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The Aging Brain 2.0
P.O. Box 739 • Forest, VA 24551 • 1-800-526-8673 • www.AACC.net
The Aging Brain 2.0
Light University 2
Welcome to Light University and “The Aging Brain 2.0” program of study. Our prayer is that you will be blessed by your studies and increase your effectiveness in reaching out to others. We believe you will find this program to be academically-sound, clinically-excellent and biblically-based. Our faculty represents some of the best in their field—including professors, counselors, and ministers who provide students with current, practical instruction relevant to the needs of today’s generations. We have also worked hard to provide you with a program that is convenient and flexible, giving you the advantage of “classroom instruction” online and allowing you to complete your training on your own time and schedule in the comfort of your home or office. The test material can be found at www.lightuniversity.com and may be taken open book. Once you have successfully completed the test, which covers the units within this course, you will be awarded a certificate of completion signifying you have completed this program of study. Thank you for your interest in this program of study. Our prayer is that you will grow in knowledge, discernment, and people-skills throughout this course of study. Sincerely,
Ron Hawkins, D.Min., Ed.D. Dean, Light University
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The American Association of Christian Counselors
Represents the largest organized membership of Christian counselors and caregivers in the world, having just celebrated its 30th anniversary in 2016.
Known for its top-tier publications (Christian Counseling Today and Christian Counseling Connection), professional credentialing opportunities offered through the International Board of Christian Care (IBCC), excellence in Christian counseling education, an array of broad-based conferences and live training events, radio programs, regulatory and advocacy efforts on behalf of Christian professionals, a peer-reviewed Ethics Code, and collaborative partnerships such as Compassion International, the AACC has become the face of Christian counseling today.
The AACC also helped launch the International Christian Coaching Association (ICCA) in 2011, and has developed a number of effective tools and training resources for Life Coaches.
Our Mission
The AACC is committed to assisting Christian counselors, the entire “community of care,” licensed professionals, pastors, and lay church members with little or no formal training. It is our intention to equip clinical, pastoral, and lay caregivers with biblical truth and psychosocial insights that minister to hurting persons and help them move to personal wholeness, interpersonal competence, mental stability, and spiritual maturity.
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Our Vision
The AACC’s vision has two critical dimensions: First, we desire to serve the worldwide Christian Church by helping foster maturity in Christ. Second, we aim to serve, educate, and equip 1,000,000 professional clinicians, pastoral counselors, and lay helpers throughout the next decade. We are committed to helping the Church equip God’s people to love and care for one another. We recognize Christian counseling as a unique form of Christian discipleship, assisting the Church in its call to bring believers to maturity in the lifelong process of sanctification—of growing to maturity in Christ and experiencing abundant life. We recognize some are gifted to do so in the context of a clinical, professional and/or pastoral manner. We also believe selected lay people are called to care for others and that they need the appropriate training and mentoring to do so. We believe the role of the helping ministry in the Church must be supported by three strong cords: the pastor, the lay helper, and the clinical professional. It is to these three roles that the AACC is dedicated to serve (Ephesians 4: 11-13).
Our Core Values
In the name of Christ, the American Association of Christian Counselors abides by the following values:
VALUE 1: OUR SOURCE We are committed to honor Jesus Christ and glorify God, remaining flexible and responsive to the Holy Spirit in all that He has called us to be and do. VALUE 2: OUR STRENGTH We are committed to biblical truths, and to clinical excellence and unity in the delivery of all our resources, services, training, and benefits. VALUE 3: OUR SERVICE We are committed to effectively and competently serve the community of care worldwide—both our membership and the Church at large—with excellence and timeliness, and by over-delivery on our promises. VALUE 4: OUR STAFF We are committed to value and invest in our people as partners in our mission to help others effectively provide Christ-centered counseling and soul care for hurting people. VALUE 5: OUR STEWARDSHIP We are committed to profitably steward the resources God gives to us in order to continue serving the needs of hurting people.
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Light University
Established in 1999 under the leadership of Dr. Tim Clinton—has now seen nearly 300,000 students from around the world (including lay caregivers, pastors and chaplains, crisis responders, life coaches, and licensed mental health practitioners) enroll in courses that are delivered via multiple formats (live conference and Webinar presentations, video-based certification training, and a state-of-the-art, online distance teaching platform).
These presentations, courses, and certificate and diploma programs offer one of the most comprehensive orientations to Christian counseling anywhere. The strength of Light University is partially determined by its world-class faculty—more than 150 of the leading Christian educators, authors, mental health clinicians and life coaching experts in the United States. This core group of faculty members represents a literal “Who’s Who” in Christian counseling. No other university in the world has pulled together such a diverse and comprehensive group of professionals.
Educational and training materials cover more than 40 relevant core areas in Christian counseling, life coaching, mediation, and crisis response—equipping competent caregivers and ministry leaders who are making a difference in their churches, communities, and organizations.
Our Mission Statement
To train one million Biblical Counselors, Christian Life Coaches, and Christian Crisis Responders by educating, equipping, and serving today’s Christian leaders.
Academically Sound • Clinically Excellent • Distinctively Christian
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Video-based Curriculum
Utilizes DVD presentations that incorporate more than 150 of the leading Christian educators, authors, mental health clinicians, and life coaching experts in the United States.
Each presentation is approximately 50-60 minutes in length and most are accompanied by a corresponding text (in outline format) and a 10-question examination to measure learning outcomes. There are nearly 1,000 unique presentations that are available and organized in various course offerings.
Learning is self-directed and pacing is determined according to the individual time parameters/schedule of each participant.
With the successful completion of each program course, participants receive an official Certificate of Completion. In addition to the normal Certificate of Completion that each participant receives, Regular and Advanced Diplomas in Biblical Counseling are also available.
The Regular Diploma is awarded by taking Caring for People God’s Way, Breaking Free, and one additional Elective among the available Core Courses.
The Advanced Diploma is awarded by taking Caring for People God’s Way, Breaking Free, and any three Electives among the available Core Courses.
Credentialing
Light University courses, programs, certificates, and diplomas are recognized and endorsed by the International Board of Christian Care (IBCC) and its three affiliate Boards: the Board of Christian Professional & Pastoral Counselors (BCPPC); the Board of Christian Life Coaching (BCLC); and the Board of Christian Crisis & Trauma Response (BCCTR).
Credentialing is a separate process from certificate or diploma completion. However, the IBCC accepts Light University and Light University Online programs as meeting the academic requirements for credentialing purposes. Graduates are eligible to apply for credentialing in most cases.
Credentialing involves an application, attestation, and personal references.
Credential renewals include Continuing Education requirements, re-attestation, and occur either annually or biennially depending on the specific Board.
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Online Testing
The URL for taking all quizzes for this course is: http://www.lightuniversity.com/my-account/.
TO LOG IN TO YOUR ACCOUNT
You should have received an e-mail upon checkout that included your username, password, and a link to log in to your account online.
MY DASHBOARD PAGE
Once registered, you will see the My DVD Course Dashboard link by placing your mouse pointer over the My Account menu in the top bar of the Web site. This page will include student PROFILE information and the COURSES for which you are registered. The LOG-OUT and MY DASHBOARD tabs will be at the top right of each screen. Clicking on the > next to the course will take you to the course page containing the quizzes.
QUIZZES
Simply click on the first quiz to begin.
PRINT CERTIFICATE
After all quizzes are successfully completed, a “Print Your Certificate” button will appear near the top of the course page. You will now be able to print a Certificate of Completion. Your name and the course information are pre-populated.
