The Relation of Diet, Exercise, Stress and Alzheimer’s Disease

I believe it’s important sometimes to cover a subject that ties my expertise to something outside my field of expertise. And since diet and exercise have such a profound effect on so many aspects, it’s important to look for these connections.

This is not an article about Alzheimer’s disease per se, but rather on many contributing factors that we have control over. It’s clear that Alzheimer’s disease is multifaceted in that there are many factors that contribute to its onset.

So I want to look at the aspects we have control over. And trust me, we have a lot of control in how we care for our bodies.

The basics of Alzheimer’s disease

No doubt most of you already know that Alzheimer’s disease is associated with memory loss. And that there are other symptoms that accompany memory loss, which include:

• Misplacing personal belongings
• Difficulty with common tasks
• Getting lost in places with which one’s familiar
• Difficulty with lifelong financial skills

There are a few more, but I want to look more into some of the physiological changes that promote the onset of Alzheimer’s disease. And then some of the external factors that can expedite the physiological changes leading to Alzheimer’s. Got all that?

Let’s break this down into the important aspects of the disease.

First, what are tau proteins?

One cannot discuss Alzheimer’s disease without mentioning tau proteins. So what are they?

The simplest explanation is a group of proteins associated with the microtubules of axons in the neurons. One Tau protein in particular is found in abundance in individuals with Alzheimer’s disease.

The Tau protein I’m referring to is called neurofibrillary tangles if you’re curious. They become that way because they are hyperphosphorylated. What that means is not relevant, but please know that it occurs from both environmental toxins, poor diets, and insulin resistance. They are predominantly found in areas that are affected by Alzheimer’s disease.

Specifically, a diet that’s both high in sugar and fat. For years, and I mean many years, I have said to avoid excessive sugar intake. The combination will do you nothing but disservice.

This is yet another negative factor that is associated with a poor diet.

Treatments

Yes, there are pharmaceuticals that can slow the progression of Alzheimer’s disease. But we do not yet know how to stop or reverse the damage. This is a common statement in all of the literature about Alzheimer’s disease.

This article is not about treatments, but rather how we can diminish our risk of falling victim to Alzheimer’s disease.

Dietary effect

Genetics may play the most prominent role in developing Alzheimer’s disease. But our food choices may also be near the top of the list. These choices play a role in a few factors that are connected to the development or worsening of Alzheimer’s disease. They are:

• Type 2 diabetes
• Chronic inflammation
• Cardiovascular disease
• Hypertension

In fact, Sheih states, “Studies show that chronic type II diabetes mellitus (DM) is closely associated with neurodegeneration, especially Alzheimer’s disease.”

Sugar and Alzheimer’s Disease

This is the main reason I did a literature review on this subject. And selfishly to learn more since the disease is prevalent in my family tree.

I’ve stood high on my soapbox for decades about the dangers of eating too much sugar. And here again, the literature piles up supporting the consumption of much less sugar.

You see, sugar is a major culprit behind a lot of the diseases listed below that can result in a greater incidence of Alzheimer’s disease.

Type 2 Diabetes and Alzheimer’s Disease

First, let me be very clear. Type 2 diabetes does not cause Alzheimer’s disease. But it can increase one’s risk. And it appears to be by a large factor.

So, after a thorough review, I’ve concluded that the exact mechanism connecting the two is not yet agreed upon. Multiple levels of involvement from mitochondrial dysfunction to elevated cortisol levels have been introduced as partial explanations.

But one thing is relevant. There is a connection between the two. In fact, the term Diabetes Mellitus 3 has been coined in reference to the neurally degenerative effects of insulin resistance.

One more reason to eat well and exercise!

Cardiovascular disease and Alzheimer’s disease

There are definitely connections in the literature between the two. Common elements include blood pressure, cholesterol, and diabetes. In other words, the complications from both cardiovascular disease and diabetes promote or increase one’s risk for Alzheimer’s disease.

Some of the connections include:

• Chronic hypertension’s effect on the vascular tissue in the brain, as well as the blood-brain barrier
• Elevated cholesterol can interfere with synaptic plasticity

Inflammation and Alzheimer’s Disease

There is a connection between inflammation in the brain from insulin resistance and Alzheimer’s disease.

But does Alzheimer’s disease cause inflammation in damaged neural tissue or the reverse. It’s a valid question.

Walker states,

Human and animal studies suggest that inflammation occurring outside the central nervous system (systemic inflammation) may play a key role in promoting neurodegeneration, Alzheimer’s disease pathology, and cognitive decline in older adults.

