Sunday, November 17, 2024

DIAGNOSTIC PROGRAM: OCCUPATIONAL CANCERSCAN THROUGH ADVANCED LAB TESTING

This testing program is designed by Dr. Roberta Kline exclusively for BARDDIAGNOSTCS and its patients.

OCCUPATIONAL HEALTH TESTING PROGRAM
For the many Americans who dedicated an extended period of their careers to potentially toxic exposures, this comprehensive clinical testing program offers direct insight into their genetic predispositions for potentially adverse responses to occupational exposures.  The selected testing also identifies predisposition to common cancers, chronic diseases, and other health issues.  

Along with their DNA predisposition profiles, the client also receives personalized guidance about how this gathered information applies to their actual healthcare approach, and proactive strategies they can take to mitigate the impact on their health. 

PHASE 1: GENETIC PREDISPOSITION 
The first phase of this program establishes a client's actual genetic blueprint rendering the foundation of a personalized approach to minimizing exposure risks and optimizing health. 

1) GENETIC TESTING: Genetic testing and interpretation of inherited mutations for common cancers (including breast, prostate, pancreatic, ovarian, colorectal, stomach, and melanoma) and cardiovascular disease.  

2) NUTRITIONAL GENOMICS TESTING: Genomic testing and interpretation of SNPs in many systems underlying health, including the processing of environmental toxins, nutrition, sleep, heart disease, brain health, mood, diabetes, inflammation, oxidative stress, mitochondrial health, hormones, cancers, exercise and injury, bone density.   

3) PHARMACOGENOMIC TESTING: Genomic testing and interpretation of SNPs in genes associated with medication response, including adverse reactions and effectiveness.  


PHASE 2: BIOLOGICAL & HEALTH IMPACT 

The next segment of this program assesses the impact of toxin exposures as they interact with genetic predisposition and affecting the biological systems that support health. Each client also receives personalized guidance and strategies for addressing any ongoing exposures and improving biological functioning and health. 

  1. 1) TOXIN TESTING: Specialized testing to assess current levels of a wide variety of toxins encountered in the workplace and home environments, with personalized strategies for supporting your internal detoxification systems to reduce their levels and impact. 


  1. 2) EPIGENETIC TESTING: Epigenetic testing and interpretation to assess how environmental exposures, diet, and lifestyle are interacting with your genetic predispositions, impacting real-time gene expression and health risks including how fast your cells are aging, general cancer and disease risks, immune health, smoking and alcohol exposures. 


  1. 3) FUNCTIONAL LAB TESTING: Additional specialized lab tests to assess areas identified as potential targets of toxins, directly or indirectly. Personalized to each client, these can include assessments of hormones, mitochondria, oxidative stress, microbiome, stress, sleep and more. 



Monday, May 13, 2024

INSIDE GENETIC PREDISPOSITION

PART 1: MUTAGEN HEREDITY AND ENVIRONMENTAL CANCER EXPOSURES

By: Lennard M. Gettz, Ed.D  /  Edited by: Roberta Kline, MD


First responders of every branch (police, firefighters, paramedics), as well as construction cleanup contractors, were exposed to the many toxic hazards around the World Trade Center (WTC) as a result of the events on 9/11/2001.  For the more than 91,000 individuals involved in this massive response and cleanup effort [1], exposure to the toxicants from dust, smoke, and incendiary chemicals has led to concerns for cancer, diseases, and other health injuries post-exposure.  The James Zadroga 9/11 Health and Compensation Act enacted the World Trade Center Health Program, a federal commitment to offer comprehensive care for 9/11-related conditions. [2]

Numerous environmental contaminants have been shown to have potential carcinogenic (cancer-causing) consequences. [3] Events such as 9/11 are just some of the scenarios that have alerted government agencies, the medical community, and individuals to study the types of common cancers from each scenario.  These exposures also bring new (and heightened) concerns for gene mutations that may be inherited or passed down to the next generations of those directly impacted.

"Learning about how cancer and other illnesses work... I would hate to contract this on the job and give this to my kids", states FDNY Ret. FF Sal Banchitta- 9/11 responder. "Firefighters get a lot of training and gear to protect us from exposure- but let's face it... part of the risk of the job is that there IS no 100% guarantee- ever!  Looking back on all this, from the local house fires of burning plastics and PVC's to the many chemicals and airborne poisons in ground zero-- exposure came from anywhere.  You can only hope that you're not someone who's predisposed, but you never know." 

According to the NCI (National Cancer Institute), up to 10% of all cancers may be caused by inherited genetic changes. Cancer itself (or genetic changes in tumor cells) cannot be inherited by children of cancer patients but a genetic change or mutation that increases the risk of cancer can be passed down (inherited) if it is present in a parent's egg or sperm cells. It is for this reason why cancer may sometimes appear to run in families.  [4]


WTC-RELATED CANCERS: There are now more than 15 cancers specifically associated with exposure to the WTC toxins, with prostate and breast cancer being among the top 3. [5]. Not only do survivors have higher rates of these cancers, but they are often more aggressive. Recent research has demonstrated that DNA mutations and epigenetic changes due to toxin exposures may play a role. [6, 7, 8] 


PART 2: TODAY'S GENETICS

In an exclusive interview about the science of gene expression, genomic specialist Dr. Roberta Kline, professor at the University of Western States, offered clarity on the fundamentals of the human blueprint: what DNA is, what it does, the impact of alterations to DNA on health, and how this is influenced by environmental exposures. 