Continuing Education The AACC is approved by the American Psychological Association (APA) to offer continuing education for psychologists. The AACC is a co-sponsor of this training curriculum and a National Board for Certified Counselors (NBCC) Approved Continuing Education Provider (ACEPTM). The AACC may award NBCC approved clock hours for events or programs that meet NBCC requirements. The AACC maintains responsibility for the content of this training curriculum. The AACC also offers continuing education credit for play therapists through the Association for Play Therapy (APT Approved Provider #14-373), so long as the training element is specifically applicable to the practice of play therapy. It remains the responsibility of each individual to be aware of his/her state licensure and Continuing Education requirements. A letter certifying participation will be mailed to those individuals who submit a Continuing Education request and have successfully completed all course requirements.
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Presenter for
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Presenter Biography Timothy R. Jennings, M.D., is a Christian psychiatrist, master psychopharmacologist, author, international speaker, past president of the Tennessee & Southern Psychiatric Associations, Distinguished Fellow of the American Psychiatric Association, Fellow of the Southern Psychiatric Association, and has a private practice in Chattanooga, Tennessee. Dr. Jennings obtained his M.D. degree in 1990 from the University of Tennessee College of Medicine in Memphis, Tennessee, and completed his psychiatric residency at D.D. Eisenhower Army Medical Center in Augusta, Georgia. He is board certified in psychiatry by the American Board of Psychiatry and Neurology. Dr. Jennings is the author of a number of books, including The God-Shaped Brain and The God-Shaped Heart, and has a weekly television program, The Dr. Tim Jennings Show, which can be viewed at timjenningsmd.com.
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The Aging Brain 2.0
Table of Contents:
TAB 101: The Problem of Aging .............................................................................................. 11
Timothy R. Jennings, M.D., DFAPA
TAB 102: Lifestyle and Aging .................................................................................................. 32
Timothy R. Jennings, M.D., DFAPA
TAB 103: Dementia ................................................................................................................ 49
Timothy R. Jennings, M.D., DFAPA
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TAB 101:
The Problem of Aging
Timothy R. Jennings, M.D., DFAPA
This presentation was originally recorded as one of AACC’s CounselTalk Webinars. As such, the
presenter may mention PowerPoint slides and refer to the presentation as a Webinar. Your
course notes are equivalent to the PowerPoint; any graphics mentioned are displayed on the
video.
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Summary
This lecture explores what aging is and the impact our mindset, worldview and mental stress
have on aging and dementia risk. Participants will learn how the choices we make in life can
either accelerate loss or retain abilities.
Learning Objectives
1. Participants will describe aging, what it is, and what happens as we age.
2. Participants will identify early life risk factors that accelerate aging.
3. Participants will examine the impact our beliefs and thought patterns have on the brain,
and discover methods to reduce risk of dementia.
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I. Understanding the Risk Factors
A. The Car Metaphor
1. Many risk factors–but don’t be overwhelmed
2. Consider metaphor of keeping your car in shape to the risk factors of breakdown or
accident
3. Driving a poorly constructed vehicle—being born with genetic or epigenetic
vulnerabilities to aging
4. Driving a vehicle in poor condition—people who don’t exercise or fail to maintain
healthy nutrition
5. Driving a vehicle with defective or worn out brakes—people who have impaired
ability to calm themselves or slow themselves down
6. Driving a vehicle with bald tires—overly emotional individuals who are not grounded
in reality and who easily slip and slide as the emotional weather changes
7. Distractions such as texting, changing the radio station, or other people in the
vehicle—caught up in entertainment, alcohol, drugs, addictions such that one
doesn’t attend to their health
8. Poor vision—lack of education, insight, or understanding
9. Wet, snowy, or icy conditions—toxins, pollution, industrial exposures that accelerate
aging
10. Purposeful sabotage—victims of abuse, war, and crime
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11. Sleeping at the wheel—failure to listen and learn, ignoring healthy guidance when
presented
12. Addressing one or more risk factors does not guarantee our cars will never break
down or we will never have an accident, but it reduces the risk
13. Nor does having one or more of these problems mean we are certain to get into an
accident or have a breakdown; however, the more factors, the greater the risk
14. So, too, with aging and risk of dementia
B. What is Aging?
1. Chronologically growing older?
2. Functionally growing older?
Slow decline in vitality and ability
3. We all move through time at the same rate—but we don’t all age at the same rate
C. Understanding Design Law
1. Principles, protocols, upon which life is built to operate—laws of health
2. Why don’t you put water in the tank of your car?
3. This type of thinking is counter to human organizations—they impose laws
4. Immature think that it’s okay to smoke tobacco or marijuana as long as it is legal
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5. The mature recognize that legalizing marijuana doesn’t make it healthy
6. It is not possible to be healthy in violations of the laws of health
II. Genetic Entropy
A. 2nd Law of Thermodynamics
1. Entropy – if energy isn’t put into a system it slowly decays
Leave your home for 20 years and return
Allow a car to sit for 20 years
2. Human genome?
If mankind is disconnected from God, is there a slow, gradual entropy to our
genome?
Are we degrading or evolving to higher forms?
The Bible says that when Adam sinned, “dying you will die.”
B. The Human Genome
1. An instruction manual containing a library of information
DNA molecules = letters
Clusters of these molecules = words
Words group to form genes = chapters
Chapters/genes group into Chromosomes = volumes
Volumes/Chromosomes group into genome = library containing 3.2 billion base
pairs in 23 pairs of chromosomes or 46 chromosomes
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C. Genetic Entropy
Mutation Type Mutations per person per generation
Mitochondrial <1
Nucleotide substitution <100-300
Satellite mutations <100-300
Deletions <2-6% (plus)
Duplications/insertions <2-6% (plus)
Inversions/translocations Numerous
Conversions Thousands?
Total/person/generation >1000
D. Genetic Mutations
1. A person at 65 will have in his/her DNA up to 6,000 point mutations that were not
there at birth
2. Each generation receives up to 1,000 new mutations that the previous generation
did not
3. There has not been one mutation found that has actually added genetic information
or improved the species
4. The human genome is slowly degrading
III. Telomeres
A. Research History1
1. 1965 – cells with short telomeres didn’t divide in culture
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2. 1990 – each time a human cell divides the telomeres shorten until cannot divide
3. 2006 – people with mood d/o’s have shorter telomeres
4. 2011 – institutionalized children have shorter telomeres
5. 2012 – telomere length predicts remaining lifespan
B. Telomere Length Declines in Dividing Cells as We Age
Telomere Length in Base Pairs (Human Blood Cells)
C. Telomeres
1. Shorter in males than females (but not at birth)2
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2. Heredity accounts for 80% environ 20%
3. Negative effect
Childhood adversity3
Mood disorders
Hostility
4. Positive effect
Healthy Diet
Doubling the amount of carotenoids lengthened telomeres by 2%4
Carotenoids – highest levels had telomeres 5-8% longer4
Plant based diet increased telomerase acitivity5
5. Older father when conceived6
6. Exercise7
IV. Understanding Aging
A. Longevity
1. Percent of Newborns Living to 65
0% 20% 40% 60% 80% 100%
1997 Girls
1997 Boys
1900 Girls
1900 Boys39%
43%
7
86
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2. Why are more people living longer over the last 100 years if the genome is
deteriorating?
Reduced infections
Clean water
Safe food
Sanitation
Better nutrition
Vaccinations
Antibiotics
Improved dental care
B. Causes of Death
1. 1900s 30% of all deaths from:
Pneumonia and Influenza
Tuberculosis
Diarrhea and Enteritis
2. 1990s 60% of all deaths from:
Heart Disease
Cancer
Stroke
3. Causes of death today:8
Cardiovascular Dz – 28.2%
Cancer – 22.2%
Stroke – 6.6%
Chronic Lung Dz – 6.2%
Alzheimer’s Dz – 4.2%
Diabetes – 2.9%
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Flu and Pneumonia – 2.6%
Accidental Injury – 2.2%
All Other Causes – 24.9%
C. Aging Trends in America9
1. 1950 – 12 Million (8%) >65
2. 2002 – 36 Million (12%) >65
3. According to the CDC, by 2030 there will be 71 million people in the U.S. >65
4. 1950-2002 an 8x increase >85
5. 2020 – 7 Million >85
6. 2040 – 14 Million >85
7. Living longer – more illnesses of aging
V. Mindset
A. Factors that Increase the Risk of Dementia
1. Mindset – Unhealthy beliefs
2. For as he thinks in his heart, so is he (Proverbs 23:7, NKJV).
B. Expectations Mindset10
1. 1979 – Men 75 years old
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2. One week at a retreat, no material dated later than 1959
3. One week they were to pretend it was 1959
4. Given ID’s with their 55 y/o picture
5. Tested before and after: physical strength, posture, perception, vision, cognition,
memory.