And on top of that, Lee comments that:

Neuroinflammation has been known to play a critical role in the pathogenesis of chronic neurodegenerative disease in general, and in AD in particular.

Can strength training help prevent Alzheimer’s disease?

Indirectly, yes. Not only does strength training improve insulin resistance, but it also helps improve circulation to the brain.

It’s abundantly clear that strength training minimizes the risk of most of the diseases that promote or worsen Alzheimer’s disease. It helps:

• Strengthen peripheral vascular tissue
• Improve glucose tolerance
• Promote balanced hormones (maybe not a real phrase, but think of it as keeping your hormones at a healthy level)
• Minimize stress
• Promote better quality sleep

So, strength training is one more tool at your disposal for lowering your risk for Alzheimer’s disease.

Does cardiovascular exercise help with Alzheimer’s disease?

Again, cardiovascular exercise indirectly helps improve Alzheimer’s disease. Much like the list above for strength training, cardiovascular exercise helps:

• Strengthen peripheral vascular tissue
• Improve the pulmonary system
• Improve glucose tolerance
• Promote balanced hormones (maybe not a real phrase, but think of it as keeping your hormones at a healthy level)
• Minimize stress
• promote better quality sleep

The last note leads to the next section. There’s certainly a connection between exercise and sleep quality. And poor sleep quality amplifies and expedites the onset of Alzheimer’s (along with a lot of other factors that can make it worse).

Sleep and Alzeihmer’s

It’s now long agreed that abnormal sleep patterns emerge prior to the onset of Alzheimer’s disease. And this introduces a new downward cycle of complexities to the equation.

There’s a great deal of research that’s looking at quality sleep as a treatment for many age-related diseases.

In fact, Holth states “Abnormal tau is the earliest observable AD-like pathology in the brain with abnormal tau phosphorylation in many sleep-regulating regions…” This ties together the earlier discussion about tau proteins and Alzheimer’s disease.

Regardless, I guess one could state that quality sleep is the new anti-aging drug!

Does a high-stress level make Alzheimer’s worse?

There is certainly an agreed-upon connection between midlife hypertension, cardiovascular disease, and the development of Alzheimer’s disease.

We also know that chronic stress contributes to inflammation. And we learned earlier that systemic inflammation can contribute to the development of Alzheimer’s disease.

Further, we know that inflammation promotes tau hyperphosphorylation… that entanglement thing discussed above. Their presence is always found in diseased tissue from Alzheimer’s disease.

Mushrooms and Alzheimer’s disease

In a recent article I did entitled The Health Benefits of Mushrooms [A Definitive Guide], I found some interesting research being done on the Lion’s Mane mushroom.

It contains high levels of erinacines and hericenones. These two compounds are believed to stimulate nerve growth factor. This could be an important additional compound added to one’s arsenal in preventing Alzheimer’s disease.

How can you diminish your risk of Alzheimer’s disease if it’s in your family tree?

There are steps you can take during your adult life to minimize your risk of Alzheimer’s disease. Or push it off as far into the future as possible. For some, it’s not a matter of if, but when. In other words, live your life in a way to push it forward as far as possible into the future.

So, bottom line, what can you do based on a thorough literature review?

1. Most importantly, minimize your sugar intake as well as excess carbohydrates to lower your risk of type 2 diabetes.
2. Genuinely work on controlling your stress levels. Depression and anxiety from stress can really disrupt sleep. And the elevated levels of cortisol can wreak havoc on neural tissue.
3. Add strength training for a multitude of reasons. Even if it’s just light to moderate intensity.
4. Do cardiovascular exercise at least three times a week even if it’s just walking at a pace that is slightly above your norm.
5. Take the necessary steps to improve sleep quality. A few simple steps include:
   • minimizing caffeine in the afternoon,
   • eliminating alcohol before bed (yes, day drink)
   • leaving 3-4 hours between your last meal and bed
   • diminish your intake of liquids a few hours before bed
   • meditating while stretching right before bed

   Conclusion

   There is most certainly a connection between many of the diseases that occur from poor lifestyle habits and the onset of Alzheimer’s disease. The term is called comorbidity.

   In fact, over the years, I frequently see a connection between so many of the more commonly known diseases. One promotes the other and so on.

   This begs the question as to whether Alzheimer’s disease (and dementia) is something that would be far less prevalent without the presence of the other diseases.

