[Videos] - These 5 independent Medical Doctors all separately say NO to both taking and prescribing Statins for High Cholesterol

[16/8IF]

Just saw this research paper today regarding statin :-

Findings In this meta-analysis of 21 randomized clinical trials in primary and secondary prevention that examined the efficacy of statins in reducing total mortality and cardiovascular outcomes, there was significant heterogeneity but also reductions in the absolute risk of 0.8% for all-cause mortality, 1.3% for myocardial infarction, and 0.4% for stroke in those randomized to treatment with statins compared with control, with relative risk reductions of 9%, 29%, and 14%, respectively. A meta-regression was inconclusive regarding the association between the magnitude of statin-induced LDL-C reduction and all-cause mortality, myocardial infarction, or stroke.

Meaning The study results suggest that the absolute benefits of statins are modest, may not be strongly mediated through the degree of LDL-C reduction, and should be communicated to patients as part of informed clinical decision-making as well as to inform clinical guidelines and policy.

Conclusions and Relevance The results of this meta-analysis suggest that the absolute risk reductions of treatment with statins in terms of all-cause mortality, myocardial infarction, and stroke are modest compared with the relative risk reductions, and the presence of significant heterogeneity reduces the certainty of the evidence. A conclusive association between absolute reductions in LDL-C levels and individual clinical outcomes was not established, and these findings underscore the importance of discussing absolute risk reductions when making informed clinical decisions with individual patients.

Those who wants to read the full article , the link is below ;-


https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2790055

 

[Taloona]

if really depends, some people like me who has extremely high LDL cholesterol, 69% reduction is only just nice after reduction.

there are other pcsk9 inhibitor which doesn't have such high reduction.

it is simply dangerous to advise patients to stop stain without understanding their actual condition, eating habit and lifestyle. it is not just a concern of heart attack alone but stroke as well.


Read HWZ Forum Rules!

Yup, I think there is this genetic condition where super high bad cholesterol runs in the family and it starts at toddler stage. I remember reading about this in the ST last year and everyone in the family has to start on statins at a young age.

I asked my friend, who is a professor in pharmaceutical science about his opinion on this debate. He said he himself is also on statins!

 

[fortunecat]

So what is the alternative and is this alternative evidence based and benefits outweigh the harm?

I'm not here to discuss medical knowledge. I'm just saying what's the behaviour of most doctors. And I never say if they are right or wrong

 

[Mecisteus]

What I meant is precisely what this thread is about. Why do the doctors in the video said no to the medicine? They probably found out more and feel the side effect is worse than helping. But most doctors won't think so much, they will just prescribe it if they see the patient has this condition etc

Usually people who had stroke or heart attack before will understand the needs of statins.

Because the worst case scenario of NOT taking is just another heart attack or stroke.

 

[testerjp]

I'm pretty sure there are tonnes of people on statins and they don't have heart attacks again. So believe what you will. It's always fun to believe what you want to believe in.

Think alot of "experts" think they know how things work simply by watching some YouTube videos but are totally clueless on the mechanism of what cholesterol does to the body.

Even if the cholesterol level is not high, the plaque is still forming albeit slower.
There are also hundreds of doctors out there who think that the amount of statin given is too little and too late because the cleaner the blood the slower the plaque will form. Because we are talking about long term heart condition, forming slowly will still choke the vessels eventually.

There's also no way to dissolve or clear the plaque without risk. Suppose the plaque somehow release from the walls, it will flow to somewhere and could choke another spot. Causing a stroke or heart attack.

Cholesterol linked to dementia, rct and meta analysis have numbers to prove that statin associated with reducing chance of dementia. Meta analysis is a compilation of many researches and hundreds of thousands of patients. Use backside to think also know, how can more garbage in the blood be good for your brain.

But nahsayers can instead get some youtube videos to prove that statin can cause dementia instead.

Last thing statin has many types with generics available. In short they are cheap like fug. They are no monopoly and no control over the doctors decisions.

 

[Checkyrmed]

Think alot of "experts" think they know how things work simply by watching some YouTube videos but are totally clueless on the mechanism of what cholesterol does to the body.

Even if the cholesterol level is not high, the plaque is still forming albeit slower.
There are also hundreds of doctors out there who think that the amount of statin given is too little and too late because the cleaner the blood the slower the plaque will form. Because we are talking about long term heart condition, forming slowly will still choke the vessels eventually.

