The Protocol: Optimized, Efficient, Effective
The Vital Structure Method is structured across two complementary training days designed to hit all major functional muscle groups.
Day 1: Heavy Foundation (Building Kinetic Armor)
Objective: Maximal loading (80-85% of 1 rep max to stimulate bone density, preserve lean mass and support kinetic joint health [1, 5].

Day 2: Vital Power (Velocity & Fall Prevention)
Objective: High velocity with 40-60% external load to target Rate of Force Development,  fast-twitch Type II motor units, and fall-interception reflexes [3, 4, 11].

Integrating Exercise with Clinical Performance Medicine
Exercise is a potent medical intervention that synergizes with cardiorespiratory fitness (Zone 2 endurance and VO2Max training) [13]:

• Metabolic Health: Skeletal muscle is our largest metabolic organ. Increasing lean mass (ALMI) expands glucose disposal capacity, improving insulin sensitivity and helping reduce Visceral Adipose Tissue. [1, 6].
• Bone Mineral Density: Heavy axial loading during Day 1 exercises forces bone stimulating osteoblast activity to protect against osteopenia and osteoporotic fractures [1, 5].
• Fall Prevention & Cognitive Resilience: Explosive lateral bounding (Skater Jumps) trains rapid motor unit recruitment. If you lose your balance, your nervous system responds in milliseconds to catch you [3, 4, 11]. Furthermore, maintaining high muscle mass and physical fitness is strongly linked to preserved executive function and cognitive health as we age [1, 1].

Implementation Framework
To translate these principles into your personal routine:

1. Establish Your Baseline: Obtain a baseline body composition DEXA scan and functional strength evaluation.
2. Prioritize Form Over Load: Focus on full range of motion and joint control before increasing resistance.
3. Progress Step-by-Step: Add set volume (moving from 3 sets to 4 sets per exercise) before increasing weight.
4. Allow Recovery: Maintain 24-48 hours between Day 1 (Heavy Foundation) and Day 2 (Vital Power) workouts to ensure central nervous system restoration.
5. Fuel Muscle Protein Synthesis: Ensure adequate protein intake distributed across meals to support muscle recovery and counteract anabolic resistance [12].

By taking deliberate steps today to build strength, power, and movement quality, you lay the foundation to remain active, energetic, and resilient for years to come.
References

1. Sayer AA, Cruz-Jentoft A. Sarcopenia. Lancet. 2022;399(10323):406-410.
2. Clark BC, Manini TM. Sarcopenia =/= dynapenia. J Gerontol A Biol Sci Med Sci. 2008;63(8):829-834.
3. Metter EJ, Talbot LA, Schrager M, Conwit R. Skeletal muscle strength as a predictor of all cause mortality in healthy men. J Gerontol A Biol Sci Med Sci. 2002;57(10):B359-B365.
4. Fielding RA, Vellas B, Evans WJ, et al. Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. J Am Med Dir Assoc. 2011;12(4):249-256.
5. Leenders M, Verdijk LB, van der Hoeven L, et al. Elderly men and women benefit equally from prolonged resistance type training. Med Sci Sports Exerc. 2013;45(8):1569-1578.
6. Tessier A, Wing SS, Rahme E, Morais JA, Chevalier S. Association of Low Muscle Mass With Cognitive Function During a 3-Year Follow-up Among Adults Aged 65 to 86 Years in the Canadian Longitudinal Study on Aging. JAMA Netw Open. 2022;5(7):e2219926. doi:10.1001/jamanetworkopen.2022.19926
7. Leong DP, Teo KK, Rangarajan S, et al. Prognostic value of grip strength: findings from the Prospective Urban Rural Epidemiology (PURE) study. Lancet. 2015;386(9990):266-273.
8. Celis-Morales CA, Welsh P, Lyall DM, et al. Associations of grip strength with cardiovascular, respiratory, and cancer outcomes and all cause mortality. BMJ. 2018;361:k1651.
9. Fragala MS, Kraemer WJ, Staron RS, et al. Physiological neuromuscular adaptations to resistance training in aging. J Appl Physiol. 2019;126(3):713-731.
10. Wolfe RR. The underappreciated role of muscle in health and disease. Am J Clin Nutr. 2006;84(3):475-482.
11. Aagaard P, Suetta C, Caserotti P, et al. Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure. Scand J Med Sci Sports. 2010;20(1):49-64.
12. Morton RW, Murphy KT, McKellar SR, et al. A systematic review, meta-analysis and meta-regression of the effect of protein supplementation on resistance training-induced gains in muscle mass and strength in healthy adults. Br J Sports Med. 2018;52(6):376-384.
13. Mandsager K, Harb S, Cremer P, et al. Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Netw Open. 2018;1(6):e183605.

