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Do you really need to watch your salt intake? The science is much more nuanced than Doctors think - Wisdom Wednesdays · Hardiness with Dr Paul Taylor

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  Speaker 1: Hey, everyone, welcome to another edition of Wisdom Wednesdays. Now,
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  Speaker 1: for decades, we've been told that the key to controlling
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  Speaker 1: blood pressure is simple, eat less salt or sodium. And
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  Speaker 1: in fact, the us Diartry guidelines still recommend limiting sodium
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  Speaker 1: intake to about two point three grams per day, and
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  Speaker 1: here in Australia it's two grams per day. But when
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  Speaker 1: you dig into the science, the story is actually a
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  Speaker 1: lot more complicated. Some long term studies have actually found
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  Speaker 1: something quite surprising that lower sodium intake can sometimes associate
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  Speaker 1: with higher blood pressure. And there's another curious observation is
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  Speaker 1: that people with obesity tend to be.
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  Speaker 2: Far more salt sensitive than lean individuals.
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  Speaker 1: So the big question is why Today we're going to
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  Speaker 1: explore that and through a fascinating piece of research that
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  Speaker 1: may provide a completely new way of thinking about high
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  Speaker 1: blood pressure. And it really involves a complex interaction between
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  Speaker 1: body fat, the brain, and the nervous system. So most
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  Speaker 1: people think about body fat really think of it as
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  Speaker 1: a passive energy storage, but biologically speaking, fat is actually
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  Speaker 1: an endocrine organ and I've talked about this before. That
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  Speaker 1: means that it releases its own hormones that communicate with
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  Speaker 1: other parts of the body, and one of the most
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  Speaker 1: important of these hormones is something called leptin. Now, leptin's
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  Speaker 1: classic role is to signal the brain how much energy
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  Speaker 1: we've actually stored, and when fat mass increases, leptin levels rise.
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  Speaker 1: And what leptin does is two things. Two main things.
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  Speaker 1: One is that it's about cessation of eating. It tells
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  Speaker 1: you you've had enough eating. And it actually drives voluntary
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  Speaker 1: physical activity. And when they block the leptin gene in
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  Speaker 1: healthy mice and rats, they stop moving and they over eight.
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  Speaker 2: Right. And this is why you don't see a.
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  Speaker 1: Fat rattlesnake or a fat line, because leptin is actually
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  Speaker 1: a very powerful controller of body weight. But because we
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  Speaker 1: have appetite and we have all these ultra processed foods
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  Speaker 1: and center frey lifestyles, our leptin control system can become dysfunctional.
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  Speaker 1: And that is a state where we continue to accumulate
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  Speaker 1: leptin as we're accumulating body fat, and that is known
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  Speaker 1: as hyper leptinemia. Right, So very high levels of leptin,
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  Speaker 1: and there's actually research showing that you can get leptin resistance.
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  Speaker 1: The higher the leptin, the less effective it comes. And
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  Speaker 1: as I said, Other studies show consistently that higher leptin
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  Speaker 1: levels then also correlate with high blood pressure.
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  Speaker 2: So is it correlation or is it causation.
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  Speaker 1: Now, one pretty cool study that I just read published
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  Speaker 1: in Cell Metabolism, really answers this question, and they examined
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  Speaker 1: whether leptin itself might trigger changes in the brain that
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  Speaker 1: eventually lead to hypertension.
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  Speaker 2: So let's talk about this study.