There's also no way to dissolve or clear the plaque without risk. Suppose the plaque somehow release from the walls, it will flow to somewhere and could choke another spot. Causing a stroke or heart attack.

Cholesterol linked to dementia, rct and meta analysis have numbers to prove that statin associated with reducing chance of dementia. Meta analysis is a compilation of many researches and hundreds of thousands of patients. Use backside to think also know, how can more garbage in the blood be good for your brain.

But nahsayers can instead get some youtube videos to prove that statin can cause dementia instead.

Last thing statin has many types with generics available. In short they are cheap like fug. They are no monopoly and no control over the doctors decisions.

The real risk drivers in cardiovascular disease are insulin resistance, Lp(a), triglyceride-to-HDL ratio, and systemic inflammation. Statins can lower LDL, but they also have a tendency to raise insulin resistance, which moves the needle toward higher long-term risk. That is why LDL itself sits at the bottom of the list of meaningful markers. Focusing only on LDL reduction without correcting insulin resistance will not meaningfully lower the chances of stroke and may even worsen the problem over time. The question is whether one is actually treating the root cause or simply applying a band aid.

 

[rogze79]

Think alot of "experts" think they know how things work simply by watching some YouTube videos but are totally clueless on the mechanism of what cholesterol does to the body.

Even if the cholesterol level is not high, the plaque is still forming albeit slower.
There are also hundreds of doctors out there who think that the amount of statin given is too little and too late because the cleaner the blood the slower the plaque will form. Because we are talking about long term heart condition, forming slowly will still choke the vessels eventually.

There's also no way to dissolve or clear the plaque without risk. Suppose the plaque somehow release from the walls, it will flow to somewhere and could choke another spot. Causing a stroke or heart attack.

Cholesterol linked to dementia, rct and meta analysis have numbers to prove that statin associated with reducing chance of dementia. Meta analysis is a compilation of many researches and hundreds of thousands of patients. Use backside to think also know, how can more garbage in the blood be good for your brain.

But nahsayers can instead get some youtube videos to prove that statin can cause dementia instead.

Last thing statin has many types with generics available. In short they are cheap like fug. They are no monopoly and no control over the doctors decisions.

Are you smoking pot?

You seems to know about the mechanism of cholesterol. Please share your knowledge. We will be really keen to know more.

Why and how does the plaque forms? Please enlighten all.

Please provide the science linking high cholesterol to dementia. You can also link the rcts and what ever analysis to prove your point.

Find out how profitable statins before saying how cheap it is

 

[Mecisteus]

Even if the cholesterol level is not high, the plaque is still forming albeit slower.

This is very true.

But there are some studies which prove plagues regression is possible when LDL is super low.

 

[rogze79]

This is very true.

But there are some studies which prove plagues regression is possible when LDL is super low.

Really? Please share the studies?

 

[Emperor_Hippo]

ah yes, Youtube, the most trustworthy source of medical information. thank you

Is it no surprise that ppl are getting dumber?

singapore will one day, walk the shoes of americans.

 

[0nePunchm@n]

who dare to gambling life with stroke paralysis ??

 

[born2fly]

if you kept watching all these online than you will end up resisting any medical intervention.
3 of my friends die of heart attack in the last 10 years 42-53 age. If you want to take the chance go ahead.
Btw they also tell ppl not to do chemo for cancer..... my 2 colleagues with breast cancer stage 3-4 did chemo and thanks to chemo still alive after 20 years! Steve Job delay chemo thinking he will used diet to put it down for almost a year before it spread to his liver and stomach if not he might be still around.

 

[Emperor_Hippo]

This is very true.

But there are some studies which prove plagues regression is possible when LDL is super low.

That's one nice thought.

for starters, a pointer in a peer reviewed medical journal would be appreciated.

 

[Mecisteus]

Really? Please share the studies?

Man of substance should be able to google easily.

That's one nice thought.

for starters, a pointer in a peer reviewed medical journal would be appreciated.

Wait for above man of substance.

 

[rogze79]

Man of substance should be able to google easily.

Wait for above man of substance.

I did not make the claims. You did.

Prove it. Or else, you are just farting mindlessly.

