Dyslipidemia and elevated cholesterol levels - causes and possible solutions
Articles
Dyslipidemia is a disorder of fat metabolism in which blood levels of cholesterol or triglycerides are elevated. Most often it is raised LDL cholesterol, which can build up in the artery walls and contribute to atherosclerosis, heart attack and stroke. High cholesterol usually does not hurt and goes unnoticed for a long time, so it is important to know your values and how to keep them in range. This article explains which cholesterol values are desirable, what raises cholesterol and how to lower it through diet, lifestyle and targeted support from dietary supplements.
What will you learn in this article?
- What is cholesterol?
- The link between cholesterol and cardiovascular disease
- What are the normal cholesterol values?
- Symptoms of high cholesterol
- Causes of dyslipidemia and what raises cholesterol
- How cholesterol is tested
- How to lower cholesterol: diet and lifestyle
- Which supplements can support healthy lipid levels
- Key takeaways
What is cholesterol?
Cholesterol is a fatty substance the body genuinely needs. It is found in every cell, where it forms part of the cell membranes. From cholesterol the body makes steroid hormones, that is the sex hormones (testosterone, estrogens and progesterone) and the stress hormone cortisol. The largest share of cholesterol is used to make bile acids, which help digest fats. In the skin, vitamin D is formed from it with the help of sunlight.
The body makes most of its cholesterol itself, and a smaller part (about 20 %) comes from the diet. Cholesterol travels in the blood in lipoprotein particles, complexes of fats and proteins. The four main groups of lipoproteins are:
Chylomicrons form in the small intestine and deliver energy-rich fats from food to muscles or store them in fat cells. They also carry cholesterol from the intestines to the liver.
VLDL (very-low-density lipoprotein) carries triglycerides, phospholipids and cholesterol from the liver to fat cells.
LDL (low-density lipoprotein), commonly called "bad cholesterol", carries cholesterol into the tissues. It can also be deposited in the artery walls and contribute to atherosclerosis and cardiovascular disease. LDL particles contain apolipoprotein B100 (Apo-B100).
HDL (high-density lipoprotein), often called "good cholesterol", carries cholesterol from the tissues back to the liver, where it is reprocessed or excreted as bile salts. This process is called reverse cholesterol transport. HDL particles contain apolipoprotein A-I (Apo-A1).
The link between cholesterol and cardiovascular disease
The synthesis and use of cholesterol must be regulated to prevent its excessive accumulation in the body. The deposition of cholesterol and LDL particles in the coronary arteries is particularly important. This deposition can lead to atherosclerosis, the main factor contributing to coronary artery disease. [1]
How damaging LDL particles are to the artery walls is shaped by metabolic processes, especially oxidation and glycation. Free radicals cause oxidative damage to LDL particles. During glycation a sugar binds to the LDL molecule and glycated LDL particles form. Glycation of LDL depends on blood sugar concentration, can play a direct role in the development of atherosclerosis and makes the LDL molecule more susceptible to oxidation. [2] Elevated LDL therefore does not threaten the artery walls directly. It does mean, however, that more LDL particles are available to oxidize or otherwise change, and so more likely to damage the vessels. You can read more in the article Blood Sugar Levels: How to Keep Them Stable and Why It Matters for Health.
What are the normal cholesterol values?
Blood lipids are measured from a fasting sample and expressed in mmol/l. The values below are approximate desirable values for an adult with no additional risk factors.
