Is Inflammation the real cause of Heart Disease? | Prof. Kausik Ray
Is Inflammation the real cause of Heart Disease? | Prof. Kausik Ray
What role does inflammation play in heart disease, plaque growth and risk of heart attacks? If we keep inflammation in check, is that enough to keep our heart disease risk down? Is inflammation the “real cause” of heart disease or one factor among many?
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References:
1-https://academic.oup.com/eurheartj/ar…
2-https://www.atherosclerosis-journal.c…
3-https://www.jrheum.org/content/32/7/1…
4-https://www.sciencedirect.com/science…
5-https://www.nejm.org/doi/full/10.1056…
6-https://www.jacc.org/doi/epdf/10.1016…
7-https://www.sciencedirect.com/science…
8-https://www.ahajournals.org/doi/full/…
https://www.sciencedirect.com/science…
9-https://www.thelancet.com/journals/la…
10-https://www.nejm.org/doi/full/10.1056…
Disclaimer: The contents of this video are for informational purposes only and are not intended to be medical advice, diagnosis, or treatment, nor to replace medical care. The information presented herein is accurate and conforms to the available scientific evidence to the best of the author’s knowledge as of the time of posting. Always seek the advice of your physician or other qualified health provider with any questions regarding any medical condition. Never disregard professional medical advice or delay seeking it because of information contained in Nutrition Made Simple!.
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0:00 Intro
1:10 Is inflammation necessary for Heart Disease?
2:45 Can we stop inflammation?
4:00 Do statins work by reducing inflammation?
5:19 Summary and Takeaways
Content
0 -> does inflammation cause heart disease? does it
speed it up? is inflammation necessary? if we
6.06 -> keep it under control, are we safe from heart
disease or can we still get it? we get these
11.22 -> questions all the time and I recently got the
chance to discuss this topic with the president
17.82 -> of the European atherosclerosis Society,
Professor kausik Ray. Professor Ray is a
23.22 -> cardiologist and a professor of Public Health at
Imperial College London. he received his medical
28.32 -> degree from the University of Sheffield, a
masters from Cambridge and also completed
33.36 -> a postdoctoral fellowship at Harvard before
becoming a professor at Imperial. Professor Ray
38.94 -> has published over 200 peer-reviewed studies in
cardiovascular disease treatment and prevention,
44.58 -> including dozens of seminal clinical trials,
many of which we've covered here on the channel
50.34 -> over the years. he's one of the top experts in
cardiovascular disease on the planet so it was
56.1 -> really a privilege to have him on and discuss
many topics with him including the role of
62.34 -> inflammation in atherosclerotic cardiovascular
disease. here's that part of our conversation
72.14 -> [Music]
73.14 -> we know that when you get cholesterol in the
vessel wall, the body responds by producing
79.62 -> an inflammatory response in the vessel
wall. if you have, let's say, generalized
88.8 -> inflammation, what happens is the vessel wall
becomes more likely to attract inflammatory
98.94 -> cells, potentially you may get these particles
entering the wall, so if you have inflammation
108.84 -> you accelerate this process, so it's an
accelerant in that case, in that situation,
115.62 -> but similarly, if that wasn't true, if you
didn't have inflammation accelerating that
124.02 -> process, if you had zero inflammation, you'd
still get atherosclerosis but what would happen
129.12 -> is the particles get into the wall and your body
produces an inflammatory response. so inflammation
136.32 -> accelerates the whole thing in the same way
that diabetes accelerates the whole thing.
141.54 -> so the inflammation would still be triggered
locally, just in the localized, in the plaque,
146.46 -> in the artery wall, as a secondary event to the
cholesterol being, to the lipoproteins being
153.06 -> retained, is that right? yes. yes. and there
is no... is there any way that someone could,
158.58 -> once there is a high concentration of lipoproteins
and those particles are being retained, is there
165.18 -> any way to stop the process at that point and
prevent the cascade to the inflammation? well, so,
174.24 -> thinking about this in a slightly different
way, so what we know, to date there's only one
184.02 -> therapy that's really been clearly proven
that targeting inflammation is beneficial,
192 -> but when you look at the people, they had a high
inflammatory drive, their C-reactive proteins were
198.12 -> above 2 but the risk reduction was 15 percent,
it wasn't like, okay, you've got a really high
205.74 -> CRP and I just abolish inflammation and I dropped
that now by 50 percent. and these were people with
214.02 -> vascular disease already, so they've got that in
the vessel wall, the furring of the blood vessels,
219.12 -> you've got all of that going on, so you can slow
that down, reversing it is much much harder and
226.38 -> the only thing that we've seen that reverses that
whole process is getting your cholesterol levels
232.98 -> really very very low with combination therapies.
