Monday, September 23, 2013

Why do we humans live so long? And, oh, the problems at old age!

From our own lives, from the stories of our own families, and from scientists, we know all too well that we humans are living longer and longer and longer.  This Scientific American piece explores why we live such long lives:
Most researchers chalk up our supersized life span to the advent of vaccines, antibiotics and other medical advances, the development of efficient urban sanitation systems, and the availability of fresh, nutritious vegetables and fruit year-round. Indeed, much demographic evidence shows that these factors greatly extended human life over the past 200 years. But critical as they were to extending human life, they are only part of the longevity puzzle, Finch warrants. Marshaling data from fields as diverse as physical anthropology, primatology, genetics and medicine, he now proposes a controversial new hypothesis: that the trend toward slower aging and longer lives began much, much earlier, as our human ancestors evolved an increasingly powerful defense system to fight off the many pathogens and irritants in ancient environments. 
We need to keep in mind that our lifespan even now is supersized:
Our kind is remarkably long-lived compared with other primates. Our nearest surviving relatives, the chimpanzees, have a life expectancy at birth of about 13 years. In contrast, babies born in the U.S. in 2009 possessed a life expectancy at birth of 78.5 years. 
Of course, those who do not believe that the chimpanzees are our relatives won't bother with such scientific inquiry anyway!

Apparently it could come down to one "apolipoprotein E (APOE) gene":
APOE e4's DNA sequences closely resemble those in chimpanzee APOE, strongly suggesting that it is the ancestral human variant that emerged near the beginning of the Homo genus more than two million years ago and thus may have had the earliest effect on our longevity. Differing in several critical amino acids from the chimp version, APOE e4 vigorously ramps up the acute phase of inflammation. It boosts the production of proteins such as interleukin-6, which helps to increase body temperature, and tumor necrosis factor–alpha, which induces fever and inhibits viruses from replicating. Equipped with this supercharged defense system, children in ancient human families had a better chance of fighting off harmful microbes that they unwittingly ingested in food and encountered in their surroundings. “When humans left the canopy and went out onto the savanna,” Finch notes, “they had a much higher exposure to infectious stimuli. The savanna is knee-deep in herbivore dung, and humans were out there in bare feet.”
Moreover, early humans who carried APOE e4 most likely profited in another key way. This variant facilitates both the intestinal absorption of lipids and the efficient storage of fat in body tissue. During times when game was scarce and hunting poor, early APOE e4 carriers could draw on this banked fat, upping the odds of their survival.
Even today children who carry APOE e4 enjoy an advantage over those who do not. In one study of youngsters from impoverished families living in a Brazilian shantytown, APOE e4 carriers succumbed to fewer bouts of diarrheal disease brought on by Escherichia coli or Giardia infections than noncarriers did. And they scored higher on cognitive tests, most likely as a result of their greater absorption of cholesterol—a dietary requirement for neurons to develop in the brain
How does this all lead up to the old age problems that the blog post title drew you in?  Blame it on the same apolipoprotein E (APOE) gene!
APOE e4 carriers, with their enhanced immune systems, tended to survive many childhood infections. But they experienced decades' worth of chronic high levels of inflammation in the pathogen-rich environment—levels that are now linked to several deadly diseases of old age, including atherosclerosis and Alzheimer's. ...“And while it might be pushing it to say the senile plaques of Alzheimer's are some form of scab, like the plaques on artery vessels, they have many of the same components,” Finch suggests.
The apolipoprotein E (APOE) gene might turn out to have been one heck of a Faustian bargain we made with evolution!

One of the awful downsides to this long life is Alzheimer's.  (Yes, an issue that I have blogged about before, like here and here.)

As lifespans increase, we can expect more of us to be afflicted with this awful disease:
More than 35 million people worldwide live with dementia today, according to a new report. By 2050, that number is expected to more than triple to 115 million. The majority require constant care; they're dependent -- and that dependence can impact their loved ones in unmeasurable ways.
You might think that 115 million in a population of nine billion wouldn't matter much.  But, it will.
the problem is getting worse. Increasing life expectancies and an aging population are creating a group of seniors that's bigger than the working-age population that supports them, the report says. Approximately 4% of the population in developed countries now is currently over the age of 80; in 2050, experts predict, that number will rise to 10%. ...
People with Alzheimer's live on average four to eight years after they're diagnosed, but some may live 20 years beyond their initial diagnosis.
So, hey, here is the bottom-line: Enjoy the good life and be thankful for it.  You never know how things might be when you reach 75.

And treat our chimp relatives well!

4 comments:

Shachi said...

interesting data and hypothesis, but why Alzheimer's again :(?

Sriram Khé said...

Yeah, why Alzheimer's, right?
Not merely because it is my obsession ;)

I have come to understand that modern medicine can treat so many ailments that sidelined us before, or even killed us outright. And, there is a lot we can also try to avoid with good practices. Even many types of cancer we have treatment protocols in place.

But, alzheimer's/dementia, ... a completely different ballgame. And, as we live longer, the odds of dementia increase. As the population with dementia increases, it will require a tremendous amount of resources.

This usually won't be a worry if our lifespans were only about 40 years as was the case even only a few centuries ago, right? Hence, I refer to this as a Faustian Bargain!

Ramesh said...

Yes, Shachi, this Prof is rather fascinated with dementia. From his writings, it is clear that he already "demented" ; so perhaps this is not surprising :):):):)

Yes sir, we live probably a tad too long. Longevity per se is not the issue, the deteriorating quality of life as we age is the problem. But then, early on in business school, I was taught an invaluable piece of wisdom - if there are no alternatives, there is no problem ! Since we cannot choose how long we live (other than deliberately shortening it by things like smoking), who cares :)

Sriram Khé said...

Hmmm ... that's the bottom-line, eh--no alternatives means no problems? Was that in the business school, or are you describing the life that was in the Soviet Union? hehehe!

Most of us humans do not seem to understand and appreciate the potential hassles that come with longer and longer lifespans. It is one heck of a mixed blessing. I want to talk about that now and not when we are all really, really old because by then I would have lost my senses ;)