AGING is a natural process that is associated with biological changes that lead to a progressive decline in physiological functioning. These changes start as early as the mid-20's, and accelerate in the mid-40's and again at around age 60. While aging is inevitable, the rate at which it occurs can be faster or slower depending on multiple factors, including the interactions of genetics with diet, lifestyle, environment, and stress. It is also impacted by resilience.
Without a doubt, everyone will experience aging. It’s a biological process that begins at birth, and it is inevitable. But how we age is not. We are redefining aging, celebrating it as a time of new opportunities, deeper connections, and ongoing learning. It’s a time where we are actively engaging life with joy and purpose.
WHAT IS RESILIENCE?
Resilience is the ability to “bounce back” from an adverse event or experience, large or small. This is influenced by biological factors (including genetics) as well as psychological ones, and both forms of resilience can be cultivated. As people with higher levels of biological and psychological resilience tend to experience improved health and quality of life as they age, this heightens its importance for better aging.
Health is created from physical, emotional, mental, spiritual, and energetic balance. But balance is not static. It requires constant adjustment in response to changes and challenges in your inner and outer worlds - and often changes throughout your lifetime. Resilience helps you bounce back and regain balance. Here are 8 simple strategies to help you cultivate resilience so you can handle whatever challenges come your way in a way that helps you thrive.
8 Easy Tips for Better Aging Starts with RESILIENCE
By: Roberta Kline MD
Focus on fresh whole foods, with an emphasis on colorful vegetables and low-sugar fruits, fish, poultry, nuts, non-wheat whole grains, and cold-pressed olive oil. Adding herbs and spices boosts your food power. Avoid fried foods, processed red meat, trans-fats, and saturated fats, sugars, sweets, and baked goods; swapping sugar substitutes may be worse than sugars, so avoid those too.
Aim for 150 minutes a week of moderate to vigorous exercises, such as walking, swimming, biking, dancing, tennis, strength training, gardening, or yoga. House cleaning, gardening, and yard work count too! Ideally, it’s something that you enjoy. Moving throughout the day is just as important. If you have a sedentary job, make sure to get up and move at least 10 minutes every hour if you can.
Playing chess, solving crossword puzzles, reading books, and learning a new language or skill are examples of brain-boosting activities. Mixing up your daily routine is another great way to increase cognitive resilience. This can include: exploring new neighborhoods or trying out a new coffee shop.
Identify stressors in your life and reduce or eliminate the ones you can control, and have strategies to manage the impact of the ones you can’t. Tai chi, meditation, music, art, yoga and other exercise, being in nature, finding moments of awe, experiencing joy and laughter - these are just some of the ways that can help you cultivate resilience.
Aim for going to bed by 10 pm, and getting 7-8 hours of restful sleep nightly. Even one night of insomnia or getting inadequate sleep can have an impact on your resilience. If you snore or don’t feel refreshed when you wake up in the morning, consider getting checked for a sleep disorder such as sleep apnea.
Having strong social connections - whether a few or many - along with having meaning in our lives, can be one of the most powerful strategies. This does not include social media or other virtual interactions - there is something about the brain that needs interaction with the actual person or people.
Heart disease, diabetes, chronic pain, and other chronic health issues can reduce your resilience. Staying proactive in managing all aspects of your health can help increase your resilience and minimize their impact.
Having a sense of purpose and connection to a greater meaning is a fundamental human need. So is joy. Identify things that bring you joy. Find something that gives you a reason to be excited about the day. Purpose doesn’t necessarily mean a grand vision - it can be big or small. Whether it’s through your work, your family, or your community, it’s important to feel you are loved and valued and are contributing to something that is meaningful to you.
Aim for incorporating at least 4-5 of these strategies. They each build on each other, so the more you of these you do, the more resilience you’ll have and the more your health will benefit. Every bit counts. As you take steps to improve your resilience, you’ll also be supporting your overall health of mind, body and spirit - feeling better and having more energy to keep doing the things you love! Start small. But you don’t have to feel overwhelmed - incorporating just one of them into your daily habits helps. Start with the change that feels the easiest first. Then build on your success to incorporate all 10 if you can!
