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Dealing with Dyslipidemia via Targeted Nutrition

by Annalouise O’Connor, PhD, RD

Dyslipidemia is defined as an abnormal level of lipids in the blood and is often described most simplistically as greater levels of total or low-density lipoprotein (LDL), the “bad” cholesterol or particle number, or lower levels of high-density lipoprotein (HDL), the “good” cholesterol. Dyslipidemia is linked with cardiovascular risk and is highly prevalent: The minority of adults (46.6%) in the US have on-target total cholesterol levels (<200mg/dL).1 With cardiovascular disease (CVD) responsible for one in every three deaths in the US, getting to grips with modifiable risk factors such as dyslipidemia is important for risk management.

Dyslipidemia details

Primary dyslipidemias, such as familial hypercholesterolemia (FH), are genetic conditions and are relatively rare; for example, FH impacts 0.5% of the US adult population.2 Far more common are secondary dyslipidemias that occur as a result of factors such as obesity, adverse diet and lifestyle, abnormal glucose and insulin control, hypothyroidism, steroid therapies, chronic infection, or an inflammatory environment.3-4

Dyslipidemia can be defined by traditional lipid profile cutoffs. For those at low risk of atherosclerotic cardiovascular disease (ASCVD), LDL <130mg/dL, nonHDL <160mg/dL have been advised as maximum cutoff points, although these guidelines become stricter as CVD increases.3 For example, for individuals at very high risk of ASCVD (such as those with established or recent hospitalization for acute coronary syndrome, vascular disease, or a 10-year risk >20%), LDL <70mg/dL, nonHDL <100mg/dL, and apoB <80mg/dL have been advised.3

– Traditional and advanced testing: Looking at these traditional markers of lipid profile is one aspect of risk assessment, but with access to more sophisticated lipid profiling, it is also possible to get a better understanding of risk and dysfunction. Evaluating modified LDL, for example oxidized or glycated LDL, is interesting, as these are taken up by macrophages and can lead to foam cell formation, an early event in atherosclerosis development.5 Looking at LDL particle number (LDL-P) can provide improved risk prediction and management than LDL-C.6

– HDL…quality over quantity: When it comes to HDL, there is more to be understood than a simple HDL-C read-out shows. Studies have shown that across individuals with similar HDL-C, differences are seen in cholesterol efflux capacity7 (a critical protective activity of HDL, and an independent predictor of CVD risk).8 So it is clear that quality over quantity is important with HDL, not just because nonfunctional HDL is less effective, but because HDL can have two faces, and nonfunctional HDL can be pro-oxidative and proinflammatory in nature.9

What can you do?

– Dietary pattern, the foundation of management: Diet and lifestyle modification are the cornerstone of lipid management, and it been estimated that 80-90% of CV and DM risk could be prevented by an appropriate diet pattern.10-11 In the past, low-fat advice became the standard for lipid management, but several dietary patterns have been shown to benefit lipid profile. Diet patterns of the Mediterranean region,12 the DASH diet, a pattern rich in fruits and vegetables and low-fat dairy with reduced saturated and trans fats, as well as others such as vegetarian diets, the Portfolio diet, and a Nordic Diet pattern have been shown to be beneficial.13 More recently, very-low-carbohydrate ketogenic approaches have been studies in individuals with metabolic disease. For example, the one-year data from Virta Health shows a significant reduction in plasma triglycerides and an increase in HDL-C; although there was a modest increase in LDL-C (~10mg/dL), there was a reduction in sdLDL, highlighting the importance of advanced lipid testing.14

– Multi-pathway action of targeted nutrients: Phytonutrients and other nutritional ingredients impact lipid metabolism and profile in multiple ways, including acting as natural inhibitors of intestinal cholesterol absorption, inhibiting hepatic cholesterol synthesis, enhancing clearance of LDL, reducing modified LDL levels, and enhancing HDL functionality. Some examples of targeted nutrition actives demonstrated to improve lipid metabolism include:

  • 1-4 g/day of niacin has been shown to reduce apoB and plasma TG, reduce LDL-C and LDL particle size, and increase HDL levels15
  • Berberine has been shown to upregulate the LDL receptor and down-regulate PCSK9 and clinically to reduce plasma triglycerides and LDL, and increase circulating HDL-C16
  • Plant sterols or stanols (AKA phytosterols) at a dose of ~2 g/day are well established to reduce LDL17
  • Soluble fiber, found in foods such as psyllium, oats, and barley, can absorb water in the intestine and can also bind cholesterol and bile acids, thus enhancing their removal from the body at doses of ~10g/day16
  • Citrus bergamot has been shown clinically to reduce LDL and sdLDL18
  • Flavonoids have been demonstrated clinically to augment HDL functionality19
  • Red yeast rice supplementation can significantly reduce LDL by 20-30% and triglycerides by 10-20%20
  • Flax seeds, a source of the essential omega-3 fatty acid alpha-linolenic acid (ALA), fiber, and lignans, has been linked with reductions in LDL-C, plasma triglycerides, and overall cardiovascular risk21
  • Omega-3 fatty acids EPA and DHA dose-dependently reduce plasma triglycerides, at 2-4 g/day22

