Right.
Kind of shifting back just for a moment to the to the fasting topic, we've talked
a lot about metabolically unhealthy people with Type 2 diabetes, or perhaps
obesity, or animal models of such, and the benefits of intermittent fasting
in those, you know, people or animals.
How much can, you know, a healthy person who perhaps is not, you know, at
risk for obesity or metabolic syndrome benefit from intermittent fasting?
Yeah, that's a complicated answer.
I'll expand a little bit how much and in what ways.
There have been far fewer studies in humans of intermittent fasting on
normal weight, you know, healthy people.
In animals, the control group is always fed ad libitum and they're sedentary.
So, really, in the animal studies, the control group is couch potatoes.
And that's why, I would say in extrapolating the animal data to
humans, I'm very comfortable in saying intermittent fasting will have very
clear, measurable, highly significant benefits for overweight people.
But since all the animal studies, the control group is couch potatoes, and
we're seeing good effects on the couch potatoes, we can't say, you know, that
does apply to humans of normal weight.
But there have been studies in normal weight healthy humans.
Looking at some health indicators, blood glucose levels and insulin, and looking
at ability to maintain and build muscle mass, so resistance training studies,
several published studies where they found that with daily time-restricted
eating, people were able to maintain and build muscle just as well as people who
weren't on daily time-restricted eating.
But it's undoubtedly, the magnitude of any beneficial effects on health
in people that already have a healthy body weight are going to be less
than on people who are overweight.
And the effects on improving glucose regulation in people with Type 2 diabetes,
who already have insulin resistance, are going to be quantitatively much
greater than people who have, you know, already have normal insulin sensitivity.
So, you know, I would say that there will be some benefits, but it's
going to be quantitatively less.
Does that make sense?
Quantitatively difficult.
It does.
Like, difficult to even measure, you know, because as you've been discussing
throughout the podcast, the benefits of metabolic switching, the production of
ketone bodies like beta-hydroxybutyrate, and their signaling effects on BDNF,
you know, increasing BDNF, and also producing less reactive oxygen species,
because they're more energetically favorable or easier by the mitochondria.
It seems as though activating autophagy, as you mentioned, you know, the
clearing away of damaged stuff and organelles and things within a cell.
Like those, you know, sorts of effects happening, even if
the magnitude isn't as great.
It seems as though like that has to be beneficial long term in terms
of like activating stress response pathways, that are going to help you
deal with the stresses of aging better.