6. Results?
In every measure they improved
Greater flexibility
Better posture
Much improved hand strength
Eyesight improved by 10%
Memory improved by 10%
More than half had improved IQ scores
Appeared younger when before and after pictures were shown to random
strangers
7. Social Security – fosters belief that productivity ends at 65
8. We must educate that life doesn’t end at 65
C. NPTX2 Gene/Protein
1. Activates with new learning
2. Organizes and synchronizes brain circuits to form new memories
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3. Turning this gene off makes one vulnerable to dementia
4. Keeping this gene on reduces dementia risk
5. What keeps this gene on?
6. Activity in the neurons—new learning—so retirement with the mindset of “I am
done now” and nothing new to challenge… shuts this gene off and accelerates
cognitive decline11
D. Unhealthy Beliefs
1. I’m no good…
2. Trying to control outcomes/worry about future
3. Fear inducing God-constructs
4. Increased worry, stress, anxiety, fear
Activates brain’s fear circuitry
Increases inflammatory factors
E. Overactive Amygdala12
1. Activates sympathetic nervous system
2. Which activates macrophages – Why?
3. Which release cytokines – IL1, IL6, TNF
4. Which damage:
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Insulin receptors, glucocorticoid receptors, interfere with NE, 5HT, DA signaling
5. Resulting in:
Increased DM, obesity, high cholesterol, MI, Stroke, depression
All of which increase dementia
VI. Dysfunctional Relationships
A. Source of the Dysfunction
Regardless of the source of the dysfunction (i.e., a child who is abused is not the source
of the dysfunction but will still suffer damage from the dysfunction)
B. Animal Studies
1. Pups of nurturing mothers (licking/grooming) compared to pups of mothers who
didn’t nurture
Pups without attentive mothers had altered brain development causing
overactive amygdalas and social impairments
2. When pups of neglectful mothers were reared by nurturing mothers, their brain
development was the same as the pups of the nurturing mother
C. Child Abuse and Gene Expression in Brain Tissue13
1. 41 Canadian men (25 severe abuse, 16 controls)
2. DNA examined from hippocampal neurons
3. 362 alterations in gene expression
4. Those most significantly affected where genes which regulated neuronal plasticity
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D. Childhood Adversity Represents a Risk for Adulthood Disease
1. Adults who were abused as children
Have higher rates of medical illnesses
Have higher rates of mental illnesses
Have higher suicide rates
Have higher alcohol/drug problems
Thus, more disability and death
2. The Bible’s promise of long life for those with healthy family relationships is not
magic or special divine intervention… it is the natural outcome of living in harmony
with God’s design
VII. Lack of Spirituality/Altruism
A. The Bible Teaches to Love and Love is Life
1. The entire law is summed up in a single command: “Love your neighbor as yourself”
(Galatians 5:14).
2. Love “is not self-seeking” (1 Corinthians 13:5).
3. In the way of righteousness there is life; along that path is immortality (Proverbs
12:28).
4. He who pursues righteousness and love finds life, prosperity and honor (Proverbs
21:21).
5. The law of the Lord is perfect, reviving the soul (Psalm 19:7).
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B. Altruism Promotes Better Health
1. Adults who volunteer (after accounting for variables such as education, baseline
health, smoking, etc.)
2. Live longer, have less illness, less disability, less depression, less dementia and live
independently longer than those who did not.2
C. The REST Gene – Repressor Element 1 – Silencing Transcript
1. Cell Conductor – turning genes on and off
2. Impacts neuronal and brain circuitry development
3. Protects memory circuits – low levels increased risk of dementia
4. Turned off my chronic mental stress
5. Turned on by meditation and healthy spirituality14
D. How Healthy Spirituality Helps Slow Aging
1. Activates PFC and ACC, calms amygdala, lowers inflammatory response resulting in
improved mental and physical health
2. Altruistic activities result in better mental and physical health
3. Reduced anxiety and worry
4. Healthier lifestyle so reduced oxidative stressors
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5. Healthier relationships lower stress
VIII. Two Grand World Views: Belief Systems
A. Test the Premises of Origins
1. Godless Origin
Something came from nothing
Order came from chaos without intelligent input
Life comes from non-living matter
DNA gains information through mutation
2. God Created Origin
Something came from something
Order came from chaos with intelligent input
Life comes from another living organism
DNA degrades through mutation
B. Greatest False Belief in Science
1. Abiogenesis—life originating in non-living matter—on its own without intelligent
input
2. Can anyone demonstrate this in science?
3. Living organisms REQUIRE three elements:
Matter—atoms, proteins etc.
Energy—ionic and other molecular actions
Organized usable data—the coded information contained in our DNA
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4. Scientists who deny an intelligent Creator focus entirely on physical matter and
energy—but ignore the data
5. Where did the coded information come from?
6. Some atheists recognize this and postulate that aliens seeded life on earth
7. Genesis 1:1 in modern language: “Earth began when an extraterrestrial Intelligence
came and terraformed it, establishing a viable atmosphere and a stable planet.”
8. If science is more consistent with creation—why do so many honest people prefer a
godless view? Because the historic view of God is worse!
9. “The God of the Old Testament is arguably the most unpleasant character in all
fiction: jealous and proud of it; a petty, unjust, unforgiving control-freak; a
vindictive, bloodthirsty ethnic cleanser; a misogynistic, homophobic, racist,
infanticidal, genocidal, filicidal, pestilential, megalomaniacal, sadomasochistic,
capriciously malevolent bully.” – Richard Dawkins15
C. The Healthiest Worldview
1. A belief in a benevolent/trustworthy God
2. Next healthiest worldview?
3. Belief in no God but moral humanism
4. Worst worldview?
5. Belief in a wrathful punishing God
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IX. Improper Medical Care
A. Overuse of Medications
1. Medication use in >65
People >65 years of age compose only about 12% of the U.S. population
One-third (33%) of all drugs are prescribed for them
Consume more than 50% of over-the-counter medicines as well
More than 80% of all older people take at least one medication daily
2. Distribution of meds in body
↓ total body water
↓ lean body mass
↑ body fat
↓ serum albumin (protein)
Altered protein binding
Decreased liver and kidney function, decreased metabolism and clearance
Drugs may last longer, have higher concentrations, cause greater risk of harm
3. Fat soluble drugs last longer
Valium (diazepam)
Volume of distribution of diazepam is increased almost twofold in older patients
The elimination half-life is prolonged from 24 hours in young patients to almost
90 hours in older patients
Increased risk of falls, confusion, memory and cognitive problems, accidents,
interaction with other meds and/or alcohol
4. Water soluble drugs higher concentration
Less water, thus less dilution, so higher concentration with same dose
Older patients need lower doses of meds
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Digoxin
Aminoglycosides (gentamycin, neomycin, streptomycin, etc.)