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  Speaker 1: It was published in Cell Metabolism, and the researchers fed
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  Speaker 1: mice a high sugar, high fat diet that was designed
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  Speaker 1: to induce obesity, and what they find is that the
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  Speaker 1: blood pressure didn't increase immediately. Something else happened. First, as
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  Speaker 1: the mice gained with it, the researchers noticed structural changes
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  Speaker 1: occurring in the brain and specifically in the hypothalmis. Now
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  Speaker 1: you may well know that the hypothalmis is essentially the
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  Speaker 1: body's physiological control center or command center. We know that
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  Speaker 1: hypothalmis regulates hunger and satiety, It regulates hormones, it regulates temperature,
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  Speaker 1: it regulates fluid balance, it regulates the stress response, and importantly,
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  Speaker 1: it regulates blood pressure. Now, the hypothalmis does this partly
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  Speaker 1: by controlling your sympathetic nervous system the classic fighter flight response,
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  Speaker 1: and when the sympathetic nervous system is activated chronically, it
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  Speaker 1: can reise blood pressure by increasing heart rate, constricting blood vessels,
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  Speaker 1: and altering kidney function and fluid retention. So what these
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  Speaker 1: researchers wanted to know was could obesity some high be
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  Speaker 1: altering the structure of this hypothomas of the control center,
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  Speaker 1: And remarkably, that.
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  Speaker 2: Is exactly what they find.
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  Speaker 1: Before the mass developed high blood pressure, the researchers observe
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  Speaker 1: major remodeling of blood vessels around the hypothalmus first, and
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  Speaker 1: these changes included an increase in a number of blood vessels,
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  Speaker 1: also a thickening of the vessel basement membranes and increased
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  Speaker 1: vascular permeability.
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  Speaker 2: Now what all that.
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  Speaker 1: Means is that the micro architecture of the hypothalmus was
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  Speaker 1: literally being rewired by an increase in body fat. And crucially,
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  Speaker 1: these changes occurred before the rise in blood pressure was noticed,
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  Speaker 1: so was cause causative not correlation. And even more interesting
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  Speaker 1: was that the vascular remodeling occurred at exactly the same
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  Speaker 1: time that leptin levels in the blood street began to
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  Speaker 1: increase as the animals became obese. So the researchers really suspected,
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  Speaker 1: as you would imagine, that leptin might well be the
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  Speaker 1: actual trigger. So let's break down the mechanism a little bit.
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  Speaker 1: So the first step begins with expanding the fat tissue.
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  Speaker 1: As your fat mass increases, fat sales increase the amount
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  Speaker 1: of leptin that they release into the bloodstream. Step two
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  Speaker 1: then occurs in the brain. Leptin crosses into the hypothalmis
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  Speaker 1: and interacts with astrocytes. These are victualized support cells that
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  Speaker 1: help regulate the blood brain barrier and the local micro.
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  Speaker 2: Environment around your neurons.
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  Speaker 1: And these astrocytes actually respond to leptin by activating a
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  Speaker 1: molecular signaling pathway. It involves hifon and VGF. Now VEGF
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  Speaker 1: you may have heard me talk about this before. This
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  Speaker 1: stands for vascular endothelial growth factor, and as the name suggests,
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  Speaker 1: it stimulates the formation of new blood vessels.
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  Speaker 2: And in step three was angiogenesis.
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  Speaker 1: This is the growth of new microvessels within the hypothalmus,
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  Speaker 1: and this remodeling changes what sciencests call the gliovascular interface,
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  Speaker 1: which is the structural relationship between the brain cells and
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  Speaker 1: the blood vessels. Step four is where and it gets
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  Speaker 1: really gikky here. But this is where the physiology becomes
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  Speaker 1: really interesting. The altered vascular in environment changes how the
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  Speaker 1: neurons in the hypothalmis process signals that regulate the sympathetic
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  Speaker 1: nervous system, and the result is a persistent increase in.
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  Speaker 2: Sympathetic nerve activity.
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  Speaker 1: And chronic activation of the sympathetic nervous system is one
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  Speaker 1: of the classic drivers of hypertension.
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  Speaker 2: And not only does.
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  Speaker 1: It do that, but it really has widespread effects throughout
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  Speaker 1: your body. You do not want to be in chronic
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  Speaker 1: activation of your sympathetic nervous system. That is basically being
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  Speaker 1: in a stressed state. So obesity actually causes a stress
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  Speaker 1: on the body.
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  Speaker 2: And here's how it works.
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  Speaker 1: Basically, obesity causes higher leptin, which causes hypothalmic vascular remodeling,
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  Speaker 1: which causes sympathetic overactivity, which then causes the increased blood pressure.
