From Climate Change Reconsidered, a work of the Nongovernmental International Panel on Climate Change
The past two centuries have witnessed a significant degree of global warming as the earth recovered from the Little Ice Age and entered the Current Warm Period. Simultaneously, the planet has seen an increase in its atmospheric CO2 concentration. What effect have these trends had on human longevity? Although no one can give a precise quantitative answer to this question, it is possible to assess their relative importance by considering the history of human longevity.
Tuljapurkar et al. (2000) examined mortality over the period 1950-1994 in Canada, France, Germany (excluding the former East Germany), Italy, Japan, the United Kingdom, and the United States, finding that “in every country over this period, mortality at each age has declined exponentially at a roughly constant rate.” In discussing these findings, Horiuchi (2000) notes that the average lifespan of early humans was about 20 years, but that in the major industrialized countries it is now about 80 years, with the bulk of this increase having come in the past 150 years. He then notes that “it was widely expected that as life expectancy became very high and approached the ‘biological limit of human longevity,’ the rapid ‘mortality decline’ would slow down and eventually level off,” but “such a deceleration has not occurred.” “These findings give rise to two interrelated questions,” says Horiuchi: (1) “Why has mortality decline not started to slow down?” and (2) “Will it continue into the future?”
Some points to note in attempting to answer these questions are the following. First, in Horiuchi’s words, “in the second half of the nineteenth century and the first half of the twentieth century, there were large decreases in the number of deaths from infectious and parasitic diseases, and from poor nutrition and disorders associated with pregnancy and childbirth,” which led to large reductions in the deaths of infants, children, and young adults. In the second half of the twentieth century, however, Horiuchi notes that “mortality from degenerative diseases, most notably heart diseases and stroke, started to fall,” and the reduction was most pronounced among the elderly. Some suspected this latter drop in mortality might have been achieved “through postponing the deaths of seriously ill people,” but data from the United States demonstrate, in his words, that “the health of the elderly greatly improved in the 1980s and 1990s, suggesting that the extended length of life in old age is mainly due to better health rather than prolonged survival in sickness.”
Additional support for this conclusion comes from the study of Manton and Gu (2001). With the completion of the latest of the five National Long-Term Care Surveys of disability in U.S. citizens over 65 years of age—which began in 1982 and extended to 1999 at the time of the writing of their paper—these researchers were able to discern two trends: (1) disabilities in this age group decreased over the entire period studied, and (2) disabilities decreased at a rate that grew ever larger with the passing of time. Over the 17-year period of record, the percentage of the group that was disabled dropped 25 percent, from 26.2 percent in 1982 to 19.7 percent in 1999. The percentage disability decline rate per year for the periods 1982-1989, 1989-1994, and 1994-1999 was 0.26, 0.38, and 0.56 percent per year, respectively. Commenting on the accelerating rate of this disability decline, the authors say “it is surprising, given the low level of disability in 1994, that the rate of improvement accelerated” over the most recent five-year interval.
Looking outside the United States, Oeppen and Vaupel (2002) reported that “world life expectancy more than doubled over the past two centuries, from roughly 25 years to about 65 for men and 70 for women.” They noted that “for 160 years, best-performance life expectancy has steadily increased by a quarter of a year per year,” and they emphasized that this phenomenal trend “is so extraordinarily linear that it may be the most remarkable regularity of mass endeavor ever observed.”
These observations demonstrate that if the increases in air temperature and CO2 concentration of the past two centuries were bad for our health, their combined negative influence was minuscule compared to whatever else was at work in promoting this vast increase in worldwide human longevity. It is that “whatever else” to which we now turn our attention.
It is evident that in developed countries, the elderly are living longer with the passing of time. This phenomenon is likely due to ever-improving health in older people, which in turn is likely the result of continuing improvements in the abilities of their bodies to repair cellular damage caused by degenerative processes associated with old age, i.e., stresses caused by the reactive oxygen species that are generated by normal metabolism (Finkel and Holbrook, 2000).