| Marker | Desirable value |
|---|---|
| Total cholesterol | < 5.0 mmol/l |
| LDL cholesterol | < 3.0 mmol/l |
| HDL cholesterol | > 1.0 mmol/l (men), > 1.2 mmol/l (women) |
| Triglycerides | < 1.7 mmol/l |
| Non-HDL cholesterol | < 3.8 mmol/l |
The target LDL value is not set by age but by overall cardiovascular risk. Cholesterol does rise naturally with age, but the target depends on which risk group a person belongs to (based on age, sex, blood pressure, smoking, diabetes and other factors). According to the 2019 ESC/EAS recommendations, these LDL targets apply:
| Cardiovascular risk | LDL target |
|---|---|
| Low | < 3.0 mmol/l |
| Moderate | < 2.6 mmol/l |
| High | < 1.8 mmol/l (and at least a 50 % reduction) |
| Very high | < 1.4 mmol/l (and at least a 50 % reduction) |
Which risk group you belong to and which target is right for you is assessed by a doctor or qualified practitioner. [12]
Symptoms of high cholesterol
High cholesterol itself does not hurt and most often causes no symptoms. Many people learn about a raised level only from a blood test or after a cardiac or vascular event. That is why dyslipidemia is sometimes called a "silent" risk factor.
Visible signs appear mainly in markedly elevated, often inherited forms. They include yellowish fatty deposits in the skin (xanthomas), deposits around the eyelids (xanthelasma) or a greyish ring at the edge of the cornea (arcus corneae) in younger people. These signs are less common, and their absence does not rule out high cholesterol. Cholesterol levels are reliably revealed only by a blood test.
Causes of dyslipidemia and what raises cholesterol
Primary dyslipidemia includes genetically determined disorders of lipid metabolism, such as familial hypercholesterolemia, familial hypertriacylglycerolemia or familial hyperlipoproteinemia. These inherited disorders are among the most common and affect about 1 in every 500 people. [3]
In familial hypercholesterolemia the cause is a defect in the LDL cholesterol receptor in the liver. Normally the liver cell takes up LDL cholesterol, it binds to the LDL receptor and the liver receives a signal to stop making cholesterol. A damaged LDL receptor does not pass on this signal and cholesterol production continues. Damage to LDL receptors also occurs commonly with age and in some diseases, most notably diabetes.
Cholesterol therefore tends to rise with age. A diet high in saturated fat further reduces the number of LDL receptors and weakens the feedback mechanism that tells the liver cell to curb cholesterol production. [3]
Secondary dyslipidemia arises as a result of another condition, for example diabetes, liver, biliary tract or kidney disease, or thyroid dysfunction. For that reason it is advisable to check the thyroid in patients with dyslipidemia. [4] Over 90 % of people with hypothyroidism have dyslipidemia, but only about 4 % of people with dyslipidemia have hypothyroidism. [5]
Cholesterol and triglycerides are also raised by lifestyle factors: excessive alcohol consumption, obesity and lack of exercise. During a bacterial or viral infection triglyceride levels usually rise, so testing lipids shortly after illness is not suitable. A lipid panel is recommended about 3 weeks after a milder illness and 3 months after a more serious one. [6]
How cholesterol is tested
Dyslipidemia is most often detected at a preventive check-up from a blood test, the lipid panel. Regular monitoring is advisable for people with an inherited disorder of lipid metabolism in the family and for those at higher cardiovascular risk. The basis is measuring total, LDL and HDL cholesterol and triglycerides.
In some cases it is useful to add further markers. One is apolipoprotein B (Apo-B), a protein component of lipoproteins that indicates the number of all atherogenic particles in circulation. Many studies have shown that elevated Apo-B predicts cardiovascular risk better than the traditional markers [7], so many expert societies recommend it for risk assessment. [11]
Another marker is C-reactive protein (CRP), made by the liver, which reflects the level of inflammation. The development of atherosclerosis is linked to inflammation in the vessel walls, so the hs-CRP level can signal cardiovascular risk. CRP correlates with the extent of atherosclerosis, and its rise in patients with dyslipidemia tends to go with higher triglycerides and higher BMI. [8]
How to lower cholesterol: diet and lifestyle
The basis of managing dyslipidemia is non-pharmacological measures, that is changes to diet and lifestyle. These include regular physical activity (at least 150 minutes per week), optimizing body weight (BMI 20 to 25 kg/m², waist circumference under 94 cm in men and under 80 cm in women), not smoking and limiting alcohol. [12]
Diet plays a key role, ideally a Mediterranean-style pattern. Several authorised European Union health claims about the effect of food components on cholesterol apply here [13]:
Unsaturated fats instead of saturated: replacing saturated fats with unsaturated fats contributes to the maintenance of normal blood cholesterol levels. Replace butter and lard with olive oil, nuts and oily fish.
