Alternative Title: Living Life in Power Saving Mode – Less Function, Longer Battery Life?
As a nutritionist, I’ve been most heavily influenced by 3 paradigms/schools of thought over the last couple of years (much more so than the current versions of Paleo) – the holy trinity, as it were.
- The Protein Leverage Hypothesis
- Acellular vs. Cellular Carbohydrates
- Fat in food is always of a mixed composition
Between these three lines of thinking, many of the current, ongoing, and tedious debates in nutrition get largely resolved.
In plain English, our primary appetite is for protein, and we are probably metabolically optimised consuming a bit more than current dietary guidelines would have you believe; carbohydrates, when they are pulverised and ground down into flour mess our metabolic regulation up, and we are thus far better off consuming them in an “ancestral” form – sticking them in our gobs in an intact cellular form; and all naturally-occurring fats in our food are almost always of a mixed composition – saturated and unsaturated – and thus, in the context of eating whole, cellularly-intact foods, we don’t need to overthink or sweat these fats.
Overlay concepts like seasonality, sustainability, and food miles, and you get pretty close to a reasonable prescription for how to eat like an unfucked human being (cue Keto Jihadists, Paleo Pyramid Schemers, Big 80’s Hair High-Fatists, and Dietetic Industry Troughers reaching for the pitchforks and telling me how wrong I am).
Of these three paradigms, I have the most interest in Dr Ian Spreadbury’s take on carbohydrates and Professor David Raubenheimer’s (et al) Protein Leverage Hypothesis . Thus, I was pee-my-pants excited to have both of them speak at #AHSNZ15 (sadly, we had to beam Dr Spreadbury in via a series of 0’s & 1’s, but I did get to meet him in person just a couple of months back in Boulder, Colorado).
The talk from Prof Raubenheimer at AHSNZ is unfortunately not available for public viewing (a similar talk is here), but if it were, you would see a curious shift in tack that he took after making his case for a protein intake optimised in the 20-25% total energy intake band (though I much prefer Professor Donald Layman’s approach of expressing this as an absolute amount relative to body weight). Professor Raubenheimer, based on work he and others had been doing, put forward the case for REDUCING protein intake down to 10% of total energy intake in order to chase a bit more longevity in the human lifespan (often spoken of like achieving immortality status).
Presenting data on the Okinawan diet, Prof Raubenheimer referred to this paper, summarised as:
We also plotted the composition of the diet of the longest-lived human population, the traditional Okinawan diet; might it be that their exceptional life-span is achieved through mild protein restriction coupled with high carbohydrate intake? This analysis should give pause to those lightly adopting or recommending macronutrient-imbalanced diets for specific purposes, such as weight loss.
Upon hearing the above, I guess I was mildly pissed to be honest. I struggle to see how you can make a case for better health in the here and now of everyday life, only to quickly dismiss this with vague and heavily confounded research pointing to increased longevity [“immortality”]. Just to make my personal position clear – everybody dies – and everybody should. Some will last longer than others, but every beginning has an end. It’s reasonably well known that by the time you make it into your twilight years, you aren’t seeking to extend things out even more – there is an acceptance that the end is coming.
But not everybody lives, and especially those whose bodies, from a seemingly earlier and earlier age, is in such a state of disrepair, or whose minds are so full of angst and anxiety, that they are virtually paralysed during what should be their most vibrant, active, and productive years. These are the humans I care and worry about. I’d much rather see people live full and active lives before popping their clogs at 70, than to live like broken, lifeless, half-starved zombies, just to “brag” about hitting triple digits (seriously, we need to get the fuck over ourselves and this whole misplaced desire to become centenarians – though I’m sure all the neoliberals love the idea of having more humans consuming for longer).
With the above in mind, I decided to dig a little deeper into Professor Raubenheimer’s references…
From his paper “Putting the Balance Back in Diet” :
the diet composition that sustained longest life led to a lower intake of protein than needed to support maximal reproductive success. When allowed to compose their own diet by selecting among complementary food pairings, flies chose to mix a diet maximizing reproductive output rather than lifespan. Subsequent studies have shown that the trade-off between lifespan and reproduction is not obligatory or causal, but simply reflects differing nutritional optima for the two traits
Mice, like other animals, possess separate macronutrient appetites, and when these were forced to compete by restricting animals to a single diet composition, total food intake was driven principally by protein, increasing as percent protein in the diet fell (consistent with compensatory feeding to stabilize protein intake). Compensatory feeding for carbohydrate was also apparent, with intake increasing as percent carbohydrate fell in the diet but to a somewhat lesser degree than for protein. Unlike protein and carbohydrate, however, the concentration of dietary fat had little influence over total food intake. Consequently, total food and energy intakes were maximal on diets combining low percent protein with high percent fat.
The above quote is interesting in that it would suggest that mice have specific appetites for protein (primarily) and carbohydrate. Thus, feed mice diets where the protein is altered (and typically supplied via casein – more on that in a bit), and carbohydrate is restricted in favour of fat, and they get fat. Interesting implications when using mouse models for human diet manipulations.
