What’s in your lipid profile?
https://www.nature.com/articles/s41569-024-01111-0
(I actually gave the full document my best effort but had to retire hurt 
)
Mind you, it seems like it was just as topical over a decade ago🤔…
It is very clear for many people that as they age statins matter a great deal.
I go by what practically does help most people.
Errr…no. Quite the reverse, in fact, if looking at preventing the development of a disease as opposed to scrambling to fix it when it’s taken hold.
What would help most people would be to identify early on those folk who’re at most risk… regardless of how exemplary their future lifestyle choices might be… and manage accordingly. The tools to do this easily are becoming readily available…along with knowledge of their existence.
1 Like
This key point caught my attention:
“Different species of apolipoprotein B-containing lipoproteins are not equally atherogenic; triglyceride-rich lipoproteins and their remnants and lipoprotein(a) are markedly more atherogenic than LDL.”
Few articles about cardiovascular disease mention the role of triglycerides. While lipoprotein(a) is genetically-determined and not modifiable by lifestyle factors, triglycerides are definitely modifiable by lifestyle.
I have treated myself to a complete blood test every year for the past 20+ years. It’s not expensive and doesn’t need a doctor’s order.
About 15 years ago I began to drink a couple of glasses of ginger ale every day. I figured that it was a harmless indulgence. Not like I was drinking alcohol, right?
Wrong. The blood test showed that my blood triglycerides suddenly spiked to 175, above the danger zone of 150. The high-fructose corn syrup in the ginger ale spiked my triglycerides.
I cut out the ginger ale and most other carbs while I was at it. I lost 15 pounds and my triglycerides dropped to 95 without medication.
It takes decades for atherosclerosis to become entrenched and life-threatening. Young people can easily change their food selections and prevent a world of problems later. Then they won’t need statins.
Data point: my angiogram showed that my coronary arteries are clear (except for one spot of 40% blockage in my LAD which the cardiologist considers insignificant). The top-line bill for that day in the hospital (including the angiogram and some tests around it) was $14,300.
Wendy
6 Likes
Yes they can…provided that it’s their food selection/lifestyle choices that are responsible for that world of problems. Granted, folk like myself…who have followed a healthy eating/drinking lifestyle for well over half a century (not counting the time on my mother’s watch)…are few and far between but they do exist and are increasingly likely to have their risks ignored in spite of more opportunity to identify and manage them simply because of the assumption that lifestyle choices will make a difference for everyone.
For myself, I’ve never seen my triglycerides higher than/HDL lower than 80 mg/dL.or so. Regardless of whether there’s much emphasis on their roles in the pathogenesis of ASCVD for the lay public to read, I think it’s reasonable to expect those we seek out to help us manage our health and wellbeing to have enough of a take to respond to an unexpected Red Flag (however modest) appropriately…regardless of how much those who’ve been responsible for their own ill health dictate the narrative.
That is your situation. Mine was becoming a type 2 diabetic at age 49. I was immediately given statins as at risk.
My dad at age 55 was seen as at risk for cholesterol problems. He was put on a statin but they did not know statins could protect against plaque. It just worked out for him.
1 Like
Well, yes. “Folk like me” are the ones I was referring to…good custodians of their bodies whose personal risk factors tend not to be noticed simply because they’re doing everything right. It’s your good fortune that you were prescribed statins at 49. However, let’s be honest, if you were finally diagnosed with T2D.at that age, there were a good few years (decades, even) prior to that when it was surely obvious that you were heading away from healthy homeostasis.
Not sure what you mean about your dad. No matter how soon after statins were introduced that he got them, of course “they” knew statins were protective against atheroscleosis…that’s exactly why there was a hunt for lipid lowering agents in the first place (including drugs that were less successful before they were discovered/developed)
I forgot. What was the genetic variation that predisposed you to atherosclerosis?
On the standard lipid panel I’ve had done over the years, my LDL-C tended to register as “mildly elevated” and toggled around 125-135 mg/dL give or take. A few years back I started to wonder and also started to read/listen to podcasts mentioning that some lipoprotein particles are more atherogenic than others…and that these can be measured. I actually asked for this so-called “advanced” testing and my new to the practice PCP added Apo-b and Lp(a) to the Usual Suspects (I could tell she wasn’t convinced) but both came back super high. Likewise my CAC score, and my subsequent CT angiogram showed significant blockage of 3 coronary arteries and some random lower blockage scattered about. Absolutely no symptoms whatsoever!!
So the Apo-b can be modified by lifestyle…meaning craptaculous eating habits and sedentary behaviour can raise it, and fixing those habits can lower it. Obviously, if it’s elevated in someone who has taken care of business and it’s a result of a poor genetic hand being dealt, then medication is the only option.
