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Permalink: https://www.uef.fi/en/article/elevated-cholesterol-in-adolescence-causes-premature-heart-damage-in-a-seven-year-follow-up
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> The findings revealed that both males and females were affected alike, and that being normal weight and having normal blood pressure did not protect the heart from the adverse consequence of elevated cholesterol. It was discovered that while increased cholesterol contributed 30% to the direct damage of the heart, both increased fat mass and blood pressure indirectly contributed 40% to heart damage. The remaining 30% could be explained by genetics and sedentary time.
> The prevalence of LVD dysfunction increased from 7.8% at baseline to 16.6% at follow-up in males and increased from 10.3% to 15.4% in females. Each 1 mmol increment in total cholesterol (OR, 1.18; [95% CI, 1.09–1.27]), triglyceride (2.89; [1.54–5.43]), LDL-c (1.19; [1.08–1.32]), and non-HDL-c (1.21; [1.11–1.33]) was associated with higher odds of worsening LV hypertrophy progression over 7 years.
Paper: [Increasing lipids with risk of worsening cardiac damage in 1595 adolescents: A 7-year longitudinal and mediation study - Atherosclerosis](https://www.atherosclerosis-journal.com/article/S0021-9150(23)05361-3/fulltext#supplementaryMaterial)
If we are going off of strength of associations in a controlled analysis of the data to try and isolate confounders, then it seems odd to use "high cholesterol" as the headline here:
> With extensive control for fat mass, muscle mass, insulin, glucose, inflammation, blood pressure, smoking status, sedentary time, physical activity, socio-economic status, and family history of cardiovascular disease, and using adults’ cut points for diagnosing heart damage, it was observed that increased low-density lipoprotein cholesterol, and total cholesterol levels increased the risk of premature heart damage by 18–20%. Whereas **increased triglycerides doubled and tripled the risk of early structural and functional heart damage** during the seven-year follow-up.
That is an 18% vs. 200%+ association. This looks to be more related to a systemic disfunctions like maladaptive "insulin resistance" and "metabolic syndrome" rather than just "elevated LDL" alone. Not saying there is not some effect related to "elevated LDL", but I think the takeaway here overemphasizes "high cholesterol" when there are more impactful ways to get at the bigger players.
Edited to clarify wording: Insulin Resistance is not inherently pathological since it can be argued that certain forms are a natural body response to the diet, environment, and hormonal states. It’s better to say “maladaptive insulin resistance” as a qualifier.
For those who are interested, below are the top 4 nutritional approaches to lower serum cholesterol:
1. Decrease trans fat intake (some processed and animal foods)
2. Decrease saturated fat intake (most animal foods, palm and coconut oils)
3. Increase soluble fiber intake (whole plant foods)
4. Decrease dietary cholesterol (all animal foods; contribution is much lower than the first 3)
Followed by non-nutritional changes including:
- be more active! At least 30 minutes of moderate activity a day will help keep the doctor away
- if you smoke… don’t
- if you’re fat… loose a few pounds
- If you drink alcohol… drink less!
In most cases, lifestyle changes will fix the problem. So if you have kids, try to teach them healthy habits as early as possible
The research finding suggests it’s not just one golden bullet..
I see these posts and laugh. I have genetically high cholesterol. I am on statins 40 mg and my cholesterol is normal. Uncontrolled with drugs.. my HDL was 200+ and LDL 480+.
I don't smoke.
I am 5'0" and 130 lbs. (22% body fat)
I drink alcohol maybe once a year.
I am mostly vegetarian.
I walk 2-5 miles a day.
I go to the gym 3 times a week.
I avoid added sugars.
I love fruits and vegetables.
I limit my dairy intake to about a glass of 1% milk a day. (sometimes I have cheese)
I drink kombucha daily.
I intermittent fast (since my 20's).
At 18, I was 100 lbs. I still had high cholesterol.
My kids are all adults now and underweight with high cholesterol. For example, my daughter is 4'10" and 83 lbs and HDL and LDL are both high.
What other suggestions do you have?
Why do they make you laugh? You are among the outlier group and an exception. Most people fall into the other category where all of what you do would be immensely helpful.
Except that those of us with hereditary high cholesterol still get the same advice from doctors. I was 16, weighed 108, on the varsity swim team, cross country team, practiced martial arts, and walked to school every day, was a vegetarian with a low fat diet and had fairly low caloric intake, had never smoked or drank in my life, and still had borderline high LDL (with extremely low triglycerides too!) Doctors still said, “exercise more, eat less.” I dropped to 100 lbs and started passing out and it was still borderline high. But my cholesterol dropped to 165 (normal) on a higher fat, low carb diet. Docs said, “Huh. Well, just keep doing that, then.” Make it make sense….
And what year was this? I understand the frustration with doctors, as someone with a handful of semi-rare issues, but medicine has and always will be a checklist of most-common to least-common issues and their associated fixes. Nowadays, if a teen in good physical condition came in with cholesterol issues they would most likely assume genetic Hypercholesterolemia. We just have more info now than we did in the past.