5. Side effects
Older patients experience adverse outcomes about twice as often as younger
patients
Older patients experience more adverse reactions than younger patients
regardless of the number of drugs they use
6. Medications in elderly
Use sparingly and in low doses
Minimize number
Avoid sedating medications
B. Lack of Preventative Care
1. Routine checkups and screenings
2. Vaccines
3. Dental care
Failing to care for teeth increases dementia risk (one study those with fewest
teeth had highest risk of dementia)16, 17
4. Hearing aids
5. Glasses/cataract surgery, etc.
6. Walkers and safety aids
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C. Action Plan to Reduce Risk of Illness and Dementia as We Age
1. Develop a healthy mindset and belief system
2. Live a healthy lifestyle:
Exercise, healthy diet, avoid toxic substances
3. Engage in healthy spirituality
Embrace love and become a giver, volunteer
4. Develop healthy relationships
Minimize medications
5. Maintain preventative care
Cancer screen, glasses, hearing aids, dental care, vaccines
6. Create a safe environment
References 1
http://psychnews.psychiatryonline.org/doi/full/10.1176/pn.47.17.psychnews_47_17_18-a.
2 Okudo, K., et al. (2002). Telomere length in the newborn, Pediatric Research, 52, 377-381.
3 Shalev, I., et al. (2012). Exposure to violence during childhood is associated with telomere erosion from 5 to 10
years of age: a longitudinal study, Molecular Psychiatry, 18, 576–581; doi:10.1038/mp.2012.32.
4 Min, K.B., & Min, J.Y. (2017) Association between leukocyte telomere length and serum carotenoid in U.S. adults.
Eur J Nutr, 56(3):1045-1052. https://doi.org/10.1007/s00394-016-1152-x.
5 Ornish, D., et al. (2013). Effect of comprehensive lifestyle changes on telomerase activity and telomere length in
men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study. The Lancet
Oncology, 14(11), 1112-1120.
6 Eisenberg, D.T., Hayes, M.G., & Kuzawa, C.W. (2012). Delayed paternal age of reproduction in humans is
associated with longer telomeres across two generations of descendants. Proc Natl Acad Sci USA, 109(26),
10251-6.
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7 Sjögren, P., Fisher, R., Kallings, L., Svenson, U., Roos, G., & Hellénius, M. (2014). Stand up for health – avoiding
sedentary behaviour might lengthen your telomeres: Secondary outcomes from a physical activity RCT in
older people. Br J Sports Med, 48(19), 1407-9.
8 http://www.cdc.gov/chronicdisease/resources/publications/aag/aging.htm.
9 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1751014/.
10 Langer, E. (2009), Counterclockwise: Mindful Health and the Power of Possibility. New York: Ballentine.
11 Reti, I.M., et al. (2002). Prominent Narp expression in projection pathways and terminal fields. J Neurochem,
82(4), 935-44.
12 Miller, A.H., Maletic, V., & Raison, C.L. (2009). Inflammation and its discontents: The role of cytokines in the
pathophysiology of major depression. Biol Psychiatry. 65(9):732-741.
13 Labonté, B., Suderman, M., Maussion, G., et al., (2012). Genome-wide epigenetic regulation by early-life trauma.
Arch Gen Psych, 69(7):722-731. doi:10.1001/archgenpsychiatry.2011.2287.
14 Ashton, N., Hye, A., Leckey, C., et al. (2017). Plasma REST: A novel candidate biomarker of Alzheimer’s disease is
modified by psychological intervention in an at-risk population. Transl Psychiatry, 7(6): e1148.
15 Dawkins, R. (2006). The God delusion. Boston: Houghton Mifflin, p. 51.
16 Yamamoto, T., et al. (2012). Association between self-reported dental health status and onset of dementia: A 4-
year prospective cohort study of older Japanese adults from the Aichi Gerontological Evaluation Study
(AGES) Project. Psychosomatic Medicine, 74(3), 241-48, https://doi.org/10.1097/PSY.0b013e318246dffb.
17 Stein, P.S., et al. (2007). Tooth loss, dementia and neuropathology the Nun Study. Journal of the American Dental
Association, 138(10), 1314-22.
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TAB 102:
Lifestyle and Aging
Timothy R. Jennings, M.D., DFAPA
This presentation was originally recorded as one of AACC’s CounselTalk Webinars. As such, the
presenter may mention PowerPoint slides and refer to the presentation as a Webinar. Your
course notes are equivalent to the PowerPoint; any graphics mentioned are displayed on the
video.
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Summary
In this lecture, participants will examine the factors that contribute to obesity, the impact of
obesity on brain health, and how exercise, fasting, sleep, mental rest, and getting back to
nature can slow the aging process and decrease dementia risk.
Learning Objectives:
1. Participants will identify factors that increase oxidative stress, accelerate aging, and
increase dementia risk.
2. Participants will describe the impact various lifestyle interventions have on body and
brain health.
3. Participants will formulate an action plan to reduce oxidative stress and, thereby,
reduce dementia risk.
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I. Aging and Oxidative Stress
A. What Contributes to Functional Decline as We Age?
B. What is Oxidative Stress?
1. It is the damage to DNA, proteins and lipids (fatty substances) caused by oxidants,
which are highly reactive substances containing oxygen.
2. This is why we hear so much about “anti-oxidant” substances that prevent oxidation.
II. Obesity
A. What Increases Oxidative Stress?
1. Obesity: Adipose tissue produces reactive oxygen species (ROS) and reduces the
production of antioxidant enzymes1
2. At age 70
Obese: 8% less brain volume and look 16 years older
Overweight: 4% less brain volume and look 8 years older
3. Overweight or Obese2
55-64: obese: men 40.4%; women 42.4%
65-74: obese: men 36.6%; women 35.6%
>75: obese: men 25.6%; women 25.9%
55-64: overweight or obese: men 80.5%; women 69.4%
65-74: overweight or obese: men 79.1%; women 69.6%
>75: overweight or obese: men 70.8%; women 61.3%
4. Why are the percentages decreasing with age?
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B. What Contributes to Obesity?
1. Epigenetics
Males who GF smoked before age 11, higher rates of obesity3
If mother had famine conditions while pregnant4
2. Childhood abuse, neglect, severe trauma5
3. Sleep deprivation—alters body’s hormones6
2009 CDC survey – 35% of Americans sleep less than seven hour per night7
National Sleep Foundation – 20% of Americans sleep less than six hours per
night8
4. Change in types of fats consumed9
Up until 100 years ago, 1% of caloric intake from linoleic acid (omega 6 fatty
acid)
Now 8% of our diet is linoleic acid (LA)
LA is precursor to brain derived marijuana-like compounds called
endocannabinoids, which affect appetite, satiety, and food craving
Soy beans are 50% LA by weight
1% omega 3 (DHA/EPA) reversed the increased endocannabinoids
5. Bacteria in the gut10
Obese people less bacteroidetes and more firmicutes as compared to lean
people11
Wrong bacteria can make calories typically inaccessible to humans accessible
(fiber)12
High sugar and animal fats in diet increased growth of the bad bacteria13, 14
These changes in bacteria were associated with increased inflammation15
Plant based diets increased growth of good bacteria16
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Gastric by-pass surgery changes gut bacteria17
6. Brown vs. White Fat
Brown fat – high mitochondria regulate temperature – burns fat
White fat – stored fat – obesity
Immune system (iNKT) activates protein (fibroblast growth factor-21), which
turns white fat to brown fat = weight loss18, 19
High fat, high sugar diet decreased iNKT20
Plant-based diets changed bacteria in gut, which increased iNKT contributing to
weight loss20
C. Obesity
1. Adipose tissue produces reactive oxygen species (ROS) and reduces the production
of antioxidant enzymes1
2. What contributes to obesity
Unhealthy diet
Failure to exercise
Genetics
Drugs/medications
Stress
III. Advanced Glycation End Products (AGEs)
A. Glycation
1. Glycation is the process of sugars, in a non-enzymaticly controlled way, binding to
proteins and DNA significantly altering their structure and function. The altered
protein/DNA is an AGE.