⚠️ EDUCATIONAL DISCLAIMER: This content is strictly for educational and informational purposes and does not constitute medical advice, diagnosis, treatment, or a physician-patient relationship.

This contrast is exactly why we need to change the story about creatine.

I am a preventive and lifestyle medicine physician, not a competitive bodybuilder. And yet, creatine is one of the very few daily recommendations I make regularly, particularly as we age.

Here is the truth, stripped of the gym hype: Creatine is one of the most thoroughly researched, cost-effective, clinically validated, and safe tools available for supporting cellular energy, protecting your brain, and preserving your muscles as you get older. It isn't a steroid. It's a bioenergetic health tool. Let’s unpack the science.

What Creatine Actually Is (A Quick Biology Lesson)
You don’t have to get lost in biochemistry to understand how creatine works. You just need to understand how your cells create energy. The single energy currency that powers every action in your body—from blinking your eyes to holding a difficult yoga pose like Dancer’s Pose is ATP (Adenosine Triphosphate).

ATP provides energy by "tripping" a phosphate group, changing ATP into ADP (Adenosine Diphosphate). When this shift happens, energy is released. To keep moving, ADP must immediately become ATP again. Think of it as a dead battery that needs to be recharged instantly. Your body does this in several ways (including breathing oxygen and burning fuel), but the fastest, most effective way to "recharge the battery" is with Phosphocreatine.
By supplementing with creatine, you increase your body’s stores of phosphocreatine. This acts as an immediate energy reserve, allowing your cells to recycle energy rapidly. The high-demand tissues that benefit most? Your muscles and your brain.

Creatine for Muscle Vitality: Strength & Cell Volumization:
As we age, we all confront a serious clinical challenge: Sarcopenia, or the involuntary loss of muscle mass, strength, and function.
Starting around age 30, muscle mass begins to decline, and the rate accelerates after 60. This is not about aesthetics. Healthy muscle tissue is vital because it is a major driver of metabolic health and insulin sensitivity, your best structural insurance against falls, and the literal framework of physical independence and vitality.
This is where creatine is helpful operating through two critical mechanisms.

The Performance Boost: Rapid Energy
Countless clinical studies of older adults show that creatine supplementation, when paired with regular resistance training, improves muscle mass and real-world functional strength far more than training alone. Maximizing your energy reserves allows you to do the consistent, foundational work required to keep doing the activities you love, longer.

The Hydration Signal: Intracellular Cell Volumization
This second mechanism is vital to understand. Creatine is an osmolyte, or an "osmotically active compound," which means it has a natural ability to attract and bind water molecules.
To pull creatine inside, your cells use specialized transporters. As they accumulate creatine, they must maintain balance, triggering osmosis. Water follows the creatine into the muscle, a process known clinically as Intracellular Cell Volumization. Crucially, Intracellular means water is stored inside the actual muscle cells, contrasting sharply with the "bloat" that patients fear, which refers to extracellular water retention under the skin.

This specialized cellular hydration isn't just cosmetic; it act as a powerful anabolic (muscle-building) and anti-catabolic (anti-breakdown) signal. Research suggests that swelling a muscle cell stimulates pathways for protein synthesis and reinforces its structural stability—which directly contributes to counteracting the muscular decline associated with aging.

Look again at that picture of me of holding a yoga balance on uneven rock on a high-altitude peak. That functional stability and structural integrity are not "gym bro" goals; they are goals for life. Integrating creatine monohydrate is a high-yield optimization to preserve that vitality.

