Why is my LDL Cholesterol so high?

There are many myths within the health industry, with a big one based around LDL cholesterol. Any individual which goes to the doctor with high cholesterol immediately gets written a prescription for a statin while being rushed out of the doctor’s room so they can move onto the next patient. The statin will help lower someone’s blood cholesterol levels, but it won’t be a permanent fix. In order to address high cholesterol, the root cause needs to first be determined. There are multiple factors which cause elevated cholesterol levels and can be seen as an interplay between; Thyroid, Infections, Triglycerides and Leaky Gut. This blog is going to focus on explaining the physiology  behind how each of these factors are related to increases LDL cholesterol.

 

Thyroid:

The thyroid is a vital hormone gland which plays an important role on the synthesis, absorption and metabolism of lipids. Low levels of thyroid function may lead to higher levels circulating cholesterol(1). It does this by increasing the intestinal absorption of cholesterol(2). The thyroid also increases the amount of LDL receptors which uptake LDL in the liver and tissues, although when thyroid levels get too low, the number of LDL receptors begin to decrease(3). This in turn leads to an inability to clear LDL from the blood, thus increasing the amount of circulating LDL. This increases the potential risk of developing heart disease.

 

Infections:

During infection we see changes in lipoprotein metabolism to allow for the redistribution of nutrients to cells that are important in host defense or tissue repair(4). Studies have found infection to decrease cholesterol transport back to the liver, which may help conserve cholesterol in macrophages and other cells that play key roles in host defence(5). Infections have also been found to increase lipoprotein and lipid production to protect the host from toxic effects of microorganisms(6). These factors lead to an increase in circulating LDL and attribute to a greater risk of cardiovascular disease.

 

Triglycerides:

LDL is a cholesterol transport protein, used to take cholesterol from the liver to cells where they perform various functions. These LDL molecules not only carry cholesterol but triglycerides and antioxidants as well. When we eat refined carbohydrates and sugars, our blood sugar levels begin to spike(7). This causes the pancreas to release insulin to pull the sugars into our cells. Although when our glycogen stores are full, insulin then begins to convert the sugars into triglycerides to be stored in adipose tissue(8). We then need to transport these triglycerides from the liver to the tissues. Unfortunately the LDL molecule can only fit in a certain amount of cholesterol and triglycerides. With the increase in triglycerides the body then needs to produce more LDL to transport them(9). This again increases the amount of circulating LDL molecules in the blood, increasing the risk of developing heart disease.

 

Leaky gut:

The digestive system acts as a barrier between your gut and bloodstream, preventing harmful substances from leaving the gut. The intestines contain tight junctions, which allow nutrients to pass into the blood stream. In leaky gut, these tight junctions begin to loosen, allowing harmful substances to enter the blood stream(10). A common endotoxin which enters the blood stream is called lipopolysaccharide which is produced by certain gut bacteria(11). The release of this endotoxin causes an immune reaction triggering widespread inflammation. The immune reactions trigger an increase in LDL molecules as they have anti-microbial effects(12). A protein called LPS-binding protein circulates with LDL, binding to LPS and removing it from circulation(13). This action increases the amount of circulating LDL win order to fight off endotoxins.

 

To conclude, there are various factors at play contributing to increased levels of LDL Cholesterol. These include Thyroid function, Infections, Triglycerides, and Leaky gut. From this it can be made evident that we need to start viewing the body as a whole, understanding the roles of various systems in the body and how they play their parts in disease manifestation.  There are times therapeutic drugs do have their place in disease treatment, although the underlying causes of a disease need to be addressed in order to bring an individual back to health.

