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Wisdom Wednesdays: Anti-aging strategies part 12: Improving mitochondria function · Hardiness with Dr Paul Taylor

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  Speaker 1: Hey, everyone, welcome to another edition of Wisdom Wednesdays and
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  Speaker 1: to the last of twelve of our series of anti
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  Speaker 1: aging strategies. And today we are goining to talk about
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  Speaker 1: mitochondrial dysfunction, and it's basically.
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  Speaker 2: The power failure behind aging.
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  Speaker 1: That's power for people who can't understand my accent, and
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  Speaker 1: so mitochondrial dysfunction for me is probably the most important one,
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  Speaker 1: just in my opinion, of those twelve hallmarks of aging,
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  Speaker 1: because we know that the mitochondria are implicated in almost
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  Speaker 1: every one of the major causes of death, and they
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  Speaker 1: are also implicated in pretty much every mental health condition
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  Speaker 1: that there is. Doctor Chris Palmer, who's a psychiatrist at
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  Speaker 1: Harvard University, has written a brilliant book called Being Brain Energy,
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  Speaker 1: and basically he shows quotes all of the studies that
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  Speaker 1: show that damaged mitochondria or suboptimal mitochondria are present in
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  Speaker 1: every mental health condition that there is. Now, let's get
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  Speaker 1: back to the mitochondria. They are often known as the
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  Speaker 1: powerhouses of the cell because they create the energy within
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  Speaker 1: the cell, but their rules extend far beyond energy production
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  Speaker 1: and understanding how that influences aging and really provides insights
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  Speaker 1: into how we can maintain our vitality, increase our health span,
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  Speaker 1: and prevent chronic diseases. So what are they? They are
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  Speaker 1: specialized organelles. Organell is just a fancy name for a
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  Speaker 1: substructure of the cell that has one or more and
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  Speaker 1: are one and more clear functions. And so these are
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  Speaker 1: specialized organelles within our cells, and they're responsible for producing ATP.
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  Speaker 1: ATP is the primary energy currency of our cells and
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  Speaker 1: therefore of us, and they achieve this ATP through something
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  Speaker 1: called oxidative phosphorolization.
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  Speaker 2: So there's going to be a few big words. That's
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  Speaker 2: just a little bit of a warning.
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  Speaker 1: But that's basically how we convert nutrients from food into energy,
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  Speaker 1: and it's through something called or part of it's through
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  Speaker 1: something called the CREB cycle. So cells with high energy
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  Speaker 1: demands think about neurons in the brain and muscle cells,
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  Speaker 1: they have numerous mitochondria to meet their energy needs. So
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  Speaker 1: the more energy hungry a cell is, the more mitochondria
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  Speaker 1: they tend to have. But they don't just the energy production.
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  Speaker 1: They're also involved in critical processes like calcium signaling, which
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  Speaker 1: is really important for keeping us alive, apoptosis, which is
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  Speaker 1: that programmed sale death that we talked about in previous episodes,
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  Speaker 1: and also the generation of reactive oxygen species. And their
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  Speaker 1: unique feature is that they actually possess their own DNA
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  Speaker 1: called mitochondrial DNA, and it's inherited maternally, so it comes
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  Speaker 1: from the mum and that encodes essential components.
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  Speaker 2: For their function.
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  Speaker 1: And this really sets your mitochondria out from everything else,
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  Speaker 1: the fact that they have their own DNA which you
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  Speaker 1: actually get from the mother. And let's talk about mitochondrial
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  Speaker 1: dysfunction and why it's important in aging. So as we
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  Speaker 1: age this, the efficiency of our mitochondria actually declines, and
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  Speaker 1: that leads to reduce the AT production atp sorry production
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  Speaker 1: and increased reactive oxygen species generation. If you remember reaction
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  Speaker 1: of oxygen species, they can create inflammation and all sorts
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  Speaker 1: of nasty things. They basically cause oxidative damage to cellular
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  Speaker 1: components including lipids, proteins in DNA within the cell and
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  Speaker 1: that contributes to cellular senescence and tissue dysfunction. So if
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  Speaker 1: you remember back cellular sinescence, that's like the zombie cells.
