Why a low protein diet for longevity is flawed

One of the pushbacks that can come up when discussing higher protein diets and if they are healthy, is the research that supports a low protein diet for longevity. It’s an interesting juxtaposition. On the one hand, there is clear clinical data that early mortality from falls has a high prevalence among older individuals, due to frailty and potential adverse effects from polypharmacy (taking multiple medications) and the research shows not only that a higher protein diet (in addition to resistance training – which is at least as important) helps offset this risk, but that an already frail adult can improve their outcome from increasing both protein and their weight-bearing exercise load. On the other hand? Studies suggest a lower protein intake helps offset the ageing process and we live longer if we limit our intake of protein, particularly because of the potential for mTOR (mammalian target of rapamycin, a signalling process) to be upregulated due to protein intake, which proliferates growth and as such, is pro-cancer and pro-ageing. Let’s look at the two of these theories.

When we age and lose muscle function and mass (called sarcopenia) we lose the ability to balance, hold ourselves steady and generally move properly in everyday life. You only need to go outside on a busy street to see older individuals and how they move. A lot of this can be overcome when we put the work into increasing and maintaining lean muscle tissue through weight-bearing exercise and resistance training, and optimising protein intake. As I have said in previous emails, we become resistant to the impact of protein as we age (anabolic resistance), which means the messages the brain receives from a protein load is dimmed down, and we need more protein to get the same signal. Without it we don’t optimise our ability to preserve and build muscle.

 For everyone, regardless of age, it is about reaching the leucine threshold (leucine being a branched chain amino acid, BCAA) for this to occur. Younger individuals (college age and younger) can do this on 15g of protein at a single meal, whereas research suggests those older than 45-50y need 40g of protein (equating to almost double the current recommendation for leucine). This reflects the blunting of muscle protein synthesis and, as such, as we age, we just need more.

 What about mTOR then? mTOR refers to two complexes, one of which (mTORC1) gets messages from nutrients and calories, along with growth factors such as insulin growth-like factor (IGF-1) to initiate anabolism– i.e. growth when energy is aplenty, and muscle breakdown when it is not. Over many years mTOR has been studied for its role in ageing and cancer risk, with research showing involvement in cancer cell proliferation and tumour growth. Thus, mTOR inhibitors are also studied to determine whether their ability to dial down the mTOR signal reduces the growth of cancer cells. Researchers in the field of longevity also propose that, due to mTOR being signalled by energy (calories), sugar and amino acids, a low protein intake is required to dim the signal to mTOR and reduce the risk of accelerated ageing and reduced lifespan. Indeed there is plenty of preclinical work to indicate that calorie restriction and protein restriction impacts on biomarkers of ageing and extends lifespan. Studies also show that calorie restriction in humans reduce risk factors associated with ageing. Therefore those in the longevity research argue that low protein is important to offset the damaging impact of accelerated ageing. This is clearly at odds with the information above regarding the importance of protein as we age.

Some of the pushback that occurs with the low protein recommendation is that it is impossible to determine from the short-term studies in the longevity space that there is an increased health and lifespan when living in a calorie deficit and with a low protein intake over many years, as a study like this cannot be done in humans. Researchers in the protein field respectfully reject the premise of a low protein approach.

What is the deal, then, with mTOR, protein, and the apparent conflicting theories here?

It appears that, actually, it isn’t mTOR itself that is the issue, and signalling of mTOR, it is instead the dysfunction of the mTOR signalling. There is a difference between acute, short term spike in response to a stressor (such as a hit of protein, or undergoing a training programme) and dysregulated signalling that is not able to be switched off. This inappropriate response that might precipitate diseases such as cancer can be attributed to insulin resistance. Dietary habits (and other lifestyle factors) that lead to elevated insulin – such as excess carbohydrate, inflammation, high sugar and excess calories over time – can result in the body requiring more insulin to deliver nutrients into cells. This resistance to insulin means we have more insulin in our bloodstream, and signals an increase in mTOR action. But it is a low-level continual switching on, and never switching off, rather than a pulsatile effect of a protein dose that is the issue.

And there may also be a difference in the tissue specific signalling of mTOR, and the dysregulation of mTOR may be more of an issue if in organs such as liver, kidneys and/or brain, rather than muscle which requires mTOR signalling for preventing sarcopenia. Further, another important trigger for mTOR is resistance training, and those who are experts in the field of physique science argue that if mTOR signalling truly was an issue, and something that we need to downregulate, we would see an increase in cancer rates in people who spend decades optimising both protein and resistance training in physique sports. Yet that isn’t what we see.

Protein and resistance training are key to staying healthy into our older years, maintaining muscle function and health. mTOR dysregulation is at the heart of cellular proliferation and potentiating cancer under certain conditions. This is different from the important role it plays in preserving muscle health. If concerned about mTOR signalling, it makes more sense to ensure you are protecting yourself from insulin resistance, and instead focusing on reducing inflammation and excess refined carbohydrate. Preclinical trials show that a ketogenic diet including medium chain fatty acids reduce inflammation and dysregulation of the mTOR signalling pathway.