The Contribution of Decreasing Cancer Mortality to Gains in Life Expectancy

This study provides an assessment of the impact of improvements in cancer prevention and cancer therapies over the past few decades, based on observed changes in life expectancy. In the opinion of the authors, better prevention is the more important contribution to these results - which doesn't say much for the current high level strategy in cancer research aimed at production of better therapies, given the vast sums devoted to that industry. Because of its focus on cancer, an unusual life expectancy construct is used in this study, considering only ages 40 to 84; cancer has a very low incidence at younger ages, and the risk declines again in late life, both absolutely, and in comparison to other causes of death.

Cancer is surpassing cardiovascular disease (CVD) as the leading cause of death in many high income populations and is projected to become a leading cause of morbidity and mortality worldwide in the coming decades. While substantial progress in reducing mortality from CVD has been shown, equivalent global assessment of cancer remains challenging, requiring a multifaceted and multi-indicator approach. Cancer mortality rates are declining in most highly developed countries, largely due to recent successes in the control of common cancers through programs of effective prevention, early detection, and treatment. In contrast, mortality rates of many types of cancer, including breast cancer and prostate cancer, are still increasing in transitioning countries, or at best stabilizing.

There is a need to quantify and better understand the position of cancer among other leading causes of avoidable death, including CVD, and the specific impact of major cancers as barriers to attaining old age. In this study, we quantify the contributions of changing cancer mortality rates on changes in life expectancy in ages 40-84 (LE40-84) over the period 1981-2010, adjusting for other causes of deaths, while making benchmark comparisons with equivalent gains achieved through the reduction of CVD mortality rates.

Only ages 40-84 were included, as individuals within this age group comprise the majority of cancer cases. In addition, in this age group there is also a lower probability of the causes of death being misreported and the existence of comorbid conditions compared with in those aged 85 or more, reducing bias related to competing causes of deaths. As a sensitivity test, we replicated the analysis for ages 0-39 and found that the contributions of cancer to change in life expectancy are negligible in this age group. Accordingly, LE40-84 throughout this article refers to life expectancy in ages 40-84, the expected number of years lived between ages 40 and 84, whereas we truncated years lived above age 85.

An overall decrease in mortality rates from all causes led to a noticeable increase in LE40-84 over the study period. In particular, very high Human Develpment Index (HDI) populations experienced gains of on average 3.7 and 2.5 years in LE40-84 among men and women, respectively, while respective values for medium and high HDI populations were lower, at 1.1 and 1.4 years. Decline in mortality rates from CVD was the main contributor, accounting for an average of more than 60% and 50% of declines in overall mortality rates in very high and medium and high HDI populations, respectively. Although decreasing overall cancer mortality rates were observed, they were greater in very high HDI populations (declines of 20% and 15% over the 30 year period for men and women, respectively) compared with medium and high HDI populations (4% and 5% decreases, respectively).

The past three decades have been marked by several triumphs in cancer control, which are clearly reflected in our results. For example, the increase in LE40-84 among men can be considered partly the result of corresponding declines in lung cancer mortality rates linked to improved tobacco control measures. Gains in life expectancy from a reduction of stomach cancer mortality rates links socioeconomic advancement to successes in combating infectious diseases through both "unplanned" prevention as well as treatment. In most of the very high HDI populations, the progress seen in terms of reductions in mortality rates from breast, prostate, and colorectal cancer can be related to a broad spectrum of cancer control interventions, including early detection, improved diagnosis, and better access to effective treatment.



Improved longevity (in the real sense of antisenescence) can only be achieved after cancer has been cured at the root cause. I say this because ultimately cancer appears to be the result of aging of the individual's genome as the result of random errors accumulated over time. Granted some errors may be inherited, and some points on the chromosomes may be more sensitive to error than others (just as a small nick on your engine timing chain is far more disastrous than the same-sized nick on your engine block) but over-all it's just accumulated error.

Given that some organisms do not appear to become senescent, there are probably only one or two error-correcting "machines" that are missing from our (aging) cell-lines that were possibly caused by the genetic bottleneck during the Cambrian extinction event, when small, short-lived animals were favored over larger ones.

Therefor, I think that we should be pursuing these strategies.
1) Promote research into "root cause" treatment of cancer to the exclusion of medical-types of treatments that are VERY adequately funded already. This will be necessary once antisenescence is developed.
2) Promote research into identifying the cellular mechanism for genetic error correction that mammals, and a variety of other organisms, do not have by looking at pairs of related organisms that have senescent and non-senescent members. (I believe such organism pairs exist).
3) Find ways to introduce/adapt this mechanism into cells that lack it.

Posted by: Benjamin Wade at June 29th, 2017 1:45 PM

1) No, you don't need to eliminate mutations to eliminate cancer, only to eliminate telomere elongation.

2) No, negligibly senescent organisms do suffer mutations (otherwise, they couldn't evolve).

3) No, we can't use their strategy to deal with cancer (being asexual organisms with no somatic cells but only germline cells).

Posted by: Antonio at June 29th, 2017 4:38 PM

@antonio - thanks for responding with a clear and concise reply.

Re: cancer - there are loads of systems out there to deal with it indefinitely, humans just don't have any of these in high enough fidelity (yet) because from an evolutionary pressure perspective, there is no pressure to improve in an pre-agrarian environment where most people are dead by 40 from infectious disease.

Naked Mole rats are almost completely cancer proof, and not through better telomere control, they just have some other system with much higher fidelity, probably for some reason unrelated to cancer. I say this because I think I detect a bit of hand wringing in Benjamin Wades comment along the lines of "cancer is near invincible, best just to make our peace with it". Cancer is not nearly invincible if naked mole rats can beat it.

Posted by: Jim at June 29th, 2017 5:42 PM
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