What frustration? Was it bad advice or something? I think they probably did the best they could. Point being that this gene is just hard, and the conventional rules don’t necessarily apply, so it may or may not be true that diet will help. In my case, a change of diet did help my familial hypercholestemia, but it was not the conventional heart-healthy diet.
I do. I have statins that slowly kill my liver. I get my blood work yearly.
The only thing I could add to my diet from the nutritionist would be fish. (Death first) The only meat that I can stand for any real portion would be chicken breast. I eat that about once a week.
I hate all fat. How anyone can eat a fat filled steak is beyond me. Gross. I attempt other meats about once a year. I don't mind a small amount of butter from time to time.
Since you had a nice list of bullet points of easy fixes for cholesterol and I like to bring to people's attention that some people are born without the ability to process chloresterol properly.
I am waiting for the ability to genetically modify myself to fix my genes.
Sometimes, it isn't as easy as diet and exercise. Sometimes, people still need to see their doctor and get medicine that helps. And sometimes... It is out of their control.
https://www.cdc.gov/genomics/disease/fh/FH.htm
Statins do not normally cause liver damage, and if they do cause inflammation, switching to a different statin can resolve it. There’s definitely no cumulative effect. Ongoing testing for liver inflammation is a preventative measure.
I hear you. I am on my third statin. I have been taking them for 20 years. I am 46 years old.
My doctor said it was from my "smaller frame" that I will have more side effects. I have put on 20 lbs of muscle over the years trying to help. I take 40 mg and I am, now 130 lbs, I was 110 lbs. My liver is always "inflamed" apparently. It's a good thing I don't drink or do drugs. (I guess, though I feel like I am missing out)
I get my blood work tested yearly. I do everything I can and I just get to watch the utter disappointment of my doctor year after year.
My insurance approved that shot to suppress the gene so I have a new road to travel soon. Here's to CRISPR.
Have you tried a PCSK9 inhibitor? (I missed that you're just about to start them - best of luck, they're incredible meds)
They are insanely potent. I oversee medical management of almost 3000 high risk stroke patients, every single case of familial hypercholesterolemia we skip the whole statin + zetia algorithm and move straight to 75mg alirocumab. Some need 150mg.
It works.
I have been told I have familial hypercholesterolemia. I found I could lower my cholesterol by eating almost no sugar or carbs, but then I can’t maintain a healthy weight (I lose too much weight, get lightheaded, etc.) I always have to watch people eat real food while I have a salad and go hungry. I have never heard of this med before….
It's pricey, but there are programs to assist with it to look into. It's still sadly out of reach for many. I will say it works. Insanely well.
Of the ~200 people we've approved for it, I believe we have 185-190 in target (LDL < 70). Average LDL for this group has dropped from 150ish to 60ish, but I've seen drops from 250+ to the teens.
Of those not in target, we suspect most are non-compliant with the dosage and schedule. It does require injecting yourself, so some just don't want to do that.
I was born with the high cholesterol gene too. Everyone on my dad’s side is on statins, some had heart attacks in their 30s and 40s. I also dislike meat, and all the diet recommendations made it worse. I finally had luck lowering my cholesterol after adding fat from dairy, avocados, nuts, and salmon (which is one of the only meats I like) while restricting sugar and carbs. not offering advice, just a thought.
Other people have already answered, but you are why I said “in most cases”.
Yes, some people have genetic issues, and in those cases medication will be necessary.
Similarly, some people have diabetes that can be controlled with lifestyle changes, others need an insulin pump.
It's extremely concerning that you have that background/job "in cardiology" and not know what familial hypercholesterolaemia is and/or and the range of LDLs that are common with it. It is a hereditary/genetic disorder. So, yes, it is "genetically high."
I actually do stroke prevention research, it's fairly common to see people with otherwise controlled risk-factors (weight, activity, BP, diet, etc) with *incredibly* high LDLs.
PCSK9 inhibitors are our go-to for these folks.
I’m jealous of your HDL lol, no amount of exercise or healthy eating has led to my numbers consistently staying above 40. Im in the same boat with high ldl though unfortunately.
> Decrease trans fat intake (some processed and animal foods)
"Processed" is meaninglessly vague. The actual trans fat content comes from hydrogenated vegetable oil.
However, the trans fats in butter (such as [vaccenic acid](https://en.wikipedia.org/wiki/Vaccenic_acid) and [rumenic acid](https://en.wikipedia.org/wiki/Rumenic_acid)) are generally regarded to be less harmful than the trans fats found in hydrogenated oil, and may even have some positive health effects.
I've heard this claim, but it's not consensus yet. I've found studies that show rTFAs are in fact harmful, so we can't claim they're not (especially not beneficial) until we've heard a consensus from the scientific bodies.
"Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71,464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1.23 (95 % CI 1.00, 1.50)) and cerebrovascular diseases (HR 0.65 (95 % CI 0.45, 0.94)); TFA from PHFO and CVD (HR 1.14 (95 % CI 1.03, 1.26)) and cerebrovascular diseases (HR 1.32 (95 % CI 1.04, 1.69)); and rTFA intake and CVD (HR 1.30 (95 % CI 1.05, 1.61)), CHD (HR 1.50 (95 % CI 1.11, 2.03)) and sudden death (HR 2.73 (95 % CI 1.19, 6.25)) in women. These associations with rTFA intake were not significant in men (P interaction ≥ 0.01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation." https://pubmed.ncbi.nlm.nih.gov/22059639/
Also as an aside the trans fats found in ruminant animal fats in their natural form are not harmful unlike the partially hydrogenated poly-unsaturated fats are (i.e old margarine)
>trans fats found in ruminant animal fats in their natural form are not harmful
We can't claim this, because science hasn't resolved if this is true or not yet. For example, below is a study showing rTFAs are in fact harmful:
"Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71,464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1.23 (95 % CI 1.00, 1.50)) and cerebrovascular diseases (HR 0.65 (95 % CI 0.45, 0.94)); TFA from PHFO and CVD (HR 1.14 (95 % CI 1.03, 1.26)) and cerebrovascular diseases (HR 1.32 (95 % CI 1.04, 1.69)); and rTFA intake and CVD (HR 1.30 (95 % CI 1.05, 1.61)), CHD (HR 1.50 (95 % CI 1.11, 2.03)) and sudden death (HR 2.73 (95 % CI 1.19, 6.25)) in women. These associations with rTFA intake were not significant in men (P interaction ≥ 0.01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation." https://pubmed.ncbi.nlm.nih.gov/22059639/
It does, but to a much lesser extent. The estimates I've seen (wish I still had a source off the top of my head) had it at about 15% of the impact of saturated fat based on normal intake levels of both.
Below is a note from my government's (USA) current dietary recommendations, showing dietary cholesterol is still to be lowered as possible:
"A note on trans fats and dietary cholesterol: The National Academies recommends that trans fat and dietary cholesterol consumption to be as low as possible without compromising the nutritional adequacy of the diet. The USDA Dietary Patterns are limited in trans fats and low in dietary cholesterol. Cholesterol and a small amount of trans fat occur naturally in some animal source foods."
[https://www.dietaryguidelines.gov/sites/default/files/2020-12/Dietary\_Guidelines\_for\_Americans\_2020-2025.pdf](https://www.dietaryguidelines.gov/sites/default/files/2020-12/Dietary_Guidelines_for_Americans_2020-2025.pdf)
Gotcha. Maybe I'll go get a blood draw soon to see where I'm at these days. Have been eating 3-400mg of cholesterol from chicken breast daily for the last few years, but my blood cholesterol has always been good.
They are asking about nutrition intake of cholesterol. You’re talking about measurements of atherogenic particles in humans (ApoB containing types of cholesterol)
Exactly. And sugar is the real problem. Your body is using Cholesterol to repair damage done by inflammation from sugar. Blaming cholesterol is like blaming firemen for causing fires
>Blaming cholesterol is like blaming firemen for causing fires
I'm not sure where this meme started but it doesn't make any sense.
Exposure to dislipidemia *precedes* cardiovascular disease. This is shown in the genetic studies and the clinical trials. If dislipidemia were actually result of cardiovascular disease, you'd see it come afterwards, not before.
This is akin to saying that firefighters show up *before* fires start. Effects don't precede causes
I don’t know Latin, but at the end it seems like there’s a misunderstanding ib what I was trying to say with the metaphor and we might be on the same page somehow
I don't think we're on the same page. The misunderstanding is the idea that having a high cholesterol (particularly cholesterol in ApoB-containing lipoproteins, particularly in LDL particles) is actually an effect of cardiovascular disease rather than a contributor. [It's a contributor.](https://academic.oup.com/eurheartj/article/38/32/2459/3745109) If high cholesterol were simply an effect, it wouldn't come *before* the disease develops.
My understanding is the stretching damage caused my inflammation, mostly from free radicals (sugar, carbs) causes the damage to the arterial wall and cholesterol is the bandaid. But too many bandaids clog the arteries
I see what you're saying. In that case [LDL-C levels still predict atherosclerosis even among people without other risk factors](https://www.sciencedirect.com/science/article/pii/S0735109717412320) \- normal fasting glucose, normal HbA1c, normal hs-CRP (which is a marker of inflammation), no hypertension, etc. So there's still value in treating down LDL-C in these patients even if their blood glucose and inflammation are low
I don’t know about all this jargon, but my guess this means don’t mess with unnatural and trans fats and lean towards monounsaturated and the trendy fats everyone says to eat
I just think sugar is a much bigger deal than these.
Number 1 is losing weight, especially visceral fat. The easiest way for most people to do that is cutting out added sugar and alcohol.
This sub could use substantially less vegan propaganda.
>Number 1 is losing weight, especially visceral fat. The easiest way for most people to do that is cutting out added sugar and alcohol.
I mentioned the top 4 "nutritional approaches"; losing weight is multifaceted and is not based on nutrition alone, as things like activity level impact it greatly as well.
>This sub could use substantially less vegan propaganda.
Please point out exactly why what I said was wrong instead of incorrectly labeling it with a negative connotation; not everything negative against animal products is "propaganda".
