When I had a stent placed six or so years ago, despite my perfect “numbers” my doctor wanted me on a statin for one year post-op because the science said I was statistically more likely to be alive after that year if on a statin, despite cholesterol numbers.
For a year I had muscle cramps nearly every night. After the year was up, I stopped taking the statin and felt much better.
I appreciate your detailed response, Qadgop. Do any tests exist that could indicate how much damage (if any) my hyperlipidemia has caused so far?
Actually, there is a LOT of research being done into this, because familial hypercholesterolemia is common enough to warrant it. (It’s believed to affect about 1% of the population.)
Some people talk about statins like they should be put into the water supply (and I’m only slightly exaggerating) but for the OP, I personally think it’s not a bad idea. Using natural remedies like eating oatmeal doesn’t hurt, either; I have a friend who was diagnosed with FH in her early 20s, when she found out her cholesterol was >400, and she lowered it 40 points in a month just by adding that to her diet, per her doctor’s recommendation.
Thank you, nearwildheaven. Do you know if it’s possible to inherit
the gene for this from a grandparent or great-grandparent? My parents’ cholesterol numbers were perfect.
FH is a dominant gene, so you would have to inherit it from a parent, unless you had a spontaneous mutation. Plus, FH shows up very early in life, so you probably don’t have it. Cholesterol numbers, and the risks associated with them, do increase with age.
That is very interesting! Thank you, nearwildheaven.
Some indirect tests like checking ankle/brachial index, or doing carotid flow studies (to name but a few) can check for blockage, but that’s not all that helpful unless you’re having symptoms. As screening tests, they don’t help improve health so much for the typical person.
Preventive cardiologists can be useful to determine overall risk in a situation like yours. Finding one can be a challenge though.
I appreciate your knowledge so much! If I knew how much arterial plaque I have compared to what a person my age with normal cholesterol should have – would that be helpful?
One more question: is it possible to have inherited a recessive gene for hyperlipidemia? My parents’ cholesterol numbers were normal.
Thank you, Quadgop!
This. I’ve been misdiagnosed or put on medications that have had horrible side effects before that took months and even years to correct because the doc wasn’t thorough. It happens. Even with my Simvastatin situation, the nurse suggested they’d put me on muscle relaxers if I get blocked up again. I know from experience that muscle relaxers also relax my ability to work. Not a solution. The doctor needs to hear what the patient is saying. I do understand my risk here but what good am I to anyone, self included, if I cannot function due to the drugs that are keeping me alive?
No, comparing plaque isn’t really useful. That’s where the preventive cardiologist can best assess risk.
And there are a variety of different genes you can have that alter cholesterol production/levels etc. You may have inherited them from your parents, but they didn’t really get activated in them for whatever reason, while they did with you. You may have a new mutation. Maybe that reading was a lab error; have you had other cholesterol readings in recent years? doesn’t hurt to recheck. What were your triglycerides. All questions a preventive cardiologist (or a thorough internist, though those are fewer these days) would ask and address the results.
It’s complicated, it’s complex, and statins reduce plaque formation even in folks with normal cholesterol levels (and low levels too) who form plaque for other reasons
Thank you so much for this response.
These results were from Oct. 2020. Triglycerides were 117 mg/dL.
The ratio of HDL to total was 4.6.
On my last test in 2017, Triglycerides were 66. Total cholesterol: 301,
HD: 87, and LDL: 194.
So I think the recent results were reliable. 
Actually, there is - for very specific gene variations. There isn’t for all of the ones that exist, however.
Generally, you don’t need to do a “genetic analysis” to make the diagnosis, though - looking at the patient’s cholesterol numbers is sufficient in most cases.
Not a doctor, just someone whose family had a hypercholestereolemia gene in many members. So far as I know, all FH genes are dominant - none are recessive, they don’t skip a generation. You can have a spontaneous mutation of your very own.
FH is the big dramatic issue. As Qadgop mentioned, there are numerous genes that can affect cholesterol levels and how your body handles it. How the body handles (or doesn’t) cholesterol is actually pretty complicated and I’m not sure it’s fully understood by anyone.