Wentworth et al. (2003) report they found “evidence for the production of ozone in human disease,” specifically noting that “signature products unique to cholesterol ozonolysis are present within atherosclerotic tissue at the time of carotid endarterectomy, suggesting that ozone production occurred during lesion development.” According to Marx (2003), “researchers think that inflammation of blood vessels is a major instigator of plaque formation,” that “ozone contributes to plaque formation by oxidizing cholesterol,” and that the new findings “suggest new strategies for preventing atherosclerosis.” Also according to Marx, Daniel Steinberg of the University of California, San Diego, says that although it’s still too early to definitively state whether ozone production in plaques is a major contributor to atherosclerosis, he expresses his confidence that once we know for sure, we’ll know which antioxidants will work in suppressing plaque formation. [[ Reactive oxygen species]] (ROS) generated during cellular metabolism or peroxidation of lipids and proteins also play a causative role in the pathogenesis of cancer, along with coronary heart disease (CHD), as demonstrated by Slaga et al. (1987), Frenkel (1992), Marnett (2000), Zhao et al. (2000) and Wilcox et al. (2004). However, as noted by Yu et al. (2004), “antioxidant treatments may terminate ROS attacks and reduce the risks of CHD and cancer, as well as other ROS-related diseases such as Parkinson’s disease (Neff, 1997; Chung et al., 1999; Wong et al., 1999; Espin et al., 2000; Merken and Beecher, 2000).” As a result, they say that “developing functional foods rich in natural antioxidants may improve human nutrition and reduce the risks of ROS-associated health problems.”
Consider, in this regard, the common strawberry. Wang et al. (2003) report that strawberries are especially good sources of natural antioxidants. They say that “in addition to the usual nutrients, such as vitamins and minerals, strawberries are also rich in anthocyanins, flavonoids, and phenolic acids,” and that “strawberries have shown a remarkably high scavenging activity toward chemically generated radicals, thus making them effective in inhibiting oxidation of human low-density lipoproteins (Heinonen et al., 1998).” They also note that Wang and Jiao (2000) and Wang and Lin (2000) “have shown that strawberries have high oxygen radical absorbance activity against peroxyl radicals, superoxide radicals, hydrogen peroxide, hydroxyl radicals, and singlet oxygen.” And they say that “anthocyanins have been reported to help reduce damage caused by free radical activity, such as low-density lipoprotein oxidation, platelet aggregation, and endothelium-dependent vasodilation of arteries (Heinonen et al., 1998; Rice-Evans and Miller, 1996).”
Our reason for citing all of this information is that Wang et al. (2003) have recently demonstrated that enriching the air with carbon dioxide increases both the concentrations and activities of many of these helpful substances. They determined, for example, that strawberries had higher concentrations of ascorbic acid and glutathione when grown in CO2-enriched environments. They also learned that “an enriched CO2 environment resulted in an increase in phenolic acid, flavonol, and anthocyanin contents of fruit.” For nine different flavonoids there was a mean concentration increase of 55 percent in going from the ambient atmospheric CO2 concentration to ambient + 300 ppm CO2, and a mean concentration increase of 112 percent in going from ambient to ambient + 600 ppm CO2. Also, they report that “high flavonol content was associated with high antioxidant activity.”
There is little reason to doubt that similar concentration and activity increases in the same and additional important phytochemicals in other food crops would occur in response to the same increases in the air’s CO2 concentration. Indeed, the aerial fertilization effect of atmospheric CO2 enrichment is a near-universal phenomenon that operates among plants of all types, and it is very powerful (e.g., Mayeux et al., 1997; Idso and Idso, 2000). There must have been significant concomitant increases in the concentrations and activities of the various phytochemicals in these foods that act as described by Wang et al. (2003).
Could some part of the rapid lengthening of human longevity reported by Oeppen and Vaupel (2002) be due to enhanced CO2 in the air putting more antioxidants in our diets? Two recent experiments showing the positive effects of antioxidants on animal lifespan provide some additional evidence that this may be the case.
