What Causes High LDL (Bad Cholesterol)?
It’s important to know what causes high LDL (low-density lipoproteins) or bad cholesterol. Knowing what increases LDL levels and eliminating these cholesterol-raising factors can prevent LDL numbers from climbing and thereby help maintain good health. Here are the culprits that can raise LDL cholesterol, and as a result, increase the risk of heart disease.
Epidemiological studies have not shown a clear relationship between dietary cholesterol intake and CHD risk. Some studies show a positive relationship, whereas several others show a neutral relationship. Clinical studies have demonstrated that dietary cholesterol increases total and LDL cholesterol, but to a lesser degree than saturated and trans fatty acids. Taking in an additional 100 mg/day of cholesterol increases total cholesterol by about 2.4mg/dL and LDL by 2.1 mg/dL. Sources of dietary cholesterol include animal products, for example, eggs, dairy products, and meats. Eggs contribute the most cholesterol to the diet, about 213 mg cholesterol/egg. Reducing dietary cholesterol is recommended to lower LDL, especially in individuals with high LDL levels. The mechanism by which dietary cholesterol elevates LDL appears to be through increased LDL synthesis, and decreased breakdown (4).
Saturated and Trans Fats
Saturated fatty acids (SFA) increase LDL cholesterol in a dose-dependent fashion, meaning that higher consumption of saturated fats results in higher LDL levels. Significant sources of SFA include fatty red meats and full-fat dairy products. High amounts of SFA are also found in tropical oils like palm oil, palm kernel oil, coconut oil. SFA intake has been shown to be associated with coronary heart disease (CHD) risk. A meta-analysis of clinical trial results shows that for every 1% increase in energy from SFA, LDL rises by 1.8 mg/dL. Lowering SFA consumption to less than 7% of energy and cholesterol consumption to less than 200 mg/day lowers LDL by 9% to 12% compared with baseline or a Western-type diet with higher SFA and cholesterol (1). Animal studies have shown that SFA increases LDL by inhibiting LDL receptor activity and increasing lipoprotein production (2).
Trans fatty acids (TFA) increase LDL to a similar degree as saturated fatty acids, but also lower HDL. Consequently, the LDL:HDL ratio is increased two-fold higher following the consumption of TFA compared to the consumption of SFA. Clinical trials have shown that TFA intake is associated with increases in the LDL:HDL ratio. Furthermore, studies have shown that individuals with high TFA intake have a higher risk of CHD. TFA is found naturally in small amounts in certain foods including dairy products, beef, and lamb. Additionally, small amounts of TFA are formed during the refining of liquid vegetable oils such as canola and soybean oil. TFA is also made by a process called partial hydrogenation, which adds hydrogen to unsaturated fatty acids. This process turns liquid oil into a semi-solid form such as shortenings and margarines, which are the most common sources of TFA. Other sources include commercially fried foods, baked goods, and savory snack foods (1). TFA can elevate LDL by decreasing LDL breakdown (3).
It is well established that whole-body cholesterol synthesis increases with obesity. Data from one study showed that increases in weight are accompanied by increases in LDL. In addition, a few studies demonstrated that in both young men and women, LDL increases with increasing BMI (5). However, the association between obesity and LDL may lessen with age (6).
In general, obesity is not always associated with increases in blood levels of total or LDL cholesterol, but it is associated with increases in blood triglycerides and decreases in HDL. Additionally, there seems to be a change in the composition of LDL particles in obese individuals. They have higher levels of small dense LDL particles. These particles contain less cholesterol than normal-sized LDL particles and are more atherogenic or more likely to cause atherosclerosis. This is because they are more readily oxidized and glycated, which makes them more likely to invade the arterial wall (7). Weight loss and exercise can improve cholesterol levels and thereby reduce cardiovascular disease risk.
