2013).

Niacinamide: (Not to be mistaken as niacin) is a form of vitamin B3. High doses of niacinamide have essentially “cured” mice with Alzheimer’s disease. It is suggested to take relatively high doses and to take them frequently (Xie et al., 2019).

Phosphatidyl Serine (PS): This nutrient is naturally produced in the brain, and plays a vital role in neuron health and healing. Unfortunately, we produce less of it as we age; thus the need to supplement (Moré, Freitas, & Rutenberg, 2014).

Tocotrienols: As a member of the vitamin E family, this supplement speeds up brain healing by repairing cells and reducing oxidative stress (Chin & Tay, 2018).

Prevention will always be your best approach to avoiding any disease. Remember that, and you are on your way to being able to remember everything else as you and your loved ones age.

Remember, I am not a medical professional. Do not create a treatment plan based on this newsletter. Let this be a stepping stone of knowledge for you to continue on the path of informed prevention and care for you and your loved ones.

Citations:

Bachiller, S., Jiménez-Ferrer, I., Paulus, A., Yang, Y., Swanberg, M., Deierborg, T., & Boza-Serrano, A. (2018). Microglia in neurological diseases: a road map to brain-disease dependent-inflammatory response. Frontiers in cellular neuroscience12, 488.

Chin, K. Y., & Tay, S. S. (2018). A review on the relationship between tocotrienol and Alzheimer Disease. Nutrients10(7), 881.

Cummings, J. L., Morstorf, T., & Zhong, K. (2014). Alzheimer’s disease drug-development pipeline: few candidates, frequent failures. Alzheimer’s research & therapy6(4), 37.

Ferreira, G. C., & McKenna, M. C. (2017). L-Carnitine and acetyl-L-carnitine roles and neuroprotection in developing brain. Neurochemical research42(6), 1661-1675.

Gargouri, B., Carstensen, J., Bhatia, H. S., Huell, M., Dietz, G. P., & Fiebich, B. L. (2018). Anti-neuroinflammatory effects of Ginkgo biloba extract EGb761 in LPS-activated primary microglial cells. Phytomedicine, 44, 45-55.

Gudala, K., Bansal, D., Schifano, F., & Bhansali, A. (2013). Diabetes mellitus and risk of dementia: A meta‐analysis of prospective observational studies. Journal of diabetes investigation4(6), 640-650.

Heneka, M. T., Carson, M. J., El Khoury, J., Landreth, G. E., Brosseron, F., Feinstein, D. L., … & Herrup, K. (2015). Neuroinflammation in Alzheimer’s disease. The Lancet Neurology14(4), 388-405.

Jaroudi, W., Garami, J., Garrido, S., Hornberger, M., Keri, S., & Moustafa, A. A. (2017). Factors underlying cognitive decline in old age and Alzheimer’s disease: the role of the hippocampus. Reviews in the Neurosciences28(7), 705-714.

Matsunaga, S., Kishi, T., & Iwata, N. (2014). Combination Therapy With Cholinesterase Inhibitors And Memantine For Alzheimer’s Disease: Systematic Review And Meta-Analysis. Alzheimer’s & Dementia, 10(4), pyu 115.

Moré, M. I., Freitas, U., & Rutenberg, D. (2014). Positive effects of soy lecithin-derived phosphatidylserine plus phosphatidic acid on memory, cognition, daily functioning, and mood in elderly patients with Alzheimer’s disease and dementia. Advances in therapy31(12), 1247-1262.

Paillard, T., Rolland, Y., & Barreto, P. D. (2015). Protective Effects of Physical Exercise in Alzheimer’s Disease and Parkinson’s Disease: A Narrative Review. Journal of Clinical Neurology, 11(3), 212-219.

Passamonti, L., Tsvetanov, K. A., Jones, P. S., Bevan-Jones, W. R., Arnold, R., Borchert, R. J., … & Rowe, J. B. (2019). Neuroinflammation and functional connectivity in Alzheimer’s disease: interactive influences on cognitive performance. Journal of Neuroscience39(36), 7218-7226.

Patrick, R. P. (2019). Role of phosphatidylcholine-dha in preventing apoe4-associated alzheimer’s disease. The FASEB Journal33(2), 1554-1564.

Profenno, L. A., Porsteinsson, A. P., & Faraone, S. V. (2010). Meta-analysis of Alzheimer’s disease risk with obesity, diabetes, and related disorders. Biological psychiatry67(6), 505-512.

Reiman, E. M., Chen, K., Alexander, G. E., Caselli, R. J., Bandy, D., Osborne, D., … & Hardy, J. (2004). Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer’s dementia. Proceedings of the National Academy of Sciences101(1), 284-289.

Seo, D. Y., Heo, J. W., Ko, J. R., & Kwak, H. B. (2019). Exercise and neuroinflammation in health and disease. International Neurourology Journal23(Suppl 2), S82.

Wang, J., Liu, Y., Zhou, L. J., Wu, Y., Li, F., Shen, K. F., … & Liu, X. G. (2013). Magnesium L-threonate prevents and restores memory deficits associated with neuropathic pain by inhibition of TNF-alpha. Pain physician16(5), E563-75.

Winblad, B., Amouyel, P., Andrieu, S., Ballard, C., Brayne, C., Brodaty, H., … & Fratiglioni, L. (2016). Defeating Alzheimer’s disease and other dementias: a priority for European science and society. The Lancet Neurology15(5), 455-532.

Xie, X., Gao, Y., Zeng, M., Wang, Y., Wei, T. F., Lu, Y. B., & Zhang, W. P. (2019). Nicotinamide ribose ameliorates cognitive impairment of aged and Alzheimer’s disease model mice. Metabolic brain disease34(1), 353-366.

Yang, X., Zhang, Y., Xu, H., Luo, X., Yu, J., Liu, J., & Chuen-Chung, R. (2015). Neuroprotection of Coenzyme Q10 in Neurodegenerative Diseases. Current Topics in Medicinal Chemistry, 16(8), 858-866.

Zhang, K., Chen, M., Du, Z., Zheng, X., Li, D., & Zhou, R. (2018). Use of curcumin in diagnosis, prevention, and treatment of Alzheimers disease. Neural Regeneration Research, 13(4), 742-752.

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