Deep Dive: Understanding Cholesterol—LDL, HDL, and What the Numbers Mean

Cholesterol and cholesterol levels are often associated primarily with cardiovascular diseases. However, cholesterol is, first and foremost, a vital component of our bodies: among other things, it is a component of cell membranes and a precursor to various hormones and bile acids.

Therefore, what matters is not only how high the cholesterol levels in the blood are, but also which lipoproteins transport the cholesterol and what the individual’s overall cardiovascular risk is.

In particular, elevated levels of atherogenic lipoproteins play an important role in the development of atherosclerosis. The body of genetic, epidemiological, and clinical data supports a causal role for LDL in atherosclerotic cardiovascular disease.

But what do LDL and HDL cholesterol actually mean? What additional information do ApoB and lipoprotein(a) provide? How can elevated cholesterol levels be managed? What role do diet, gut microbiota, and lifestyle play—and when are medications such as statins used?

A look at the current body of research shows why cholesterol should be viewed in a much more nuanced way.

LDL, HDL, and Triglycerides: What Do These Cholesterol Levels Mean?

If you want to understand your cholesterol levels, you should first know how cholesterol is transported in the body.

Cholesterol is a fat-like substance. Since cholesterol and other lipids cannot be transported freely in the aqueous blood, they are transported throughout the body in what are known as lipoproteins.

A standard lipid profile includes, among other things:

• LDL cholesterol (LDL-C)
• HDL cholesterol (HDL-C)
• Triglycerides

1. LDL cholesterol (LDL-C)

LDL particles transport cholesterol to various tissues throughout the body. If there are consistently too many atherogenic lipoproteins in the blood, they can enter the vessel wall and trigger processes there that contribute to the formation of atherosclerotic plaques. Elevated LDL-C is therefore not merely a statistical marker: the totality of genetic, epidemiological, and clinical evidence points to a causal relationship between LDL and atherosclerotic cardiovascular disease. While the commonly used term “bad cholesterol” is easy to understand, it does not adequately reflect these relationships.

2. HDL cholesterol (HDL-C)

HDL performs various functions in lipid metabolism and is involved, among other things, in the transport of cholesterol back to the liver. In observational studies, higher HDL-C levels are often associated with a lower risk of cardiovascular disease. However, this does not automatically mean that the highest possible HDL level protects against cardiovascular disease. The common term “good cholesterol” is therefore also an oversimplification. Anyone who wants to understand the difference between LDL and HDL should not simply label the two as “bad” and “good.” For risk assessment, HDL-C is only one part of a much more complex overall picture.

3. Triglycerides

Triglycerides primarily serve as a source of stored energy for the body. Elevated levels may be associated with the following factors, among others:

• Overweight
• Diabetes
• Alcohol consumption
• certain dietary habits
• genetic factors

Triglyceride-rich lipoproteins and their remnant particles are also taken into account when assessing cardiovascular risk. The current U.S. guidelines from 2026 explicitly account for this expanded consideration of atherogenic lipoproteins.

ApoB and Lipoprotein(a): What Do the Levels Indicate?

In addition to the standard lipid profile, other laboratory test results can provide additional information about an individual's risk.

1. ApoB – How many atherogenic particles are circulating?

Apolipoprotein B (ApoB) is a structural protein of atherogenic lipoproteins. Each LDL particle carries one ApoB molecule; ApoB is also found, for example, on VLDL and remnant particles. While LDL-C describes how much cholesterol is transported within LDL particles, ApoB can provide an approximate indication of the number of atherogenic lipoprotein particles. This can provide additional information, particularly when LDL-C levels and particle count do not correlate well—for example, in cases of elevated triglycerides or certain metabolic conditions. The 2026 ACC/AHA guidelines also recommend selective ApoB measurement to improve risk assessment and treatment management.

2. Lipoprotein(a)—a predominantly genetically determined risk factor

Lipoprotein(a), or Lp(a) for short, is structurally similar to an LDL particle but also contains apolipoprotein(a). Lp(a) levels are primarily genetically determined and can generally be modified only to a limited extent through conventional lifestyle measures. An elevated Lp(a) level can increase the risk of atherosclerotic cardiovascular disease. In the 2025 European ESC/EAS Update, an Lp(a) level above 50 mg/dl or 105 nmol/l is considered a cardiovascular risk factor. Lp(a) may be particularly relevant for risk stratification in individuals with moderate risk or who are nearing a treatment decision.

The 2026 U.S. guideline also recommends measuring Lp(a) in adults at least once.

How Does Atherosclerosis Develop?

Atherosclerosis usually develops over many years.

Atherogenic lipoproteins can enter the vessel wall and become trapped there. This triggers complex biological and inflammatory processes. Over time, these processes can lead to the development of atherosclerotic plaques. These plaques can progressively narrow the vessel lumen. 

If a plaque becomes unstable, ruptures, or erodes, leading to the formation of a blood clot, blood flow can be acutely impaired—with potential consequences such asa heart attack or stroke. For this reason, modern prevention is not based solely on whether a single lab result appears “normal” or “too high.” 