The evidence supporting the role of chronic stress in raising LDL cholesterol is inconsistent. A few studies show that stress can increase LDL levels. There are also studies that look at the effects of stress management on cholesterol levels. Data from two studies demonstrate that stress relief is associated with a reduction in LDL levels. However, there are a number of studies that show no relationship between stress and LDL levels (8).
The mechanism whereby stress can potentially increase LDL levels has been worked out to some degree. Stress leads to increased levels of cortisol, catecholamines, and fatty acids in the blood. Both cortisol and fatty acids can increase triglyceride synthesis and stimulate VLDL secretion from the liver. The increased secretion of VLDL is potentially atherogenic since each VLDL particle is metabolized to IDL or LDL. These are cleared mainly by the liver LDL receptor (this receptor is involved in removing IDL and LDL from the circulation), which is increased by insulin and decreased by cortisol. Insulin also decreases VLDL secretion. Catecholamines can stimulate fatty acid metabolism, decrease VLDL secretion and increase LDL uptake, thus having a protective effect opposite to those of cortisol. These effects contribute to exercise-induced stress.
Stress that is not accompanied by an increase in energy expenditure and metabolism of fatty acids can lead to the increased effects of cortisol and fatty acids relative to insulin (9). Although speculative, this type of stress may also be associated with the increased effects of cortisol and fatty acid relative to catecholamines.
Smokers have higher blood total cholesterol, triglyceride, and LDL levels, and lower HDL than non-smokers. Although LDL is higher in smokers, the amount of LDL raised by smoking is only 1.7%. The mechanism responsible for increasing LDL cholesterol in smokers is not fully understood. Quitting smoking will result in an increase in HDL levels within 17 days and will continue to improve as long as smoking cessation is maintained. In certain individuals, weight gain is associated with quitting, but HDL levels still rise toward normal despite this gain (10).
Blood total and LDL cholesterol is increased in older people. LDL cholesterol increases by about 40% from 20 to 60 years of age. The mechanism for this change in cholesterol is unclear. The aging effect on cholesterol is associated with decreased elimination of cholesterol as bile acids and reduced clearance of blood LDL (11).
Other Factors That Can Raise LDL Levels (12, 13)
· Familial hypercholesterolemia
Hormones and Gender
· Reduced estrogen levels (occurring in postmenopausal women)
· Type 2 diabetes
· Nephritic syndrome
· Obstructive liver disease
· Polycystic ovarian syndrome
· Lack of exercise
· Some steroids
· Some antihypertensive drugs
It is well established that saturated and trans fats, and, to a lesser extent, dietary cholesterol can all raise LDL levels. Aging has also been proven to increase LDL values. Obesity, stress, and smoking may increase LDL levels but the evidence for this is weak or inconsistent. A number of other factors like genetics, hormones and gender, some diseases, lack of exercise, and some drugs can also increase LDL levels. Some of these factors can be controlled such as diet, smoking, stress, physical activity, and medications, whereas others like aging, gender, some diseases, and genetics can’t be controlled.
The following suggestions may help improve cholesterol levels.
First, eliminate trans fats. Limit consumption of saturated fats by cutting back on red meat and full-fat dairy foods and replace them with beans, nuts, poultry and fish and low-fat dairy foods. Use liquid vegetable oils, for example, olive oil, canola oil, sunflower oil, safflower oil, corn oil and peanut oil, which are high in polyunsaturated and monounsaturated fats, in cooking and dipping instead of butter. Eat fish, walnuts, canola or soybean oil, ground flax seeds or flaxseed oil to increase intake of heart-protective omega-3 fats (14).
Add more soluble fiber, nuts, soy protein, and plant sterols to reduce LDL levels.
Exercise a little bit (about 30 minutes) most days of the week. Go for a walk, a jog or a swim to improve cholesterol numbers.
Quit smoking to help raise good HDL cholesterol. Try to reduce stress to avoid potential increases in LDL.
Ask for alternative drugs that don’t affect cholesterol levels if possible. Following these suggestions may help prevent LDL levels from rising and thus reduce the risk of heart disease.