Implementing these strategies can greatly improve your success in developing resilience for better aging.
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Age-related dysfunction of the brain can escalate in aggressiveness and complexity over time as the victim progresses toward the end of life. ALZHEIMER’S DISEASE (AD) is currently viewed as a progressive neurodegenerative disease that is uniformly fatal. The most common form is termed Late-Onset Alzheimer’s Disease (LOAD), which primarily impacts people over the age of 65 and is the focus of this article. In addition to its devasting impact on individuals with AD, it has a wide-reaching impact that touches every aspect of our society. But there is hope. In the following pages, we’ll review the current state of the science and clinical approaches to AD, and introduce promising new ways to approach prevention and treatment. Making these changes will require a fundamental shift in how we approach not only AD but our health and healthcare as a whole.
All stakeholders must work together to change the tide in this global epidemic. From individuals, families, and communities to healthcare, research, and private and government institutions, we all have the opportunity to be part of the solution. It won’t be easy, but to keep going in the same direction is unthinkable.
Without a drastic – and rapid- change in our approach, caring for people with dementia, particularly Alzheimer’s disease, is predicted to bankrupt this country’s healthcare systems by the year 2050. Currently, we spend more than $321 billion in direct healthcare costs caring for the more than 6 million Americans living with Alzheimer’s. In large part due to the increase in our aging population, that number is expected to increase to 13.8 million, with costs projected to be over $1 trillion by 2050. [1] Evidence shows that taking a more holistic approach can improve quality of life [2 but this requires a different mindset and strategy. In addition to the staggering cost of healthcare, there is a hidden cost that often fails to receive attention: unpaid caregiving.
More than 11 million unpaid caregivers spend an estimated 18.4 billion hours a year caring for family members with Alzheimer's or other dementias. The value of these unpaid services is estimated at $350 billion [2], exceeding the direct healthcare costs. However, this number is even greater in terms of total impact, as it does not account for the emotional, physical, and social toll, nor does it include lost wages and related benefits due to caregiving responsibilities.
AGING DISEASE
Alzheimer's disease is fatal and is the fifth‐leading cause of death among Americans aged 65 and older. [3] This number does not include those with Alzheimer’s who die of other diseases first, but where Alzheimer’s was likely a contributing factor. While people aged 65 and older only survive an average of four to eight years after diagnosis, some can live as long as 20 years. [3]
Twice as many women as men are diagnosed with Alzheimer’s disease, and women account for almost 2/3 of the approximately 7 million Americans currently living with Alzheimer’s. [3e] Ethnicity also plays a role. Black/African American individuals have twice the risk of Alzheimer’s disease compared to Non-Hispanic white individuals, and Hispanic/Latino individuals are just slightly lower at 1.5x. [4]
When looking at people 65 and older, the highest prevalence of AD is among Black/African American individuals at 13.8%, with Hispanic/Latino individuals at 12.2%, non-Hispanic white individuals at 10.3%, American Indian and Alaska Native individuals at 9.1%, and the lowest group being Asian American and Pacific Islander individuals at 8.4%. [4] The U.S. Census Bureau has predicted that the U.S. minority population will increase from 20% to almost half by 2060. Despite these statistics, most research has been conducted with non-Hispanic white populations, hampering both understanding of underlying causes as well as treatments for an increasing demographic. There are currently no good treatments in the conventional medical model, and thus people with Alzheimer’s are often led to believe that there is nothing they can do. Ending up in a nursing home often seems inevitable.
