As always with such associations, reverse causality is a consideration. Perhaps those who had fatal or MACE outcomes were just sicker and less capable of physical activity.
I say this as I just skipped a heavy exercise session, because my knee was bothering me, and I didn’t want to risk an injury. I’m off rapa for another couple of weeks. As soon as I feel better, I will resume my exercise program. Meanwhile an observer could say, “gee, he’s exercising less intensively, and we see that his knee is bothering him, he should’ve been exercising intensively”.
All of this on a much bigger scale, of course. The runner who developed terminally bad knees, quits running, while the one who because of lucky genetics has good knees, continues running.
Now, if you get intervention studies, we can try to chicken and egg this association.
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This is a great 5 minute presentation on hsCRP and CVD, and why it’s important to tackle this issue.
Universal Screening for hsCRP commentary by Dr. Paul Ridker, MD, MPH
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amuser
#1918
Counterpoint: Universal screening for IL6?
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This dovetails very nicely with the studies showing Lp(a) as a risk factor in the context of hsCRP and IL-6. There were a number of studies showing that elevated Lp(a) was highly MACE causative when hsCRP is elevated (above 2mg/L) - an example is a paper @BarryAllen posted in the thread “CVD and high Lp(a) levels”:
High-sensitivity C-Reactive Protein Modifies the Cardiovascular Risk of Lipoprotein (a): Multi-Ethnic Study of Atherosclerosis
“Lp(a)-associated ASCVD risk is observed only with concomitant elevation of hsCRP. Individuals with concomitant presence of elevated Lp(a) and systemic inflammation have greater ASCVD risk and all-cause mortality, thus may merit closer surveillance and more aggressive ASCVD risk management.”
However, things are not so simple as I noted in that thread. First, I cited a paper that found that:
“In both primary and secondary prevention populations, higher Lp(a) was associated with increased cardiovascular risk independent and regardless of hs-CRP”
https://jamanetwork.com/journals/jamacardiology/fullarticle/2814836
But also, and this is where IL-6 is tied in:
Inflammation, Lp(a) and cardiovascular mortality: results from the LURIC study
“Participants were predominantly male, with a mean age of 62.6 years. Extremely high Lp(a) (> 100 mg/dL) was associated with increased cardiovascular mortality (HR 1.5, 95% CI 1.06-2.12) compared to Lp(a) < 50 mg/dl. Both hsCRP (> 2 mg/L, HR 1.39, 95% CI 1.08-1.79 third vs. first interval) and more so IL-6 (HR 1.92, 95% CI 1.64-2.23, upper vs. lower half), were independently associated with higher CVD mortality. While hsCRP did not increase the Lp(a)-CVD mortality in stratified analysis, high IL-6 conferred an increased risk at Lp(a) levels > 100 mg/dL (HR 1.25, 95% CI 1.09-1.44).”
Bottom line, IL-6 is certainly a key inflammatory marker which appears causative in CVD. The poster @BarryAllen also provided a link on how to control IL-6 in that thread.
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More good news on the Shingles vaccine:
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adssx
#1921
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IMO, I don’t think hsCRP and IL-6 is a something where you need to choose or decide which is better. It’s likely that they both move in the same direction a lot of the time, but one might be a more useful biomarker for acute or chronic conditions. Obviously CRP is a bit more “standard” to measure on most blood test menus, but IL-6 isn’t particularly difficult either. The issue IMO is that both are incredibly non-specific; they’ll raise after a vigorous workout session, or if you catch a respiratory infection, or if you have auto-immune issues, etc etc. They’re also not specifically bad or harmful. Both of them are biologically important; CRP itself is part of the immune response, and IL-6 also plays a lot of roles in responses to injury and infection. So seeing a rise in IL-6 could be a perfectly normal thing because you’re effectively dealing with some infection or other.
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Beth
#1923
For whatever reason, I got the old-timey shingles vax aprox 15 years ago (before I was 50, and I just walked into the drugstore with no rx).
Last year I also got Shingrix because I learned the old timey one was not nearly as effective. I was previously thinking, darn, I got a vax that wasn’t that helpful, and too bad I didn’t wait for the invention of Shingrix… And now I feel extra lucky I got two kinds and maybe this has slightly decreased my chance of an MI.
For those having trouble getting the vax if you are under 50, do you really need an rx if you are in the US, and you can’t simply walk into the drugstore and say I’m immunocompromised? I didn’t’ t have an rx for Shingrix, but I was over 50 for that one.
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Paul
#1924
interesting, mine are also quite low since starting jardiance
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adssx
#1925
SGLT2i are well known to lower uric acid.
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And yet:
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Plenty of people, who should know better, still deny the link. Maybe because it isn’t very sexy.