On a related note people ask if the benefit of
239.7 -> statins is, because they have an anti-inflammatory
role in addition to lowering ApoB,
245.58 -> how much of the benefit is... I think
we used to think about that a lot more,
250.38 -> so people refer to this as pleiotropic, so
what statins do, like bempedoic acid does,
256.98 -> it reduces production of C-reactive protein in
the liver. that's very different from saying
265.5 -> that something reduces inflammation i.e.
something that's causing a problem and by
271.74 -> reducing that causal driver and then going to
basically reduce the risk. so there is data
277.56 -> both from genetics and also from trials that when
you standardize for LDL difference by different
285 -> ways of lowering LDL cholesterol, whether
it's genes that mimic pcsk9 lowering, statins,
293.1 -> ezetimibe, you get exactly the same benefit,
and the same is true when you look at randomized
299.22 -> trials, so that's basically telling you that
actually the bulk of the clinically meaningful
304.38 -> effect in a general population is related to the
magnitude of the LDL lowering and the duration
312.24 -> of that lowering, and nature doesn't care how you
lower LDL cholesterol. I'll make a quick summary
319.08 -> of everything that was said, I think Professor
Ray was pretty clear but you guys always ask for
324.24 -> a brief summary at the end so here it is. we can
have generalized inflammation throughout the body,
329.94 -> for example with inflammatory conditions,
autoimmune disease, inflammatory bowel disease,
336 -> that kind of thing, and that tends to accelerate
cardiovascular disease, plaque formation. for
342.42 -> example, it can cause more lipoproteins to
cross into the artery wall where they can get
348.24 -> stuck. but even in someone without generalized
inflammation, with normal inflammatory markers,
355.02 -> when lipoproteins cross into the artery wall
and get stuck, that triggers an inflammatory
361.14 -> process that's localized just in the plaque. so
inflammation is not a necessary precondition for
368.46 -> plaque to begin. if there's a lot of inflammation
everywhere in the body, that's clearly worse.
374.22 -> if there isn't, that's clearly better, but
plaque can still form if ApoB is high and if
381.18 -> those lipoproteins can cross into the artery
wall and get stuck. for example in clinical
386.76 -> trials that lower cholesterol and ApoB, we see
reduction in heart attacks whether people have
394.26 -> elevated inflammatory markers or not. also,
lowering apoB without significantly affecting
400.38 -> inflammatory marker levels still lowers risk,
still reduces heart attacks. and this goes both
406.38 -> ways, people who have heart disease, who lower
their cholesterol with a Statin for example,
412.32 -> can sometimes have high inflammatory markers,
and they can have what's called residual risk,
417.84 -> so that's the fraction of risk that's left
after you address the lipids. so generalized
424.26 -> inflammation and high cholesterol or apoB are
independent risk factors, they're additive.
431.28 -> having both is worse, having one is better and
having neither is ideal. and in fact, addressing
438.48 -> both lipids and inflammation is something that's
getting a lot of increased attention in the
444.18 -> cardiovascular field recently. how do we lower our
inflammation and ApoB? there are pharmaceutical
450.84 -> tools and there are lifestyle strategies. the main
lifestyle strategies to control inflammation are
456.9 -> maintaining healthy body weight, not smoking
and addressing any underlying inflammatory
462.36 -> diseases. those are not the only factors but
they are the main ones as far as lifestyle,
466.92 -> and we have more content in the pipeline coming
very soon on diet, nutrition and inflammation.
473.7 -> as far as lowering ApoB, we covered a lot of
lifestyle strategies in this previous video, so
479.94 -> check that out, let me know your questions below,
take care, I'll catch you guys next week, bye
Source: https://www.youtube.com/watch?v=NU7rfhGi-T4