According to the CDC, as of 2020 there were more than 15,000 nursing homes serving more than 1 million residents, and for-profit companies owned 70%. [6] One of the top three reasons older people are placed in assisted living facilities and nursing homes is dementia, with Alzheimer’s being the most common type and accounting for almost half of all nursing home residents; this rate is even higher for Medicare beneficiaries. As people with Alzheimer’s disease age, they are often found to have other forms of dementia as well. [3]
Research shows that those who are in nursing homes do better when provided with more specialized services. However, less than 5% of nursing home “beds” are in facilities that provide these. [6] But nursing home care is not inevitable. More than 60% of people with Alzheimer’s disease and related dementias live at home, half of them living alone. [6] This concept of “aging in place” may help alleviate the burden of nursing home care. It also can help slow the progression of the disease, as people are kept in familiar environments that provide a sense of belonging and purpose. This continued connection to their community also provides better opportunities for social and cognitive engagement.
As women are often the primary caregivers, they are much more likely to disproportionately suffer additional consequences. Women from historically minority and marginalized groups with fewer resources and access to services are even more impacted. [3]
 |
| Age distribution of AD in 2023. [3] |
LEADING CAUSES OF ALZHEIMER’S DISEASE
Alzheimer’s disease is a complex interplay of genetic and environmental factors.
1. AGE: Age is the single largest risk factor for AD. The vast majority (90-95%) of people with AD are over age 65, with risk increasing with age.
2. GENETICS: Specific forms of the APOE gene are associated with late onset Alzheimer’s disease (LOAD), the most common type that typically affects individuals after age 60. People carrying the E4 variant of the APOE gene have the largest genetic risk, based on research involving individuals primarily of European descent. Those with two copies of the APOE4 gene are estimated to have about a 60% risk of developing AD by age 85, and recent research suggests that the form of disease may be different than AD in those with normal APOE genes. [7]
Interestingly, this study also found that almost everyone with two copies of APOE4 developed brain changes in beta-amyloid and tau consistent with Alzheimer’s Disease by age 55. But previous studies have estimated that almost half—40%—of people with two copies of APOE4 don’t develop Alzheimer’s disease, so it’s not necessarily inevitable. [8]
Variants in genes regulating the inflammatory response have been implicated in AD. In 2013, a variant in the TREM2 gene was found to account for the next highest risk after APOE4. [9] Recently, a variant in the FMNL2 gene appears to link the connection between vascular disease in the brain with Alzheimer’s disease by reducing the clearance of amyloid in the brain. [10]
Research has revealed a number of other gene variants that are associated with AD more specifically in individuals with African heritage. Variants in genes linked to the immune response, and vascular systems were found to account for up to 30% of the heritability of AD in Black Americans. [11] A different APOE variant on APOE3, normally thought to be protective, was associated with an increased risk for African Americans if they also carried APOE4. New gene variants in ABCA7 have an even greater impact on AD risk for individuals with African ancestry vs European ancestry. [12] It is likely that ongoing research will continue to refine the genetic contributors for various populations, increasing our understanding of the disease and potential treatments.
We can’t change our genes, but they are not the only cause. While approximately 60% of patients with AD have APOE4 or other identifiable genetic risk factors, 40% don’t. [13] This is likely due to a combination of other genes that have recently been identified, along with dietary, lifestyle, and environmental factors. [8]
As with many other chronic diseases, this illustrates the importance of understanding how the interactions between our genes and environment can increase or decrease genetic predisposition for disease. These insights are crucial to finding clues that may help accelerate better options for treatment and even prevention.
4. ACCUMULATION OF BETA-AMYLOID AND TAU: The prevailing theory of why people develop Alzheimer’s Disease has been focused on the role of specific protein alterations in the brain called beta-amyloid plaques and, more recently, tau neurofibrillary tangles. While these changes are thought to be the hallmark of AD in the brain, the limited focus on this “amyloid hypothesis” ignores scientific research into other biological mechanisms that contribute to the disease process.