The key factor is the individual’s overall cardiovascular risk. European guidelines use SCORE2 or SCORE2-OP, among other tools, for risk assessment. The higher the individual’s risk, the more aggressively LDL-C reduction is generally pursued.

The ESC/EAS LDL-C target levels have remained unchanged in the 2025 Focused Update.

Influencing Cholesterol: What Role Do Diet and Lifestyle Play?

Regardless of whether additional medication is necessary, lifestyle factors play an important role in cardiovascular health. It’s less about individual “good” or “bad” foods and more about long-term dietary patterns.

• Dietary fiber:
  A high-fiber diet, especially one that includes soluble or viscous dietary fiber, may help lower LDL cholesterol.
  Examples of sources include:
  • Oats
  • Barley
  • Legumes
  • Psyllium husks
    
    
• Fat Quality:
  The composition of the fats you consume also plays a role. Replacing some saturated fatty acids with unsaturated fatty acids can have a beneficial effect on LDL-C.
  
  
• Movement:
  Regular exercise affects numerous cardiovascular risk factors, including:
  • Blood Pressure
  • Insulin sensitivity
  • Body weight
  • various parameters of lipid metabolism

Anyone who wants to lower their cholesterol should therefore consider their diet and lifestyle as a whole.

However, it is important to note that lifestyle changes and drug therapy are not fundamentally mutually exclusive.

The measures required depend on individual baseline values and, in particular, on the overall risk.

Gut Microbiota and Cholesterol: What Does the Research Tell Us?

The relationship between the gut microbiota and cholesterol metabolism is a growing area of research.

The gut microbiota—often referred to colloquially as gut flora —comprises the community of microorganisms in the gut.

Bile acids play a particularly interesting role in this context.

From Cholesterol to Bile Acids

The liver uses cholesterol as a starting material for the production of bile acids. These are released into the intestines via bile, where they aid, among other things, in the digestion and absorption of fats.

The vast majority of bile acids are subsequently reabsorbed and transported back to the liver. This cycle is known as the enterohepatic cycle.

Where does the gut microbiota come into play?

Intestinal bacteria can chemically modify bile acids, thereby influencing the composition of the bile acid pool and its biological activity.

Bile acids are not merely aids to digestion. They also act as signaling molecules and interact with various receptors, which in turn can influence different metabolic processes.

This creates a complex interplay between:

Cholesterol metabolism → Bile acids → Gut microbiota → Bile acid signaling → Metabolism

However, this does not mean that a specific composition of the gut microbiota—or “gut flora”—automatically leads to lower cholesterol levels. Which changes in the gut microbiota have clinically relevant effects on cholesterol metabolism and, ultimately, on cardiovascular risk is the subject of ongoing research.

Statins for High Cholesterol: How Do They Work?

If an individual's cardiovascular risk warrants pharmacological LDL-C reduction, statins are among the most thoroughly studied classes of drugs.

These include, for example, atorvastatin and rosuvastatin.

Statins inhibit the enzyme HMG-CoA reductase in the liver, which is involved in the body’s own cholesterol synthesis. In response, the liver increases the number of LDL receptors on the surface of its cells, thereby enabling it to take up more LDL particles from the blood. European guidelines continue to recommend statins as the first-line pharmacological option for lowering LDL-C. If individual target levels are not achieved with statins, or if statins cannot be used adequately, other classes of drugs or combination therapies are available.

Statins and Muscle Pain: How Should We Interpret the Evidence?

Muscle symptoms are among the most frequently discussed potential side effects of statins. It is important to make a distinction here. Muscle symptoms can occur during statin therapy. At the same time, a temporal association does not necessarily mean that the statin is actually the cause of the symptoms.

If statin intolerance is suspected, a doctor can therefore determine whether, for example:

• a different dosage,
• another statin or
• an alternative dosing regimen

is a possibility.

Complete statin intolerance is significantly less common than partial intolerance. The goal should therefore not be to downplay muscle symptoms or automatically attribute them to the medication, but rather to investigate possible causes on a case-by-case basis.

Lowering Cholesterol: What Treatment Options Are Available Besides Statins?

Not everyone can achieve their individual LDL-C target levels with a statin alone. Furthermore, in some cases, statins cannot be tolerated or can only be tolerated to a limited extent.

In that case, other classes of active ingredients are available.

• Ezetimibe:
  Ezetimibe inhibits the absorption of cholesterol in the intestine. It can be used alone or in combination with a statin.
  
  
• Bempedoic acid:
  Bempedoic acid inhibits cholesterol synthesis in the liver through a different mechanism of action than statins. The active ingredient is converted into its active form primarily in the liver. This distinguishes it pharmacologically from statins—but does not mean that muscle-related side effects are completely ruled out. The 2025 ESC/EAS Update recommends bempedoic acid, among other things, for patients who cannot take statins and require additional LDL-C reduction. In cases of high or very high cardiovascular risk, it may also be considered as an adjunct to the maximum tolerated lipid-lowering therapy.
  
  
• PCSK9 inhibitors:
  Monoclonal antibodies against PCSK9 increase the availability of LDL receptors in the liver. This allows more LDL to be taken up from the blood. They can provide a significant additional reduction in LDL-C and are used in particular when patients are at high risk and have not achieved their target levels.
  