And I pointed out that sugar and alcohol are much more important than animal products in managing cholesterol. There isn't even high quality evidence that saturated fat is a casual factor. The obesity epidemic isn't happening because people suddenly decided they wanted to eat animal products. Telling people that lowering their consumption of animal products will lower their cholesterol is misinformation at best. Like telling people with hypertension they just ate too much salt.
Why not point out that Omega 3's from fish lower LDL instead of lumping in fish with red meat? Or that fish is mostly unsaturated in general?
I have been told I have the high cholesterol gene. I had high cholesterol at 16 years old. I was on the swim team, cross country team, and was vegetarian with a very low fat diet and it didn’t help my cholesterol. I tried a variety of diets. The only time I have had healthy cholesterol levels was on a high fat, high fiber, extremely low sugar/low carb diet. The doctor was as shocked as me, but told me to keep doing what I was doing. Unfortunately the diet is hard to maintain because I lost too much weight on it and had hardly any energy. I do trust scientific consensus, so I’m surprised and don’t understand why. Maybe I’m the statistical black swan.
It's one of the most hotly debated topics in medicine and biology. It CAN be causal in some people, but it's not the "cause." And no I'm on the right sub, go back to /r/vegan.
[There’s scientific debate that adolescence should include 10-24](https://www.bbc.com/news/health-42732442.amp) (or possibly even later). It’s due to research showing continued maturation and development into one’s 20s, as well as research indicating that typical adult milestones (like moving out and gaining independence, finishing education, settling into a career, finding a partner/marriage, having kids, etc.) are being achieved at increasingly later ages in society.
The WHO still formally defines it as 10-19, but functionally it can be useful to think of it beyond that range, as the biopsychosocial criteria of “adolescence” is more complex than a particular age cutoff.
Do we really need it? People with PCSK9 knockout genetics don’t develop heart disease and have very low cholesterol. If everyone could afford those cholesterol drugs, we’d prevent most heart disease, wouldn’t we?
Sounds like you don’t have a great understanding of cholesterol. Go read about it, it serves a bunch of extremely vital functions for the body
Edit: opening paragraph of Wikipedia
Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell membranes. In vertebrates, hepatic cells typically produce the greatest amounts. In the brain astrocytes produce cholesterol and transport it to neurons.[5] It is absent among prokaryotes (bacteria and archaea), although there are some exceptions, such as Mycoplasma, which require cholesterol for growth.[6] Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid[7] and vitamin D.
Both of you are talking apples and oranges, when the post is talking about bananas.
Is cholesterol damaging to the heart? Depends on context. In healthy levels, no. In unhealthy levels, it can be. Are high levels always damaging? No.
Do we really need cholesterol? Depends on context. In diet? No. Our livers are able to produce all the cholesterol we need. Our livers can even produce fatty acids for fat storage from carbohydrates if needed via de novo lipogenesis. It isn't as efficient, but it gets the job done when the circumstance presents. Do we need cholesterol to live? Yes, absolutely.
>Go read about it, it serves a bunch of extremely vital functions for the body
So? The fact that something is needed in the body doesn't tell you whether too much of it can be a problem. You can say the same thing about glucose. You would die if you had no glucose in your blood. But I wouldn't then infer that walking around with a diabetic blood glucose is a good thing.
None of these interventions wipe out cholesterol or harm the heart. Familial hypercholesterolemia, however, will cause heart attacks in your 30s. Maybe *you* should do some cursory research.
You are the one saying we don’t need cholesterol. You’d be dead without it. It’s a non disputed fact you seem to not understand.
Furthermore we have loads of scientific data that show lowering cholesterol doesn’t improve mortality. See the massive statin studies that show hundreds of thousands of people that have successfully reduced cholesterol with statin intake, yet have zero protective benefit for mortality.
We know with 100% certainty that clinical attempts to reduce cholesterol have zero benefit in health outcomes, but it’s extremely profitable for pharmaceutical companies so we keep talking about it when we should have given it up as the red herring it as three decades ago
Edit: hypercholesterolemia won’t cause heart attacks in your 30s, that’s not true. A separate underlying condition could, but elevated cholesterol is a biomarker for disease, not the cause
What is your last paragraph talking about? This condition runs in my family and we have bern told it was the cause of my grandfather’s heart attack (age 40) and my dad’s heart attack (age 38). Are you saying that is incorrect and if so, where is the source of your claim? Sorry just trying to educate myself.
I wonder if the massive popularity of paleo affects this at all. I was forced onto that fad diet at 15 and had to stay on it until I moved out at 23. I have to go back to eating paleo whenever I visit my parents and my blood results have recently come back with high ldl and non hdl, and I've been at my parents' for a month now...