Creatine for Cognitive Resilience: Your Brain as a Metabolic Powerhouse
The most exciting, emerging data around creatine isn't about muscles at all. It's about your brain. While the brain makes up only about 2% of your body mass, it demands up to 20% of your total metabolic output. To maintain neural processing, focus, and memory, your brain requires staggering amounts of constant energy.

Modern evidence indicates that neurons utilize creatine similarly to muscles to maintain energy homeostasis. While general whole-body hydration is always key for clear thinking, for the brain, the therapeutic driver of the cognitive benefits seen in clinical trials is not cellular hydration, but bioenergetic buffering.

Supplementing with creatine maximizes your brain’s pool of phosphocreatine. This energy tap allows neurons to instantly recharge ATP at lightning speed during mental surges such as mental fatigue or sleep deprivation, where the neuron's standard stream of energy synthesis is insufficient. This support of brain bioenergetics provides a critical resilience against cognitive decline as you age.

The "Filter": Debunking the Social Media Scares:
When my patients are hesitant about creatine, it is rarely the science they are worried about. It’s the viral rumors they read online. Let’s clear those up from a clinical perspective.

The Kidney Scare:
This is the single most common concern. It likely comes from confusing a normal, safe marker of muscle metabolism (creatinine) with a marker of kidney function. Modern, randomized clinical studies confirm that creatine monohydrate supplementation is perfectly safe for kidney function in healthy individuals when taken at standard doses.

The Hair Loss Myth:
This scare is based on one old (2009), single study that showed a slight increase in DHT (a hormone associated with male pattern baldness). That study was never replicated, and zero rigorous clinical trials on the actual compound creatine have ever linked it to actual hair loss in humans. It is an unverified theory, not a medical fact.

The "Bloat" Concern:
We addressed this above. Creatine does pull water into the muscle cell (Intracellular Cell Volumization), which is a key mechanism for muscle health. For most people on a standard dosage (not a bodybuilder "loading" phase), this results in a temporary, minor weight gain on the scale, but minimal systemic bloat or puffiness. You are simply optimizing the hydration status of your vital functional tissues.

How Creatine is typically Integrated:

I want to move you past the confusing "stacking" protocols of the past. The plan is simple.

• Choose the Right Type:  Creatine Monohydrate. It is the cheapest, most effective, and most widely researched form. Don't be fooled by expensive "new" versions with zero comparative data.
• The Dosage: Most Research has suggested 3-5 grams daily.
• What You Will Notice: This is not a stimulant like caffeine. You will not "feel" anything immediately. The benefit is cumulative, supporting recovery, energy output during training, and overall brain energy homeostasis over time.
  
  

In an era of viral, low-yield wellness trends, creatine stands as a rare, evidence-backed powerhouse for cellular health. In an era of viral, low-yield wellness trends, creatine stands as a rare, evidence-backed powerhouse for cellular health.

Summary:
It is time to look past the bodybuilding magazines and recognize creatine as a  tool for preserving muscle strength, maintaining cellular integrity, and supporting brain energy as we age. For a vibrant life like the one visualized in my balancing pose, protecting your muscles and your brain energy must be proactive. Integrating creatine can be helpful.

🧬 Clinical Reference: Forbes, S. C., et al. (2023). Creatine Supplementation and Aging: A Review of Potential Mechanisms and Practical Applications. Nutrients, 15(19), 4255. doi:10.3390/nu15194255
⚠️ Medical Disclaimer: This content is strictly for educational and informational purposes only and does not constitute individual medical advice or a substitute for professional medical expertise. Supplements can interact with medications. Always consult with a qualified healthcare provider before making changes to your supplement routine.

The foundation of this practice is lifestyle medicine. Lifestyle medicine uses lifestyle factors to promote healthy aging.  The 4 drivers of healthspan and longevity are:

• Activity
• Sleep
• Nutrition
• & Mental Wellbeing

Below, I will discuss each of these fundamentals: 


Activity is the single most important factor of healthspan. We have seen that even 10 minutes a day of exercise could add years to a person's life (Church, 2007). And perhaps less newsworthy, but certainly interesting, was a study published in 2014 that showed runners were far less likely to die of heart disease regardless of BMI or smoking status (Artero, 2014). In an article published in the Journal of the American Medical Association, the Cleveland Clinic analyzed 23 years of patient data and 122,007 patients. They evaluated the association of all-cause mortality (death for any reason) and cardiorespiratory fitness. They also evaluated age, gender, race/ ethnicity, and co-morbidities such as diabetes, hypertension, smoking and coronary artery disease (CAD).