 

[IntelFlash]

Prompt:
Find me solid evidence (with high quality research including systematic, reviews, meta-analysis, RCT), whether high or low cholesterol likely linked to dementia

ChatGPT thinking
What high-quality evidence actually shows about cholesterol and dementia:


– Midlife high cholesterol (esp. LDL) → higher later-life dementia risk. A 2023 systematic review/meta-analysis of 17 cohort studies (≈1.2M people) found: elevated mid-life cholesterol → 14% higher all-cause dementia risk; every +1 mmol/L LDL → +8% all-cause dementia risk; and +17% Alzheimer’s risk. PubMed Central
– Very large real-world cohort confirms this. In >1.8 million UK adults, LDL measured before age 65 was modestly but robustly associated with dementia >10 years later; authors argue LDL belongs on the list of modifiable dementia risks. The Lancet+2PubMed+2


– Late-life “low cholesterol looks risky” is mostly reverse causation. Lipids tend to fall in the prodromal years before a dementia diagnosis, which can make low late-life cholesterol look harmful; longitudinal work shows declining cholesterol precedes dementia rather than causes it. PubMed Central+1


– HDL shows a U-shape in older adults. In a large Neurology cohort, both low and high HDL-C were linked to higher dementia risk; LDL associations were modest in this older population. Translation: don’t chase extreme HDL. PubMed+1


– Randomized trials (statins started in later life) don’t prevent dementia. The Cochrane review of RCTs (26,340 participants) plus major trials (PROSPER; HOPE-3) found no reduction in incident dementia or cognitive decline from late-life statin initiation. Cochrane+2PubMed+2


– Genetic (Mendelian randomization) evidence doesn’t support harm from lower LDL. Lifelong genetically lower LDL via HMGCR/PCSK9 variants did not increase dementia risk; point estimates even trend toward lower AD risk with lower LDL. PubMed

What this means in practice​

– Target the midlife window. High LDL/TC in midlife is the signal linked to later dementia. Keeping LDL in guideline ranges through lifestyle and, when indicated, meds is reasonable brain-health strategy—even though RCTs haven’t yet proved dementia prevention when starting therapy late. PubMed Central+1
– Don’t infer that “higher is safer” in old age. Apparent late-life links between low cholesterol and dementia are likely illness-driven lipid drop, not protection from high cholesterol. PubMed Central+1
– Avoid HDL extremes. Extremely low or very high HDL in seniors tracks with higher risk; focus on overall cardiometabolic health, not pushing HDL to extremes. PubMed

Key studies you can cite (by design)​

– Wee et al., 2023 systematic review/meta-analysis (midlife dyslipidemia → ↑ dementia; per-mmol LDL effects). PubMed Central
– Iwagami et al., Lancet Healthy Longevity 2021 (LDL in <65 y → later dementia). The Lancet
– Ferguson et al., Neurology 2023 (U-shaped HDL–dementia in older adults). PubMed
– Cochrane Review 2016 (statins started late don’t prevent dementia). Cochrane
– PROSPER RCT (pravastatin, no cognitive benefit). PubMed
– HOPE-3 cognitive substudy (rosuvastatin, no cognitive benefit). PubMed
– Benn et al., BMJ 2017 Mendelian randomization (genetically lower LDL not increasing dementia; possibly lower AD risk). PubMed

Bottom line​

– High LDL/TC in midlife is the cholesterol pattern most consistently linked to higher dementia risk.
– Late-life “low cholesterol” signals likely reflect preclinical disease, not benefit from keeping cholesterol high.
– Starting statins late hasn’t shown dementia prevention in RCTs, but lifelong lower LDL (genetically or from earlier control) does not appear harmful and may be beneficial. Cochrane+3PubMed Central+3The Lancet+3




Deepseek Deep research
Based on high-quality evidence, the relationship between cholesterol and dementia is complex and depends significantly on when cholesterol is measured during a person's life. Midlife high cholesterol, particularly high LDL ("bad" cholesterol), is linked to an increased risk, while the relationship in late life is less clear.

The table below summarizes the key findings from systematic reviews and large-scale studies.

Life Stage	Cholesterol Level	Association with Dementia Risk	Key Evidence
Midlife (before ~65)	High LDL-C and Total Cholesterol	Increased Risk	A 2023 meta-analysis of 17 studies (1.2M participants) found midlife high cholesterol increased the risk of all-cause dementia and mild cognitive impairment. Another meta-analysis confirmed high LDL-C specifically increases Alzheimer's disease risk.
Late Life (after ~65/70)	Low Total Cholesterol	Increased Risk (but likely a consequence, not a cause)	A 32-year study found that a decline in cholesterol from midlife to late life was a better predictor of risk than a single measurement. Low levels may be a sign of underlying illness or weight loss that can occur before dementia diagnosis.
Late Life	High Cholesterol	No Consistent Association	A 2021 individual patient meta-analysis of over 21,000 older adults (avg. age 76) found no clear link between high cholesterol and subsequent cognitive decline or dementia.