Beta-glucans: beta-glucans from oats and barley contribute to the maintenance of normal blood cholesterol levels. The beneficial effect is obtained with a daily intake of 3 g, roughly one portion of porridge.
Plant sterols and stanols: contribute to the maintenance of normal blood cholesterol levels. The beneficial effect is obtained with a daily intake of at least 0.8 g, usually from fortified foods.
Reducing saturated fat: reducing the intake of saturated fat contributes to the maintenance of normal blood cholesterol levels.
What to include and what to limit is summarized in the table below.
| Worth including | Worth limiting |
|---|---|
| Oats and barley (beta-glucans) | Fatty meat and processed meats |
| Legumes | Butter and lard (saturated fat) |
| Olive oil | Fried food and fast food |
| Nuts and seeds | Industrial baked goods and trans fats |
| Oily fish (salmon, mackerel) | Excess sugar and white flour |
| Vegetables and fruit | Alcohol in larger amounts |
Individual foods often come up too. For eggs, the effect on blood cholesterol used to be overestimated. According to a large analysis, moderate consumption, about one egg a day, is not associated with higher cardiovascular risk in most people. [14]
Supplements with red yeast rice (monacolin K) were once linked to lowering cholesterol. Since 2022, however, the European Union has significantly limited the monacolin K content for safety reasons, and the earlier health claim is no longer used. If non-pharmacological measures are not enough, treatment (including statins) is guided by a doctor.
Which supplements can support healthy lipid levels
Dietary supplements do not replace dietary changes or treatment, but they can complement them. We have selected the following key supplements from our portfolio to focus on in the case of dyslipidemia.
Omega-3 fatty acids
Omega-3 fatty acids help maintain the balance between omega-3 and omega-6 fatty acids, whose disruption is linked to inflammatory processes. EPA and DHA contribute to the normal function of the heart; the beneficial effect is obtained with a daily intake of 250 mg of EPA and DHA. DHA and EPA contribute to the maintenance of normal blood triglyceride levels at a daily intake of 2 g.
The amount of omega-3 in the body can be assessed with the Omega-3 Index, used as an independent marker of cardiovascular risk. How the dry-blood-spot method works is explained in the article DBS method or dry blood spot analysis.
Magnesium
Magnesium is one of the frequently missing minerals. It contributes to a reduction of tiredness and fatigue and to normal energy-yielding metabolism, and is depleted more during periods of stress. Research also explores the relationship of magnesium to the enzyme HMG-CoA reductase, which is involved in cholesterol production (the same enzyme targeted by statins). [15] These effects are not yet among the authorised health claims.
Vitamin E
Vitamin E contributes to the protection of cells from oxidative stress, and so helps protect LDL particles from oxidation. It is the name for a group of eight compounds, four tocopherols and four tocotrienols. Full-spectrum vitamin E with tocotrienols, found in ProLife, is also a subject of research in cholesterol metabolism: studies look at the ability of tocotrienols to influence the enzyme HMG-CoA reductase. [9] These effects are not an authorised health claim.
Vitamin D
Studies observe an association between low vitamin D levels and an unfavourable lipid profile, along with other risk factors such as hypertension and diabetes. [10] These are observed associations, not a proven causal effect on cholesterol. Every cell in the body has a receptor for vitamin D.
Before setting a dose, it is advisable to have your vitamin D level measured and then personalise supplementation.
Key takeaways
Dyslipidemia raises cardiovascular risk: elevated LDL cholesterol can build up in the artery walls and contribute to atherosclerosis, heart attack or stroke.
Know your values: desirable is total cholesterol below 5.0 mmol/l and LDL below 3.0 mmol/l; the LDL target, however, is set by cardiovascular risk, not by age.