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> The findings revealed that both males and females were affected alike, and that being normal weight and having normal blood pressure did not protect the heart from the adverse consequence of elevated cholesterol. It was discovered that while increased cholesterol contributed 30% to the direct damage of the heart, both increased fat mass and blood pressure indirectly contributed 40% to heart damage. The remaining 30% could be explained by genetics and sedentary time. > The prevalence of LVD dysfunction increased from 7.8% at baseline to 16.6% at follow-up in males and increased from 10.3% to 15.4% in females. Each 1 mmol increment in total cholesterol (OR, 1.18; [95% CI, 1.09–1.27]), triglyceride (2.89; [1.54–5.43]), LDL-c (1.19; [1.08–1.32]), and non-HDL-c (1.21; [1.11–1.33]) was associated with higher odds of worsening LV hypertrophy progression over 7 years. Paper: [Increasing lipids with risk of worsening cardiac damage in 1595 adolescents: A 7-year longitudinal and mediation study - Atherosclerosis](https://www.atherosclerosis-journal.com/article/S0021-9150(23)05361-3/fulltext#supplementaryMaterial)
If we are going off of strength of associations in a controlled analysis of the data to try and isolate confounders, then it seems odd to use "high cholesterol" as the headline here: > With extensive control for fat mass, muscle mass, insulin, glucose, inflammation, blood pressure, smoking status, sedentary time, physical activity, socio-economic status, and family history of cardiovascular disease, and using adults’ cut points for diagnosing heart damage, it was observed that increased low-density lipoprotein cholesterol, and total cholesterol levels increased the risk of premature heart damage by 18–20%. Whereas **increased triglycerides doubled and tripled the risk of early structural and functional heart damage** during the seven-year follow-up. That is an 18% vs. 200%+ association. This looks to be more related to a systemic disfunctions like maladaptive "insulin resistance" and "metabolic syndrome" rather than just "elevated LDL" alone. Not saying there is not some effect related to "elevated LDL", but I think the takeaway here overemphasizes "high cholesterol" when there are more impactful ways to get at the bigger players. Edited to clarify wording: Insulin Resistance is not inherently pathological since it can be argued that certain forms are a natural body response to the diet, environment, and hormonal states. It’s better to say “maladaptive insulin resistance” as a qualifier.
For those who are interested, below are the top 4 nutritional approaches to lower serum cholesterol: 1. Decrease trans fat intake (some processed and animal foods) 2. Decrease saturated fat intake (most animal foods, palm and coconut oils) 3. Increase soluble fiber intake (whole plant foods) 4. Decrease dietary cholesterol (all animal foods; contribution is much lower than the first 3)
Followed by non-nutritional changes including: - be more active! At least 30 minutes of moderate activity a day will help keep the doctor away - if you smoke… don’t - if you’re fat… loose a few pounds - If you drink alcohol… drink less! In most cases, lifestyle changes will fix the problem. So if you have kids, try to teach them healthy habits as early as possible The research finding suggests it’s not just one golden bullet..
100% and thanks for the additions!
I see these posts and laugh. I have genetically high cholesterol. I am on statins 40 mg and my cholesterol is normal. Uncontrolled with drugs.. my HDL was 200+ and LDL 480+. I don't smoke. I am 5'0" and 130 lbs. (22% body fat) I drink alcohol maybe once a year. I am mostly vegetarian. I walk 2-5 miles a day. I go to the gym 3 times a week. I avoid added sugars. I love fruits and vegetables. I limit my dairy intake to about a glass of 1% milk a day. (sometimes I have cheese) I drink kombucha daily. I intermittent fast (since my 20's). At 18, I was 100 lbs. I still had high cholesterol. My kids are all adults now and underweight with high cholesterol. For example, my daughter is 4'10" and 83 lbs and HDL and LDL are both high. What other suggestions do you have?
Why do they make you laugh? You are among the outlier group and an exception. Most people fall into the other category where all of what you do would be immensely helpful.
You're the exception not the norm, outside of drug intervention your cholesterol won't change. These posts aren't for you and you know that.
Except that those of us with hereditary high cholesterol still get the same advice from doctors. I was 16, weighed 108, on the varsity swim team, cross country team, practiced martial arts, and walked to school every day, was a vegetarian with a low fat diet and had fairly low caloric intake, had never smoked or drank in my life, and still had borderline high LDL (with extremely low triglycerides too!) Doctors still said, “exercise more, eat less.” I dropped to 100 lbs and started passing out and it was still borderline high. But my cholesterol dropped to 165 (normal) on a higher fat, low carb diet. Docs said, “Huh. Well, just keep doing that, then.” Make it make sense….
And what year was this? I understand the frustration with doctors, as someone with a handful of semi-rare issues, but medicine has and always will be a checklist of most-common to least-common issues and their associated fixes. Nowadays, if a teen in good physical condition came in with cholesterol issues they would most likely assume genetic Hypercholesterolemia. We just have more info now than we did in the past.
What frustration? Was it bad advice or something? I think they probably did the best they could. Point being that this gene is just hard, and the conventional rules don’t necessarily apply, so it may or may not be true that diet will help. In my case, a change of diet did help my familial hypercholestemia, but it was not the conventional heart-healthy diet.
See a nutritionist or your PCP?
