Can we preserve our cells' energy through nutrition? The fascinating case of phosphatidylcholine

It focuses on a fundamental phenomenon of ageing: the progressive loss of efficiency of our mitochondria. And at the centre of this story is a molecule you have probably heard little about: phosphatidylcholine.

Let's start with the mitochondria

To understand the significance of this study, we first need to understand what mitochondria are. Our cells need energy to function. And mitochondria play a central role in this energy production.

They are involved in converting the energy contained in nutrients into ATP, the form of energy that our cells can directly use.

But mitochondria are not small, isolated, immobile structures. They form extremely dynamic networks. In particular, they can continuously fuse, divide and remodel their organisation in response to the cell's energy needs and the stress it faces.

This mitochondrial dynamics is essential to their proper functioning. Yet, with age, this capacity for adaptation progressively deteriorates. It is one of the hallmarks of cellular ageing.

What the researchers discovered

They studied various mechanisms that could explain this mitochondrial deterioration during ageing. To do so, they used several highly modern approaches: proteomics, lipidomics, genetics, transcriptomics and metabolomics.

And one of the elements that emerged from their work is an age-related decrease in the synthesis of an essential phospholipid: phosphatidylcholine.

Phosphatidylcholine is one of the major constituents of biological membranes. And this is fundamental. Because we talk a great deal about proteins, vitamins, hormones or antioxidants… but far less often about the quality of the membranes of our cells and our organelles. Yet, without functional membranes, our cells cannot function properly.

The membrane is not simply the cell's envelope

We sometimes imagine the cell membrane as a kind of bag that holds the cell's components together. It is far more complex than that. Membranes are dynamic biological structures.

They are involved in particular in cell communication, receptor functioning, exchanges between the cell and its environment, signalling, molecular transport and the functioning of mitochondria.

The lipid composition of these membranes is therefore extremely important. And phosphatidylcholine constitutes a major element of it.

What happens when phosphatidylcholine decreases?

This is precisely what the researchers studied. Their results suggest that an age-related decrease in phosphatidylcholine synthesis contributes to disorganising the mitochondrial network.

Mitochondria then lose part of their ability to maintain their dynamics and metabolic flexibility. In other words: a change in lipid composition can contribute to a decline in the quality of mitochondrial function.

And since mitochondria play a central role in energy production, this can contribute to the decrease in metabolic resilience observed with age.

But the most interesting experiment comes next.

The researchers asked themselves: what happens if we restore the availability of this phosphatidylcholine?

In their animal model — the nematode Caenorhabditis elegans — increasing phosphatidylcholine through diet improved mitochondrial integrity at an advanced age.

They also conducted experiments on human cells in culture. Here again, their results suggest that improving phosphatidylcholine availability can restore certain metabolic capacities and enhance cellular resilience in the face of stress.

This is fascinating. But this is precisely where I want to make an essential distinction.

Does this mean that eating eggs rejuvenates our cells?

No. We cannot claim that today. And it is important to me to tell you this.

This study provides an extremely interesting biological mechanism. It shows results in a model organism and in human cells in the laboratory. It also provides human data showing that phosphatidylcholine metabolism changes with age.

But it does not constitute a clinical trial demonstrating that eating more phosphatidylcholine slows or reverses aging in human beings.

We must always distinguish three things: a mechanistic finding; a therapeutic or nutritional hypothesis; and a demonstrated clinical efficacy in human beings. We are here primarily in the first two stages. And that is already exciting.

So why are we talking about egg yolk?

Because nutrition naturally plays a role in phosphatidylcholine metabolism. Choline is an essential nutrient and an important precursor for phosphatidylcholine synthesis.

And the egg — particularly the yolk — is an excellent dietary source of choline and phospholipids. It is also found in various foods, notably offal, certain meats and fish, soy and its derivatives, as well as, in varying proportions, other foods of animal and plant origin.

This does not mean: 'Eat two egg yolks a day and you will rejuvenate your mitochondria.' That would be scientifically incorrect.

This means something much more interesting: our diet provides the elements necessary for building and renewing essential cellular structures. And this places nutrition in a far deeper perspective than the simple calculation of calories.

A calorie does not tell the whole story of a food

This is a message I care deeply about. For years, we reduced nutrition to an equation: calories consumed versus calories expended.

This equation remains important for energy balance. But it does not describe everything a food does in our body.

We also eat to provide amino acids to build our proteins, fatty acids for certain membranes and signalling pathways, vitamins and minerals for enzymatic reactions, hormonal precursors, molecules necessary for the nervous system, and phospholipids required for cell membranes.

We therefore do not eat energy alone. We also eat the materials with which our body maintains its cells.

And what about women around the time of menopause?

The study also reports particularly interesting observations regarding sex- and age-related differences. The human analyses identified changes in phosphatidylcholine metabolism with ageing, with particularly noteworthy variations in women around the postmenopausal period.

This is a fascinating research avenue. But here again, let us be rigorous. This does not allow us today to assert that a reduction in phosphatidylcholine is responsible for menopausal fatigue, or that phosphatidylcholine supplementation constitutes a treatment for menopause.

It is a biological association and a mechanistic lead that now deserves to be studied clinically.

And what about phosphatidylcholine supplements?

They exist. There are also various forms of choline and other phospholipids marketed as dietary supplements.

But this study does not allow us to conclude that everyone should start taking a phosphatidylcholine supplement. That would be moving far too quickly.

The optimal dose, bioavailability, long-term effects, the populations likely to benefit, and above all the clinical outcomes in humans, remain to be determined. A promising discovery is not yet a prescription. That is a fundamental rule when we talk about longevity medicine.

What this study changes in the way we view ageing

For me, the most interesting message lies elsewhere. For a long time, we regarded certain mitochondrial changes associated with ageing as an almost inevitable consequence of age.

This study suggests that part of this deterioration may be linked to modifiable biological mechanisms. And that is precisely what makes research on ageing so fascinating.

Ageing remains inevitable. But not all of the biological mechanisms that accompany ageing are necessarily immutable.

Take care of your membranes

That may sound like an odd piece of advice. We talk a great deal about taking care of our heart, our brain, our skin, our microbiome. But rarely about our cell membranes.

Yet their composition depends in part on our metabolic and nutritional environment. A high-quality diet providing sufficient protein, essential fatty acids, choline, vitamins, minerals, and other indispensable nutrients therefore remains one of the cornerstones of healthy ageing.

And alongside that, it is reasonable to limit a diet dominated by ultra-processed products and fats that have been repeatedly heated or oxidised. Not because any particular food 'destroys your mitochondria', but because metabolic health is built upon the totality of our nutritional environment.

And that is precisely why I enjoy presenting this type of study to you: not to turn a scientific finding into a miraculous promise, but to show you how research allows us, gradually, to better understand the mechanisms of ageing. Longevity is not about searching for a miracle food. It is about understanding our biology well enough to take better care of it.