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2. AGEs react with body tissues to produce free radicals and Reactive Oxygen Species
(increased oxidative stress).
3. AGE’s Impact
Damage collagen (skin thins, wrinkles, loses elasticity)
Binds with oxidized LDL in endothelium (arterial walls causing inflammation and
obstruction) and prevents HDL from removing the LDL
Interact with IgG altering immune response
Interact with cellular membranes altering membrane function
In vitro they interact with DNA – potential to alter DNA expression
4. Two Primary Sources of AGEs
Food: Browned, fried, and charred foods (30% absorption)
Body metabolism (high blood sugar levels increase AGEs): Hgb A1c – glycated
hemoglobin
B. How to reduce AGE’s and Slow Aging
1. Reduce Consumption of Sugar
Average American consumes 125-150 pounds per year
Stabilize blood sugar levels, eat complex carbs and proteins, high fiber diet,
exercise
2. Eat vegetables and fruits raw, boiled or steamed
Water prevents sugar from binding to proteins
3. Limit consumption of browned, caramelized, deep fried foods – this cooking
technique creates AGEs
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4. Limit meat, but when used cook at low temperature and slowly cook. High temps
create AGEs.
5. Avoid high fructose corn syrup (10x more reactive than glucose in the body).
6. Drink water. For many, the greatest sources of excess sugar are soft drinks.
7. Stop smoking.
Smoking has long been associated with cancer and cardiovascular health
concerns. Recent research has clearly shown a significantly higher level of serum
AGEs in smokers and especially diabetic smokers.
8. Scavenger of AGE
Rhodiola rosea, green tea, grape seed extract, omega-3 fatty acids, carnosine,
vitamin B6, alpha lipoic acid (plant sources of alpha-lipoic acid include broccoli,
spinach, collard greens, chard, and brewer’s yeast)
IV. Reducing Oxidative Stress: Diet
A. What Reduces Oxidative Stress and Slows Aging?
1. Diet
Designed to reduced AGEs
Apples, broccoli, spinach, kale, peaches, cabbage, cauliflower, tomatoes, carrots,
citrus fruits, most berries and omega-3 fatty acids
B. Neurology 2011: Nutrients Improve Brain Volume and Cognitive Function
1. Three, distinct nutrient biomarker patterns (NBPs) in blood related to cognitive
performance and (MRI) measures of brain aging
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2. 2 Diet patterns with favorable cognition and brain volume
High in plasma B vitamins (B1, B2, B6, folate, and B12), as well as vitamins C, D,
and E (fruits, nuts, grains, vegetables)
High in plasma marine omega-3 fatty acids (oily fish)
3. Diet with less favorable cognition and brain volume
A diet in high trans-fat pattern (fast food, junk food)
C. Neurology 2014: Omega-3 FA Slow Brain Atrophy21
1. After age 70, the brain shrinks by 0.5% per year
2. 1,111 women age 70 – no dementia at the beginning of the study
3. Eight years later – women with the highest EPA and DHA blood levels at the study’s
outset had brains that were about two cubic centimeters larger overall than women
with the lowest levels
4. Hippocampus was 2.7% larger in women who had fatty acid levels twice as high as
the average
5. The analysis adjusted for other factors that could influence the women’s brain size,
including education, age, other health conditions, smoking, and exercise
D. Vegetarian Diet
1. According to the American Diabetic Association, vegetarians have lower:
Heart disease
Colorectal, ovarian, and breast cancers
Diabetes
Obesity
Hypertension (high blood pressure)
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E. Fast or Calorie Restriction
1. Oxidation is damage resulting from free radicals and other reactive oxygen species
2. Mitochondria especially susceptible to damage and releasing more free radicals
if not removed, release toxic proteins that kill cells
3. Caloric restriction or intermittent fasting removes and recycles damaged cellular
components (cellular trash) like damaged mitochondria, thus reducing toxic stress22
4. Results in less disability, better cognition, increased longevity23, 24
F. How to Implement Diet Change
1. Plan meals ahead of time to ward off unhealthy temptations
2. Replace unhealthy ingredients with healthy ones
3. For example, an omelet made with egg whites and vegetables is healthier than one
heaped with cheese and sausage
4. Serve yourself smaller portions
5. Slow down when you eat
6. Change one item at a time, on a schedule
7. Remove sodas and drink water
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8. Remove red meat and eat fish (wild)
V. Tobacco and Drugs of Abuse
A. Impact on the Brain
1. Suppress antioxidant enzymes
2. Disrupt mitochondrial function
3. Increase the production of super oxides and free radicals
4. Activates the brain’s HPA (stress response)
B. Alcohol/Ethanol
1. Harmful to fetus
2. Harmful in developing brains
3. Harmful in brains with dementia
4. No benefit from distilled spirits in any amount
5. Harmful in amounts greater than the equivalent of 2.5 beers per day
6. Multiple studies show cardiac and brain benefit and lower dementia risk “mild to
moderate drinkers”
7. Strongest evidence from wine
8. But same benefits from regular, non-alcoholic grape juice
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9. Likely from antioxidant molecules and not the alcohol (polyphenols and flavonoids)
VI. Reducing Oxidative Stress: Exercise
A. Exercise
1. IL-10 is anti-inflammatory cytokine that reduces inflammation
2. Increases all neurotrophins
3. Older people who exercise regularly saw 2% growth in hippocampus reversing
effects of aging
4. Older adults who exercise are 40% less likely to experience disability25
5. Increased IL-10 and decreased inflammation26
6. Turns on all neurotrophins27
7. Older people who exercised saw 2% growth in hippocampus reversion – two years of
aging28
8. Older people walking 15 min./day decreased AD29
9. People who exercise have better cognitive abilities, sharper memory, and larger
brains29
10. People with MCI who participated in 12-week supervised exercise program
compared against healthy controls:
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MCI who exercised had increased neural connections in 10 brain regions
Healthy controls did not30
B. Exercise Recommendations
1. How to get started:
See your doctor
Start low and go slow
Find an exercise you enjoy
Stay balanced – extreme exercise is not healthy
2. Moderate Aerobic exercise five days per week, 30 minutes each day (10 minute
bouts) or Vigorous Aerobic exercise three days per week, 20 minutes per day
Sitting = 0; All Out = 10
Moderate = 5; Vigorous = 7-8
3. Strength training at least two days per week
8-10 different exercises; at least one set of 10-12 reps each
4. Flexibility two days per week, 10 minutes per day
VII. Reducing Oxidative Stress: Rest
A. Sleep
1. OSA – Cognitive impairments, mood disorders and loss of gray matter which
reversed with treatment31
2. Sleep disorders double the risk of depression32
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3. During sleep, the brain cells contract, expelling metabolic waste and increasing
clearance from brain, including beta amyloid33
4. Benzodiazepines increase memory problems34
B. Sabbath Rest
1. Blue Zones
Ikaria, Greece
Nicoya, Costa Rica
Okinawa, Japan
Sardina, Italy
Loma Linda, California
2. What is unique about Loma Linda?
Heterogeneous
Seventh-day Adventists
3. From Blue Zone Web site
Lessons from Loma Linda: “Find a sanctuary in time to decompress. …
Observance of the Sabbath strictly occurs from Friday to Saturday night, giving
Adventists a weekly time to focus on family, friends, God and nature.”35
4. Seventh-day Adventists also:
Eat healthy (high percent of vegetarians)
Don’t smoke, use alcohol or illegal drugs
Exercise more than most
Have less obesity
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C. Time in Nature
1. Reduced stress hormones, decreased heart rate, improved mental, physical health
and learning36, 37, 38, 39
2. Touching the earth provides electrons that reduce ROS, decreases inflammation,
improves the body’s anti-oxidant enzymes, improves blood flow, sleep, energy, and
reduces pain40, 41, 42
3. Outdoor exercise may be better43
D. Action Plan to Reduce Dementia Risk
1. Develop a healthy mindset and belief system
2. Live a healthy lifestyle
Veggie or Mediterranean Diet
Clean air and water
Regular exercise
Regular sleep 7-8 hours per night
3. Engage in healthy spirituality
Embrace love and become a giver, volunteer
Weekly mental rest (Sabbath)
Time in nature
4. Develop healthy relationships
Forgive
Healthy boundaries
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References
1 Furukawa, S., et al. (2004). Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin
Invest, 114(12), 1752-1761.
