Life Spans

Jacob Schor ND, FABNO

September 20, 2015



I’ve been walking down to City Park on my own this past week.  Our dog Poppy is having trouble, a pulled muscle that has been slow to heal; she’s been hopping about on three legs, crying in pain. I skipped walking for the first few weeks of her invalid-hood, but of late I sneak out our back gate for my regular walk.


I’ve made the same morning circuit around Ferril Lake for nearly a quarter century now, varying it on occasion, some days going clockwise on other days, counterclockwise.  Back in the 1990s, when I ran the loop, I would make multiple laps.  With Poppy, a single lap, about two and half miles, has been distance enough most mornings.  Of late though our normal walk has been impossible for her.


I need the routine as it gives me much needed time to process my thoughts.  Watching Poppy’s sudden transition from being a middle-aged but active dog into an old dog has left me pondering this business of aging, most specifically the fact that we have a lifespan. 


The lifespan of dogs appears to vary by size.  The big breeds are shorter lived than the small breeds. 

Does the same hold true for humans?  A number of older studies claimed that taller people live longer, suggesting that men over 6 feet tall had lower risk of death from heart disease than shorter men.  Yet a paper by Thomas Samaras and colleagues solidly counters this notion and concludes that larger size in humans was associated with increased risk of both heart disease and cancer. [1]   Kind of like with dogs.


Watching the dog age reminds me that I’ve aged quite a bit during this span of years.  There was a time in which three laps around the lake were required to count as exercise, one lap now is totally adequate to start my day with.  I’m not getting younger either.


Almost all living things have life spans. 


There are several different ways that we measure or describe life span.  Maximum span is usually defined to be the mean life span of the most long-lived 10% of a given cohort.  It is also sometimes defined as the age at which the oldest known member of a species or an experimental group has died.  We can also talk about mean life span, average life span and so on.  They are all descriptors of the same phenomenon though.  All living things die sooner or later and most species appear to have a clearly defined time period within which boundaries their life is lived.


It is curious to note that the hearts of most mammals, from mouse to elephant to human, are good for approximately the same number of beats in their lives, an average of 7.3 +/- 5.6 x 10(8) heart beats/lifetime.[2]    [A fact that should make you wonder midway through your next cardio workout; ‘Is this really a good idea?’]

[NOTE: This idea may not be quite accurate and we shouldn’t repeat it here but it’s a common and interesting thought.]



Some animals appear to have relatively long life spans, including Koi (200 years), Greenland Sharks (200+ years), Galapagos tortoises (190 years), and Bowhead Whales (200 years).  The longest lived animal to date was a now deceased member of that Arctica islandica species of edible clam that apparently was 507 years old when examined by biologists a few years ago. [3]  

Plants may have short one-year life spans, in which case they are called annuals, or longer life spans.  Some trees appear to have tremendously long lives; certain Giant Sequoia trees are estimated to be over 3,000 years old, a Great Basin Bristlecone Pine is supposedly 4,846 years old and a Quaking Aspen colony in Utah is about 80,000 years old.  Actually they may not have defined life spans at all.



Why is it that people rarely live past 100?


That people have defined and limited spans to their existence is curious; few ‘healthy’ people, given the choice, would chose to have a shorter life.  Most people want to live as long as possible, or at least that’s what it seems, given the effort, financial resources and commitment people in middle age and later invest toward preservation of their health. 


We aren’t alone in wondering about this.  People have obviously pondered this question for eons.  Of late the scientists are creating mathematical models to justify the hard facts of life.


Aging is a genetic mechanism that prevents humans and other organisms from living as long as they could, or might want to. In a June 2015 article in Science, Justin Werfel, Donald E. Ingber and Yaneer Bar-Yam suggested that “… age-related ailments provide the evolutionary benefit of shortening life span, which conserves resources for future generations…. relatively short-lived organisms fare better over time than longer-lived and even immortal competitors….. shortened life spans are ubiquitous in nature, including in humans. If people are programmed to die…., then scientists should focus on discovering and deactivating the genetic mechanism. Instead of treating age-related diseases, we can address them by intervening in the process of aging.” [4] 


Aging appears to be evolution’s attempt at planned obsolescence, a way to get older members of a species off the road, so to speak. 


The idea that science may in the future be able to intervene in the process of aging comes with a certain amount of irony and also some horror to this writer.  The irony is that there is a fair degree of overlap between those people who invest in living healthy lives so they can live longer and those people who are deeply opposed to research on genetic modification.  What will happen if the answer to life extension turns out to be becoming your own genetically modified organism?  The horror of course is that offering genetic modification to those in society with the most resources would counter evolution’s goal of getting those that consume an inordinate share of resources out of the way.  Only the richest could afford immortality; what if Trump got to live forever?