The material presented in this article is only for your information. Before you make any changes to your diet and lifestyle, please consult your physician. Your doctor will be able to give you appropriate advice on what will help you manage your lipid levels.
1. Katcher HI, Hill AM, Lanford JLG, Yoo JS, Kris-Etherton PM. Lifestyle Approaches and Dietary Strategies to Lower LDL-Cholesterol and Triglycerides and Raise HDL-Cholesterol. Endocrinology and Metabolism Clinics of North America. 2009;38(1):45-78.
2. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Curr Atheroscler Rep. 2010;12(6):384-90.
3. Matthan NR, Welty FK, Barrett PH, Harausz C, Dolnikowski GG, Parks JS, et al. Dietary hydrogenated fat increases high-density lipoprotein apoA-I catabolism and decreases low-density lipoprotein apoB-100 catabolism in hypercholesterolemic women. Arterioscler Thromb Vasc Biol. 2004;24(6):1092-7.
4. Packard CJ, McKinney L, Carr K, Shepherd J. Cholesterol feeding increases low-density lipoprotein synthesis. J Clin Invest. 1983;72(1):45-51.
5. Howard BV, Ruotolo G, Robbins DC. Obesity and dyslipidemia. Endocrinology and Metabolism Clinics of North America. 2003;32(4):855-67.
6. Tonstad S, Despres J-P. Treatment of lipid disorders in obesity. Expert Review of Cardiovascular Therapy. 2011;9(8):1069-80.
7. Nesto RW. LDL Cholesterol Lowering in Type 2 Diabetes: What Is the Optimum Approach? Clinical Diabetes. 2008;26(1):8-13.
8. Strauss-Blasche G, Ekmekcioglu C, Marktl W. Serum lipids responses to a respite from occupational and domestic demands in subjects with varying levels of stress. Journal of Psychosomatic Research. 2003;55(6):521-4.
9. Brindley DN, McCann BS, Niaura R, Stoney CM, Suarez EC. Stress and lipoprotein metabolism: modulators and mechanisms. Metabolism. 1993;42(9 Suppl 1):3-15.
10. Campbell SC, Moffatt RJ, Stamford BA. Smoking and smoking cessation‚ÄîThe relationship between cardiovascular disease and lipoprotein metabolism: A review. Atherosclerosis. 2008;201(2):225-35.
11. Galman C, Matasconi M, Persson L, Parini P, Angelin B, Rudling M. Age-induced hypercholesterolemia in the rat relates to reduced elimination but not increased intestinal absorption of cholesterol. Am J Physiol Endocrinol Metab. 2007;293(3):E737-42.
12. Wattoo FH, Memon MS, Memon AN, Wattoo MH, Tirmizi SA, Iqbal J. Estimation and correlation of stress and cholesterol levels in college teachers and housewives of Hyderabad-Pakistan. J Pak Med Assoc. 2008;58(1):15-8.
13. Step 3: What causes high cholesterol? 2012 [updated December 31, 2012]; Available from:
14. The Nutrition Source. Fats and Cholesterol: Out with the Bad, In with the Good. 2012 [updated September 19, 2012]; Available from: http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-full-story/.
This content is accurate and true to the best of the author’s knowledge and does not substitute for diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed health professional. Drugs, supplements, and natural remedies may have dangerous side effects. If pregnant or nursing, consult with a qualified provider on an individual basis. Seek immediate help if you are experiencing a medical emergency.
Questions & Answers
What does LDL stand for?
LDL stands for low-density lipoproteins. It is a class of lipoprotein particles, which are molecules made of protein and fat. LDL particles consist of a core of triglycerides and cholesterol in a shell of phospholipids, free cholesterol and protein. They transport cholesterol and fats through the blood to the tissues. They are low density because they have more lipids than proteins (lipids are less dense than protein).Helpful 5