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Most doctors, in my experience, don’t understand, promote or encourage people to reduce risk. My mother’s doctor doesn’t care that her LDL-C is 180 mg/dl. When I went to my family doctor with LDL-C of >200 mg/dl at age 32, she pulled up the QRisk and said my 10y risk was low, so don’t worry.
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A lot of patients still are weirdly reluctant to treatment. I have friends, colleagues (biomedical researchers, scientists) with high LDL-C who insist they’ll handle it by just cutting back on some junk food.
I think people just don’t like this idea that something which is “natural” is also bad for you, and you can benefit from exogenous (and un-natural) molecules to fix it.
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Dr. Brad weighs in on preventing CVD.
He advocates for low dose statin + Ezetemibe. It’s good to see this.
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RonPut
#1929
Wow! So many here with high lipids! And a few who still argue that it doesn’t matter…, until it does.
As Carville said, “It’s The Diet, Stu**d!” Sure, drugs help, but more often than not they help at a cost, and I don’t mean financial cost, although that matters for the rest of society that has to support poor eating habits.
Unless one has hypercholeteromia or some other issue, there is no excuse for having super high lipids. It’s the heavy meat and dairy diet, and all the junk food that most seem to be eating.
Attia is full of BS, he is a charlatan who milks the obese with $150k+ consierge fees and often spouts unsupported claims that give comfort to those who know little and want to do little – pill popping is as easy as it gets. To an extent, so does Dayspring – he makes millions from pharma to push drugs, although recently he has scaled back a little on his insistence that dietary cholesterol doesn’t matter (it does, enough).
For the vast majority it’s as simple as eating a whole foods plant-based diet, and enough movement to maintain muscle and balance the calories. If it’s too boring for some, they will die prematurely, and will cost the rest of society dearly while dying.
Cheers.
adssx
#1930
Do you have any evidence that Dayspring is making “millions from pharma to push drugs”?
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AnUser
#1931
There are benefits to reducing levels even further than what can be achieved through diet alone:
A recent meta-analysis published in JAMA Cardiology suggests that it is both safe and effective to lower LDL below 70 mg/dL. The authors reviewed a large database of CVD patients with LDL levels averaging 70 mg/dL or less at the start of the studies. On average, there was a 20% drop in CVD risk seen for every 39 mg/dL drop in LDL cholesterol. In other words, a drop in LDL from 70 mg/dL down to 31 mg/dL was associated with 20% fewer CVD events such as heart attack or stroke.
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Diet and exercise, lifestyle and all non-drug interventions just optimize what you already have. It’s like the objective is to move across a distance as fast as possible, and you diligently train and eat to run as fast as you can. There’s a limit.
This site is dedicated to moving beyond that. It says: it is wise to optimize your non-drug interventions, but ultimately, you need an assist to move faster. A horse. A bicycle. A car. An airplane. A rocket. A wormhole transporter/jk/.
So, rapamycin.news - because rapamycin is the horse in this analogy… or at least we hope it is.
Diet/exercise will only get your ApoB so low. For more, you need the horses and the bicycles of something more: drugs - statins, ba, eze, pcsk9i.
One day we’ll get to the cars and airplanes of genetic manipulation and design, and rockets of man-machine bodies.
Until then, drugs, the ponies.
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Very well said. As much as I love taking full advantage of what interventions we have available to us now, I want more funding, research and development of new longevity interventions that either slow down aging, reverse the damage of aging, both, or some unforeseen other thing we’ve not thought of.
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What cost when one has no side effects? Higher risk of diabetes? Not every statin has that. Long-long-long term risk that hasn’t been detected in half a century of usage?
Besides, many people can’t control their cholesterol with diet alone. The human body is not perfect and never was.
pill popping is as easy as it gets.
Because it works and telling people to “just exercise and eat better bro” has a success rate of <1%.
To an extent, so does Dayspring – he makes millions from pharma to push drugs,
Source?
For the vast majority it’s as simple as eating a whole foods plant-based diet, and enough movement to maintain muscle and balance the calories. If it’s too boring for some, they will die prematurely, and will cost the rest of society dearly while dying.
Or you take medication and more than mitigate all the damage.
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Paiva
#1935
Just sharing my personal experience in this topic:
Five days ago i put my second CORONARY STENT 14years after my first one in 2011.
All this 14years I keep my healthy routine (diet, exercise, good sleep, etc) and ldl colesterol around 60-70mg/dc taking statin, benpedoic acid (recently) and ezetimibe.
As my CVDs family history is bad ( my father and mother died of it); six months ago, afther read dr Peter Atilla book OUTLIVE, I change statins to pcsk9 inibitor. Since then, my LDL droped to 28mg/dc on the last sample days ago. I hope, keeping this “aggresive number”, stay out for another stent… Im male, 73y, BMI 20,6.
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