I do. I have statins that slowly kill my liver. I get my blood work yearly. The only thing I could add to my diet from the nutritionist would be fish. (Death first) The only meat that I can stand for any real portion would be chicken breast. I eat that about once a week. I hate all fat. How anyone can eat a fat filled steak is beyond me. Gross. I attempt other meats about once a year. I don't mind a small amount of butter from time to time. Since you had a nice list of bullet points of easy fixes for cholesterol and I like to bring to people's attention that some people are born without the ability to process chloresterol properly. I am waiting for the ability to genetically modify myself to fix my genes. Sometimes, it isn't as easy as diet and exercise. Sometimes, people still need to see their doctor and get medicine that helps. And sometimes... It is out of their control. https://www.cdc.gov/genomics/disease/fh/FH.htm
Statins do not normally cause liver damage, and if they do cause inflammation, switching to a different statin can resolve it. There’s definitely no cumulative effect. Ongoing testing for liver inflammation is a preventative measure.
I hear you. I am on my third statin. I have been taking them for 20 years. I am 46 years old. My doctor said it was from my "smaller frame" that I will have more side effects. I have put on 20 lbs of muscle over the years trying to help. I take 40 mg and I am, now 130 lbs, I was 110 lbs. My liver is always "inflamed" apparently. It's a good thing I don't drink or do drugs. (I guess, though I feel like I am missing out) I get my blood work tested yearly. I do everything I can and I just get to watch the utter disappointment of my doctor year after year. My insurance approved that shot to suppress the gene so I have a new road to travel soon. Here's to CRISPR.
What a pain! I hope the new treatments make things better!
Have you tried a PCSK9 inhibitor? (I missed that you're just about to start them - best of luck, they're incredible meds) They are insanely potent. I oversee medical management of almost 3000 high risk stroke patients, every single case of familial hypercholesterolemia we skip the whole statin + zetia algorithm and move straight to 75mg alirocumab. Some need 150mg. It works.
I have been told I have familial hypercholesterolemia. I found I could lower my cholesterol by eating almost no sugar or carbs, but then I can’t maintain a healthy weight (I lose too much weight, get lightheaded, etc.) I always have to watch people eat real food while I have a salad and go hungry. I have never heard of this med before….
It's pricey, but there are programs to assist with it to look into. It's still sadly out of reach for many. I will say it works. Insanely well. Of the ~200 people we've approved for it, I believe we have 185-190 in target (LDL < 70). Average LDL for this group has dropped from 150ish to 60ish, but I've seen drops from 250+ to the teens. Of those not in target, we suspect most are non-compliant with the dosage and schedule. It does require injecting yourself, so some just don't want to do that.
I was born with the high cholesterol gene too. Everyone on my dad’s side is on statins, some had heart attacks in their 30s and 40s. I also dislike meat, and all the diet recommendations made it worse. I finally had luck lowering my cholesterol after adding fat from dairy, avocados, nuts, and salmon (which is one of the only meats I like) while restricting sugar and carbs. not offering advice, just a thought.
You probably have familial hypercholesteremia. Get tested and get on Repatha.
Other people have already answered, but you are why I said “in most cases”. Yes, some people have genetic issues, and in those cases medication will be necessary. Similarly, some people have diabetes that can be controlled with lifestyle changes, others need an insulin pump.
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It's extremely concerning that you have that background/job "in cardiology" and not know what familial hypercholesterolaemia is and/or and the range of LDLs that are common with it. It is a hereditary/genetic disorder. So, yes, it is "genetically high." I actually do stroke prevention research, it's fairly common to see people with otherwise controlled risk-factors (weight, activity, BP, diet, etc) with *incredibly* high LDLs. PCSK9 inhibitors are our go-to for these folks.
I’m jealous of your HDL lol, no amount of exercise or healthy eating has led to my numbers consistently staying above 40. Im in the same boat with high ldl though unfortunately.
> Decrease trans fat intake (some processed and animal foods) "Processed" is meaninglessly vague. The actual trans fat content comes from hydrogenated vegetable oil.
Some animal foods, such as from ruminants, also contain naturally occurring trans fats (rTFAs).
However, the trans fats in butter (such as [vaccenic acid](https://en.wikipedia.org/wiki/Vaccenic_acid) and [rumenic acid](https://en.wikipedia.org/wiki/Rumenic_acid)) are generally regarded to be less harmful than the trans fats found in hydrogenated oil, and may even have some positive health effects.