2 Go, A.S, et al. (2013). Heart disease and stroke statistics—2013 update: A report from the American Heart
Association. Circulation, 127:e6-e245. http://www.heart.org/idc/groups/heart-
public/@wcm/@sop/@smd/documents/downloadable/ucm_319574.pdf.
3 Pembrey, M.E., et al. (2006). Sex-specific, male-line transgenerational responses in humans. Eur J Hum
Genet. 14(2), 159-66.
4 Heijmans, B., et al. (2008). Persistent epigenetic differences associated with prenatal exposure to famine in
humans, PNAS, 105(44), 17046-17049.
5 Danese, A., et al. (2009). Adverse childhood experiences and adult risk factors for age-related disease: depression,
inflammation, and clustering of metabolic risk markers, Arch Pediatr Adolesc Med., 163(12), 1135-1143.
6 Copinschi, G. (2005). Metabolic and endocrine effects of sleep deprivation. Essential Psychopharmacology, 6(6),
341-7.
7 https://www.cdc.gov/sleep/data_statistics.html.
8 Quoted from http://www.webmd.com/sleep-disorders/features/toll-of-sleep-loss-in-america.
9 Alvheim, A., et al. (2012). Dietary linoleic acid elevates endogenous 2-ag and anandamide and induces obesity.
Obesity, 20(10), 1984-1994.
10 Ley, R., et al. (2006). Microbial ecology: Human gut microbes associated with obesity, Nature 444, 1022-1023.
11 Tilg, H., & Kaser, A. (2011). Gut microbiome, obesity, and metabolic dysfunction. J Clin Invest, 121(6), 2126-2132.
12 Thomas, F., et al. (2011). Environmental and gut bacteroidetes: The food connection. Front Microbiol, 2, 93.
13 David. L., et al. (2014). Diet rapidly and reproducibly alters the human gut microbiome, Nature 505(7484), 559-
563.
14 Wu, G., et al. (2011). Linking long-term dietary patterns with gut microbial enterotypes, Science, 334(6052), 105-
108.
15 de La Serre, C.B., et al. (2010). Propensity to high-fat diet-induced obesity in rats is associated with changes in
the gut microbiota and gut inflammation, American Journal of Physiology – Gastrointestinal and Liver
Physiology, 299(2), G440-G448.
16 Tilg, H., & Kaser, A. (2011). Gut microbiome, obesity, and metabolic dysfunction. J Clin Invest, 121(6), 2126-2132.
17 Harris, K., et al. (2012). Is the gut microbiota a new factor contributing to obesity and its metabolic disorders?
Journal of Obesity 2012, Article ID 879151, 14 pages.
18 Lynch, L., et al. (2016). iNKT cells induce FGF21 for thermogenesis and are required for maximal weight loss in
GLP1 therapy, Cell Metabolism, 24(3), 510-519.
19 Lukens, J., et al. (2012). Fat chance: Not much against NKT cells, Immunity, 37(3), 574-587.
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20 Wieland Brown, L.C, Penaranda, C., Kashyap, P.C., Williams, B.B., Clardy, J., Kronenberg, M., et al. (2013).
Production of α-galactosylceramide by a prominent member of the human gut microbiota. PLoS Biol
11(7), e1001610.
21 Pottala, J.V., Yaffe, K., Robinson, J.G., Espeland, M.A., Wallace, R., & Harris, W.S. (2014). Higher RBC EPA + DHA
corresponds with larger total brain and hippocampal volumes: WHIMS-MRI study. Neurology, 4(82), 435-
42.
22 http://aging.ufl.edu/files/2011/01/UF-scientists-reveal-how-dietary-restriction-cleans-cells-_-UFShands-The-
University-of-Florida-Academic-Health-Center.pdf.
23 Singh, R., et al. (2012). Late-onset intermittent fasting dietary restriction as a potential intervention to retard
age-associated brain function impairments in male rats. Age (Dordr), 34(4), 917-33.
24 Davis, L.M., Pauly, J.R., Readnower, R.D., Rho, J.M., & Sullivan, P.G. (2008). Fasting is neuroprotective following
traumatic brain injury. J Neurosci Res., 86(8), 1812-22.
25 Ettinger Jr., W.H., et al. (1997). A randomized trial comparing aerobic exercise and resistance exercise with a
health education program in older adults with knee osteoarthritis. The Fitness Arthritis and Seniors Trial
(FAST). JAMA, 277(1), 25-31.
26 Helmark, I., et al. (2010). Exercise increases interleukin-10 levels both intraarticularly and peri-synovially in
patients with knee osteoarthritis: a randomized controlled trial. Arthritis Research & Therapy, 12(4), R126.
27 Jin, K., et al. (2002). Vascular endothelial growth factor (VEGF) stimulates neurogenesis in vitro and in vivo, PNAS,
99(18), 11946-50.
28 Fahnestock, M., et al. (2001). The precursor pro-nerve growth factor is the predominant form of nerve growth
factor in brain and is increased in Alzheimer's Disease, Molecular and Cellular Neuroscience, 18(2), 210-
220.
29 Liang, K.Y., Mintun, M.A., Fagan, A.M., et al. (2010). Exercise and Alzheimer's disease biomarkers in cognitively
normal older adults. Ann Neurol., 68(3), 311-318.
30 Chirles, T.J., Reiter, K., Weiss, L.R., Alfini, A.J., Nielson, K.A., & Smith, J.C. (2017). Exercise training and functional
connectivity changes in mild cognitive impairment and healthy elders. Journal of Alzheimer’s Disease,
57(3), 845-856.
31 Canessa, N., et al. (2011). Obstructive sleep apnea: Brain structural changes and neurocognitive function before
and after treatment. American Journal of Respiratory and Critical Care Medicine, 183(10), 1419-1426.
doi: 10.1164/rccm.201005-0693OC.
32 Peppard, P.E., Szklo-Coxe, M., Hla, K.M., & Young, T. (2006). Longitudinal association of sleep-related breathing
disorder and depression. Archives of Internal Medicine, 166(16), 1709-15.
33 Xie, L., et al. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156), 373-377.
34 Pariente, A., et al. (2016). The Benzodiazepine-Dementia disorders link: Current state of knowledge. CNS Drugs.
30(1), 1-7. doi: 10.1007/s40263-015-0305-4.
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35 http://www.bluezones.com/live-longer/education/expeditions/loma-linda-california/.
36 Morita, E., et al. (2007). Psychological effects of forest environments on healthy adults: Shinrin-yoku (forest-air
bathing, walking) as a possible method of stress reduction, Public Health, 121(1), 54-63.
37 Lee, J., et al. (2011). Effect of forest bathing on physiological and psychological responses in young Japanese
male subjects, Public Health, 125(2), 93-100.
38 Stigsdotter, U., et al. (2010). Health promoting outdoor environments: Associations between green space, and
health, health-related quality of life and stress based on a Danish national representative survey, Scand J
Public Health, 38(4), 411-417.
39 O’Brien, L. (2009). Learning outdoors: the Forest School approach, Education 3-13, 37(1), 45-60.
40 Oschman, J.L. (2008). Perspective: Assume a spherical cow: The role of free or mobile electrons in bodywork,
energetic and movement therapies, Journal of Bodywork and Movement Therapies, 12(1) 40-57.