Specific Cholesterol Types and Statins​

Research provides more detailed insights into different types of cholesterol and the effect of cholesterol-lowering medication.

• "Bad" vs. "Good" Cholesterol: The strongest evidence points to high levels of Low-Density Lipoprotein (LDL-C), often called "bad" cholesterol, as a risk factor in midlife. The evidence for High-Density Lipoprotein (HDL-C, "good" cholesterol) and triglycerides is less consistent.
• Role of Statins: Statins, drugs that lower cholesterol, are associated with a reduced risk of dementia. A large 2025 meta-analysis of 55 studies concluded that statin use was linked to a 14% lower risk of all-cause dementia and an 18% lower risk of Alzheimer's disease. The benefit is thought to come from both improving cardiovascular health and other protective effects on the brain.

Understanding the Complex Link​

The reason for the differing risk based on age is an area of active research. Key proposed mechanisms include:

• Vascular Health: High cholesterol contributes to atherosclerosis (hardening of the arteries), which can impair blood flow to the brain and contribute to vascular dementia.
• Amyloid-Beta Production: Some research suggests that high cholesterol may promote the production of amyloid-beta, the protein that forms plaques in the brains of people with Alzheimer's disease. It's important to note that cholesterol in the blood does not directly enter the brain; the brain produces its own. However, cholesterol-byproducts like bile acids, which can cross into the brain, may be involved.
• Reverse Causation in Late Life: The link between low cholesterol in old age and higher dementia risk is often explained by "reverse causation." This means that the disease process of dementia (e.g., weight loss, poor diet, general ill health) may cause cholesterol levels to drop, rather than low cholesterol causing dementia.

Conclusion and Recommendations​

In summary, the solid evidence indicates:

• Manage Midlife Cholesterol: Having high cholesterol, especially LDL-C, in midlife (before age 65) is a recognized risk factor for developing dementia later in life.
• Don't Worry About High Cholesterol in Late Life: For older adults, high cholesterol is not consistently linked to a higher risk of cognitive decline.
• Statins are Beneficial: If prescribed statins to manage cholesterol, taking them is associated with a reduced risk of dementia.

The most effective approach to reducing dementia risk is maintaining good cardiovascular health throughout life, which includes managing cholesterol, blood pressure, and weight through a healthy diet and regular exercise.

 

[IntelFlash]

Prompt
Find me solid evidence (with high quality researches including systematic, reviews, meta analysis, RCT, whether extremely low LDL regress plaque in blood vessels


ChatGPT thinking

Here’s the straight, evidence-first read on whether pushing LDL very low actually regresses atherosclerotic plaque (direct imaging endpoints; RCTs + meta-analyses):


– PCSK9 inhibitor added to statin (LDL ≈ 20–40 mg/dL) → consistent regression (RCTs).
– GLAGOV (JAMA 2016): Evolocumab + statin drove time-weighted mean LDL to 36.6 mg/dL vs 93.0 and reduced percent atheroma volume (PAV) −0.95% vs +0.05%; plaque regression in 64.3% vs 47.3%. PubMed
– PACMAN-AMI (JAMA 2022): Alirocumab + high-intensity statin achieved ~23.6 mg/dL LDL and produced greater PAV regression (−2.13% vs −0.92%) at 52 weeks, with improved OCT/NIRS features (↑ fibrous-cap thickness; ↓ lipid burden). JAMA Network
– HUYGENS (JACC Imaging 2022): Evolocumab + statin (mean on-treatment LDL 28.1 vs 87.2 mg/dL) increased minimum fibrous-cap thickness and reduced maximum lipid arc vs placebo—key stabilization markers at very low LDL. PubMed


– High-intensity statins alone (LDL ≈ 60–70 mg/dL) → measurable regression (RCTs).
– SATURN (NEJM 2011): Rosuvastatin 40 mg vs atorvastatin 80 mg: median PAV −1.22% vs −0.99% (regression in both arms; achieved LDL roughly mid-60s to ~70 mg/dL). American College of Cardiology
– ASTEROID (JAMA 2006; open-label, blinded endpoints): Rosuvastatin 40 mg lowered LDL to ~61 mg/dL with significant regression across IVUS measures. (Seminal but not randomized.) PubMed+1