The findings were remarkable. Their findings on typical risk factors were consistent with what we often see. Having diabetes, CAD, smoking, or hypertension conferred approximately a 1.2-1.4X mortality risk or an approximately 20-40% increase risk of death from any cause, but here is the remarkable aspect, being out of shape or having low fitness conferred a 5.0X mortality risk that is a 400% increase risk of death from any cause over any time period. In other words being out of shape was 3 to 4 times worse than smoking, having diabetes or having CAD.  (Mandsager, 2018) (For more information see my post on VO2 max)

Sleep
Sleep has become the new currency. Studies have shown that adequate sleep lowers the risk of some cancers (Thompson, 2011; Irwin,1994; Hakim, 2014), the risk of diabetes (Knutson,2007; Sheen,1996)  and helps maintain heart health. One study showed that 6 or less hours of sleep led to a 200-300% increased risk of coronary artery calcification (King, 2008). Proceedings of the National Academy of Sciences (PNAS) published an article that found limiting sleep to less than 6 hours for 1 week changed the activity of 711 genes or about 3% of the total genome (Möller-Levet, 2019). It found that the sleep reduction down-regulated genes that were associated with healthy immune functioning and up-regulated genes associated with chronic inflammation and tumor production. (For more information see my post on sleep.)

Nutrition:
Nutrition is a loaded term. It has a different meaning to different groups of people. From a healthspan perspective, there are many ways to eat well. I believe the most important thing we can do is to keep sugars low. According to the 2010 Dietary Guidelines advisory committee our top sources of calories for North Amercians come from: 

1. Grain-based desserts (cakes, cookies, donuts, pies, crisps, cobblers, and granola bars)
2.  Yeast breads
3.  Chicken and chicken-mixed dishes
4.  Soda, energy drinks, and sports drinks
5.  Pizza
6.  Alcoholic beverages
7.  Pasta and pasta dishes
8.  Mexican mixed dishes
9.  Beef and beef-mixed dishes
10.  Dairy desserts

 

When our top sources of calories are grain based desserts, processed foods and sodas, we are setting ourselves up for long term health consequences. High sugar foods and processed foods containing sugars are known risk factors for diabetes, obesity, metabolic syndrome, cancers, autoimmune diseases and chronic inflammation (Ma, 2022). Once we have minimized sugars  we can begin to look at timing and quantity of food, fiber and protein intake based on genetics, labs, activity and goals. (For more information please see this post.)

Emotional health and mental wellbeing:
Maintaining emotional health takes many forms. There is no one size fits all. For some meditation may be an important factor for others, community gives them a sense of wellbeing.  

Meditation practices as short as 3-4 minutes have been shown to increase parasympathetic tone, decreasing our sympathetic tone with improvements seen in blood pressure, immune function and digestion (Creswell, 2017).  Many studies demonstrate that meditation can change the balance of our autonomic nervous system (the part of our nervous system we don’t control)  from that of fight or flight (sympathetic) to that of rest, healing and digestion (parasympathetic) (Koopman, 2011; Amihai, 2015).  When our sympathetic nervous system is over activated for days, weeks or months we experience more stress and our bodies experience more inflammation (Bellinger, 2018).

Community has also been implicated in longevity. Many years ago there was a town in Pennsylvania where people seemed to have unusual longevity. Harvard researchers looked for many years as to why these people had such unusual longevity.  They evaluated the foods, water, genetics among other things and could not find anything that differed significantly from neighboring towns, except, that this town had an unusually strong family and community relationships. Sadly, over the years, as the town modernized and the cohesiveness dissolved, the longevity seen in this town regressed to that of neighboring towns (Egolf, 1992). (For more information on mental wellbeing please see this post.)

Lifestyle medicine is meant to be practiced as a form of preventative not reactive medicine. While it is helpful to start lifestyle measures at any point, it is optimal to start early with relative consistency, understanding perfection is not possible.

I hope you found this helpful.