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  Speaker 1: So the big question here is the damage permanent. And
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  Speaker 1: this is where it gets encouraging because the researchers wanted
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  Speaker 1: to know that, so they performed a follow up experiment
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  Speaker 1: and they took these obese mice and they switched them
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  Speaker 1: back to a normal diet, which caused the animals to
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  Speaker 1: lose weight and lower their leptin levels, and when they
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  Speaker 1: did that, they saw that the abnormal blood pressure growth
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  Speaker 1: in the hypothalm was actually reversed, so the microvascular structure
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  Speaker 1: returned almost completely to what was seen in lean animals.
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  Speaker 1: In other words, these brilling changes weren't permanent, at least
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  Speaker 1: in the mouse model. Now we don't know if they
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  Speaker 1: were obese, if they'd been left to be obese for
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  Speaker 1: months and months and months, whether that remodeling would actually
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  Speaker 1: have happening. But what it does suggest is that obesely
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  Speaker 1: might leave what some scientists referred to as a metabolic scar,
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  Speaker 1: but that scar may still be modifiable if the underlying
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  Speaker 1: environment actually improves. So for me, this research provides an
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  Speaker 1: intriguing explanation for something that doctors have observed for years
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  Speaker 1: is that people with obesity often exhibit salt sensitive hypertension,
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  Speaker 1: and that means that blood pressure rises much more dramatically
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  Speaker 1: in response to sodium intake than it doesn't lean individuals.
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  Speaker 1: And one possibility here, a very clear one, is the
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  Speaker 1: hypotholic remodeling that we've just discussed actually alters the neural
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  Speaker 1: circuits that regulate kidney sodium handling. So remember, the sympathetic
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  Speaker 1: nervous system directly affects the kidneys, and if sympathetic activity increases,
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  Speaker 1: the kidneys tend to retain more sodium and water, which
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  Speaker 1: raises blood pressure. And by the way, this is why
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  Speaker 1: chronic stress can also reaise blood pressure, because it's the
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  Speaker 1: sympathetic nervous system then influencing the kidneys to retain more
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  Speaker 1: sodium and water.
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  Speaker 2: So I think this research really does converge.
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  Speaker 1: So really, obesity may prime the brain in a way
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  Speaker 1: that makes the body much more reactive to sodium intake.
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  Speaker 1: In other words, the problem is not just salt alone,
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  Speaker 1: but how the brain interprets salt signals when influenced by
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  Speaker 1: excess body fat.
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  Speaker 2: So what does it all mean.
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  Speaker 1: It means that hypertension, particularly in obesity, is not simply
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  Speaker 1: about a dietary sodium problem. It involves these complex neuroendocrime
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  Speaker 1: pathways that link fat tissue, the brain, vascular system, and
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  Speaker 1: the nervous system. Now, all of this doesn't mean that
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  Speaker 1: sodium intake is irrelevant. But if you're metabolically healthy and
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  Speaker 1: if you're lean, do you really need to manage your
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  Speaker 1: salt intake or is it just people who are overweight
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  Speaker 1: who need to manage the salt intake. And this really
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  Speaker 1: ties in with research that shows that the single best
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  Speaker 1: way to lower your blood pressure if you're overweight is
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  Speaker 1: to actually lose weight. And now we understand the mechanisms. So,
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  Speaker 1: if you're lean, do you really need to follow the
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  Speaker 1: Diar Tree guidelines around salting tick? I certainly don't, but
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  Speaker 1: you can make your own call. But if your obease
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  Speaker 1: or overweight, then managing your weight would be the first step.
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  Speaker 1: But understand that if you are overweight, you are much
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  Speaker 1: more likely to be much more salt sensitive than lean individuals. So,
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  Speaker 1: like everything in the dietary guidelines, and there is no
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  Speaker 1: one size fits all, we read a much more nuanced approach.
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  Speaker 2: So that's it for this week, folks, Catch you next time.