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  Speaker 1: So basically, when your mitochondria loser efficiency, we get more
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  Speaker 1: damage inside the cell and the cell turns into zombie cells,
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  Speaker 1: and this decline in mitochondrial function is associated with a
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  Speaker 1: whole host of age related diseases such as metabolic syndrome,
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  Speaker 1: and metabolic syndrome basically increases your risk for a huge
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  Speaker 1: amount of diseases, including cardiovascular disease, the biggest killer, and
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  Speaker 1: we know that in powered mitochondrial function, it disrupts energy metabolism,
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  Speaker 1: contributes to insulin resistance and obesity, which are hallmarks of
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  Speaker 1: metabolic syndrome, but also kind of mitochondrial function and contributes
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  Speaker 1: to neurodegenerative diseases because are neurons, because they're so energy hungry,
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  Speaker 1: they are particularly vulnerable to mitochondrial dysfunction. And we know
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  Speaker 1: now that defective mitochondria can lead to synaptic failure and
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  Speaker 1: the death of neurons, as we see in Alzheimer's disease
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  Speaker 1: and Parkinson's disease. And the other big thing that it
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  Speaker 1: contributes to is cardiovascular diseases. So mitochondal dysfunction in cardiac
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  Speaker 1: cells impers your heart function and contributes to hypertension, atherosclerosis,
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  Speaker 1: and overall cardiovascular disease. And if you take those collectively,
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  Speaker 1: cardiovascular disease neurodegenerate disease and metabolic syndrome, and in the
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  Speaker 1: knock on effects of metabolic syndrome, that actually.
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  Speaker 2: Accounts for a huge portion of death.
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  Speaker 1: And that's why I think mitochondrial dysfunction is the most
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  Speaker 1: important hallmark of aging. And we have this theory called
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  Speaker 1: the mitochondrial free radical theory of aging, and that suggests
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  Speaker 1: that a cumulative oxidative damage from these reactive oxygen species
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  Speaker 1: over time leads to the functional decline of our mitochondria
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  Speaker 1: and that drives the aging process. So let's talk about
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  Speaker 1: the stuff that we can actually do. And first up,
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  Speaker 1: of course, is regular physical activity. There is probably nothing
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  Speaker 1: that you can do better for your mitochondria than regular
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  Speaker 1: physical activity.
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  Speaker 2: Engaging in in.
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  Speaker 1: Regular exercise is a cornerstone for bolstering mitochondrial health. Physical
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  Speaker 1: activity has been shown over and over again to improve
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  Speaker 1: mitochondrial function and induce mitochondrial biogenesis, which is the creation
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  Speaker 1: of new mitochondria.
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  Speaker 2: And so it has two things.
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  Speaker 1: It enhances the efficiency of your existence mitochondria and it
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  Speaker 1: creates new mitochondria. And this adaptation is crucial for meeting
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  Speaker 1: increased energy demands and improving our metabolic health.
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  Speaker 2: And we know that.
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  Speaker 1: Both aerobic training, particularly zone two, which is that's that
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  Speaker 1: heart rate of sixty to seventy percent of your max.
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  Speaker 1: But from a non technical perspective, you're exercising, you can talk,
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  Speaker 1: but you can't sing, So you can talk in sentences,
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  Speaker 1: but you're kind of breathing heavily and you can't sing.
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  Speaker 1: If you can sing, you're in zone one. If you
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  Speaker 1: can't talk in sentences, you're in zone three.
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  Speaker 2: A higher heart rate zone.
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  Speaker 1: And we know that this zone two, you it's basically
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  Speaker 1: where aerobic metabolism is dominant, and that has been shown
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  Speaker 1: to improve our mitochondrial health, can contribute a little bit
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  Speaker 1: to mitochondria biogenesis. And interestingly, I read a study recently
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  Speaker 1: where they took a bunch of people who weren't fit,
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  Speaker 1: and they put half of them straight into resistance training,
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  Speaker 1: and half of them they did eight weeks of aerobic
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  Speaker 1: training in zone two before they went into resistance training.
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  Speaker 2: And then they looked at their.
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  Speaker 1: Strength training gains and muscle sized gains, and it turns
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  Speaker 1: out that the people who'd done the aerobic training first
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  Speaker 1: actually increased their strength and muscle maths quicker than the
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  Speaker 1: people who went straight into the resistance training. And the
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  Speaker 1: thinking is the aerobic training gave them a better functioning
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  Speaker 1: mitochondria and some more mitochondria, and then that translated to
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  Speaker 1: quicker benefits from the strength training. So let's talk about
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  Speaker 1: high physical activity. Actually, oh sorry before we do that.