– Systematic reviews / meta-analyses: regression is real and clinically relevant.
– JAMA Cardiology 2023 meta-analysis (23 imaging trials; ~7,400 pts): Each 1% PAV reduction associated with ≈25% lower odds of MACE, supporting that imaging regression from intensive LDL lowering is not just cosmetic. JAMA Network+1
– American Journal of Preventive Cardiology 2024 meta-analysis & meta-regression: Lipid-lowering therapies (statins ± ezetimibe/PCSK9) significantly regress PAV and TAV and improve plaque phenotype (↓ lipid arc; ↑ fibrous-cap thickness). Benefits observed at both <70 mg/dL and ≥70 mg/dL achieved LDL, with greater regression at lower LDL. PMC

Bottom line​

– Yes. Multiple randomized, double-blind imaging trials show that driving LDL to very low levels (~20–40 mg/dL) with PCSK9 + statin produces larger plaque regression and more stable plaque features than statin monotherapy. High-intensity statins alone (LDL ~60–70 mg/dL) still yield modest regression. Meta-analytic data link each 1% drop in PAV to materially lower clinical event risk. JAMA Network+4PubMed+4JAMA Network+4





Deepseek Deep research

Comprehensive analysis of high-quality evidence confirms that achieving very low LDL cholesterol levels can lead to regression of atherosclerotic plaque. The most significant plaque regression occurs with intensive lipid-lowering therapy, particularly high-intensity statins, which reduce plaque volume and increase plaque stability .

The table below summarizes key LDL-C targets for plaque regression identified in major meta-analyses.

LDL-C Target Level	Observed Effect on Plaque	Key Supporting Evidence
< 70 mg/dL	Significant regression of Total Atheroma Volume (TAV) and Percent Atheroma Volume (PAV) .	2021 Meta-analysis of 31 studies (4,997 patients)
< 80 mg/dL (with HDL > 45 mg/dL)	Significant reduction in Total Atheroma Volume (TAV) .	2021 Meta-analysis of 31 studies
~78 mg/dL	Significant regression of coronary atherosclerotic plaque volume .	2014 Systematic review of 20 trials (5,910 patients)

How Low Should LDL Go?​

Large-scale systematic reviews have helped establish specific LDL-C targets for achieving plaque regression:

• A 2021 meta-analysis in Scientific Reports concluded that to regress coronary plaques, LDL should be reduced to < 80 mg/dL, and HDL should be increased to > 45 mg/dL for the best effect on total plaque volume .
• An earlier 2014 systematic review found that intensive LDL-C lowering—by more than 40% or to a target level below approximately 78 mg/dL—could lead to significant plaque regression when sustained for over 17 months .

Most Effective Therapies for Plaque Regression​

Not all lipid-lowering therapies are equally effective at causing plaque regression. A 2024 meta-analysis of 51 studies involving 9,113 adults provided a direct comparison .

• High-Intensity Statins (HIS) were identified as the most effective treatment, driving significant reductions in both percent and total atheroma volume .
• Combination Therapies, such as statins combined with ezetimibe or EPA (eicosapentaenoic acid), also promote regression, though the effect on total atheroma volume is primarily driven by high-intensity statins .

How Does Plaque Regression Work?​

Plaque regression is not just about shrinking size; it also involves stabilizing the plaque to make it less likely to rupture and cause a heart attack or stroke. The biological mechanisms include :

• Lipid Removal: Therapies enhance reverse cholesterol transport, where cholesterol is removed from plaque deposits in the artery walls and transported to the liver for elimination .
• Plaque Stabilization: As lipids are removed, the plaque becomes more stable. Key changes include an increase in fibrous cap thickness and a reduction in the inflammatory lipid core, making the plaque less vulnerable to rupture .

Important Considerations and Limitations​

While the evidence for LDL-lowering is strong, it is important to consider the full picture:

• LDL-C is Necessary but Not Always Sufficient: In rare cases, individuals with genetically very low lifelong LDL-C (e.g., below 40 mg/dL) can still develop atherosclerosis if other risk factors like diabetes and hypertension are present, highlighting that managing overall cardiovascular risk is essential .
• Therapies Work Over Time: Plaque regression is a gradual process observed over months to years of sustained therapy .