Now, you see, while that’s elevated it’s not the highest possible.
My mother, for instance - on maximum statin dose her lowest total cholesterol reading was 600 something and it was usually over 800. That’s what some FH genes can do to your cholesterol levels.
Fun fact - my mom was part of the clinical trials for statins. They did help her, and it was fortunate she tolerated them well. She took them from the 1980’s onward. Used to be, her form of the disease tended to kill people in their mid-40’s. Mom lived to 77. So, in her case, a win. They can be life-saving. It’s unfortunate that not everyone can tolerate them or find them beneficial.
Broomstick, this is so interesting! Thank you.
Sounds like she was homozygous for type II familial hyperlipidemia. I saw a 9 year old girl with that back at the Lipid Research center. She had a cholesterol level of 1200 and her body was covered with xanthomas. The only treatment was plasmapheresis back then. She was one of the first to get statins.
I’m heterozygous for type II myself, and my cholesterol level as as high as 400 at times. Now with modern meds, my total cholesterol runs about 150.
I am not going to comment on a personal case since this is between you and your doctor.
Plenty of people have high levels of LDL cholesterol and over time this puts them at risk for narrow arteries, stroke and heart problems.
Many people can improve their levels by eating healthier, but in some people the problem is with the liver and not their diet. These people would still have high levels of cholesterol regardless of how well they eat.
Your body needs some cholesterol to make cell membranes, steroids and hormones. It’s there for a reason.
There are many types of cholesterol. HDL levels are seen as good. No one talks about chylomicrons, various Apos or VLDL so the mass media discussion is a simplified version of reality. Triglyceride levels also likely contribute to risk, but exactly how much is not definitively understood.
Statins were originally tested for people up to age 75, and more recent studies have shown a benefit in veterans beyond this age.
I think they are clearly beneficial in people with elevated LDL cholesterol with other risk factors: diabetes, smokers, high blood pressure, family history, obesity, minimal exercisers. They are beneficial for many people approaching these categories too, like those with high-normal values. Exactly where the cutoff is between who benefits and who does not is not always clear to me despite guidelines. If you have had heart problems being on a statin makes good sense if it is tolerated.
They are good drugs. Niacin is too, in my mind, despite two big studies showing the sustained release version (which includes another medicine) are not helpful in terms of reducing mortality. The plain version of niacin is still helpful, and reduces arterial deposits, but is tough for many to take as it causes flushing and itching at therapeutic doses.
Statins reduce mortality. There are other drug classes that also work but seem to show less benefit for that. Still, it’s a gestalt, you could reduce mortality with more exercise and healthier lifestyle choices too.
I have been reading this thread with interest as I have been tracking my cholesterol levels for about the past 10 years, after my company started this wellness program and I did a lipid panel, which led to the discovery my levels were outside of the recommended ranges.
My doctor suggested statins but I wanted to try to resolve the issue on my own thru diet and exercise. I do not have many of the risk factors: non-smoker, not obese, not a regular drinker, and AFAIK no family history. Back then, I was very active - running half marathons and a lot of bicycling. My doctor suggested I increase my exercise level - but I literally could not - I was already exercising 5-6 days a week. Diet was (and is) more of the challenge, and while I have made strides it was not enough, and finally around 2018 I accepted atorvastatin (20mg, which I tolerated well), and my levels improved such that all went into the recommended ranges (except triglycerides and HDL, which I never got in range).
This year I decided to give it another try, and consulting with my doctor I went off the statin for the last 6 months to see if I could manage things without. I am still active but not running half-marathons right now, and have been eating a healthy diet. The result was disappointing - all levels went back to their pre-statin levels, which, while not terrible, are still not within the recommended ranges. My pharmacist friend suggested the sudden stoppage of the statin in the spring may have triggered my body to produce more than normal since then. I dunno.
Anyway, I have a consult with my Dr next week and I am sure he will suggest going back on the statin, which I will accept (again).