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  Speaker 1: And high intensity interval training has shown to be very
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  Speaker 1: very potent in stimulating mitochondrial biogenesis of the creation of
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  Speaker 1: new mitochondria. So let's talk about the mechanism. One is AMPK,
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  Speaker 1: and so basically AMPK stimulates mitochondrial biogenesis and enhances oxidative metabolism.
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  Speaker 1: And the other thing, again we're getting a bit giky.
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  Speaker 1: Here is PGC one alpha upregulation and PGC one alpha
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  Speaker 1: If you really want to know what it is, it's
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  Speaker 1: perioxysome proliferator activated receptor gamma coactivator one alpha, and this
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  Speaker 1: is a master regulator of mitochondrial genesis. And this PGC
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  Speaker 1: one alpha pathway is hugely important in our health and
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  Speaker 1: studies have shown as I said, that both aerobic training
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  Speaker 1: and high intensity interval training and resistance training improves our
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  Speaker 1: mitochondrial content and function in our muscle, leading to improved
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  Speaker 1: intinal insensitivity and reduce.
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  Speaker 2: Risk of metabolic disorder.
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  Speaker 1: And we also know that fasting and exercise both stimulate
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  Speaker 1: mitochondria biogenesis and stress resistance in muscle cells and through
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  Speaker 1: calcium signaling an AMPK activation.
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  Speaker 2: Right, that's geeky enough for the minute.
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  Speaker 1: Let's talk about calorie restriction and intermittent fasting, So reducing
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  Speaker 1: your caloric intake without going into malnutrition or doing implement
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  Speaker 1: intermittent fasting or time restricted feeding as some people call it.
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  Speaker 2: They have been associated with.
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  Speaker 1: Enhanced mitochondrial function and increase lifespan in various species, not
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  Speaker 1: in humans, I hasten to add. But the mechanisms by
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  Speaker 1: which this happens is that when we fast, we switch
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  Speaker 1: from burning glucose to burning fat. This what we call
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  Speaker 1: metabolic flexibility. And when you switch over to burning fat,
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  Speaker 1: it actually stimulates the production of ketone bodies like beta
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  Speaker 1: hydrox computury it and that actually serves as an energy
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  Speaker 1: substrate and signaling molecule for the mitochondria. And what fasting
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  Speaker 1: also does is it induces autopogy. I talked about that
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  Speaker 1: in earlier ones. That's the cellular clean up process by
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  Speaker 1: which the things inside the sale actually take damage mitochondria.
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  Speaker 1: This is called mitophagy. And they take that damage mitochondria
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  Speaker 1: and actually recycle them and create new mitochondria. So this
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  Speaker 1: is that's the cellular recycling plant that's actually going on.
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  Speaker 1: And this this is called cyclic metabolic switching theory. It
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  Speaker 1: suggests that health benefits of intermittent fasting may actually be
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  Speaker 1: better than those of continuous calorie restriction. And I actually
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  Speaker 1: think that's a slam dunk because of that interplay between
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  Speaker 1: ketone metabolism, mitochondrial adaptations, and autophogy.
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  Speaker 2: And I know I'm getting very.
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  Speaker 1: Geeky here, but I think it's important to understand these processes.
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  Speaker 1: Now I link to this, you'll not be surprised to
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  Speaker 1: hear that if intermittent fasting does this and through ketones,
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  Speaker 1: going on a ktogenic diet where it's it's high fat,
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  Speaker 1: low carbohydrate and moderate protein that stimulates beta hydroxy buttyate
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  Speaker 1: and other ketones which then positively influenced mitochondrial function. And
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  Speaker 1: we see this a katogenic diet really beneficial for Alzheimer's
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  Speaker 1: disease in Parkinson's disease, probably because of the impact that
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  Speaker 1: they have in the mitochondria in brain cells, and the
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  Speaker 1: mechanisms are very similar. Add to intermittent fasting enhance mitochondrial
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  Speaker 1: efficiency because the ktone bodies are really an excellent energy source.
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  Speaker 1: An increase our at B production reduced oxidative stress. But
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  Speaker 1: beta hydroxy butty in itself has actually been shown to
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  Speaker 1: stimulate antioxidant defenses, which is really really important. And a
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  Speaker 1: study combining a ketogenic diet with exercise actually showed that
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  Speaker 1: there were alterations in mitochondrial function, including increased respiratory what's
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  Speaker 1: called respiratory control ratio and ATP production in skeletal muscle,
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  Speaker 1: as well as improvements.
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  Speaker 2: In metabolic health markers.
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  Speaker 1: So together with exercise and a ketogenic diet or intermittent
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  Speaker 1: fasting can be very powerful double wami for your mitochondria.