Key Takeaways for You​

Based on the current high-level evidence:

• Yes, extremely low LDL levels can regress plaque. The most robust data supports targeting an LDL-C level of below 70-80 mg/dL .
• High-intensity statin therapy is the most effective proven strategy for achieving this regression .
• Plaque regression is a measurable phenomenon confirmed by advanced imaging techniques like intravascular ultrasound (IVUS), which shows a reduction in plaque volume and improvement in plaque composition after intensive lipid-lowering .

 

[Checkyrmed]

who dare to gambling life with stroke paralysis ??

But gambling with life is exactly what happens when treatment focuses only on LDL while ignoring the real drivers such as insulin resistance, Lp(a), inflammation and excess omega 6. Lowering LDL alone is not a guarantee against stroke or paralysis because it can create a false sense of security while the root problem continues to worsen.

 

[nachtsid.er]

So many keyboard experts bbfas here
Continue your bui bui diet and make way for higher quality immigrants

 

[Checkyrmed]

Prompt
Find me solid evidence (with high quality researches including systematic, reviews, meta analysis, RCT, whether extremely low LDL regress plaque in blood vessels


ChatGPT thinking

Here’s the straight, evidence-first read on whether pushing LDL very low actually regresses atherosclerotic plaque (direct imaging endpoints; RCTs + meta-analyses):


– PCSK9 inhibitor added to statin (LDL ≈ 20–40 mg/dL) → consistent regression (RCTs).
– GLAGOV (JAMA 2016): Evolocumab + statin drove time-weighted mean LDL to 36.6 mg/dL vs 93.0 and reduced percent atheroma volume (PAV) −0.95% vs +0.05%; plaque regression in 64.3% vs 47.3%. PubMed
– PACMAN-AMI (JAMA 2022): Alirocumab + high-intensity statin achieved ~23.6 mg/dL LDL and produced greater PAV regression (−2.13% vs −0.92%) at 52 weeks, with improved OCT/NIRS features (↑ fibrous-cap thickness; ↓ lipid burden). JAMA Network
– HUYGENS (JACC Imaging 2022): Evolocumab + statin (mean on-treatment LDL 28.1 vs 87.2 mg/dL) increased minimum fibrous-cap thickness and reduced maximum lipid arc vs placebo—key stabilization markers at very low LDL. PubMed


– High-intensity statins alone (LDL ≈ 60–70 mg/dL) → measurable regression (RCTs).
– SATURN (NEJM 2011): Rosuvastatin 40 mg vs atorvastatin 80 mg: median PAV −1.22% vs −0.99% (regression in both arms; achieved LDL roughly mid-60s to ~70 mg/dL). American College of Cardiology
– ASTEROID (JAMA 2006; open-label, blinded endpoints): Rosuvastatin 40 mg lowered LDL to ~61 mg/dL with significant regression across IVUS measures. (Seminal but not randomized.) PubMed+1


– Systematic reviews / meta-analyses: regression is real and clinically relevant.
– JAMA Cardiology 2023 meta-analysis (23 imaging trials; ~7,400 pts): Each 1% PAV reduction associated with ≈25% lower odds of MACE, supporting that imaging regression from intensive LDL lowering is not just cosmetic. JAMA Network+1
– American Journal of Preventive Cardiology 2024 meta-analysis & meta-regression: Lipid-lowering therapies (statins ± ezetimibe/PCSK9) significantly regress PAV and TAV and improve plaque phenotype (↓ lipid arc; ↑ fibrous-cap thickness). Benefits observed at both <70 mg/dL and ≥70 mg/dL achieved LDL, with greater regression at lower LDL. PMC

Bottom line​

– Yes. Multiple randomized, double-blind imaging trials show that driving LDL to very low levels (~20–40 mg/dL) with PCSK9 + statin produces larger plaque regression and more stable plaque features than statin monotherapy. High-intensity statins alone (LDL ~60–70 mg/dL) still yield modest regression. Meta-analytic data link each 1% drop in PAV to materially lower clinical event risk. JAMA Network+4PubMed+4JAMA Network+4





Deepseek Deep research

Comprehensive analysis of high-quality evidence confirms that achieving very low LDL cholesterol levels can lead to regression of atherosclerotic plaque. The most significant plaque regression occurs with intensive lipid-lowering therapy, particularly high-intensity statins, which reduce plaque volume and increase plaque stability .