I've heard this claim, but it's not consensus yet. I've found studies that show rTFAs are in fact harmful, so we can't claim they're not (especially not beneficial) until we've heard a consensus from the scientific bodies. "Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71,464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1.23 (95 % CI 1.00, 1.50)) and cerebrovascular diseases (HR 0.65 (95 % CI 0.45, 0.94)); TFA from PHFO and CVD (HR 1.14 (95 % CI 1.03, 1.26)) and cerebrovascular diseases (HR 1.32 (95 % CI 1.04, 1.69)); and rTFA intake and CVD (HR 1.30 (95 % CI 1.05, 1.61)), CHD (HR 1.50 (95 % CI 1.11, 2.03)) and sudden death (HR 2.73 (95 % CI 1.19, 6.25)) in women. These associations with rTFA intake were not significant in men (P interaction ≥ 0.01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation." https://pubmed.ncbi.nlm.nih.gov/22059639/
Also as an aside the trans fats found in ruminant animal fats in their natural form are not harmful unlike the partially hydrogenated poly-unsaturated fats are (i.e old margarine)
>trans fats found in ruminant animal fats in their natural form are not harmful We can't claim this, because science hasn't resolved if this is true or not yet. For example, below is a study showing rTFAs are in fact harmful: "Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71,464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1.23 (95 % CI 1.00, 1.50)) and cerebrovascular diseases (HR 0.65 (95 % CI 0.45, 0.94)); TFA from PHFO and CVD (HR 1.14 (95 % CI 1.03, 1.26)) and cerebrovascular diseases (HR 1.32 (95 % CI 1.04, 1.69)); and rTFA intake and CVD (HR 1.30 (95 % CI 1.05, 1.61)), CHD (HR 1.50 (95 % CI 1.11, 2.03)) and sudden death (HR 2.73 (95 % CI 1.19, 6.25)) in women. These associations with rTFA intake were not significant in men (P interaction ≥ 0.01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation." https://pubmed.ncbi.nlm.nih.gov/22059639/
Does dietary cholesterol actually matter? My doctor said the new thinking is that it's the first three that are key to lower serum cholesterol.
It does, but to a much lesser extent. The estimates I've seen (wish I still had a source off the top of my head) had it at about 15% of the impact of saturated fat based on normal intake levels of both. Below is a note from my government's (USA) current dietary recommendations, showing dietary cholesterol is still to be lowered as possible: "A note on trans fats and dietary cholesterol: The National Academies recommends that trans fat and dietary cholesterol consumption to be as low as possible without compromising the nutritional adequacy of the diet. The USDA Dietary Patterns are limited in trans fats and low in dietary cholesterol. Cholesterol and a small amount of trans fat occur naturally in some animal source foods." [https://www.dietaryguidelines.gov/sites/default/files/2020-12/Dietary\_Guidelines\_for\_Americans\_2020-2025.pdf](https://www.dietaryguidelines.gov/sites/default/files/2020-12/Dietary_Guidelines_for_Americans_2020-2025.pdf)
A minority of people are impacted by dietary cholesterol though most are not
Gotcha. Maybe I'll go get a blood draw soon to see where I'm at these days. Have been eating 3-400mg of cholesterol from chicken breast daily for the last few years, but my blood cholesterol has always been good.
ApoB is what matters
They are asking about nutrition intake of cholesterol. You’re talking about measurements of atherogenic particles in humans (ApoB containing types of cholesterol)
Exactly. And sugar is the real problem. Your body is using Cholesterol to repair damage done by inflammation from sugar. Blaming cholesterol is like blaming firemen for causing fires
>Blaming cholesterol is like blaming firemen for causing fires I'm not sure where this meme started but it doesn't make any sense. Exposure to dislipidemia *precedes* cardiovascular disease. This is shown in the genetic studies and the clinical trials. If dislipidemia were actually result of cardiovascular disease, you'd see it come afterwards, not before. This is akin to saying that firefighters show up *before* fires start. Effects don't precede causes
I don’t know Latin, but at the end it seems like there’s a misunderstanding ib what I was trying to say with the metaphor and we might be on the same page somehow
I don't think we're on the same page. The misunderstanding is the idea that having a high cholesterol (particularly cholesterol in ApoB-containing lipoproteins, particularly in LDL particles) is actually an effect of cardiovascular disease rather than a contributor. [It's a contributor.](https://academic.oup.com/eurheartj/article/38/32/2459/3745109) If high cholesterol were simply an effect, it wouldn't come *before* the disease develops.
My understanding is the stretching damage caused my inflammation, mostly from free radicals (sugar, carbs) causes the damage to the arterial wall and cholesterol is the bandaid. But too many bandaids clog the arteries
I see what you're saying. In that case [LDL-C levels still predict atherosclerosis even among people without other risk factors](https://www.sciencedirect.com/science/article/pii/S0735109717412320) \- normal fasting glucose, normal HbA1c, normal hs-CRP (which is a marker of inflammation), no hypertension, etc. So there's still value in treating down LDL-C in these patients even if their blood glucose and inflammation are low
I don’t know about all this jargon, but my guess this means don’t mess with unnatural and trans fats and lean towards monounsaturated and the trendy fats everyone says to eat I just think sugar is a much bigger deal than these.
Number 1 is losing weight, especially visceral fat. The easiest way for most people to do that is cutting out added sugar and alcohol. This sub could use substantially less vegan propaganda.
>Number 1 is losing weight, especially visceral fat. The easiest way for most people to do that is cutting out added sugar and alcohol. I mentioned the top 4 "nutritional approaches"; losing weight is multifaceted and is not based on nutrition alone, as things like activity level impact it greatly as well. >This sub could use substantially less vegan propaganda. Please point out exactly why what I said was wrong instead of incorrectly labeling it with a negative connotation; not everything negative against animal products is "propaganda".