 

References:

1. Pearce E. Update in Lipid Alterations in Subclinical Hypothyroidism. The Journal of Clinical Endocrinology & Metabolism [Internet]. 2012 [cited 7 December 2018];97(2):326-333. Available from: https://academic.oup.com/jcem/article/97/2/326/2836270

2. Lutz J. Hypothyroid and Cholesterol; Too Little Thyroid Hormone, Too Much Cholesterol. Endocrine Web [Internet]. 2018 [cited 7 December 2018];. Available from: https://www.endocrineweb.com/news/thyroid-diseases/59757-hypothyroid-cholesterol-too-little-thyroid-hormone-too-much-cholesterol

3. Moon J, Kim H, Kim H, Choi S, Lim S, Park Y et al. Decreased Expression of Hepatic Low-Density Lipoprotein Receptor–Related Protein 1 in Hypothyroidism: A Novel Mechanism of Atherogenic Dyslipidemia in Hypothyroidism. Thyroid [Internet]. 2013 [cited 7 December 2018];23(9):1057-1065. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770248/

4. Feingold K, Grunfeld C. The Effect of Inflammation and Infection on Lipids and Lipoproteins. Endotext [Internet]. 2015 [cited 7 December 2018];. Available from: https://www.ncbi.nlm.nih.gov/books/NBK326741/

5. Feingold K, Grunfeld C. The acute phase response inhibits reverse cholesterol transport. Journal of Lipid Research [Internet]. 2010 [cited 7 December 2018];51(4):682-684. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842157/

6. Infection and Inflammation-Induced Proatherogenic Changes of Lipoproteins. The Journal of Infectious Diseases [Internet]. 2000 [cited 7 December 2018];181:S462-S472. Available from: https://academic.oup.com/jid/article/181/Supplement_3/S462/2191190

7. Jenkins D, Wolever T, Taylor R, Barker H, Fielden H, Baldwin J et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. The American Journal of Clinical Nutrition [Internet]. 1981 [cited 10 January 2019];34(3):362-366. Available from: https://academic.oup.com/ajcn/article-abstract/34/3/362/4692881

8. Vynckt V. The Conversion of Carbohydrates to Triglycerides [Internet]. Healthyeating.sfgate.com. 2018 [cited 10 January 2019]. Available from: https://healthyeating.sfgate.com/conversion-carbohydrates-triglycerides-2218.html

9. Griffin B, Freeman D, Tait G, Thomson J, Caslake M, Packard C et al. Role of plasma triglyceride in the regulation of plasma low density lipoprotein (LDL) subfractions: relative contribution of small, dense LDL to coronary heart disease risk. Atherosclerosis [Internet]. 1994 [cited 10 January 2019];106(2):241-253. Available from: https://www.sciencedirect.com/science/article/pii/0021915094901295

10. Madara J. Loosening Tight Junctions. Perspectives [Internet]. [cited 10 January 2019];:1089-1094. Available from: https://dm5migu4zj3pb.cloudfront.net/manuscripts/113000/113987/JCI89113987.pdf

11. Hart A, Lammers K, Brigidi P, Vitali B, Rizzello F, Gionchetti P et al. Modulation of human dendritic cell phenotype and function by probiotic bacteria. BMJ Journals [Internet]. 2019 [cited 10 January 2019];. Available from: https://gut.bmj.com/content/53/11/1602?utm_source=TrendMD&utm_medium=cpc&utm_campaign=GUT_TrendMD-0

12. Grunfeld H, Feingold K. Effects of endotoxin on lipid metabolism. Endotoxic Shock and Metabolism [Internet]. 1995 [cited 10 January 2019];23:1013-1017. Available from: https://pdfs.semanticscholar.org/a2c1/9025573414d20d3cb2ffbe491493075834ec.pdf

13. Vreugdenhil A, Rousseau C, Hartung T, Greve J, Veer C, Buurman W. Lipopolysaccharide (LPS)-Binding Protein Mediates LPS Detoxification by Chylomicrons. The Journal of Immunology [Internet]. 2003 [cited 10 January 2019];170(3):1399-1405. Available from: http://www.jimmunol.org/content/170/3/1399.short

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