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  Speaker 1: Let's talk about pharmacological or supplement interventions. So NAD precursors
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  Speaker 1: theoretically are good for the mitrochondry because we know NAD
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  Speaker 1: plus is really important. So compounds that you'll see like
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  Speaker 1: NMN plastered all over the internet and NR they are
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  Speaker 1: thought to boost NAD levels. The fact they've been shown
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  Speaker 1: to actually do that, and that's essential for our mag
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  Speaker 1: to chondrial function. But if you don't want to spend
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  Speaker 1: a shitload of.
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  Speaker 2: Money on NMN and NR.
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  Speaker 1: You can actually just take some B vitamins because NMN
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  Speaker 1: and NAR are actually converted in the gut to vitamin
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  Speaker 1: B three, which is nicotinic acid. And so you can
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  Speaker 1: either go out and spend a shitload of money on
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  Speaker 1: NMN and NR, or you can just take vitamin B three.
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  Speaker 2: I know what I would do.
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  Speaker 1: Another supplement that's pretty promising, And actually I have started
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  Speaker 1: playing with this methylne blue because it has been shown
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  Speaker 1: to actually stimulate the mitochondria through its actions on the
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  Speaker 1: crab cycle. It actually by cut passes for those who
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  Speaker 1: are geeky, complexes one in three in the electron transport
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  Speaker 1: chain and actually stimulates the crab cycle, leading to increased
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  Speaker 1: ATP production and improves cellular energy metabolism through the mitochondria. Okay,
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  Speaker 1: now if that's not kiky enough, let's now talk about
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  Speaker 1: low level light therapy or infrared and near infrared light therapy,
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  Speaker 1: so near infrared light and that's also known as a photobiomodulation.
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  Speaker 1: That is basically applying low level red light to near
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  Speaker 1: infrared light and to stimulate cellular function. And what it
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  Speaker 1: does is it works on something called cytochrome C oxides
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  Speaker 1: and that is a key enzyme in the mitochondrial electron
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  Speaker 1: transport chain. And there is a heap of research now
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  Speaker 1: I that shows that near infrared light actually boosts the
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  Speaker 1: function of your mitochondria, and that is something I was
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  Speaker 1: so convinced by the research. And I have a panel
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  Speaker 1: that does both red light and near in for red light,
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  Speaker 1: because the research for me is very very compelling about
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  Speaker 1: improvements in mitochondrial function. And we are now even seeing
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  Speaker 1: near infrared light helmets of certain way of lengths significantly
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  Speaker 1: improving symptoms in both Parkin's disease and Alzheimer's disease. And
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  Speaker 1: basically what happens is that at light passes goes through
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  Speaker 1: your skeleton and actually stimulates goes it deep inside of
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  Speaker 1: your body and stimulates your mitochondria and certain parts of
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  Speaker 1: the electron transport chain, and that leads to increased energy
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  Speaker 1: production and improves cellular energy metabolism. And the other thing
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  Speaker 1: that near infrared light does is it releases nitric oxide,
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  Speaker 1: and that actually helps to improve blood flow and reduces
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  Speaker 1: oxidative stress.
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  Speaker 2: And studies have.
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  Speaker 1: Shown that infrared light penetrates human tissues and benefits mitochondrial
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  Speaker 1: function as I say it, and it can improve things
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  Speaker 1: like mitochondrial dynamics and quality control following ischemia, stroke, cardiac
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  Speaker 1: arras so I actually was using it post my heart
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  Speaker 1: surgery and also for overall brain function, cognitive function. It's
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  Speaker 1: actually been shown to help people recover from straight stroke
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  Speaker 1: and neuro degenerative diseases. So hink conclusion, lots of big mouthfuls,
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  Speaker 1: but basically what we know is our mitochondria are absolutely
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  Speaker 1: key to cellular health and longevity, and doing things like
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  Speaker 1: regular exercising, intermittent fasting, low carbon particularly keathogenic diets, some
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  Speaker 1: potential pharmacology, and near infrared light therapy can all really benefit.
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  Speaker 1: And while studies haven't been established it because they're really
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  Speaker 1: hard to do, I actually think that these things are
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  Speaker 1: additive because they work on slightly different pathways in our mitochondria.
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  Speaker 2: So I think if.
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  Speaker 1: You're doing all of them, you're going to get better
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  Speaker 1: benefits than if you're just doing one or two. So
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  Speaker 1: that's it for this week, folks, Catch you next time.