Amy Savagian, MD


References:

Amihai, I., Kozhevnikov, M. (2015). The Influence of Buddhist Meditation Traditions on the Autonomic System and Attention. Biomed Res Int. 731579. Published online 2015 Jun 4. doi: 10.1155/2015/731579

Artero EG, Jackson AS, Sui X, Lee DC, O'Connor DP, Lavie CJ, Church TS, Blair SN.  (2014). Longitudinal Algorithms to Estimate Cardiorespiratory Fitness: Associations with Nonfatal Cardiovascular Disease and Disease-Specific Mortality.  Journal of the American College of Cardiology, Jun, 63 (21):2289-96. doi: 10.1016/j.jacc.2014.03.008. Epub 2014 Apr 2.  

Bellinger, D.L.1, Lorton, D. (2018). Sympathetic Nerve Hyperactivity in the Spleen: Causal for Nonpathogenic-Driven Chronic Immune-Mediated Inflammatory Diseases (IMIDs)? Int J Mol Sci. 2018 Apr; 19(4): 1188. Published online 2018 Apr 13. doi: 10.3390/ijms19041188

Church TS, Earnest CP, Skinner JS et al. (2007). Effects of Different Doses of Physical Activity on Cardiorespiratory Fitness Among Sedentary, Overweight or Obese Postmenopausal Women With Elevated Blood Pressure: A Randomized Controlled Trial. Journal of the American Medical Association JAMA, 297(19), 2081-2091. https://jamanetwork.com/journals/jama/fullarticle/1108370

Creswell, David J. (2017). Mindfulness Interventions. Annual Review of Psychology. Vol. 68:491-516 (Volume publication date January 2017). First published online as a Review in Advance on September 28, 2016. https://doi.org/10.1146/annurev-psych-042716-051139

Egolf B, Lasker J, Wolf S, Potvin L. The Roseto effect: a 50-year comparison of mortality rates. Am J Public Health. 1992 Aug;82(8):1089-92. doi: 10.2105/ajph.82.8.1089. PMID: 1636828; PMCID: PMC1695733.

Hakim et al., (2014). Tumors grow more in sleep deprived mice: Fragmented sleep accelerates tumor growth and progression through recruitment of tumor-associated macrophages and TLR4 signaling. Cancer Res. Mar 1;74(5):1329-37. doi: 10.1158/0008-5472.CAN-13-3014

Irwin et al., (1994). “Sleep deprivation reduces natural killer cells: Partial sleep deprivation reduces natural killer cell activity in humans. Psychosomatic Medicine. 56(6):493–498. 


King et al. (2008). Short sleep duration and incident coronary artery calcification. JAMA 300(24):2859-66. doi: 10.1001/jama.2008.867.

Knutson et al. (2007). The metabolic consequences of sleep deprivation. Sleep Medicine Reviews. Volume 11, Issue 3, Pages 163-178. https://doi.org/10.1016/j.smrv.2007.01.002 

Koopman, F.A., Stoof, S. P., Straub, R. H. , van Maanen, M. A. , Vervoordeldonk, M. J. , Tak,  P. P. (2011) Restoring the Balance of the Autonomic Nervous System as an Innovative Approach to the Treatment of Rheumatoid Arthritis. Mol Med; 17(9-10): 937–948. Published online 2011 May 20. doi: 10.2119/molmed.2011.00065


Ma X, Nan F, Liang H, Shu P, Fan X, Song X, Hou Y, Zhang D. Excessive intake of sugar: An accomplice of inflammation. Front Immunol. 2022 Aug 31;13:988481. doi: 10.3389/fimmu.2022.988481. PMID: 36119103; PMCID: PMC9471313.

Mandsager K, Harb S, Cremer P, Phelan D, Nissen SE, Jaber W. (2018) Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Network Open. 1(6):e183605. doi:10.1001/jamanetworkopen.2018.3605
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2707428

Möller-Levet CS et al. 2019 Effects of insufficient sleep on circadian rhythmicity and expression amplitude of the human blood transcriptome. Proc Natl Acad Sci U S A. Mar 19;110(12):E1132-41. doi: 10.1073/pnas.1217154110.