Melov et al. (2000) examined the effects of two superoxide dismutase-/catalase-like mimetics (EUK-8 and EUK-134) on the lifespan of normal and mutant Caenorhabditis elegans worms that ingested various concentrations of the mimetics. In all of their experiments, treatment of normal worms with the antioxidant mimetics significantly increased both mean and maximum lifespan. Treatment of normal worms with only 0.05 mM EUK-134, for example, increased their mean lifespan by fully 54 percent. In mutant worms whose lifespan had been genetically shortened by 37 percent, treatment with 0.5 mM EUK-134 restored their lifespan to normal by increasing their mutation-reduced lifespan by 67 percent. It also was determined that these effects were not due to a reduction in worm metabolism, which could have reduced the production of oxygen radicals, but “by augmenting natural antioxidant defenses without having any overt effects on other traits.” In the words of the authors, “these results suggest that endogenous oxidative stress is a major determinant of the rate of aging,” the significance of which statement resides in the fact that antioxidants tend to reduce such stresses in animals, including man.
Another study addressing the subject was conducted by Larsen and Clarke (2002), who fed diets with and without coenzyme Q to wild-type Caenorhabditis elegans and several mutants during the adult phases of their lives, while they recorded the lengths of time they survived. This work revealed that “withdrawal of coenzyme Q from the diet of wild-type nematodes extends adult life-span by ~60 percent.” In addition, they found that the lifespans of the four different mutants they studied were extended by a Q-less diet. More detailed experiments led them to conclude that the life-span extensions were due to reduced generation and/or increased scavenging of reactive oxygen species, leading them to conclude in the final sentence of their paper that “the combination of reduced generation and increased scavenging mechanisms are predicted to result in a substantial decrease in the total cellular ROS and thereby allow for an extended life-span.”
In light of these many diverse observations of both plants and animals, there is some reason to believe that the historical increase of CO2 in the air has helped lengthen human lifespans since the advent of the Industrial Revolution, and that its continued upward trend will provide more of the same benefit. Additional information on this topic, including reviews of newer publications as they become available, can be found at http://www.co2 science.org/subject/h/humanlifespan.php.
In a related study, Matzarakis et al. (2011) developed a relationship between heat stress and all-cause mortality in the densely populated city of Vienna (Austria), using a human biometeorological index that is known as the physiologically equivalent temperature or PET. Based upon data from the period 1970-2007, and after adjusting the long-term mortality rate to account for (1) temporal variations in the size of the population of Vienna, (2) temporal changes in life expectancy, and (3) the changing age structure of Vienna's population, the three researchers found that a significant relationship existed between heat stress and mortality. Over this 38-year period, some significant decreases in heat sensitivity were found, which "could indicate active processes of long-term adaptation to the increasing heat stress.” They refer to these changes as "positive developments” in the conclusion section of their paper.
Climate Change Reconsidered: Website of the Nongovernmental International Panel on Climate Change. http://www.nipccreport.org/archive/archive.html
Chung, H.S., Chang, L.C., Lee, S.K., Shamon, L.A., Breemen, R.B.V., Mehta, R.G., Farnsworth, N.R., Pezzuto, J.M. and Kinghorn, A.D. 1999. Flavonoid constituents of chorizanthe diffusa with potential cancer chemopreventive activity. Journal of Agricultural and Food Chemistry 47: 36-41.
Espin, J.C., Soler-Rivas, C. and Wichers, H.J. 2000. Characterization of the total free radical scavenger capacity of vegetable oils and oil fractions using 2,2-diphenyl-1-picryhydrazyl radical. Journal of Agricultural and Food Chemistry 48: 648-656.
Finkel, T. and Holbrook, N.J. 2000. Oxidants, oxidative stress and the biology of ageing. Nature 408: 239-247.
Frenkel, K. 1992. Carcinogen-mediated oxidant formation and oxidative DNA damage. Pharmacology and Therapeutics 53: 127-166.
Heinonen, I.M., Meyer, A.S. and Frankel, E.N. 1998. Antioxidant activity of berry phenolics on human low-density lipoprotein and liposome oxidation. Journal of Agricultural and Food Chemistry 46: 4107-4112.
Horiuchi, S. 2000. Greater lifetime expectations. Nature 405: 744-745.
Idso, C.D. and Idso, K.E. 2000. Forecasting world food supplies: The impact of the rising atmospheric CO2 concentration. Technology 7S: 33-56.
Larsen, P.L. and Clarke C.F. 2002. Extension of life-span in Caenorhabditis elegans by a diet lacking coenzyme Q. Science 295: 120-123.
Manton, K.G. and Gu, X.L. 2001. Changes in the prevalence of chronic disability in the United States black and nonblack population above age 65 from 1982 to 1999. Proceedings of the National Academy of Science, USA 98: 6354-6359.