• Inclisiran:
  Inclisiran takes a different approach: it uses small interfering RNA (siRNA) to reduce the production of PCSK9 in the liver. This, too, increases the number of available LDL receptors and lowers LDL-C.
  
  The choice of which therapy or combination is appropriate depends on:

• • individual risk,
  • the initial values,
  • the target values,
  • Comorbidities and
  • tolerability.

Lowering Cholesterol with Dietary Supplements—What Is the Evidence?

Dietary supplements are often used with the goal of affecting cholesterol levels. However, the scientific evidence varies significantly depending on the substance, dosage, and study population.

One widely discussed study is the SPORT study. In the study, adults with an elevated 10-year cardiovascular risk were treated with, among other things, low-dose rosuvastatin, a placebo, or one of six commonly used supplements:

• Fish oil
• Cinnamon
• Garlic
• Turmeric
• Plant sterols
• Red mold rice

After 28 days, rosuvastatin 5 mg reduced LDL-C significantly more than placebo and all of the supplements studied. None of the supplements tested in this study resulted in a statistically significant reduction in LDL-C compared with placebo.

What does that mean—and what doesn't it mean?

The results show that, under the conditions of this study, the specific medications examined did not achieve an LDL-C reduction comparable to that of rosuvastatin.

However, this does not mean that all dietary supplements or nutrition-related interventions have no effect on LDL-C.

The following points, among others, are important for interpretation:

• The SPORT study lasted only 28 days.
• She examined specific products and dosages.
• It was primarily designed to compare rosuvastatin with the other groups.
• It was not designed to reliably detect small differences between each individual supplement and the placebo.

An accompanying scientific commentary therefore points out the limitations of a blanket interpretation. Furthermore, there is evidence of moderate effects on LDL-C for plant sterols and stanols, as well as for viscous soluble dietary fiber.

Dietary supplements should therefore not be evaluated across the board. At the same time, they are not a substitute for medically necessary lipid-lowering therapy.

Probiotics and Cholesterol: What Does the Research Say?

Certain probiotics are also being studied for their potential effects on lipid metabolism. Possible mechanisms include, among other things, interactions between the gut microbiota and bile acid metabolism.

However, it is particularly important here not to refer to “probiotics” as a single, uniform group.

Possible effects may depend on:

• the bacterial strain used,
• the dosage,
• the duration of study and
• of the study population.

Furthermore, changes in individual lipid parameters do not automatically indicate a reduction in cardiovascular risk. The gut microbiota is therefore an interesting area of research, but it is not currently a substitute for established treatments for elevated lipid levels.

Conclusion: What Cholesterol Levels Really Tell Us

Cholesterol is neither inherently “good” nor “bad.” It performs vital functions—yet at the same time, elevated levels of atherogenic lipoproteins play a key role in the development of atherosclerosis.

A standard lipid profile including:

• LDL-C,
• HDL-C and
• Triglycerides

...represents only part of the overall picture.

Markers such as ApoB and Lp(a) can provide additional information for individual risk assessment in certain situations. Therefore, current European guidelines take into account not only lipid levels but also the overall cardiovascular risk profile and additional risk modifiers.

Diet, exercise, and other lifestyle factors remain key components of prevention. At the same time, for individuals at elevated risk, there are well-studied medication options available for lowering LDL-C.

The connection between gut microbiota, bile acids, and cholesterol metabolism also opens up interesting avenues for research. However, many of these relationships are more complex than simple statements such as “a healthy gut microbiota lowers cholesterol” would suggest.

What matters, therefore, is not a single cholesterol reading or a single measure, but rather the individual assessment of overall cardiovascular risk.

Sources & Academic Literature

1. ESC/EAS (2025): Focused Update of the 2019 ESC/EAS Guidelines for the Management of Dyslipidemias. (Escardio)
2. ACC/AHA et al. (2026): Guideline on the Management of Dyslipidemia. ( professional.heart.org)
3. Ference BA et al. (2017): Low-density lipoproteins cause atherosclerotic cardiovascular disease. European Heart Journal. (OUP Academic)
4. Borén J et al. (2020): Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights. European Heart Journal. (OUP Academic)
5. Ridlon JM, Gaskins HR (2024): Another renaissance for bile acid gastrointestinal microbiology. Nature Reviews Gastroenterology & Hepatology. (Nature)
6. Laffin LJ et al. (2023): Comparative Effects of Low-Dose Rosuvastatin, Placebo, and Dietary Supplements on Lipids and Inflammatory Biomarkers. Journal of the American College of Cardiology, 81(1), 1–12. (JACC)
7. Maki KC, Dicklin MR (2023): Caution Against Rejecting All Dietary Supplements for LDL Cholesterol Reduction. Journal of the American College of Cardiology, 81(1), 13–15. (JACC)
   

Medical Information

This post is intended solely for general informational purposes and is not a substitute for individual medical advice, diagnosis, or treatment. Medications should not be started, stopped, or adjusted in dosage without consulting a doctor.