Sheen et al. (1996). Relationships between sleep quality and glucose regulation in normal humans. American Journal of Physiology. Volume 271, No 2,  01 AUG 1996. https://doi.org/10.1152/ajpendo.1996.271.2.E261-E270.

Thompson et al., (2011). Colorectal cancer and sleep: Short duration of sleep increases risk of colorectal adenoma. Cancer. Feb 15;117(4):841-7. doi: 10.1002/cncr.25507.
https://pubmed.ncbi.nlm.nih.gov/20936662/

​

What can we do to optimize cognitive health? We first need to generally understand the mechanisms that are believed to contribute to cognitive decline.  These include: abnormal glucose metabolism, inflammation, oxidative stress, poor trophic factor signaling, and dysfunctional calcium flux (Isaacson et al 2018). In the section below I will discuss each of these and then lifestyle factors that may modulate the mechanisms contributing to cognitive decline.

Abnormal glucose metabolism:
Poor glucose metabolism, as seen in diabetes and overfed states such as obesity are known to contribute to insulin resistance at the level of the neuron. Type 2 diabetes is generally a state of hyperinsulinemia (high insulin). This state promotes neuronal inflammation and amyloid deposition. Interestingly, a high-fat, low-carbohydrate ketogenic diet, which is known to limit insulin production, in mice that genetically over-express amyloid beta resulted in a 25% reduction of amyloid burden compared to mice on a standard diet (Van der Auwera et al., 2005).

Inflammation:
Inflammation is also thought to worsen cognitive function. Studies have shown elevated inflammatory markers in patients with Alzheimer's Disease (AD). To modulate this inflammation, we can consider decreasing dietary sugars, adding in medications or supplements to decrease inflammation and assuring adequate sleep (as sleep deprivation increases biomarkers of inflammation) (Irwin et al., 2006). Social engagement may also play a role in decreasing the risk of AD by improving immune function (Bower et al., 2003, Friedman et al., 2007).

Oxidative stress: 
Patients with AD show many signs of oxidative stress including protein and DNA oxidation as well as lipid peroxidation. The increased oxidation comes from reactive oxygen species (ROS). ROS is important for normal cellular activity, but when there is an imbalance between the production and clearance of ROS the cell undergoes oxidative stress. People with APOe4 have increased markers of oxidative stress (Jofre-Monseny et al., 2008). To decrease oxidative stress, we need to increase the clearance of ROS or decrease the production.  

Trophic Factors: 
Trophic factors are basically growth factors. They include molecules such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) that are responsible for brain plasticity and improving cellular survival by preventing activation of the caspase system. BDNF is particularly important in the hippocampus (where  memory consolidation occurs). In AD, people have less trophic factors, which in the presence of increased amyloid can lead to neuronal death. (Guo et al., 1997)

Amyloid burden:
In AD, patients are known to have increased extracellular amyloid.  The role of amyloid is not fully understood–some people liken it to scar tissue, but as it accumulates, it causes more inflammation and increases oxidative stress. Interestingly, the oxidative stress, impaired glucose metabolism and inflammation can also lead to more amyloid deposition.

Dysfunctional calcium signaling:
In AD we see increased intracellular and mitochondrial calcium. These elevated levels can increase ROS, leading to increased oxidative stress, inflammation and amyloid production. Together this leads to increased rates of cell (neuronal) death. 

Reducing risk should have a multi-factorial approach.  Each approach may reduce risk across several domains. For example treating insulin resistance may help with glucose metabolism and downstream effects of inflammation and oxidative stress. Watson and Craft (2003) demonstrated that treating insulin resistance may reduce the risk of AD.

Targeted nutrition can reduce the risk of AD through mechanisms of insulin resistance, inflammation and oxidative stress. We can improve insulin resistance by reducing processed sugars and the overfed state. Diets such as a mediterranean or low carb diet have been shown to be helpful.  (Scarmeas et al., 2009, Volek et al., 2004).

Sleep deprivation has been shown to increase inflammatory cytokines. Assuring adequate sleep will decrease inflammation, improve insulin resistance and help with calcium toxicity. 

Stress management can help reduce cortisol levels that impact insulin resistance, oxidative stress, trophic factors, calcium toxicity and amyloid burden.

Exercise both resistance and aerobic helps with glucose metabolism, insulin resistance, oxidative stress and trophic factors.

