A caterpillar in the fridge.

When I was very young I had a thing for caterpillars.  Not inch worms (though they are cool too), not silk worms, not bag worms (yuck!), and not tomato horn worms which scare me to this day.  Simple little caterpillars, fuzzy or not- I liked them.

The idea of these little critters transitioning into magnificent butterflies fascinated me.  And though I only witnessed this in person once in Mrs. Scholar’s kindergarten class, I reflected on the magic every time I saw one scurry across the footpath, or saw a swallowtail land on a Xenia flower in mom’s garden. 

I mostly liked them because they were fun to play with though.

“Catty” was my favorite of them all.  He wasn’t a particularly special caterpillar.  He wasn’t fuzzy, or striped like a monarch.    He was just plain and simple light green, camouflaged perfectly for his original home on a Sycamore tree in our back yard.I loved to play with him, and wanted him to last forever.  I knew that if he spun a chrysalis I couldn’t watch him scury about on the linoleum of the kitchen floor.  And I knew that once he turned into a butterfly he would fly far away.  I’d never see him again.  

To keep either of these from happening, and also to keep him safe, I stored him in a recycled yellow Parkay margarine tub in the refrigerator when we weren’t together.  (With a piece of lettuce for optimal nutrition to keep him strong of course!)  I figured that, if he was kept cold, he would slow down.  And if he slowed down, he wouldn’t get old very fast.  And if he aged slowly, I could keep him longer!

Move over, Sinclair, this gal’s been contemplating longevity since she was 6!

Sadly, “Catty” died after only a week or so.  My little sister stepped on him.  So the world will never know the outcome of my attempt at cryogenics.

I hadn’t thought about my biohacking endeavor for a while.  (It is a bit of a traumatic childhood memory.)  But while chasing rabbit hole tangents is typically my nemesis when doing my health research, creating unending spasticity in my thinking, I haven’t been able to resist dipping my toes into the field of longevity that frequently pops up as I explore various nutritional and metabolic concepts in depth.

Longevity and its elusiveness had fascinated mankind for centuries.  But over the past ten years it’s busted out of control.  Leading the parade towards the fountain of youth is caloric restriction.

Pardon me while my head explodes.

Okay, I’m back.

Longevity is the life expectancy of an individual living thing. It refers to how much time a person will live. Genetics, lifestyle, metabolism, and our environment are a few major factors that impact one's longevity.

The conventional theory on why species age and what dictates how long they survive is based in part on a modern version of the very old and now discredited “rate of living” (ROL) theory of aging. According to this disproven and outdated idea, aging is caused by the loss of vital substances such as water or hormones - the more rapidly the vital substances are used up the shorter the lifespan.

In 1921 Raymond Pearl (1921) hypothesized that the primary determinant of how long various species live is influenced by the relative speed of their resting metabolism. Simply stated, from this viewpoint, metabolic rate is theorized to be inversely proportional to lifespan; species that live fast will die young while those that have a slower metabolism live longer.  

In support of the ROL theory, another concept- the evolution theory- proposes that animals that face high mortality such as predation and disease must develop more quickly.  They must age and procreate quickly in order to pass their genes onto the next generation before they die. Animals that face low extrinsic mortality are enabled to delay development and reproduction, and thus live slower and longer (Kirkwood and Holliday, 1979).  And because these lower-extrinsic mortality species are also higher on the food chain, they tend to grow larger.  This led to the observation that longevity appears to be positively correlated with the size of an animal as well as its brain capacity (Sacher, 1978). 

None of these predeceasing theories carried mechanistic explanations, however.  

But in the 1950s Denham Harman suggested that cellular operation leads to the production of reactive oxygen species (ROS, also known as free radicals).  These damaging byproducts are partially reduced metabolites of molecular oxygen generated from metabolic reactions or as by-products of various cellular processes.  For decades and continuing to this day, this theory has been the most popular concept in the area of aging.