Knowledge is power. Knowing your lipid numbers is an important step to good cardiovascular health. But dyslipidemia should not be viewed in a vacuum. Interlocking risk factors such as blood pressure and endothelial dysfunction, glucose and insulin control, smoking status, body weight, and waist circumference, as well as a proinflammatory environment should be addressed in parallel—the pleiotropic effects of nutritional change and intervention can bring benefit to every area of health and wellbeing.

References

  1. AHA. Heart disease and stroke statistics-2016 update: a report from the American Heart Association. 2016;133:e38-360.
  2. De Ferranti et al. Prevalence of familial hypercholesterolemia in the 1999 to 2012 United States National Health and Nutrition Examination Surveys (NHANES). 2016;133(11):1067-1072.
  3. Jellinger et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(Suppl 2):1-87.
  4. Patel et al. Human experimental endotoxemia in modeling the pathophysiology, genomics, and therapeutics of innate immunity in complex cardiometabolic diseases. Arterioscler Thromb Vasc Biol. 2015;35(3):525-534.
  5. Chistiakov et al. How do macrophages sense modified low-density lipoproteins? Int J Cardiol. 2017;230:232-240.
  6. Allaire et al. LDL particle number and size and cardiovascular risk: anything new under the sun? Curr Opin Lipidol. 2017;28:261–266.
  7. de la Llera-Moya et al. The ability to promote efflux via ABCA1 determines the capacity of serum specimens with similar high-density lipoprotein cholesterol to remove cholesterol from macrophages. Arterioscler Thromb Vasc Biol. 2010;30:796-801.
  8. Khera et al. Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. NEJM. 2011;380:572-580.
  9. Rosenson et al. Dysfunctional HDL and atherosclerotic cardiovascular disease. Nat Rev Cardiol. 2016;13(1):48-60.
  10. Stampfer et al. Primary prevention of coronary heart disease in women through diet and lifestyle. 2000;343:16-22.
  11. Hu et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. 2001;345:790-797.
  12. De Lorgeril et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation. 1999;99:779-785.
  13. Garcia-Rios et al. New diet trials and cardiovascular risk. Curr Opin Cardiol. 2018;33(4):423-428.
  14. Bhanpuri et al. Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study. Cardiovasc Diabetol. 2018;17(1):56.
  15. Houston et al. . “Niacin doesn’t work and is harmful!” proclaim the headlines. Yet another highly publicized questionable study to discredit integrative medicine. Integr Med (Encinitas). 2014;13(5):8-11.
  16. Hunter et al. Functional foods and dietary supplements for the management of dyslipidemia. Nat Rev Endocrinol. 2017;13(5):278-288.
  17. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106(25):3143-3421.
  18. Gliozzi et al. The effect of bergamot-dervied polyphenolic fraction on LDL small dense particles and non-alcoholic fatty liver disease in patients with metabolic syndrome. Adv Biol Chem. 2014;4(2):129-137.
  19. Millar et al. Effects of dietary flavonoids on reverse cholesterol transport, HDL metabolism, and HDL function. Adv Nutr. 2017;8(2):226-239.
  20. Cicero et al. Lipid-lowering nutraceuticals in clinical practice: position paper from an International Lipid Expert Panel Nutr Rev. 2017;75(9):731-767.
  21. The role of nutraceutical supplements in the treatment of dyslipidemia. J Clin Hypertens (Greenwich). 2012;14(2):121-132.
  22. Weintraub et al. Update on marine omega-3 fatty acids: management of dyslipidemia and current omega-3 treatment options. Atherosclerosis. 2013;230(2):381-389.

Annalouise O’Connor, PhD, RD

Dr. Annalouise O’Connor is the R&D Manager for Therapeutic Platforms and Lead for Cardiometabolic and Obesity platforms at Metagenics. Her role involves research coordination, as well as developing formulas for targeted nutrition solutions and programs to assist practitioners in the optimal management of their patients’ health. Annalouise trained as an RD and worked in clinical and public health settings. Dr. O’Connor completed her PhD in the Nutrigenomics Research Group at University College Dublin (Ireland) and postdoctoral work at the UNC Chapel Hill Nutrition Research Institute.

 

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