Hormone replacement may lower amyloid burden and improve trophic factors. 

Drugs can target inflammation, oxidative stress and amyloid.  

Supplements may also play a role as it relates to insulin resistance, inflammation, oxidative stress and calcium toxicity.

Based on cognitive testing results we may also consider specific interventions that engage executive planning, motor speed, processing speed and more.

Alzheimer’s and mild cognitive impairment has a long window of brain changes before any symptoms arise. With monitoring and a targeted lifestyle plan, we can significantly reduce the risk of dementia.

References:
Alzheimer's Universe. Weill Cornell Medicine. Retrieved November 30, 2022, from https://www.alzu.org/.
 
Bower, J. E., Kemeny, M. E., Taylor, S. E., and Fahey, J. L. (2003). Finding positive meaning and its association with natural killer cell cytotoxicity among participants in a bereavement-related disclosure intervention. Ann. Behav. Med. 25, 146–155. doi: 10.1207/S15324796ABM2502_11
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Photo cred:​https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2707428

Photo cred: ​https://oss.adm.ntu.edu.sg/xloh002/activity-range/

Another way to evaluate fitness is the measure the volume of oxygen the body can use, measured in milliliters per kilogram per minute. This measurement is called VO2 max and it is the gold standard for measuring aerobic fitness. Vo2max depends on cardiac output (the pumping ability of the heart stroke volume x heart rate), air exchange in the lungs, blood flow to the muscles and atmospheric oxygen available (due to elevation). Vo2 max is measured by an exercise physiologist as the patient or athlete runs or bikes at progressively harder levels while wearing a mask connected to a machine that evaluates exhaled oxygen and carbon dioxide. Using VO2max we can evaluate relative endurance. 

To me the data on fitness argues that fitness testing, ideally a VO2max test should be a part of every person's preventative health plan. We need to understand where we are in order to implement a targeted plan to achieve our health goals.

References:
​
Ruegsegger GN, Booth FW. Health Benefits of Exercise. Cold Spring Harb Perspect Med. 2018 Jul 2;8(7):a029694. doi: 10.1101/cshperspect.a029694. PMID: 28507196; PMCID: PMC6027933.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6027933/ 

​Mandsager K, Harb S, Cremer P, Phelan D, Nissen SE, Jaber W. Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Netw Open. 2018;1(6):e183605. doi:10.1001/jamanetworkopen.2018.3605
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2707428

​Blair SN, Kohl HW, Paffenbarger RS, Clark DG, Cooper KH, Gibbons LW. Physical Fitness and All-Cause Mortality: A Prospective Study of Healthy Men and Women. JAMA. 1989;262(17):2395–2401. doi:10.1001/jama.1989.03430170057028
https://jamanetwork.com/journals/jama/article-abstract/379243

​Meyers J, Prakash M, Froelicher V et al. Exercise Capacity and Mortality among Men Referred for Exercise Testing. N Engl J Med 2002; 346:793-801. DOI: 10.1056/NEJMoa011858 https://www.nejm.org/doi/full/10.1056/NEJMoa011858

Blair S et al. Age-Specific Exercise Capacity Threshold for Mortality Risk Assessment in Male Veterans. Circulation 2014;130:653–658. 
https://www.ahajournals.org/doi/full/10.1161/circulationaha.114.009666

https://med.virginia.edu/exercise-physiology-core-laboratory/fitness-assessment-for-community-members/vo2-max-testing/
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Moore S et al. Leisure Time Physical Activity of Moderate to Vigorous Intensity and Mortality: A Large Pooled Cohort Analysis. PLOS Medicine. November 6, 2012 https://doi.org/10.1371/journal.pmed.1001335
https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1001335

Bone Density:
Bone density is an important metric as it helps us to understand risk of fractures. Fractures particularly hip fractures have a high morbidity and mortality. According to the CDC there are approximately 300,000 hip fractures per year in those 65 years and older [CDC]. Given that there are approximately 56 M Americans who are 65 years or older this gives a crude approximation of 1 hip fracture per every 187 Americans over the age of 65. Of these, studies have found that approximately 25-50% will die over the next year depending on the study. [Cui et al, Schnell et al]  This is a staggering number for something that is preventable. For those of us under 65, we should be doing all we can to prevent bone loss. A DXA reports your score for hip, femoral neck and lumbar spine as a T and Z scores. The z-score compares your bone density to others your age. The T-score is the number we care about and it compares your bone density to that of a 30-year-old. A T score of -1.0 or higher is considered normal bone density. A score of -1.0 and -2.5 is in the osteopenia range, and anything under -2.5 is considered the osteoporosis range.