I just skimmed the responses, but that LDL definitely puts you into strongly suspected heterozygous FH category. Currently genetic testing is not indicated for heterozygous FH but I know many preventative cardiologist who do it anyway. Statin therapy is definitely indicated for that level of LDL, and it very well may not be enough to get the levels down to target goals. A good chunk of my patients that fall into that FH category are also on a PCSK9 inhibitor which almost always knocks those levels down. If your PCP has not done it already, I would ask them to check you for other signs of FH such as xanthomas and other atherosclerotic disease.
I will also say that simvastatin is widely used but less favored as it tends to have more interactions with other commonly used medications (such as amlodipine). The go to statins now are more likely to be atorvastatin (Lipitor) or rosuvastatin (Crestor), or if interactions with other medications are really a concern, pravastatin (we commonly use it for transplant patients).
Edited to add: Lifestyle and diet can help modify a person’s general risk of cardiovascular disease, but it tends to have a fairly small effect on the actual cholesterol numbers. It’s also important to remember that the cholesterol itself is a risk factor for cardiovascular disease, and having low cholesterol does not equate to no risk just as having high cholesterol does not mean you are doomed to have a heart attack or stroke. A lot goes into the risk profile, and cholesterol is certainly a large contributor to it, but I have had plenty of with terrible coronary artery disease who had fairly normal cholesterol levels. An advanced lipid panel could also be done to look for other higher risk features, such as lipoprotein(a), although again in your case, it would be more for research purposes than management decisions.
I think mom was heterozygous. For one thing, if she was homozygous I should have inherited at least one FH gene but with a total cholesterol holding steady at 100-110 for last 50 years that seems highly unlikely. And that’s with a total disregard to limiting fats, lipids, cholesterol, etc. in my diet and no medications required.
I think mom’s side might just have a particularly vicious FH gene in the family tree. Mom did have xanthomas above and below her eyes, but not any other places I was aware of. She did have a crapload of lipids in her blood vessels, though. Being healthy otherwise probably helped her survive the FH problems, but in the end cardiac disease is what got her. For many years whenever she encountered a new doctor there’d be puzzlement over how a woman normal-to-underweight, low blood pressure, no sign whatsoever of diabetes, and regular exercise could have such severe heart disease from such a young age but now we know.
The way it was explained to me (and I can’t verify if it’s true or not, but it seems to make some sense) is that mom’s problem wasn’t that she was either eating too many fats, or her body making too much cholesterol, it’s that the disposal mechanism was “broken” - her body couldn’t get rid of it when done with it. So it kept building up and building up.
Dad’s side has awesome cholesterol values (I take after dad in that way). Unfortunately, in that family tree we have an autosomal dominant desmoplakin-associated arrhythmogenic right ventricular cardiomyopathy gene (I hope I have all of that correct). Which is a mouthful and not something I had ever heard of until just a few years ago but it did explain why so many people on his side of the family literally dropped dead before the age of 30 with no obvious explanation. I seem to have dodged that genetic bullet as well.
Given that mom’s problem (high cholesterol) can, with modern medicine, allow for a normal lifespan and kills you slowly enough that there is time to diagnose it and limit the damage I’d take that over dad’s family curse which all too often can strike without warning. As in, someone in their 20’s who seems perfectly healthy can just literally fall over dead with no prior symptoms (Happened to an uncle, possibly two great-uncles, and two of my nephews in fact - all falling over dead between 20 and 30. Might have also been a problem in the greater extended family tree but that’s impossible to research). Unless you get tested specifically for it, which we all have down to my latest great-nephew (he, too, dodged the bullet). There are some limited things that can be done for it, but it’s not nearly as common or well studied as FH. So, as aggravating as treating high cholesterol can be, and as annoying as it is to have as an inheritance, things could be far worse in my opinion.
audiobottle, I greatly appreciate your response. I’d like to ask if you think any screenings would be informative such as Carotid Artery Screening, Peripheral Arterial Disease Screening, or Abdominal Aortic Aneurysm? If they showed serious damage from the cholesterol, that would be a big incentive to try a Statin. Thank you!
Thanks again to everyone who replied! I’ve learned a lot.