The older we get the more we spend on healthcare: “…… health care costs increase by age with the exception of the very youngest ages. Costs, on average, are very high in the first year or two of birth and drop significantly by age five. At that point, costs increase modestly through the teen years. Female costs then begin to accelerate more quickly during child-bearing ages and flatten out in the 40s before increasing again. Male costs are relatively flat in the 20s and begin to accelerate after age 30, but remain lower on a per person basis than females in the same age group. The “cross-over age” occurs in the early 60s, when per capita spending for males exceeds that for females. Medicare ….for beneficiaries age 65 and older continue to increase with age. Males continue to have higher costs than females for whom per person costs start to decline around age 90.”[5] 



To continue with the car analogy, the older we get the more we cost to operate, especially once past warranty; our gas mileage goes down and we become the metaphorical ‘gas hogs of society.’  While we can measure the constantly increasing cost to society of older members of the species in dollar amounts, in earlier times this cost was measured in food in the pantry; no wonder evolution so favors limited life spans.


Back in 2004 when everything seems to have costs less than it does today, especially health care, “Per capita lifetime expenditure [for healthcare was] … $316,600, a third higher for females ($361,200) than males ($268,700). Two-fifths of this difference owes to women's longer life expectancy. Nearly one-third of lifetime expenditures is incurred during middle age, and nearly half during the senior years. For survivors to age 85, more than one-third of their lifetime expenditures will accrue in their remaining years.” [6]


Back in naturopathic school, this fact, that most healthcare costs were incurred at the very tail end of life was used as an argument to encourage more preventive health care, using another car analogy, we should invest more in routine maintenance. We were trained to ask people “How often do you change the oil in your car?  Shouldn’t you do as much for your health?”  This was and probably still is an idea that makes sense to young doctors and perhaps young people as well, but in the big picture, it doesn’t really make sense. 


Sure, routine automotive maintenance sounds reasonable.  Never changing your car’s oil might shorten its life span,  but the number of car washes you drive it through, the number of times you vacuum the carpets, or even how often you change the windshield wipers isn’t going to change how many miles you can put on the engine.  Cars are designed to last their lifespan and then fall apart.  Like people, they cost more and more the older they get.  That’s why we donate them to NPR once they reach a certain age.  (the cars)


FYI: The longest living person whose dates of birth and date have been verified was Jeanne Calment, who lived to 122.


In naturopathic medicine we often talk of the Vis medicatrix naturae, the healing power of nature, a concept that is all but lost to modern mainstream medicine.  We describe this Vis as a force of nature, a force that impels living organisms to restore homeostasis, to return to normal function, or what we call health.  We seek out therapies and lifestyles that stimulate the action of this Vis in order to promote a return to health.


How does the Vis medicatrix naturae change as we age?  Does it become weaker?  Does this fundamental propensity to heal from illness come into conflict with evolution’s prescription for a limited life span?  It is hard to imagine that the Vis would be at odds with evolution?


Does naturopathic medicine, the therapies that elicit the Vis, become less effective the older we get? 

Or do they tip the scales away from the evolutionary impulse to get rid of us and favor an extended lifespan?


We talk about lifespan as genetic programming but that is so last century; it ignores the advances in genetics and our current science about just how complex genetic expression is.  It is worth consideration as to what actually changes with age that sets lifespan, for surely there must be some mechanism that distinguishes between those who live to only 50 and those who live twice as long.


Recently, Lopez-Otín et al in their paper “The Hallmarks of Aging” cataloged the molecular processes that decline with advancing age and that may explain this phenomenon of aging. These processes include epigenetic changes, loss of telomere function, declining protein homeostasis, increased cellular senescence, depletion of the stem cell pool, and altered intercellular communication.


The changes in appearance that characterize aging are governed by specific shifts in the reservoirs of proteins made by the body. Therefore, the mechanisms that change gene expression that vary with age are of interest. These shifts in protein production are mainly controlled by proteins that bind DNA and RNA, as well as by a variety of noncoding (nc) RNA, both short ncRNAs (mainly microRNAs) and long noncoding (lncRNAs). Together, these many factors appear to control aging by controlling gene expression transcriptionally and post-transcriptionally in many ways.  [7,8]  


In fact this appears to be exactly the idea that Costa et al are talking about in their July 2015 paper, when they write “As the DNA content of most cells within an organism remains largely identical throughout the life span, age-associated transcriptional changes must be achieved by epigenetic mechanisms. However, how aging may impact on the epigenetic state of cells is only beginning to be understood.”[9]   The current focus of interest by scientists is  these long noncoding RNAs (lncRNA):  