The table below summarizes key LDL-C targets for plaque regression identified in major meta-analyses.

LDL-C Target Level	Observed Effect on Plaque	Key Supporting Evidence
< 70 mg/dL	Significant regression of Total Atheroma Volume (TAV) and Percent Atheroma Volume (PAV) .	2021 Meta-analysis of 31 studies (4,997 patients)
< 80 mg/dL (with HDL > 45 mg/dL)	Significant reduction in Total Atheroma Volume (TAV) .	2021 Meta-analysis of 31 studies
~78 mg/dL	Significant regression of coronary atherosclerotic plaque volume .	2014 Systematic review of 20 trials (5,910 patients)

How Low Should LDL Go?​

Large-scale systematic reviews have helped establish specific LDL-C targets for achieving plaque regression:

• A 2021 meta-analysis in Scientific Reports concluded that to regress coronary plaques, LDL should be reduced to < 80 mg/dL, and HDL should be increased to > 45 mg/dL for the best effect on total plaque volume .
• An earlier 2014 systematic review found that intensive LDL-C lowering—by more than 40% or to a target level below approximately 78 mg/dL—could lead to significant plaque regression when sustained for over 17 months .

Most Effective Therapies for Plaque Regression​

Not all lipid-lowering therapies are equally effective at causing plaque regression. A 2024 meta-analysis of 51 studies involving 9,113 adults provided a direct comparison .

• High-Intensity Statins (HIS) were identified as the most effective treatment, driving significant reductions in both percent and total atheroma volume .
• Combination Therapies, such as statins combined with ezetimibe or EPA (eicosapentaenoic acid), also promote regression, though the effect on total atheroma volume is primarily driven by high-intensity statins .

How Does Plaque Regression Work?​

Plaque regression is not just about shrinking size; it also involves stabilizing the plaque to make it less likely to rupture and cause a heart attack or stroke. The biological mechanisms include :

• Lipid Removal: Therapies enhance reverse cholesterol transport, where cholesterol is removed from plaque deposits in the artery walls and transported to the liver for elimination .
• Plaque Stabilization: As lipids are removed, the plaque becomes more stable. Key changes include an increase in fibrous cap thickness and a reduction in the inflammatory lipid core, making the plaque less vulnerable to rupture .

Important Considerations and Limitations​

While the evidence for LDL-lowering is strong, it is important to consider the full picture:

• LDL-C is Necessary but Not Always Sufficient: In rare cases, individuals with genetically very low lifelong LDL-C (e.g., below 40 mg/dL) can still develop atherosclerosis if other risk factors like diabetes and hypertension are present, highlighting that managing overall cardiovascular risk is essential .
• Therapies Work Over Time: Plaque regression is a gradual process observed over months to years of sustained therapy .

Key Takeaways for You​

Based on the current high-level evidence:

• Yes, extremely low LDL levels can regress plaque. The most robust data supports targeting an LDL-C level of below 70-80 mg/dL .
• High-intensity statin therapy is the most effective proven strategy for achieving this regression .
• Plaque regression is a measurable phenomenon confirmed by advanced imaging techniques like intravascular ultrasound (IVUS), which shows a reduction in plaque volume and improvement in plaque composition after intensive lipid-lowering .

Midlife risk factor control matters, targeting metabolic health early is more likely to reduce long term dementia and vascular risk than starting late.

Use better markers when possible, consider ApoB, triglyceride to HDL ratio, measures of insulin resistance and Lp(a) in risk assessment rather than relying only on LDL mass.

Interpret late life low cholesterol cautiously, declining lipids can be a marker of preclinical disease rather than evidence that higher cholesterol is protective. The clinical response should be comprehensive and metabolic focused, not LDL centric or reductionist.

The claim that high-intensity statins are the “most effective” therapy for plaque regression ignores the larger picture of what drives plaque formation in the first place. Lowering LDL through pharmacology may produce a modest reduction in plaque volume on imaging, but it does not address insulin resistance, chronic inflammation, endothelial dysfunction, or poor metabolic health. Those root causes are what destabilize plaques and determine long-term outcomes.

To sum this up, focusing only on high-intensity statins as “the most effective” therapy risks mistaking a band-aid for a cure. True plaque regression and vascular protection require improving insulin sensitivity, lowering inflammation, and restoring metabolic health, not simply chasing an LDL target.