It’s no secret that I’ve already written the book on metabolism — or have I? Well, I thought I had . . . until now. Don’t get me wrong, my book Master Your Metabolism is not filled with bad or incorrect info — it’s just incomplete. And this is becaus. I looked at metabolism only as it relates to body weight and, subsequently, all the lifestyle diseases associated with obesity. I didn’t look at how it is connected to aging.
Believe it or not, the ideal metabolism as it relates to age and the ideal metabolism as it relates to body weight can be in opposition.
Let me guess: you think you’re misunderstanding me, right? Isn’t a slow metabolism the worst possible thing in the world?
Well, I can tell you this: there is absolutely no question that a slower metabolism is linked to a longer life. Ever heard the saying “the candle that burns twice as bright burns half as long”? That’s a pretty solid metaphor for metabolism. But don’t panic if you have a fast metabolism — you can still live a very long and healthy life. The keys remain the same, no matter where you fall on the metabolism bell curve.
What is it about a faster metabolism that we think is so great? Just one thing: you can eat more and not gain weight, which ages you whether you gain weight or not because, hello, it causes oxidative stress. So that friend who could eat whatever she wanted and not gain weight, the one you wanted to punch in the face?
Well, guess what? That’s not so great for her overall health — despite her pant size.
And while obesity is unhealthy and linked to many life-threatening diseases, like cancer and heart disease, a slow metabolism doesn’t make you fat — if you exercise regularly and aren’t overeating. It really is that simple.
I’ve actually had a slower metabolism my entire life and thought it was a curse until now. I had to be smart about my food choices and careful not to overeat, and I managed to keep myself perfectly healthy at 16 percent body fat (give or take). Now I am so thankful that I have a slow metabolism because it forced me to be mindful about what and how much I ate and, without intention, resulted in lowering my rate of oxidative stress.
Let’s say you’re the person with the fast metabolism, and you’re thinking, “Oh my God, I’m screwed.” Not so. There are a ton of things you can do to offset this oxidative stress, but before we get into that, let’s discuss what metabolism is.
The faster your metabolism, the more calories you burn all day long, but how many calories you burn depends on a few things. You burn calories when you exercise — but you should know that already.
You also burn calories during non-exercise- activity thermogenesis (pretty much any activity you’re doing while you’re awake that’s not technically exercise). You’re burning calories when you’re at rest or asleep. And finally, you burn calories while digesting food —this is called the thermic effect of food, or TEF.
The thing is, when you metabolize food, it stresses your body. And when you overeat, you’re creating even more stress. That’s just one piece of the puzzle related to why overeating may lead to a shorter life span and a variety of age-related health issues, such as type-2 diabetes and cardiovascular disease.
But other scientists are looking at metabolism from the perspective of how the foods we eat get broken down. The reason? Because having certain nutrients, either abundant or absent in our systems, may inhibit or trigger autophagy, a process that occurs when your body needs to recycle damaged and worn-out cells for their nutrients, which in turn can reduce the risk of some of the age-related issues we experience.
No possibility is being left ignored, but does that mean that we shouldn’t rev up our metabolisms to help burn fat? I mean, if having a slower metabolism may help extend your life span, is it worth doing things that actually slow down your metabolism, like not exercising, not sleeping properly, and not eating protein- rich foods (which require more energy to digest than carbs and fats)?
No, of course not. Our goal is not to slow down our metabolism but to inhibit certain aspects of metabolism that accelerate aging and maximize aspects that help combat it.
How A Slow Metabolism Affects Your Age
Your body spends every waking second circulating blood, eliminating waste, growing and repairing cells, controlling your body temperature and hormone levels, keeping your brain and nerves firing, breathing — you name it. And all these metabolic activities to keep you alive not only take energy — they take their toll.
The very job of keeping you alive creates metabolic stress, which over time results in damage to your cells. You can avoid some of it, but you can’t stop all of it, because it only shuts off entirely when you shut off for good. And that is antithetical to our goal here.
But there’s one other thing about your metabolism that changes with age — your body’s ability to detect nutrients. Most people think the word metabolism only means one thing — how fast your body converts food into energy. But scientists understand that there are molecular events that relate to your metabolism — events that occur because of an ebb or flow of specific key nutrients that float about in your system as your metabolism does its job.
Your body is way smarter than it looks — right down to a cellular level. Your cells produce enzymes to process different nutrients (like glucose, for example), and they rely on a series of nutrient-sensing pathways to both recognize the nutrients and respond to them in the right way.
Even though you have many nutrient sensors, there are four major nutrient-sensing pathways — insulin/IGF-1 signaling (IIS), mechanistic target of rapamycin (mTOR), AMP-activated protein kinase (AMPK), and sirtuins — that really matter when it comes to what ages you.
In a nutshell, it kinda works like this: your IIS (among other things) lets your cells know when glucose is present, while mTOR is specifically sensitive to amino acids (broken down from the protein you’re eating) and lets your cells know when that’s around.
Then the two team up to signal when there’s an abundance of these nutrients available. The mTOR and IIS levels rise in relation to how much you’re eating and how often, and your cells are alerted to this smorgasbord of food.
Once your cells notice that there’s plenty of glucose and amino acids to go around, they spend less time seeking out damaged cells to break down for their nutrients. Instead, they start using all those extra nutrients to grow cells.
Eating too much as well as too often causes your mTOR and IIS levels to stay elevated all the time, and the process of autophagy (the breaking down of damaged cells) shuts off.
Your body figures, “Why get rid of damaged cells when I have plenty of nutrients and hormones floating around?” But the longer autophagy is off, the more damaged, misfolded protein cells start stacking up. This leads to protein aggregation, which can cause bad things to happen, including cell dysfunction and tissue damage that can eventually lead to disease.
The other two nutrient-sensing pathways — AMPK and sirtuins — work together as well, but in the exact opposite way. Instead of noticing when you’re swimming in nutrients, they’re more concerned with when you have fewer nutrients hanging around.
AMPK is the master regulator of cellular energy. In particular, it monitors levels of adenosine triphosphate (ATP), a chemical your cells both store and break down for the energy necessary to execute every biological reaction in your body.
Once AMPK senses you’re using up your ATP, it goes to work as a central regulator of both lipid (fat) and glucose (sugar) metabolism. The higher your energy demand, the more ATP you need, and the more your AMPK pathway is activated.
Sirtuins, on the other hand, look for high levels of nicotinamide adenine dinucleotide (NAD+), a metabolite that’s present in every cell and helps facilitate DNA repair. When they see plenty of NAD+ present, sirtuins help adjust your metabolism and regulate many metabolic functions, including keeping your genome and mitochondria stable.
But when there is less NAD+ to be found, something that naturally happens as we age, keeping those processes in working order isn’t always your sirtuin’s top priority.
So, what’s the bottom line when it comes to aging?
Science is showing that higher levels of AMPK and sirtuins extend your life span. The exact opposite is true of your IIS and mTOR pathways. When these pathways are activated and their levels are elevated, life span is reduced, but when they’re decreased — yup, guess what? There’s an increase in life span.
So the goal here is to get AMPK and sirtuins up while bringing IIS and mTOR down.
Why do scientists think these pathways affect life span?
When AMPK is activated, it inhibits mTOR,4 thereby increasing autophagy. Meanwhile, when some forms of sirtuins are activated (such as SIRT1 and SIRT3), they help heal mitochondria, improve fatty acid oxidation (so you burn more fat for fuel), and enhance the effectiveness of