Even though mice on low [protein] diets were moderately adipose (although not to the extent of low-protein, high-fat fed mice), they lived longest. Indeed, longevity mirrored the pattern seen in flies, being greatest on low [protein] diets. Markers of metabolic health (insulin, glucose tolerance) and immune function at 15 months of age were consistent with the longevity data, being best on low [protein] diets and worst on high protein and high-fat diets. By contrast, measures of reproductive potential in both males and females were highest on a higher-protein diet, consistent with results from flies.
As part of my recent Ancestral Health talks, I’ve been doing a lot of reading on developmental plasticity – our ability to change our physiological settings in response to environmental changes (such as a restrained food [protein] supply), and, importantly, how these physiological settings can be transmitted to our offspring in order to calibrate their settings to better match the environment they are potentially heading into (and the consequences when these epigenetic transmissions end up mismatched to the actual consequent environment).
It makes sense, from an evolutionary perspective, that when animals are in a constrained food environment – particularly constrained with respect to their primary appetite – protein – and when they are still of reproductive age (as is going to be the case in freshly bred research mice and flies) – that they can adjust their physiological and metabolic settings away from reproduction, and slow everything down in order to wait the constrained environment out. This is where the “longevity” comes from. It’s a form of stasis so that these animals aren’t wasting precious reproductive resources in an environment not supportive of it.
Note that in an unconstrained environment with respect to protein, they always default away from longevity and back toward reproduction.
And here is the real kicker, especially with regard to the real and messy world of modern human beings…
Whereas a low [protein] diet appears beneficial for longevity and late life health, protein leverage on such a diet tends to drive over-consumption of total energy and risk of obesity, thereby mitigating the health benefits of low-protein intake.
But ain’t nobody talking about that bombshell when selling the “lower your protein and live forever” line.
I’ve talked before about the benefits of optimising protein to stave off the likes of dynapenia, sarcopenia, and osteopenia (and how with our modern diet and lifestyles, we have real issues with these conditions, from an increasingly early age).
From a reproduction standpoint, and, looking further out, the development origins of health and disease, if you ask the population to start heavily constraining their protein intake – to 10% of total energy intake – there are going to be even more problems.
From Gluckman, et al…
Given that epigenetic mechanisms underpin developmental plasticity and that nutritional cues are important with respect to adaptive developmental plasticity, it is to be expected that a variety of nutritional cues in development will have specific epigenetic consequences. Most experimental studies of nutritional effects on the offspring have used an unbalanced maternal diet with a low protein-to-carbohydrate ratio or a global dietary restriction during pregnancy.
Initially most animal studies involved investigation of effects of unbalanced or poor maternal diet and body composition on cardiovascular and metabolic function in the offspring. The most commonly used challenge was a low-protein diet fed to the mother during pregnancy. This produced low birth weight and later growth and produced effects on offspring blood pressure, the heart, and blood vessel structure and function.
So the very diet that is thought to increase our longevity – one with a low protein-to-carbohydrate ratio – is also the very same diet considered to be unbalanced and lead to epigenetic consequences when discussing developmental plasticity. Which is it going to be? Developmentally mismatched children who go on to live longer than they should (theoretically)? Or the reverse – well-developed and active kids, who go on to be healthy adults that don’t last much longer than our historical averages?
The upshot, it seems, that you can twiddle the knobs on our machinery and extract a few more days/weeks/months out of the system. But this comes at a compromise and is NOT where all the experimental models default to. That is, flies, mice, and humans, do not self-select and optimise to longevity. They optimise to reproduction. Many of the longevity researchers/proponents are being quite mischievous/ignorant in not making this crystal clear.
Two interesting asides relating to my background reading for this post…
Gosby and colleagues (2011) showed that the 12% increase in ad libitum energy intake among subjects confined to a 10% protein diet relative to 15% or 25% protein diets was due to increased consumption of savory-flavored foods between meals.
The seeking of savory cues is indicative of protein hunger, and is reflected in increased activity in brain regions associated with reward, such as the inferior orbitofrontal cortex and striatum (Griffioen-Roose et al., 2014). These results indicate that protein status influences gustatory pathways in a way that affects protein intake in humans.
Note that when you restrict protein, total energy intake increases substantially – by 12% (Raubenheimer is quoted previously suggesting that for every 1.5% drop in protein intake below 15%, you’ll get a 14% compensation through increased carbohydrate and fat consumption).
The line “the seeking of savory cues is indicative of protein hunger” explain Tofurkey and other vegan frankenfood meat analogues.
Also noteworthy, when you pull the diet data for the mouse models used in longevity research, you soon notice that to vary protein content in diet, they vary primarily casein protein, as well as methionine (and I do believe there are potential issues with high methionine diets –http://www.benbest.com/calories/Meth.html)
Interesting that in Table 2 of the above link, the protein sources highest in methionine per 100g consumed are generally high-casein dairy foods.