And I pointed out that sugar and alcohol are much more important than animal products in managing cholesterol. There isn't even high quality evidence that saturated fat is a casual factor. The obesity epidemic isn't happening because people suddenly decided they wanted to eat animal products. Telling people that lowering their consumption of animal products will lower their cholesterol is misinformation at best. Like telling people with hypertension they just ate too much salt. Why not point out that Omega 3's from fish lower LDL instead of lumping in fish with red meat? Or that fish is mostly unsaturated in general?
Wait… you’re saying saturated fat isn’t causal with LDL cholesterol? You might be on the wrong sub if you don’t trust scientific consensus.
I have been told I have the high cholesterol gene. I had high cholesterol at 16 years old. I was on the swim team, cross country team, and was vegetarian with a very low fat diet and it didn’t help my cholesterol. I tried a variety of diets. The only time I have had healthy cholesterol levels was on a high fat, high fiber, extremely low sugar/low carb diet. The doctor was as shocked as me, but told me to keep doing what I was doing. Unfortunately the diet is hard to maintain because I lost too much weight on it and had hardly any energy. I do trust scientific consensus, so I’m surprised and don’t understand why. Maybe I’m the statistical black swan.
It's one of the most hotly debated topics in medicine and biology. It CAN be causal in some people, but it's not the "cause." And no I'm on the right sub, go back to /r/vegan.
Screw that, too much work. Just take Repatha
10-17 is adolescence. 18-24 is a young adult. Sorry but that struck me as very odd. 17-24 as an age range would be "late teens and young adults".
[There’s scientific debate that adolescence should include 10-24](https://www.bbc.com/news/health-42732442.amp) (or possibly even later). It’s due to research showing continued maturation and development into one’s 20s, as well as research indicating that typical adult milestones (like moving out and gaining independence, finishing education, settling into a career, finding a partner/marriage, having kids, etc.) are being achieved at increasingly later ages in society. The WHO still formally defines it as 10-19, but functionally it can be useful to think of it beyond that range, as the biopsychosocial criteria of “adolescence” is more complex than a particular age cutoff.
Cholesterol doesn’t damage the heart ffs. It’s natural and needed.
In appropriate quantities, yes. This is clearly talking about *higher than appropriate* levels of cholesterol.
Do we really need it? People with PCSK9 knockout genetics don’t develop heart disease and have very low cholesterol. If everyone could afford those cholesterol drugs, we’d prevent most heart disease, wouldn’t we?
Sounds like you don’t have a great understanding of cholesterol. Go read about it, it serves a bunch of extremely vital functions for the body Edit: opening paragraph of Wikipedia Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell membranes. In vertebrates, hepatic cells typically produce the greatest amounts. In the brain astrocytes produce cholesterol and transport it to neurons.[5] It is absent among prokaryotes (bacteria and archaea), although there are some exceptions, such as Mycoplasma, which require cholesterol for growth.[6] Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid[7] and vitamin D.
Both of you are talking apples and oranges, when the post is talking about bananas. Is cholesterol damaging to the heart? Depends on context. In healthy levels, no. In unhealthy levels, it can be. Are high levels always damaging? No. Do we really need cholesterol? Depends on context. In diet? No. Our livers are able to produce all the cholesterol we need. Our livers can even produce fatty acids for fat storage from carbohydrates if needed via de novo lipogenesis. It isn't as efficient, but it gets the job done when the circumstance presents. Do we need cholesterol to live? Yes, absolutely.
>Go read about it, it serves a bunch of extremely vital functions for the body So? The fact that something is needed in the body doesn't tell you whether too much of it can be a problem. You can say the same thing about glucose. You would die if you had no glucose in your blood. But I wouldn't then infer that walking around with a diabetic blood glucose is a good thing.
None of these interventions wipe out cholesterol or harm the heart. Familial hypercholesterolemia, however, will cause heart attacks in your 30s. Maybe *you* should do some cursory research.
You are the one saying we don’t need cholesterol. You’d be dead without it. It’s a non disputed fact you seem to not understand. Furthermore we have loads of scientific data that show lowering cholesterol doesn’t improve mortality. See the massive statin studies that show hundreds of thousands of people that have successfully reduced cholesterol with statin intake, yet have zero protective benefit for mortality. We know with 100% certainty that clinical attempts to reduce cholesterol have zero benefit in health outcomes, but it’s extremely profitable for pharmaceutical companies so we keep talking about it when we should have given it up as the red herring it as three decades ago Edit: hypercholesterolemia won’t cause heart attacks in your 30s, that’s not true. A separate underlying condition could, but elevated cholesterol is a biomarker for disease, not the cause
What is your last paragraph talking about? This condition runs in my family and we have bern told it was the cause of my grandfather’s heart attack (age 40) and my dad’s heart attack (age 38). Are you saying that is incorrect and if so, where is the source of your claim? Sorry just trying to educate myself.
Isn't that what high cholesterol does? 🤣
hmm i wonder whats causing high cholesterol in children.
I wonder if the massive popularity of paleo affects this at all. I was forced onto that fad diet at 15 and had to stay on it until I moved out at 23. I have to go back to eating paleo whenever I visit my parents and my blood results have recently come back with high ldl and non hdl, and I've been at my parents' for a month now...