High cholesterol usually does not hurt: it most often has no symptoms and is revealed only by a blood test, so preventive check-ups matter.
Diet and exercise are the basis: cholesterol is helped by replacing saturated fats with unsaturated ones, beta-glucans from oats and barley, plant sterols and regular activity.
Supplements are support, not a substitute: omega-3 contributes to normal heart function and normal triglyceride levels, while magnesium and vitamin E have their roles in metabolism and cell protection.
Sources:
[1] Cholesterol: Synthesis, Metabolism, and Regulation. The Medical Biochemistry Page. https://themedicalbiochemistrypage.org/cholesterol-synthesis-metabolism-and-regulation/
[2] Fournet M, Bonté F, Desmoulière A. Glycation Damage: A Possible Hub for Major Pathophysiological Disorders and Aging. Aging Dis. 2018;9(5):880-900. https://www.aginganddisease.org/EN/10.14336/AD.2017.1121
[3] Pizzorno JE, Murray MT. Textbook of Natural Medicine. 5th ed. Elsevier; 2021.
[4] Rizos CV, Elisaf MS, Liberopoulos EN. Effects of thyroid dysfunction on lipid profile. Open Cardiovasc Med J. 2011;5:76-84. https://opencardiovascularmedicinejournal.com//VOLUME/5/PAGE/76/
[5] Šatný M, Vrablík M. Sekundární dyslipidemie, přehled pro praktické lékaře. Medicína pro praxi. 2019. https://www.medicinapropraxi.cz/pdfs/med/2019/05/11.pdf
[6] Soška V. Sekundární dyslipidemie a jejich léčba. Vnitřní lékařství. 2007. https://www.casopisvnitrnilekarstvi.cz/pdfs/vnl/2007/04/14.pdf
[7] Feingold KR. Introduction to Lipids and Lipoproteins. In: Endotext. MDText.com; 2021. https://www.ncbi.nlm.nih.gov/books/NBK305896/
[8] Swastini DA, Wiryanthini IAD, Ariastuti NLP, Muliantara A. Atherosclerosis Prediction with High Sensitivity C-Reactive Protein (hs-CRP) and Related Risk Factor in Patient with Dyslipidemia. Open Access Maced J Med Sci. 2019;7(22):3887-3890. https://pmc.ncbi.nlm.nih.gov/articles/PMC7048367/
[9] Baliarsingh S, Beg ZH, Ahmad J. The therapeutic impacts of tocotrienols in type 2 diabetic patients with hyperlipidemia. Atherosclerosis. 2005;182(2):367-374. https://www.atherosclerosis-journal.com/article/S0021-9150(05)00165-6/abstract
[10] Kim MR, Jeong SJ. Relationship between Vitamin D Level and Lipid Profile in Non-Obese Children. Metabolites. 2019;9(7):125. https://www.mdpi.com/2218-1989/9/7/125
[11] Contois JH, McConnell JP, Sethi AA, et al. Apolipoprotein B and cardiovascular disease risk: position statement from the AACC Lipoproteins and Vascular Diseases Division Working Group on Best Practices. Clin Chem. 2009;55(3):407-419. https://academic.oup.com/clinchem/article-abstract/55/3/407/5629355
[12] Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J. 2020;41(1):111-188. https://academic.oup.com/eurheartj/article/41/1/111/5556353
[13] Commission Regulation (EU) No 432/2012 establishing a list of permitted health claims made on foods. Official Journal of the European Union. https://eur-lex.europa.eu/legal-content/EN/TXT/?uri=CELEX%3A32012R0432
[14] Drouin-Chartier JP, Chen S, Li Y, et al. Egg consumption and risk of cardiovascular disease: three large prospective US cohort studies, systematic review, and updated meta-analysis. BMJ. 2020;368:m513. https://www.bmj.com/content/368/bmj.m513
[15] Rosanoff A, Seelig MS. Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals. J Am Coll Nutr. 2004;23(5):501S-505S. https://pubmed.ncbi.nlm.nih.gov/15466951/
