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/

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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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Friedman, E. M., Hayney, M., Love, G. D., Singer, B. H., and Ryff, C. D. (2007). Plasma interleukin-6 and soluble IL-6 receptors are associated with psychological well-being in aging women. Health Psychol. 26, 305–313. doi: 10.1037/0278-6133.26.3.305
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Guo, Q., Sopher, B. L., Furukawa, K., Pham, D. G., Robinson, N., Martin, G. M., et al. (1997). Alzheimer’s presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid β-peptide: involvement of calcium and oxyradicals. J. Neurosci. 17, 4212–4222.
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Isaacson et al. Mechanisms of Risk Reduction in the CLinical PRactice of Alzheimer’s Disease Prevention. Front. Aging Neurosci., 10 April 2018.doi: 10.3389/fnagi.2018.00096
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Irwin, M. R., Wang, M., Campomayor, C. O., Collado-Hidalgo, A., and Cole, S. (2006). Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation. Arch. Intern. Med. 166, 1756–1762. doi: 10.1001/archinte.166.16.1756
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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:
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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.
​

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

​
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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​In New York City, the rate of cases vs infections presented by Gov. Cuomo was approximately a multiple of 12, suggesting a much lower infection fatality rate. In Los Angeles, USC completed a study using antibody testing suggesting the we had 28-55 times more infections that cases reported. These are in-line with the Stanford/ Santa Clara study suggesting they had 50X more infections that cases reported. All of these studies optimistically show a much lower hospitalization and fatality rate.  Having said that, there are problems with the antibody tests, so we need to evaluate these tests and studies with some healthy skepticism. 

For my patients, I am offering the Quest RT-PCR for active symptoms and the Abbott serology test to evaluate prior exposure.  The Abbott serology test has been tested internally at Abbott and through a separate commercial lab. From internal testing Abbott reports a sensitivity of 100% and a specificity of 99.5%.  The outside lab validated the prior testing suggesting a sensitivity of 100% and a specificity of 99.4%. When evaluating antibody tests, the accuracy is very important as many of these tests are not very accurate.  The specificity of these tests is the more important parameter, as you want as few false positives as possible.

If you are not a patient of mine, but are interested in antibody testing, the FDA has given letters of authorization to some companies.  Click here for a complete list.  [https://www.fda.gov/medical-devices/emergency-situations-medical-devices/emergency-use-authorizations#covid19ivd]

With any of the tests, they should be done in conjunction with a conversation with your doctor.  The antibodies show past exposure.  The antibody seems to offer a window of protection, though there are questions related to seroconversion and the permanence of immunity after developing antibodies.

On a separate note, I wanted to include some educational links to excellent talks on SARS-CoV-2.

The first is by Dr. Olsterholm from the MN Center of Infectious Disease Research and Policy (CIDRAP)  He has 5 excellent podcasts thus far and many webinars available at this site. https://www.cidrap.umn.edu/covid-19/podcasts-webinars

The second excellent educational talk on SARS-CoV-2 is by Dr. Pamela Bjorkman a Cal-tech professor whose lab is currently evaluating the virus.  https://www.youtube.com/watch?v=OBcc_dk9Q9U

Be well,


Amy

I have been postponing putting out this aspect of my analysis for a week now. Everyday things seem to change, and I hoped my analysis would lead me elsewhere.  I want to spend a minute discussing what flattening the curve means,  what different aspects of the curve means and why I think we will have periods of self isolation/ social distancing and re-socialization over at least the next year.

The curve represents cases over time. The area under the curve represents the total number of cases.  By flattening the curve, we prevent hospitals from being overwhelmed. But it doesn’t mean we ”eradicate” the disease. We live in a globalized society where international travel still occurs and people can travel state to state.  If we don’t want to overwhelm the medical system and the number are correct, flattening the curve means we push out our time-line. It means this ends by one of three ways, we have a vaccine, we have an effective treatment or we reach herd immunity (which is thought to occur when about 2/3’s of the population has had the disease). 

Herd immunity, assuming the numbers are correct is several years away.  I think we will have a vaccine or treatment first.  So what does this mean?  I think it means we will go through multiple periods of social-distancing/ self isolation and re-socialization.  I’m hoping our numbers are wrong and that we are significantly underestimating the number of cases we have had. There are two main factors that give me hope.   In Iceland, half the people that have tested positive were asymptomatic and if Covid began in China in November and it has the transmissibility that it seems to have, hopefully many more people have had it than have realized it.
​
Let's walk through a scenario below of how LA County could reach herd immunity without overwhelming the system, and you will see why I think we will have a vaccine or treatment before herd immunity and why this won't be over in a few months, but we will likely see multiple cycles of social distancing and re-socialization.  

We know that LA County has 10.1M people this means we need about 6.7M cases of covid to reach herd immunity. If we assume 5% of cases need a ventilator that means we will have 336,602. people needing a vent.  Average duration on vent has been variable depending on data-sets, but let's assume the average person who needs a vent requires it for 12 days. 336,602 x 12 is about 4M vent days required.  Gov. Newsom has called for 10,000 vents in CA, that means we should have about 2500 in the LA area.  If we divide 4M vent days by 2500 vents we will get the number of days required to reach herd immunity without overwhelming the system.  The answer is about 4 years.  That assumes we have our numbers of cases correct, which is a big if.  Harvard public health came out yesterday suggesting a similar scenario, though I am sure they had a much more eloquent model.  What this means if these numbers hold is that we have a long winter ahead, but with social distancing, we can prevent the system from being overwhelmed.

​
Be well,

Amy