There are numerous studies that demonstrate that ROS and oxidative damage increase with age and that reducing oxidative damage extends the lifespan of various studied organisms.  Studies also exist showing that increased production of ROS shortens lifespan.

In principal, the maximum lifespan of species should therefore be negatively correlated with tissue concentrations of ROS and positively correlated with tissue concentrations of antioxidants.  Spinning from this, a lower metabolic rate would lead, in theory, to lower ROS production, and thereby increase longevity.

Things get complicated, though, when the counter to these ROS is brought into consideration.  Antioxidants, which we all know to be “excellent” for us, have shown mixed results.  Furthermore, the aging effects of ROS have been studied in isolation, nor do their mere existence explain varying inevitability.  

You can read more on the ROS model and conflicting evidence here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901353/#!po=1.35135

So how does all this relate to calories?

The earliest studies in the field of bio gerontology observed that animals that are calorically restricted without being malnourished, live longer.  According to the metabolic ROS stress theory, calorically restricted animals live longer because a lower caloric intake should lead to a lower metabolic rate and, thereby, reductions in the quantity of damaging free radicals. 

But in recent studies, caloric reduction has been shown to have varying effects on both metabolic rate and lifespan (Sohal and Weindruch, 1996). 

In 2004, the mathematician/biologist Lloyd Demetrius postulated the newest theory of aging - referred to as the “metabolic stability-longevity hypothesis” (hereafter referred to as MSL).  

According to Demetrius, the most important factor involved in duration of life is not metabolic rate or oxidative stress, but metabolic organization and stability- the ability of cells to resist fluctuations in the steady state concentration of metabolites (ROS) within the cell.  The core argument of MSH is that longevity is correlated with stability of the resting concentrations of ROS, whereas the metabolic rate/ROS theory claims that longevity is correlated with production rates of ROS.

There are countless factors affecting the metabolic stability of cells.  In small animals, it’s speculated that the metabolic stabilizing effect of caloric restriction (and only then to a point that still maintains health and vitality) has a solid impact on the production and effect of ROS, leading to increases in lifespan.  But Demetrius’ work proposes that the relative benefits of (mild) caloric restriction should diminish in species that already have high rates of metabolic stability (long-lived animals and humans).

If Demetrius’ metabolic stability hypothesis proves valid (which it looks like it is going to) caloric restriction of any degree would most likely have little notable influence on human longevity, and certainly close to none when compared to the metabolic insults created by the consumption of poor quality foods, chemicals, and daily stress.  

In support of this, Luigi Fontana, the internist who led the largest human trial on caloric restriction at Washington University states:

“What we are finding now is that it’s not the number that matters. Genetics, the composition of the diet, when you eat, and what’s in your microbiome influences the impact of calorie restriction.”

Also backing the MSL theory, Rafael de Cabo, chief of the National Institute on Aging’s Translational Gerontology Branch, led a team that recently completed a 25-year study of calorie restriction in monkeys.  They didn’t see the drastic lifespan improvements previously seen in other primate studies. While they did observe lower rates of cancer and various other diseases, he added at the time: “But as we very well know, no one is going to be able to withstand eating so little for their entire life.”

After all, is a life drastically slowed down truly life? Even concepts regarding the potential benefits of hormetic stress revolve around an imposed external stress being the exception to “challenge” the body. When stress becomes the norm (and chronic caloric deprivation leading to cellular deregulation is certainly a metabolic stressor), the body quickly starts to shut down.

Efforts to increase longevity should focus on the same principles that govern optimal health to begin with:

• finding ways to increase the stability and wellness of our body’s cells.

• increasing the robustness of metabolic networks. 

• decreasing ongoing stressors to the physical and psychological body.

I agree with the overarching benefit of reducing calories if overabundance is commonplace, and certainly that of reducing calories coming from chemical-laden and highly processed foods. But no one will ever convince me that withholding food, the very substance of energy and life itself, is the ticket to living a longer, happier, more fruitful and meaningful life.

A slow life is no life. I’m sorry “Catty”.