Scientific research is shedding light on the complexity of Alzheimer’s disease that goes far beyond beta-amyloid plaques and tau protein tangles. In fact, these changes are now thought to be a result of the underlying biological mechanisms that can lead to AD - which likely explains why pharmaceutical companies have pursued treatment without much success. [9]
This single-minded focus on the amyloid hypothesis, excluding other theories that challenged this accepted dogma, has significantly contributed to the lack of progress in finding treatments. [9] As a result of this and other biases, Alzheimer’s Disease research has been grossly underfunded compared to other chronic diseases such as heart disease and HIV.
But even the funds invested have failed to deliver significant progress. Despite spending over $40 billion on drug development over the last 25 years, the FDA has approved only a handful of medications that are woefully inadequate in improving symptoms and disease progression. [15] None address the underlying causes and we have no cure.
Clearly, we need a different approach. Fortunately, dedicated scientific researchers have been making significant headway in understanding the underlying causes and exploring innovative approaches to treatment. With appropriate funding, these lay the foundation for more fruitful results that also address inequities in research and treatment access.
(To be continued)
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| Sponsored Infomercial: BREAKTHROUGH SOLUTIONS FOR PERSONALIZED WELLNESS ON A GENETIC AND CELLULAR LEVEL The primary culprits in aging are oxidative stress and impaired mitochondria. A modern movement in functional healing is about PERSONALIZED NUTRITION - a health strategy allowing us to better analyze and meet our body's complex needs. Arriving at more effective solutions means QUESTIONING WHAT'S OUT THERE, then undergoing more educated research as part of making better decisions. COMPLEX CELLULAR SUPPORT, (part of our NUTRIGENOMICS PLUS series) is a whole-body restorative strategy- optimizing the very heart of our body's energy production. NUTRIGENOMICS PLUS was created to be a powerful custom designed nutritional supplement for adults, recommended for anyone over 18 years old who wants to support their overall health*. It is not designed for any specific illness or disease, but instead offers a wide array of nutraceuticals including focused antioxidants, anti-inflammatories and mitochondrial support for overall wellness and longevity. This custom designed formula was developed by genomic scientists who carefully selected ingredients (antioxidants) that synergistically support the immune and mitochondrial functions. This offers a strategic balance of phytonutrients and bioactives that are recognized to address inflammatory disorders, cancer symptoms and cardiovascular health. as well as the prevention of DNA damage, and regulate hormones. (See complete info-site) |
5. NEUROINFLAMMATION: Inflammation in the brain has been associated with several neurodegenerative diseases, of which Alzheimer’s Disease is the most common. [16] In AD, this involves specialized cells in the brain called microglia. Damage to these microglia leads to dysfunction and degeneration of neurons, which then creates a circular cascade of more inflammation and more damage to mitochondria and neurons. [17]
Cytokines and the inflammasome are a central part of the neuroinflammatory process, activating numerous cascades that increase the pro-inflammatory response and deposition of beta-amyloid plaques that damage neurons.. [9]
Various toxins as well as microbiological agents including viruses, prions, parasites, and bacteria have also been associated with triggering an inflammatory response and the development of AD. [18]
(L Image): Piekut et al. Fig. 1. The pathomechanism of virus-associated neurodegeneration. Herpes simplex virus 1.
6. MITOCHONDRIAL DYSFUNCTION: Maintaining healthy mitochondria is essential for biological functions, including in the brain. Mitochondria have been implicated in the development of many age-related diseases, including Alzheimer’s disease (AD). [19] Mitochondria are considered the powerhouses of our cells, producing the energy we need to live in the form of ATP. Due to lack of energy stores in the brain for fat and glucose, which typically fuel cells, the mitochondria must produce the energy needed. Dysfunction of mitochondria has an outsized impact on the brain due to the high energy requirements of the neurons and glia. [19]
One of the mechanisms by which mitochondrial function is affected is through the connection of inflammation and oxidative stress – two biological responses that go hand in hand. The mitochondria create oxidative stress as part of the normal process of ATP production. In the face of excess energy demand, including inflammation, the level of oxidative stress can exceed the normal antioxidant mechanisms and lead to damaged mitochondria.