Below, you can see a sample report.  While osteopenia and osteoporosis are always defined by the T score of -1 and -2.5 at every age, the downtrending lines represent bone density by age (the average and +/-1 standard deviation), in essence showing the expected bone loss by year.
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Graphs derived from NHANES & GE Lunar databases.

Graphs from LEAD cohort published in Nature

To Summarize DXA scans are helpful in understanding if your fat is metabolically concerning, if you need to gain muscle and how your bone density is faring. I tried to illustrate why it is important to understand each of these factors.

If you schedule a dexa try to always schedule with the same machine, avoid calcium supplements for 24 hours before the scan and avoid food for 3 hours before the scan. Hydration can play a role with more water giving higher lean mass reading.

DXAs are important because they allow us to benchmark and determine if we need to address muscle mass, VAT or bone density. It allows us to being thinking about nutritional goals and resistance training.

I hope this was a helpful,

Amy

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References:

​Bachettini, N.P., Bielemann, R.M., Barbosa-Silva, T.G. et al. Sarcopenia as a mortality predictor in community-dwelling older adults: a comparison of the diagnostic criteria of the European Working Group on Sarcopenia in Older People. Eur J Clin Nutr 74, 573–580 (2020). https://doi.org/10.1038/s41430-019-0508-8

CDC.gov, Hip Fracture Risks, Retrieved 1/3/23 https://www.cdc.gov/falls/hip-fractures.html#:~:text=Each%20year%20over%20300%2C000%20older,are%20hospitalized%20for%20hip%20fractures.&text=More%20than%2095%25%20of%20hip,2%20usually%20by%20falling%20sideways.&text=Women%20experience%20three%2Dquarters%20of%20all%20hip%20fractures.

​Cui, Z., Feng, H., Meng, X. et al. Age-specific 1-year mortality rates after hip fracture based on the populations in mainland China between the years 2000 and 2018: a systematic analysis. Arch Osteoporos 14, 55 (2019). https://doi.org/10.1007/s11657-019-0604-3

Oudbier S, Goh J Looijaard S, Reijnierse E, Meskers C, Maier A, Pathophysiological Mechanisms Explaining the Association Between Low Skeletal Muscle Mass and Cognitive Function, The Journals of Gerontology: Series A, Volume 77, Issue 10, October 2022, Pages 1959–1968, https://doi.org/10.1093/gerona/glac121

​Schnell S, Friedman SM, Mendelson DA, Bingham KW, Kates SL. The 1-year mortality of patients treated in a hip fracture program for elders. Geriatr Orthop Surg Rehabil. 2010 Sep;1(1):6-14. doi: 10.1177/2151458510378105. PMID: 23569656; PMCID: PMC3597289.

Srikanthan P, Karlamangla AS. Muscle mass index as a predictor of longevity in older adults. Am J Med. 2014 Jun;127(6):547-53. doi: 10.1016/j.amjmed.2014.02.007. Epub 2014 Feb 18. PMID: 24561114; PMCID: PMC4035379.

Taniguchi Y, Makizako H, Kiyama R, Tomioka K, Nakai Y, Kubozono T, Takenaka T, Ohishi M. The Association between Osteoporosis and Grip Strength and Skeletal Muscle Mass in Community-Dwelling Older Women. Int J Environ Res Public Health. 2019 Apr 6;16(7):1228. doi: 10.3390/ijerph16071228. PMID: 30959864; PMCID: PMC6480005

Tessier et al. Association of Low Muscle Mass with Cognitive Function During a 3 Year Follow up Among Adults Aged 65 to 86 Years in the Canadian Longitudinal Study on Aging. JAMA Network Open 2022;5(7):e221996. doi:10.1001/jamanetworkopen.2022.19926
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