Genes are specific regions of DNA that contain the code for all of the proteins that run our biology. Gene expression is the ultimate result of this complex process, and gene expression research has greatly accelerated the study of human biology and improved the practice of medicine. Up until the completion of the Human Genome Project in 2003, much of the focus had been on studying rare mutations linked to specific inherited diseases and cancers. We now know that these alterations of the DNA code are not the only ways people can be predisposed. 

The most common types of changes in DNA are called SNPs (single nucleotide polymorphisms), and we each have millions of these. These SNPs can alter our biochemistry and biology, but they typically have a much smaller effect individually than mutations. However, the additive effect of multiple SNPs can create significant predispositions to (or protection from) most diseases, including cancer. 

The latest gene expression research has added a third layer called epigenetics. Epigenetic changes don’t affect the DNA or genetic code itself. Rather, they respond to environmental cues to control when genes are turned on or off. Therefore, epigenetic changes can be easily modified throughout a person’s lifetime.

These processes all work together, and all of them can be inherited. Depending on diet, lifestyle, exercise, stress, medications, and environmental exposures, their impact can be increased or decreased. For example, someone with mutations, SNPs, or epigenetic changes that impair their ability to detoxify environmental chemicals can have a higher risk of DNA damage that can lead to disease or cancer. Diet and lifestyle strategies can counteract some of this risk - or can make it worse. This can help explain why not everyone exposed to the same toxins is affected in the same way, and why the same dietary and lifestyle factors can affect people’s health differently.



GENETIC PREDISPOSITION TESTING

With the existence of cancers in the family, physicians may recommend genetic testing.  Inherited mutations account for approximately 10% of all cancers, and these tend to be more aggressive and occur at an earlier age. [8] Genetic mutations have been identified for certain forms of pancreatic cancer, colorectal cancer, prostate cancer, or breast or ovarian cancer.  These tests for cancers such as Breast, Ovarian, and Pancreatic are known to target pathogenic/ly pathogenic (P/LP) variants associated with increased risk (including BRCA1, BRCA2, CDH1, PALB2, PTEN, and TP53, and recommended approaches to genetic counseling/testing and care strategies in individuals with these P/LP variants. [10, 11]

Genetic testing supports proactive prevention initiatives and active surveillance for these specific cancers that continue to prevail. Gene SNP testing can further support personalized prevention and screening strategies. While epigenetics is emerging as another tool in efforts to identify predispositions and personalize strategies, it is still more informative than prognostic at this time.



Sunday, November 3, 2024

AGING IN AMERICA: REVIEW FROM SOCIETAL TO BIOCHEMICAL

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. 

Healthy aging is not just about keeping disease and disability at bay. While we’d all like to stay as healthy and functional as possible, we can age successfully and gracefully even with less-than-optimal  health.

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

Tip #1: EAT RIGHT
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.

Tip #2: MOVE
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.


Tip #3: CHALENGE YOUR BRAIN
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. 


Tip #4 MANAGE STRESS
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.


Tip #5: GET A GOOD NIGHT'S SLEEP
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. 


Tip #6: FEEL CONNECTED
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.


 Tip #7: MANAGE YOUR HEALTH
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.


Tip #8: CULTIVATE PURPOSE & JOY
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. 

 ------------------------------------------------------------------------------------------------------------


Prevention101 HealthCast Pilot episode of the "Smarter Aging" series (10/2024)


PART 3: ALZHEIMER’S DISEASE- A GLOBAL EPIDEMIC  Written By: Roberta Kline, MD  (Originally published in Journal of Diagnostic Science,©2024)

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.

ALZHEIMER’S DISEASE WILL BANKRUPT HEALTHCARE
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.


NURSING HOME VS HOME CARE
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.

Living at home requires aids and adaptations, as well as caregiver support. This brings up another challenge: “Who provides the support?” How we treat the elderly reflects our societal values. With an overemphasis on achievement and productivity, those unable to meet this standard are seen as “less important” and thus less valuable. Often, this intersects with traditionally female roles, including caretaking for the elderly, children, and those who are sick, infirm, or disabled. 

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. 

3. EPIGENETICS: Epigenetics involves changes that affect gene expression without changing the DNA sequence. It is the body’s ability to quickly respond to environmental factors, and has been identified as a significant contributing factor to many health issues including Alzheimer’s Disease. [14] It is one of the mechanisms by which diet and lifestyle factors impact genetics and contribute to AD – and how we can also leverage them to potentially reverse these processes.

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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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. 

 



DR. ROBERTA KLINE is an ObGyn physician, an award-winning author, an educational advocate, and an inspirational speaker for the professional and women’s communities. She holds a combined mission to upgrade how we approach health and deliver healthcare for women through education, globalized communication, research, and advocacy.  Dr. Kline develops and teaches CME programs, consults on gene expression project designs, and leads collaborative projects designed to advance the direction of women’s health. She is also a clinical advisor in integrative medicine and functional genomics to many health organizations including the Integrative Health Research Center. Dr. Kline is Director of Educational Programs for the Women's Health Collaborative, Editor of the Women’s Health Digest, and on faculty at the University of Western States.




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. 

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