“Aging is a process during which progressive deteriorating of cells, tissues, and organs over time lead to loss of function, disease, and death. Towards the goal of extending human health span, there is escalating interest in understanding the mechanisms that govern aging-associated pathologies. Adequate regulation of expression of coding and noncoding genes is critical for maintaining organism homeostasis and preventing disease processes. Long noncoding RNAs (lncRNAs) are increasingly recognized as key regulators of gene expression at all levels - transcriptional, post-transcriptional and post-translational. In this review, we discuss our emerging understanding of lncRNAs implicated in aging illnesses. We focus on diseases arising from age-driven impairment in energy metabolism (obesity, diabetes), the declining capacity to respond homeostatically to proliferative and damaging stimuli (cancer, immune dysfunction), and neurodegeneration.” [10]


It is interesting to note that a number of lifetyle and nutritional factors make changes in these lncRNAs.  For example Wolfberry fruit (Lycium barbarum) improves elevated blood pressure in rats by affecting these lncRNAs. [11]   Berberine improves fatty liver disease apparently through down regulation of lncRNAs.[12]    Maternal diets during gestation appear to affect these lncRNAs [13]  and this certainly provides good argument that we might be able to affect lifespan more by investing money and effort into changing maternal diets that spending money toward the end of life.  At that point, the horse is out of the barn, so to speak.



It’s been about three weeks since I began writing this letter.  Poppy has slowly, week-by-week improved, but ever so slowly.  She’s learned, much to her embarrassment, to get in and out of the car using a collapsible ramp.  She is adamant about still coming to the office on workdays.  She’s gradually increased the distance she can walk, first to the corner, then slowly around the block, then two blocks and so on.  It has been a slow process.


Yesterday morning we ramped her up into the car and drove down to City Park for a slow walk around the lake, almost a full mile.  Poppy waded into the lake and paddled about, then came ashore and immediately rolled in goose poop.


Some of you will think I’m anthropomorphizing here, but once she sat up from that roll, tail wagging, a huge grin on her face, it felt clear to me she was saying, “It is great to be alive.”


The dog may be onto something.  As we age and see that the hours or days of our lives are no longer without end, life does get a more precious, the fact that we are alive a bit more appreciated. 





1. Samaras TT, Elrick H. Height, body size, and longevity: is smaller better for the human body?

West J Med. 2002 May;176(3):206-8.  Free text:


2.  Levine HJ. Rest heart rate and life expectancy. J Am Coll Cardiol. 1997 Oct;30(4):1104-6.

Free text:


3.  Munro D, Blier PU. The extreme longevity of Arctica islandica is associated with increased peroxidation resistance in mitochondrial membranes. Aging Cell. 2012 Oct;11(5):845-55.


 4. Programmed Death is Favored by Natural Selection in Spatial Systems. June 2015


5.  accessed September 8, 2015


6.  Berhanu Alemayehu and Kenneth E Warner. The Lifetime Distribution of Health Care Costs.

Health Serv Res. 2004 Jun; 39(3): 627–642.


 7.  López-Otin C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013;153:1194–1217.[PMC free article] [PubMed]


 8. Ioannis Grammatikakis, Amaresh C. Panda, Kotb Abdelmohsen, and Myriam Gorospe. Long noncoding RNAs (lncRNAs) and the molecular hallmarks of aging. Aging (Albany NY). 2014 Dec; 6(12): 992–1009.


9.  Costa MC, Leitão AL, Enguita FJ. Noncoding Transcriptional Landscape in Human Aging. Curr Top Microbiol Immunol. 2015 Jul 22. [Epub ahead of print]


10.  Kim 1, Kim KM, Noh JH, Yoon JH1, Abdelmohsen K, Gorospe M. Long noncoding RNAs in diseases of aging. Biochim Biophys Acta. 2015 Jul 2. pii: S1874-9399(15)00136-4.


11.  Zhang X1, Yang X2, Lin Y3, Suo M3, Gong L3, Chen J3, Hui R3. Anti-hypertensive effect of Lycium barbarum L. with down-regulated expression of renal endothelial lncRNA sONE in a rat model of salt-sensitive hypertension. Int J Clin Exp Pathol. 2015 Jun 1;8(6):6981-7. eCollection 2015.


12.  Yuan X1, Wang J2, Tang X3, Li Y4, Xia P5, Gao X6. Berberine ameliorates nonalcoholic fatty liver disease by a global modulation of hepatic mRNA and lncRNA expression profiles. J Transl Med. 2015 Jan 27;13:24.


 13. Gong L, Pan YX, Chen H. Gestational low protein diet in the rat mediates Igf2 gene expression in male offspring via altered hepatic DNA methylation. Epigenetics. 2010 Oct 1;5(7):619-26.