41 Chevalier, G., et al. (2015). One-hour contact with the earth’s surface (grounding) improves inflammation and
blood flow: A randomized, double-blind, pilot study, Health, 7(8), 1022-1059.
42 Chevalier, G., et al. (2012). Earthing: Health implications of reconnecting the human body to the earth’s surface
electrons, J Environ Public Health, 291541.
43 Gladwell, V., et al. (2013). The great outdoors: How a green exercise environment can benefit all. Extreme
Physiology & Medicine, 2, 1-7. DOI: 10.1186/2046-7648-2-3.
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TAB 103:
Dementia
Timothy R. Jennings, M.D., DFAPA
This presentation was originally recorded as one of AACC’s CounselTalk Webinars. As such, the presenter may mention PowerPoint slides and refer to the presentation as a Webinar. Your course notes are equivalent to the PowerPoint; any graphics mentioned are displayed on the video.
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Summary
In this presentation, participants will examine the brain changes that occur in Alzheimer’s
Disorder (AD) and demonstrate how the various factors previously discussed contribute to the
development of AD. This lecture will also discuss how lifestyle choices can prevent this
destructive cascade.
Learning Objectives
1. Participants will differentiate Alzheimer’s dementia from other dementias.
2. Participants will link risk factors described earlier with the damaging brain changes
found in Alzheimer’s dementia.
3. Participants will formulate a plan to reduce risk to prevent dementia.
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I. Understanding Dementia
A. What is Dementia?
1. Dementia is not normal aging; it is a disease state
2. A brain disease characterized by multiple cognitive deficits, including memory and
one or more of the following:
Aphasia (language disturbance)
Apraxia (motor disturbance)
Agnosia (impaired recognition of familiar objects)
Executive function impairment
B. Prevalence1
1. Worldwide 5-7% > 60 y/o some dementia
2. Latin America 8.5%
3. Sub-Saharan Africa 2-4%
4. In 2010, approximately 35.6 million people worldwide had some form of dementia
5. Numbers projected to double every 20 years through 2050 (65.7 million in 2030,
115.4 million in 2050)
6. Three most common forms are Alzheimer’s, Vascular, and Lewy Body
C. Vascular Dementia2, 3
1. Due to decreased blood flow to brain
2. Western countries about 1.5% prevalence
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3. Risk factors:
High blood pressure
Smoking
DM-II
Obesity
Cardiovascular disease
Stroke
D. Lewy Body Dementia
1. Third most common type, 1.4 million in U.S. (rates uncertain as often misdiagnosed
as AD or Parkinson’s Dementia)4, 5
2. Caused by build-up of a toxic protein (alpha-synuclein)
3. Poorly understood and research is ongoing
E. Lewy Body vs. Alzheimer’s
1. In addition to having dementia DLB has:
2. Marked fluctuations in level of alertness, attention, and cognition
3. Recurrent visual hallucinations that are well-formed and detailed
4. Sudden appearance of Parkinson-like movement after memory and cognitive
problems
5. Symptoms of REM sleep disorder
6. Overly sensitive to medicines that can cause Parkinson-like symptoms
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F. Alzheimer’s Disease vs. Dementia
1. Disease refers to the cascade of pathological changes which damage brain tissue
2. Dementia refers to the functional loss of memory plus one of the other cognitive
abilities previously described
3. Dementia, therefore, can be caused by anything that damages the brain
4. Alzheimer’s dementia is caused by Alzheimer’s disease
G. Alzheimer's Disease (AD)6
1. 5.2 million in U.S. (5 mill> 65 y/o) – 11% of population
2. 3.2 million women/1.8 million men
3. AD is the most common cause of dementia
4. AD incidence doubles every five years after age 65
5. The prevalence of AD among the elderly is 67 per 1,000 people (Parkinson’s disease
is 9.5 per 1,000)
6. More than one in nine aged 65 and one in three aged 85 have AD (82% are older
than 75-years-old)
7. Vast majority over the age of 75 (82%)
8. 62.9% of Hispanics > 85 have AD
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9. 58.8% of African-Americans > 85 have AD
10. 30.2% of whites > 85 have AD
H. History of Alzheimer’s Disease
1. First described in 1907 by Alois Alzheimer
2. Observed in 51 y/o wf with memory loss
3. Post mortem
Neurofibrillary tangles and senile plaques
I. Two Types of Alzheimer’s Disorder
1. Early onset before age 65, usually before age 60
Three gene mutations cause this
No known cure
5% of cases
2. Late onset after 65
95% of AD cases
Due to inflammatory and oxidative stress over time
Can prevent this with lifestyle changes
II. Alzheimer’s Disorder and the Brain
A. Understanding the Brain
1. 100 billion nerve cells
2. Over one trillion supporting cells
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3. Each brain cell with up to 10,000 connections to other cells
40,000,000,000,000,000 (Forty Quadrillion)
4. 1-2% of body mass
5. Uses 20% body energy
6. High state of flux
7. Many waste products
B. When Neurons Die7, 8, 9
1. Brain removes waste products
2. Trace chemicals left behind scavenged by amyloid
3. Amyloid can become toxic if:
Misfolds (not soluble)
Binds to copper, iron, zinc
Binds to methionine
C. ApoE
1. Lipoprotein that transports fat vitamins, cholesterol into cells
2. Three gene variants: ApoE2, ApoE3, ApoE4
3. ApoE2: 7% population, increased risk of atherosclerosis
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4. ApoE3: 79% of population neutral effect
5. ApoE4: 14% of population implicated in Alzheimer’s
If two copies 10-30x increased risk
Up to 65% of people with Alzheimer’s with this gene
But one-third of Alzheimer’s without this gene
D. ApoE4 – Genetic Risk
1. The APOE ε4 is neither necessary nor sufficient to get the disease
2. A study out of Washington University found that people with APOE ε4 were not
demented and had less amyloid in their brains if they had a history of exercise.10
3. Genetics account for only one-third of the risk
4. What is the key?
5. Inflammation, which causes insulin resistance in the brain, is likely the key and
lifestyle impacts inflammation-improving insulin sensitivity
E. ApoE and Cholesterol
1. High cholesterol is associated with increased AD11
2. ApoE transports cholesterol in and out of neurons
3. Not everyone with high cholesterol gets AD
4. Not everyone with ApoE4 gets AD
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5. Could these two factors together increase risk?
6. Modulating cholesterol changes ApoE gene activity12
7. High fat diet caused insulin resistance and worsened memory and cognition in all
groups, but ApoE4 group exaggerated deficits in brain region that forms memory13
8. This reversed with one month of low fat diet13
9. Low fat diet improved cholesterol and cognition especially in those with two copies
of the ApoeE4 gene14
10. Could cholesterol-lowering meds reduce risk of AD?
11. SOME, but not all, cholesterol-lowering meds did reduce AD risk in people with two
copies of the Apoe4 gene
12. Greatest positive effect atorvastatin (P = .026)
13. Lovastatin (no significant difference found)
14. E4/E4 people with symptoms of AD, but received statin medication, had significantly
better cognitive function over the course of 10-year follow-up compared with those
who did not receive the statins (P < .01)
F. NPTX2 Gene/Protein15
1. Activates with new learning
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2. Organizes and synchronizes brain circuits to form new memories