Another consequence of inflammation and oxidative stress is the disruption of normal maintenance that includes the ability to destroy old or damaged mitochondria, as well as generate new ones. This process of mitochondrial autophagy and biogenesis has been found to be related to aging and the progression of Alzheimer’s Disease. [16]
7. VASCULAR DISEASE: Alzheimer’s disease is associated with cardiovascular and cerebrovascular disease, associated with beta amyloid plaques and neurofibrillary tau tangles in up to 70% of people with Alzheimer’s disease. [10] When blood vessels become diseased, blood flow to the brain is restricted, causing neuronal cell death. This leads to a circular cascade of inflammation and oxidative stress, and further damage to neurons in the brain.
Many diseases are associated with increased cardiovascular risk, including obesity, hypertension, hypercholesterolemia, diabetes, and metabolic syndrome. Each of these is also associated with inflammation and oxidative stress as well as mitochondrial dysfunction. It is likely a combination of the various factors, in addition to vascular dysfunction, that connect them with Alzheimer’s disease risk.
MODIFIABLE RISK FACTORS: With all of these significant contributors to Alzheimer’s disease, it’s important to remember that we have some control over many risk factors - and they are thus potentially modifiable. The brain is an incredibly complex organ, and we need to reframe our reductionist thinking to approach the brain as an evolving, complex network that adapts to biological, social, and environmental influences to create a better approach to diseases such as Alzheimer’s disease.
It is estimated that 40% of AD is related to modifiable risk factors [3], including:
• insulin resistance • glucose dysregulation
• hypertension • dyslipidemia
• obesity • physical inactivity
• hearing loss • smoking
• alcohol • traumatic brain injury
• low levels of socialization and cognitive stimulation
• air pollution
These are all potential areas where we can improve both prevention and treatment and understand the protective mechanisms that may explain why some people don’t get Alzheimer’s disease despite multiple risk factors – including genetics.
R-Image: Nday, CM et al Understanding the biological and neurological mechanisms behind resilience.
EARLY DETECTION: Currently, there is no treatment to effectively cure Alzheimer’s, and the more the disease has progressed, the more difficult it is to slow progression or even reverse course.
Early detection is a crucial component to reducing morbidity and mortality from many diseases, and this needs to be extended to Alzheimer’s Disease. It is evident that metabolic and brain changes can start 20 years or more before symptoms appear. New blood tests are emerging that may help us identify people with very early changes in brain biology – long before symptoms appear. [19] Having this information early may help to develop strategies to slow or even reverse them before a person ever develops symptoms of Alzheimer’s Disease.
Diabetes, high cholesterol, and high blood pressure are some of the most common diseases that predispose to Alzheimer’s Disease [19], and these also have altered metabolic and cellular changes that can be seen years or even decades before diagnosis. Here, too, early detection enables addressing these earlier in the disease process and can contribute to improving our approach to Alzheimer’s Disease as well. [20] While conventional medicine does not effectively address the root causes of these diseases, Personalized Genomic & Functional Medicine has been shown to do just that – especially if addressed early.
In Part 2 of this series, we’ll look at ways in which we already have many of the tools we need to make a difference in the treatment and potential prevention of Alzheimer’s disease today.
REFERENCES
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2. Gaugler JE, Yu F, Davila HW, & Shippee T. (2014). Alzheimer’s Disease And Nursing Homes. Health Affairs (Project Hope), 33(4), 650. https://doi.org/10.1377/hlthaff.2013.1268
3. 2024 Alzheimer's disease facts and figures. Alzheimers Dement. 2024 May;20(5):3708-3821. doi: 10.1002/alz.13809.
4. Lim, Aaron C., et al. "Quantification of Race/Ethnicity Representation in Alzheimer’S Disease Neuroimaging Research in the USA: A Systematic Review." Communications Medicine, vol. 3, no. 1, 2023, pp. 1-12, https://doi.org/10.1038/s43856-023-00333-6.
