Healthspan Lifestyle Change — Living Better for Our Children (II)

This is the second post in a series. In the first one, we reflected on a simple and difficult question: if we know we should change our lifestyle, why don’t we? There, I introduced the ideas of Peter Attia—a physician who has devoted his practice to understanding how we might live longer and better—and I mentioned that I would try to share some of his key insights in a simpler, clearer way.

This post is that attempt.

Both texts can be read separately, but together they form a single conversation. The intention behind both: to draw attention to how we live, and to the goal of being more present—and present for longer—for our children.

A midweek workout in the garage. They laugh, they sweat — building not just strength, but the kind of life they want to share.

Healthspan lifestyle change and metabolic health impact our body's ability to manage energy.

Let’s start with a simple image.

We eat. And why do we eat? Because it gives us the energy we need to move — not just physically, but also to keep all our bodily functions running.

We eat, and when we do, food enters our digestive system. There, a series of biochemical processes transform what we’ve eaten — say, broccoli — into usable forms of energy: carbohydrates, fats, proteins. That energy is then distributed throughout the body so that each part can use it as needed [i].

When everything is functioning properly, energy is distributed efficiently and each system gets what it needs.

But when the body starts to malfunction, that energy ends up in the wrong places — or worse, it causes harm [ii].

It’s like storing a piece of raw meat on your nightstand, next to your bed.

So, what causes that misdistribution? Why does it happen this way?

To understand this process — and where it breaks down — we need to look at one remarkable trait of animals like us. A trait that helped our species survive.

Our bodies are capable of storing unused energy for later, especially in times of scarcity or increased need [iii] — say, chasing a buffalo across the savanna.

And how do we store it? As fat. First as subcutaneous fat, just beneath the skin [iv].

The problem begins when we consume more calories than we burn on a regular basis. The body keeps storing fat. But eventually, it runs out of room under the skin.

Still, the body doesn’t stop trying to save energy — because evolutionarily, conserving energy remains a top priority. In the savanna, nothing was guaranteed. In winter, even less so. You never knew when your next meal would come.

So that excess fat starts accumulating in places it shouldn’t: first in the liver, then around the abdomen [v]. It’s like a home that’s run out of space, and now you’re stashing things anywhere — on top of the washing machine, blocking hallways, cluttering every corner.

In the liver, this accumulation is called fatty liver. At first, it simply gets in the way, like a vacuum cleaner left in the middle of a hallway. But over time, it causes inflammation, then scarring — internal damage — and gradually, the liver stops working properly. It becomes like a house where every activity requires maneuvering around piles of stuff: exhausting and inefficient.

Just consider this: the liver performs around 600 different functions in the human body [vi], including the production of bile — essential for fat digestion — and the regulation of blood sugar. When these functions are compromised, it can lead to insulin resistance (linked to type 2 diabetes) or hormonal imbalances (such as in certain cases of hypothyroidism, where slowed metabolism results from inadequate thyroid hormone production).

Visceral fat — the kind that accumulates around the abdomen — also begins to press on organs, inflame them, and disrupt their function [vii]. This buildup has been linked to both cancer and cardiovascular disease, partly because it can surround vital organs like the heart, and partly because it can enter the bloodstream, forming plaques and blockages.

Some of that fat can even reach the brain — a condition associated with increased risk of Alzheimer’s disease.

In short: when fat accumulates where it shouldn’t, it disrupts metabolic function [viii], and a vicious cycle begins. The pancreas, liver, and kidneys stop working properly; they fail to produce the necessary hormones and enzymes, which affects how we process and distribute energy — which in turn worsens our metabolic function.

Peter Attia’s thesis is that diseases like cardiovascular conditions, neurodegeneration, and cancer may all be consequences of disrupted metabolic function [ix]. But under the paradigm of Medicine 2.0, they are treated and studied in isolation — and only when the damage is already done, without ever asking what caused it in the first place… or what continues to cause it.

General Principles, Particular Decisions

Not all bodies are the same. Each body is unique [x]. This means that people vary in their ability to store subcutaneous fat [xi]. Some have very little capacity for it—their bodies quickly divert fat to organs like the liver or pancreas. Others are able to store it under the skin for longer. That’s why being thin doesn’t necessarily mean someone’s metabolism is working well [xii]. And this, Peter Attia says, is one of the most important takeaways for how we approach our life cycle.

According to him, one clear conclusion is that we need to burn more energy than we consume [xiii]. And to do that, we have to place the body under a certain amount of stress—through exercise or fasting—so that it starts using its reserves.

But let’s remember: everybody is different, and every health goal is too. This needs to be evaluated case by case. It’s not a universal or one-size-fits-all recommendation. That’s important.

Still, we can say this: when we fast or exercise, we put the body in a state where it has to dip into its reserves. In other words, we send it a signal — “there are few nutrients available.” And that signal activates cellular processes called autophagy: mechanisms that clean, recycle matter, and remove toxins. Like tidying up the house [xiv].

Of course, this is especially hard today, for at least two reasons [xv]. First, we live in a world with 24/7 food availability. We’re not in the savanna anymore. Three taps on your phone and food arrives in 30 minutes. Just walk to the kitchen and open a cupboard. Second, many of those foods are loaded with fructose and added sugar, which makes caloric intake incredibly high in very short timeframes.

So, the fundamental principle is this:

→ We have to burn what we consume.

This is one of the essential principles behind the healthspan lifestyle change we want to build in order to be more present—for longer—for our children. What to eat, and how much to eat, depends—again—on each case: how much movement there is in that family, for example; their habits, rhythms, and daily reality.

Now, we know it’s not easy to do this. The first reason to try, as we’ve said, is to be more present for our children. But it’s not just that: if we manage it, they’ll eat better too. They’ll learn a healthier lifestyle. And we’ll be able to model it for them by example.

Still, easier said than done. Each life unfolds in unique circumstances, with its own demands. That’s why, at ON Care, we treat each family as unique. We understand that the support each one needs to build a healthier life—not just physically, but emotionally and mentally—is singular, with its own path and obstacles.

Because, in the end, that’s what all of this is about. Being there when our child looks at us, like that two-year-old girl looking at her father—and making him think not about dying, but about how to live longer, and better.

If we can hold onto that desire—not as anxiety, but as a guiding light—maybe we can build a lifestyle that’s truly worth living: one that cares for us, so that we can care for them.

Notes

[i] Peter Attia and Bill Gifford, Outlive: The Science & Art of Longevity, First edition (New York: Harmony, 2023), 96.

[ii] Attia and Gifford, 97.

[iii] Attia and Gifford, 98.

[iv] Attia and Gifford, 99.

[v] Attia and Gifford, 92.

[vi] Attia and Gifford, 93.

[vii] Attia and Gifford, 103–7.

[viii] Attia and Gifford, 110.

[ix] Attia and Gifford, 110.

[x] Attia and Gifford, 31.

[xi] Attia and Gifford, 98.

[xii] Attia and Gifford, 100.

[xiii] Attia and Gifford, 107.

[xiv] Attia and Gifford, 80.

[xv] Attia and Gifford, 101.