I don’t do things by halves so, not content with this stroke of bad luck, I am one of the approx 20% of the population with elevated Lp(a) and this cannot be modified by diet, exercise or medication…yet.
My lipid lowering medications are lipitor…which got my LDL-C down to about 90mg/dL (would probably be fine if started, say, a couple of decades or so ago when menopause had kicked in) and addition of Repatha, a PCSK9 inhibitor, has me now at a nicely low 31 mg/dL as of my cardiology review a couple of weeks ago.
I blame my mum for all of this😉
3 Likes
You didn’t ask this, but I’ll point it out anyway. For pretty much anyone who’s been running a bit rich on the LDL-C stakes for any length of time, it’s worthwhile suspecting that there’s been some degree of atherogenic activity going on under the hood. Also realising that just getting back to standard range might not be enough to prevent further progression of any damage that may have been initiated.
This is one of the reasons that cholesterol denialists like to repeat the nonsense that statins don’t work or some other tomfoolery. In the unlucky few, a disease process will continue to progress unless a serious intervention is applied. Hence my aggressive lipid lowering therapy…which has landed me in that dreaded “donut hole” come November for the past 2 years.
Yes absolutely but the somewhat theoretical and somewhat unexpected is the reduction in plaque.
Nothing matters about statins if the plaque is still building up.
Dad is 86, this was 31 years ago. 1994 might as well have been a half blind time on this topic.
The Lp(a) was the piece of the puzzle I missed last time around. My cholesterol was in the 220 range and my ldl was in the 120 range prior to my decision to combine time restricted feeding with very long hill walks. Long walks after dinner, no snacks, long walks before breakfast, adding up to 2-4 hours worth of walks during my 14-16 hour fasts (plus full day mountain hikes roughly once a week). I was able to reduce my total cholesterol to151 and my ldl to 71 in about two years, but I guess I did not have the Lp(a) gene and did not know to ask the question.
1 Like
Well, there’s no reason why you should. Neither should I, for that matter. It was purely a fluke that the relevant information drifted across my radar screen and that I was interested enough to follow up on it. I’m pretty miffed about it because this isn’t brand new stuff that a halfway competent primary care physician would be in the dark about…or at least shouldn’t be.
“Heart disease” is globally the #1 cause of death…which to me means that the index of suspicion should be high for everyone who has a marginally dodgy looking lipid profile. Regardless of whether or not they conform to the stereotype of someone you’d expect to be a candidate for a heart attack.
3 Likes
It really is terrible to be in the position people are in with less care than they should have received. It is not excusable.
The drift from determining statins were lowering plaque versus the side effects was left in limbo for a long time.
At age 83 my mother was put on a statin for a bit of an increase in her cholesterol. She does not tolerate statins at all. She is on something else to protect her.
Her mother had a blockage at age 82. She had angioplasty but no stent in those days. Just a year or two early before stents became common place. She was all set and lived to age 98.
A lot of this is luck.
1 Like
Out of interest, what is she being protected from? Was it just a slight and very late mild increase…and just an automatic response for no other reason?
I’ve posted this link many times and was probably the one that was most instrumental in pushing me to request the further testing I mentioned upstream…the Lp(a), Apo-b, circulating insulin (in case a drift towards metabolic dysfunction was responsible) and CAC scan. I think I was reasonably confident that my experience would be the same as the flaneur’s.
This notion (a non invasive way to actually visualise if a long standing elevation in total cholesterol/LDL-C has resulted in actual pathology) shouldn’t be as new to the folk who ought to know about it as it was to me. As the article pointed out…not all “high cholesterol” needs to be lowered…and a reaction to introduction of statin therapy (if real) would be something to concentrate my mind on making sure lipid lowering therapy were actually necessary beyond simply tinkering with a biomarker.
This is another article from this excellent site…
There are a good few articles on this topic here and I’ve followed the board for quite a while out of general interest. It’s interesting to note that, now I “know what I know” and look back and re-read some of those articles, a lot of what I’ve stumbled across of late (last 2 or 3 years) had been mentioned frequently before. Goes to show how easy it is to ignore facts…even if interested…if we don’t think they apply to us.
We have a history of stroke in our advanced 80s and 90s.
Everything dances around the only issue which is plaque. All that study of cholesterol levels buries the matter of plaque.
It is what it is. It has taken time to add things up.
It is not really about calcium or cholesterol. It is mostly about plaque.
I’ve been utilizing CAC (also termed heart scan, coronary calcium score, or cardioscan) to help assess my patient’s risk of ASCVD for years although the procedure is not covered by insurance and until recently was not strongly endorsed by major guidelines.
The scan is good enough to see minute blockages caused by plaque. That seems to have been in doubt for a long time but the two cardiologists looking in 2020 and 2023 said I have zero plaque. I passed a stress test two summers ago.
1 Like