5. https://www.cdc.gov/nchs/fastats/nursing-home-care.htm
6. Mukamel DB, Saliba D, Ladd H, Konetzka RT. Dementia Care Is Widespread In US Nursing Homes; Facilities With The Most Dementia Patients May Offer Better Care. Health Aff (Millwood). 2023 Jun;42(6):795-803. doi: 10.1377/hlthaff.2022.01263.
7. Fortea J, Pegueroles J, Alcolea D, et al (2024). APOE4 homozygosity represents a distinct genetic form of Alzheimer’s disease. Nature Medicine, 30(5), 1284-1291. https://doi.org/10.1038/s41591-024-02931-w
8. Steele OG, Stuart AC, Minkley L, et al. A multi-hit hypothesis for an APOE4-dependent pathophysiological state. Eur J Neurosci. 2022 Nov;56(9):5476-5515. doi: 10.1111/ejn.15685.
9. Si, Zhen, et al. "Targeting Neuroinflammation in Alzheimer’S Disease: From Mechanisms to Clinical Applications." Neural Regeneration Research, vol. 18, no. 4, 2023, pp. 708-715, https://doi.org/10.4103/1673-5374.353484.
10. Lee, A.J., Raghavan, N.S., Bhattarai, P. et al. FMNL2 regulates gliovascular interactions and is associated with vascular risk factors and cerebrovascular pathology in Alzheimer’s disease. Acta Neuropathol 144, 59–79 (2022). https://doi.org/10.1007/s00401-022-02431-6
11. Benjamin, Kynon J., et al. "Analysis of Gene Expression in the Postmortem Brain of Neurotypical Black Americans Reveals Contributions of Genetic Ancestry." Nature Neuroscience, vol. 27, no. 6, 2024, pp. 1064-1074, https://doi.org/10.1038/s41593-024-01636-0.
12. Stepler KE, Gillyard TR, Reed CB, Avery TM, Davis JS, Robinson RAS. ABCA7, a Genetic Risk Factor Associated with Alzheimer's Disease Risk in African Americans. J Alzheimers Dis. 2022;86(1):5-19. doi: 10.3233/JAD-215306.
13. Fernandez F, & Andrews JL. (2020). Genetics of dementia: A focus on Alzheimer's disease. Diagnosis and Management in Dementia, 127-146. https://doi.org/10.1016/B978-0-12-815854-8.00009-4.
14. Sharma, Vivek K., et al. "Alzheimer’S Disorder: Epigenetic Connection and Associated Risk Factors." Current Neuropharmacology, vol. 18, no. 8, 2020, pp. 740-753, https://doi.org/10.2174/1570159X18666200128125641
15. Harrison J, Mitchell SL, McCarthy EP, & Mor V. (2024). Pragmatic Clinical Trials for Dementia Care: Experience from the First 5 Years of the IMPACT Collaboratory. Generations (San Francisco, Calif.), 48(2). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11429579/
16. Tran M, & Reddy PH. (2021). Defective Autophagy and Mitophagy in Aging and Alzheimer’s Disease. Frontiers in Neuroscience, 14, 612757. https://doi.org/10.3389/fnins.2020.612757
17. Marttinen M, Takalo M, Natunen T, et al. (2018). Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer’s Disease. Frontiers in Neuroscience, 12, 427638. https://doi.org/10.3389/fnins.2018.00963
18. Piekut T, Hurła M, Banaszek N, Szejn P, Dorszewska J, Kozubski W, Prendecki M. Infectious agents and Alzheimer's disease. J Integr Neurosci. 2022 Mar 28;21(2):73. doi: 10.31083/j.jin2102073.
19. Misrani, Afzal, et al. "Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’S Disease." Frontiers in Aging Neuroscience, vol. 13, 2021, p. 617588, https://doi.org/10.3389/fnagi.2021.617588.
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