Marnett, L.J. 2000. Oxyradicals and DNA damage. Carcinogenesis 21: 361-370.
Marx, J. 2003. Ozone may be secret ingredient in plaques’ inflammatory stew. Science 302: 965.
Matzarakis, A., Muthers, S. and Koch, E. 2011. Human biometeorological evaluation of heat-related mortality in Vienna. Theoretical and Applied Climatology 105: 1-10.
Mayeux, H.S., Johnson, H.B., Polley, H.W. and Malone, S.R. 1997. Yield of wheat across a subambient carbon dioxide gradient. Global Change Biology 3: 269-278.
Melov, S., Ravenscroft, J., Malik, S., Gill, M.S., Walker, D.W., Clayton, P.E., Wallace, D.C., Malfroy, B., Doctrow, S.R. and Lithgow, G.J. 2000. Extension of life-span with superoxide dismutase/catalase mimetics. Science 289: 1567-1569.
Merken, H.M. and Beecher, G.R. 2000. Measurement of food flavonoids by high-performance liquid chromatography: a review. Journal of Agricultural and Food Chemistry 48: 577-599.
Neff, J. 1997. Big companies take nutraceuticals to heart. Food Processing 58: 37-42.
Oeppen, J. and Vaupel, J.W. 2002. Broken limits to life expectancy. Science 296: 1029-1030.
Rice-Evans, C.A. and Miller, N.J. 1996. Antioxidant activities of flavonoids as bioactive components of food. Biochemical Society Transactions 24: 790-795.
Slaga, T.J., O’Connell, J., Rotstein, J., Patskan, G., Morris, R., Aldaz, M. and Conti, C. 1987. Critical genetic determinants and molecular events in multistage skin carcinogenesis. Symposium on Fundamental Cancer Research 39: 31-34.
Tuljapurkar, S., Li, N. and Boe, C. 2000. A universal pattern of mortality decline in the G7 countries. Nature 405: 789-792.
Wang, S.Y., Bunce, J.A. and Maas, J.L. 2003. Elevated carbon dioxide increases contents of antioxidant compounds in field-grown strawberries. Journal of Agricultural and Food Chemistry 51: 4315-4320.
Wang, S.Y. and Jiao, H. 2000. Scavenging capacity of berry crops on superoxide radicals, hydrogen peroxide, hydroxyl radicals, and singlet oxygen. Journal of Agricultural and Food Chemistry 48: 5677-5684.
Wang, S.Y. and Lin, H.S. 2000. Antioxidant activity in fruit and leaves of blackberry, raspberry, and strawberry is affected by cultivar and maturity. Journal of Agricultural and Food Chemistry 48: 140-146.
Wang, S.Y. and Zheng, W. 2001. Effect of plant growth temperature on antioxidant capacity in strawberry. Journal of Agricultural and Food Chemistry 49: 4977-4982.
Wentworth Jr., P., Nieva, J., Takeuchi, C., Glave, R., Wentworth, A.D., Dilley, R.B., DeLaria, G.A., Saven, A., Babior, B.M., Janda, K.D., Eschenmoser, A. and Lerner, R.A. 2003. Evidence for ozone formation in human atherosclerotic arteries. Science 302: 1053-1056.
Willcox, J.K., Ash, S.L. and Catignani, G.L. 2004. Antioxidants and prevention of chronic disease. Critical Reviews in Food Science and Nutrition 44: 275-295.
Wong, S.S., Li, R.H.Y. and Stadlin, A. 1999. Oxidative stress induced by MPTP and MPP+: Selective vulnerability of cultured mouse astocytes. Brain Research 836: 237-244.
Yu, L., Haley, S., Perret, J. and Harris, M. 2004. Comparison of wheat flours grown at different locations for their antioxidant properties. Food Chemistry 86: 11-16.
Zhao, J., Lahiri-Chatterjee, M., Sharma, Y. and Agarwal, R. 2000. Inhibitory effect of a flavonoid antioxidant silymarin on benzoyl peroxide-induced tumor promotion, oxidative stress and inflammatory responses in SENCAR mouse skin. Carcinogenesis 21: 811-816.