Science is out of control. And it needs to be put in the corner for a time-out.
In many blog entries, I’ve discussed the lack of scientific (or common-sense) validation for running shoes.
Eyal Lederman wrote an excellent article recently regarding the similar lack of scientific validation for current ideas surrounding “core stability.”
But what spurred this blog entry was a presentation by Dr. Robert Mazzeo gave to my graduate class last week about his work studying mitochondria.
“Mitochondria = Longevity”
Mitochondria are the “powerhouses” of your cells. They convert glucose and/or pyruvate into ATP, the nucleotide your cells use to do work.
Essentially, researchers have found that mitochondrial density (the number of mitochondrion per area unit) increases when rats are put on a calorically-restricted (CR) diet.
Further, they’ve shown that certain of these rats (called “responders”) live up to 40% longer than “normal” rats.
Dr. Mazzeo is a specialist in the field of cellular metabolism. I trust him when he says that there is an increase in mitochondrial density resulting from calorically restricted diets in lab rats.
But I’m more than a little confused about the connection of the research to longevity, or implications for longevity research generally.
In the past century, average lifespan in humans has increased due to preventive/treatment methods, hygiene, etc., while maximal lifespan (that is, ultimately how long people can live) has not (Lanza, et. al, abstract).
According to the Lanza paper, this is related to mitochondria, mitochondrial density, and the metabolic load (specifically, on mitochondria) associated with caloric intake. While it may be true that increase in mitochondria occurs in concert with extended maximal lifespan (in some animals), does that imply causation, or even direct correlation?
First, what about the non-responder rats? Are they “not normal?” In the studies that have been performed, non-responder rats are from a different genetic “strain” of rat.
Then, what about the rats that get “averaged out” in statistical analysis?
Why does the effect occur only when CR is introduced at a very early age in the lifespan? In all of the studies, maximal lifespan only increases when CR is introduced within the first few weeks of the rat’s life and then maintained from there.
There seem to be differences between mitochondria created in response to caloric restriction and those created in response to physical activity, and hopefully Dr. Mazzeo’s research will shed light on that question. But, again, does that mitochondrial increase (happening, simultaneous to increased maximal lifespan) imply causation? And does it transfer to human animals?
What are the other physical/metabolic structures/processes that differ between these two classes of stimulus?
The complexity of natural organism function needs to be considered when making claims like this.
To quote Booth and Laye (2009) – “Normal physiological processes are dynamic, integrated, periodic, and therefore, it is difficult to define normal physiological function by looking at a single time point or single process in a non-stressed subject” (abstract). It, I think, is far too simplistic to point at a single cellular function and make the claim that it (alone) increases maximal lifespan.
Another issue has to do with what the true maximal lifespan or caloric intake of rats is.
Human beings have been known to live as long as 122 years (as far as we’ve recorded), and people throughout history have been known regularly to live well into their 80’s. We might suppose that human “maximal lifespan” is somewhere around 125 years, given optimal genetics, environment, etc., throughout that lifespan.
There are a few populations (specifically, centenarian populations) around the world that exhibit unusual consistency in long lifespan, supposedly due precisely to “optimal conditions” (that include such a diversity of “causes” as: family, absence of smoking, largely plant-based diets usually including legumes, constant and moderate physical activity, and social engagement and the accompanying structures – see the book “Blue Zones” by Dan Buettner for his analysis of these populations).
Perhaps the researchers in rat studies have not increased the maximal lifespan of these lab rats, they’ve merely found what the maximal lifespan is for (a select strain of, “responder”) rats when those animals are isolated in ideal conditions (for lengthy lifespan).
Further, what is “caloric restriction” for rats? Animals with less “self-regulatory” mechanism frequently (naturally/evolutionarily) take advantage of large stores of calories whenever they find them. “Feast or famine” is programmed into many animals (human beings included). In these studies, are the researchers really “restricting” calories below what is “optimal” for the rats, or are they actually feeding the rats an optimal level of calories. That is, these rats are fed diets that appear to be calorically restricted based on a human understanding/analysis of “normal” rats whose natural instinct might be to eat well beyond what a human “normal” when opportunity provides for excess in a “natural” (non-lab) setting.
On a final, philosophico-theoretical note, I’m interested in what the implications would be if mitochondrial density due to caloric restriction were found to increase maximal lifespan in human beings. Why increase maximal life span? To what end? What is the quality of that lifespan? Especially with regard to increasing levels of disease in the population at large due to ever-rising pollutant/toxicity levels in everything from the air to the food we eat. Perhaps we should focus first on quality, and then on quantity. In fact, if we focus on quality, quantity might naturally follow, as found (again) in centenarian populations scattered throughout the world.
The biggest issue I have, though, has little to do with any of that.
Rather, it’s about scientists and other “authority figures” in our society presenting sentences like “caloric restriction leads to increased longevity.”
It’s not true. It’s not clear. It’s not responsible.
Very few people in our society have been given the “critical thinking” classes they’d need in order to hear news like this and use it the way they should (which is, not at all).
Again, this type of talk (authority/consumer) supports our basic ideas too, that common sense is not good enough, that the lessons of your elders are meaningless, that science (or authority in general) holds all the answers, that you can’t do it on your own.
You can. You should. And, ultimately, you do whether you believe “they” are helping you or not.
References
Booth, F.W., Laye, M.J. (2009). Lack of adequate appreciation of physical exercise’s complexitiescan pre-empt appropriate design and interpretation in scientific discovery. Journal of Physiology, Ahead of Print.
Buettner, D. (2009). The Blue Zones: Lessons for Living Longer from the People Who’ve Lived the Longest. Washington DC: National Geographic Books.
Lanza, I.R., Nair, S. (2009). Mitochondrial function as a determinant of life span. European Journal of Physiology, Ahead of Print.