3. High NPTX2 with high amyloid no dementia
4. Low NPTX2 with low amyloid no dementia
5. Low NPTX2 with high amyloid = dementia2
6. Keeping this gene on reduces dementia risk when amyloid high
7. What keeps this gene on?
8. Activity in the neurons—new learning—no new challenges… shuts down gene and
accelerates cognitive decline16
G. Insulin17
1. Peripherally regulates glucose uptake
2. In the brain – made by brain cells
Regulates amyloid clearance
Tau phosphorylation
Blood flow regulation
Inhibition of apoptosis, inflammatory responses, and lipid catabolism
Facilitates transmitter receptor trafficking
Synaptic plasticity
Memory formation
H. Similarities between Diabetes Mellitus and Alzheimer’s Disease17
1. Insulin Resistance
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2. Elevated inflammatory and oxidative stress
3. Amyloid protein deposits in brain and pancreas
4. Tau hyperphosphorylation
5. Cognitive decline
6. Type II DM increase risk of AD 60%
I. Insulin Resistance as People Age17
1. 50% of Americans aged 45-64 have peripheral insulin resistance with normal blood
sugar
2. 76% of people >65 y/o have peripheral insulin resistance
3. Triggers of insulin resistance are:
High fructose diet
High fat diet
Chronic inflammation/stress
4. Beta Amyloid, IL-6, TNF-alpha phosphorylate the insulin sub receptor in brain cells
rendering it unresponsive to insulin and is strongly associated with cognitive decline
and memory loss
J. Potential Pathways17
1. Inflammation
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2. Insulin resistance
Phosphor by IL-6 TNFa
3. Amyloid not cleared
4. Tau phosphorylation
5. Microtubule disconnect
6. Influx + ions
7. Cell death
8. More Amyloid
9. Head injury, bad genes increases amyloid
10. Insulin resistance
Phosphor by amyloid
11. Tau phosphorylation
12. Microtubule disconnect
13. Influx + ions
14. Cell death
15. More Amyloid
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K. Risk Factors for Dementia
1. Increasing age18
2. Family history
3. Oxidative stress
4. Trisomy 21
5. Alcohol/drug abuse
6. Smoking
7. Sedentary lifestyle
8. Toxic exposure
9. Head injury
#1 cause head injury in U.S.: MVA, falls, firearms
Sports
Bicycle accidents
10. Poor vascular health
Smoking doubles risk
11. DM/glucose intolerance
Doubles the risk
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12. Obesity
13. Western diet
14. HTN
15. Low intelligence
Television increases risk of dementia because it slows neural connectivity
16. Low cognitive stimuli
17. Depression
18. PTSD
19. Social isolation
20. Psychological stress
21. Chronic sleep deprivation
III. Four Keys to Alzheimer’s Dementia Prevention
A. Physical conditioning
1. Exercise increases insulin sensitivity
2. Active animals have larger hippocampi
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3. Older people who walk regularly, even as little as 15 minutes a day, have a lower risk
for AD
4. People who routinely exercise exhibit better cognitive abilities and actually have
larger brains
5. Exercise in older adults – 2% growth hippocampi reversing two years of aging
B. Mental Stimulation
1. Mentally stimulating activities and certain brain-training programs that have NEW
LEARNING are in the long-term associated with lower brain amyloid levels and a
decreased risk for AD, as are graduating from college or engaging in lifelong
learning19, 20
C. Stress Management
1. Chronic stress activates inflammatory pathways and damages the brain
2. Study of 5,000 individuals found that neuroticism—which included feelings of guilt,
anger, anxiety, and depression—was associated with a greater risk for dementia. In
contrast, conscientiousness was shown to be protective against dementia.21
3. Meditating on God of love reduces stress
4. Altruistic activities reduce dementia risk
5. Trust God with outcomes
6. Be truthful – address issues and resolve them
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7. Forgive
D. Nutrition
1. Normal weight
2. Mediterranean Diet
3. Fruits, nuts, vegies, omega-3 fatty acids
4. Avoid sugars, trans fats
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References
1 Prince, M., et al. (2013). The global prevalence of dementia: A systematic review and metaanalysis. Alzheimer’s
Dementia, 9(1), 63-75. e2.
2 Hébert, R., & Brayne, C. (1995). Epidemiology of vascular dementia, Neuroepidemiology, 14(5), n 240-57.
3 Alagiakrishnan, K. (2016). Vascular dementia, Medscape. Retrieved from
http://emedicine.medscape.com/article/292105-
overview?pa=zcEvbqaaWmxRptTGYZ0VaBgqqj5eiNbBDXnNXohGdXOY93XZtb2DI9sJMvxg9Zib8SIvl8zjYv73
GUyW5rsbWA%3D%3D#a4.
4
Lewy Body Dementia Association. https://www.lbda.org/content/incidence-lewy-body-dementias-general-
population.
5 Savica, R., Grossardt, B.R., Bower, J.H., Boeve, B.F., Ahlskog, J., & Rocca, W.A. (2013). Incidence of dementia with
Lewy bodies and Parkinson disease dementia. JAMA Neurol, 70(11), 1396-1402.
doi:10.1001/jamaneurol.2013.3579.
6 Alzheimer’s Association (2014). Alzheimer’s disease fact and figures. Retrieved from
http://www.alz.org/downloads/facts_figures_2014.pdf.
7 Lee, C-C., et al. (2007). A three-stage kinetic model of amyloid fibrillation, Biophys J, 92(10), 3448-3458.
8 Su, B., et al. (2008). Oxidative stress signaling in Alzheimer’s disease, Curr Alzheimer Res., 5(6): 525-532.
9 Lee, H.G., Casadesus, G., Zhu, X., Takeda, A., Perry, G., & Smith, M.A. (2004). Challenging the amyloid cascade
hypothesis: Senile plaques and amyloid-beta as protective adaptations to Alzheimer disease. Ann N Y
Acad Sci. 1019(1), 1-4.
10 Head, D., Bugg, J.M., Goate, A.M., et al. (2012). Exercise engagement as a moderator of the effects of APOE
genotype on amyloid deposition. Arch Neurol, 69. 636-643.
11 Jarvik, G.P., et al. (1995). Interactions of apolipoprotein E genotype, total cholesterol level, age, and sex in
prediction of Alzheimer's disease: A case-control study. Neurology, 45(6), 1092-6.
12 Petanceska, S.S., et al. (2003). Changes in apolipoprotein E expression in response to dietary and
pharmacological modulation of cholesterol. J Mol Neurosci, 20(3), 395-406.
13 Johnson, L.A., Torres, E.R., Impey, S., Stevents, J.F., & Raber, J. (2017). Apolipoprotein E4 and insulin resistance
interact to impair cognition and alter the epigenome and metabolome. Sci Rep., 7, 43701.
14
Geifman, N., Brinton, R.D., Kennedy, R.E., et al. (2017). Evidence for benefit of statins to modify cognitive decline
and risk in Alzheimer’s disease. Alzheimers Res Ther., 9:10.
15 Xiao, M.F., Xu, D., Craig, M.T., et al. (2017). NPTX2 and cognitive dysfunction in Alzheimer’s disease. eLife. 2017
March 23; 6.
16 Reti, I.M., et al. (2002). Prominent Narp expression in projection pathways and terminal fields. J Neurochem.
82(4):935-44.
17 Talbot, K. (2013). Psychiatric Times, p. 18-21.
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18 Evans, D.A., Funkenstein, H.H., Albert, M.S., et al. (1989). Prevalence of Alzheimer’s Disease in a community
population of older persons: Higher than previously reported. JAMA, 262(18): 2552-2556.
19 Belleville, S., et al. (2011). Training-related brain plasticity in subjects at risk of developing Alzheimer's disease.
Brain, 134, 1623-1634.
20 Landau, S.M., Marks, S.M., Mormino, E.C., et al. (2012). Association of lifetime cognitive engagement and low β -
amyloid deposition. Arch Neurol., 69, 623-629.
21 Low, L., Harriosn, F., & Lackersteen, S.M. (2012). Does personality affect risk for dementia? A systematic review
and meta-analysis. The American Journal of Geriatric Psychiatry, 21(8), 713-728.
http://www.ajgponline.org/article/S1064-7481(12)00031-0/fulltext.
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