   Nonetheless, it’s very clear that we have a responsibility to take care of ourselves by eating well, exercising, minimizing stress, and sleeping well. These are the things we have control over. And the choice to ignore self-care is a welcome mat to a perfect storm of so many diseases.

   I’m going to go out on a limb here and state once again how bad excess sugar is for us. The negatives just keep piling up. So why do we allow this addiction to sugar to continually diminish the quality of our lives?

   Why do we accept the onset of so many diseases with such an uproar, but yet be so cavalier about the necessary effort to prevent so many of these problems? A total head-scratcher!

   Alzheimer’s Research and References

   Akhter, F., Chen, D., Yan, S. F., & Yan, S. S. (2017). Mitochondrial Perturbation in Alzheimer’s Disease and Diabetes. Progress in Molecular Biology and Translational Science, 146, 341–361.

   Jerrah K. Holth, Tirth K. Patel, David M. Holtzman, Sleep in Alzheimer’s Disease–Beyond Amyloid, Neurobiology of Sleep and Circadian Rhythms, Volume 2, January 2017, Pages 4-14.

   Lee, Y., Han, S.B., Nam, S. et al. Inflammation and Alzheimer’s disease. Arch. Pharm. 2010, Res. 33, 1539–1556.

   Kehoe, Patrick Gavin. ‘The Coming of Age of the Angiotensin Hypothesis in Alzheimer’s Disease: Progress Toward Disease Prevention and Treatment?’ 1 Jan. 2018 : 1443 – 1466.

   Lewis H. Kuller, Oscar L. Lopez, Rachel H. Mackey, Caterina Rosano, Daniel Edmundowicz, James T. Becker, Anne B. Newman, Subclinical Cardiovascular Disease and Death, Dementia, and Coronary Heart Disease in Patients 80+ Years, J Am Coll Cardiol. 2016 Mar, 67 (9) 1013-1022.

   Mostafa Madmoli, Yasaman Modheji, Alireza Rafi, Rezvan Feyzi, Pouriya Darabiyan, Alieh Afshar Nia, Diabetes and its predictive role in the incidence of Alzheimer’s disease, Medical Science, 23(95), January – February, 2019.

   Bryce A.Mander, Joseph R.Winer, William J.Jagust, Matthew P.Walker, Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer’s Disease? Trends in Neurosciences, Volume 39, Issue 8, August 2016, Pages 552-566.

   Bryce A. Mander, Joseph R. Winer, Matthew P. Walker, Sleep and Human Aging, Neuron
   Volume 94, Issue 1, 5 April 2017, Pages 19-36.

   Moreira, Paula I., High-sugar diets, type 2 diabetes and Alzheimer’s disease, Current Opinion in Clinical Nutrition and Metabolic Care: July 2013 – Volume 16 – Issue 4 – p 440-445

   Cláudia Y. Santos, Peter J. Snydera, Wen-Chih Wud, Mia Zhange, Ana Echeverria, Jessica Albera, Pathophysiologic relationship between Alzheimer’s disease, cerebrovascular disease, and cardiovascular risk: A review and synthesis, Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, Volume 7, 2017, Pages 69-87.

   Shieh, J.C., Huang, P. & Lin, Y. Alzheimer’s Disease and Diabetes: Insulin Signaling as the Bridge Linking Two Pathologies. Mol Neurobiol 57, 1966–1977 (2020).

   Yen-Hua Shih RN, MS, Ming-Chyi Pai MD, PhD, Ying-Che Huang BSd, Jing-Jy Wang RN, PhD, Sundown Syndrome, Sleep Quality, and Walking Among Community-Dwelling People With Alzheimer Disease, Journal of the American Medical Directors Association, Volume 18, Issue 5, May 2017, Pages 396-401.

   Giacomo Tini, Riccardo Scagliola, Fiammetta Monacelli, Giovanni La Malfa, Italo Porto, Claudio Brunelli, and Gian Marco Rosa, Alzheimer’s Disease and Cardiovascular Disease: A Particular Association, Cardiology Research and Practice, Volume 2020, May 2020.

   Marcelo N.N.Vieira, Ricardo A.S. Lima-Filho, Fernanda G.De Felice, Connecting Alzheimer’s disease to diabetes: Underlying mechanisms and potential therapeutic targets, Neuropharmacology, Volume 136, Part B, 1 July 2018, Pages 160-171.

   Keenan A. Walker, Bronte N. Ficek, and Reyhan Westbrook, Understanding the Role of Systemic Inflammation in Alzheimer’s Disease, ACS Chemical Neuroscience 2019 10 (8), 3340-3342