Atherosclerosis & arteriosclerosis: Buy online dietary supplement for healthy Heart

BENEFITS OF TAKING CAVSOR FOR PATIENTS WITH ATHEROSCLEROSIS

A number of studies have documented the beneficial cardiovascular effects of increased consumption of n-3 (also called omega-3) and n-6 (omega-6) polyunsaturated fatty acids (PUFAs)[1,2,3,4]. The beneficial effects of PUFAs, in particular their ability to reduce the risk of fatal coronary heart disease and sudden cardiac death, are recognized by the Food and Agriculture Organization (FAO) of the United Nations [5]. Cavsor contains three n-3 (including eicosapentaenoic acid, or EPA, and docosahexaenoic acid, or DHA), two n-6, and one n-9 PUFAs. 

 

Atherosclerosis is a major risk factor for cardiovascular disease [6,7,8] and some of the beneficial effects of PUFAs on cardiovascular health are likely due to their antiatherosclerotic effects [1,9], in particular their anti-inflammatory effects. Although atherosclerosis was traditionally considered as a lipid (mainly cholesterol)-associated disease, the evidence accumulated since the late 1990s has resulted in its recognition as an inflammatory disease, in which both adaptive and innate immune responses play a role [10,11]. Therefore, anti-inflammatory agents are now considered promising for prevention and/or treatment of atherosclerosis. In particular, a study currently underway at the University of Oxford (UK) aims to identify the agents able to inhibit the innate immune responses and to use such agents as anti-atherosclerosis drugs [12]. A number of studies have documented the anti-inflammatory effects of n-3 PUFAs, which are likely to underlie their anti-atherosclerotic effects. Some examples of such studies are described below.

 

Effects of PUFAs on the levels of C-reactive protein

Elevated plasma levels of C-reactive protein (CRP), which is an indicator of inflammation, are a well-known risk factor for the development of atherosclerosis. Inhibitors of HMG CoA-reductase inhibitors (statins), which are used as a mainstream therapy to prevent atherosclerosis and cardiovascular disease because they reduce cholesterol levels, also reduce the levels of CRP [13,14]. Several studies suggest that PUFAs reduce the levels of CRP. A study conducted in Denmark, which enrolled 46 patients with chronic renal failure, found that supplementation with 2.4 g n-3 PUFAs daily for 8 weeks reduced the CRP levels by approximately 40%, although this effect did not reach statistical significance due to a small group of examined patients [15].

 

A study conducted in Japan (511 participants aged 21 to 67 years) found that CRP levels tended to be lower in participants taking EPA, DHA, or both, although these relationships did not reach statistical significance [16]. However, when the results in men were analyzed separately, the effects of both n-3 PUFAs and n-6 PUFAs were significant. The findings that the levels of both n-3 PUFAs and n-6 PUFAs are associated reduced CRP levels are corroborated by a more recent study conducted by the French National Institute of Health and Medical Research (INSERM) enrolling 843 participants, which examined the relationship between the intake of n-3 PUFAs, n-6 PUFAs, and vitamin E on CRP levels [17]. The authors found inverse associations between the intake of either n-3 PUFAs or n-6 PUFAs and elevated CRP levels in participants with low intake of vitamin E. Another study by the same team, which included 2031 participants, found a significant positive association between high n-6:n-3 PUFA intake ratio and elevated CRP [17].

 

Effects of PUFAs on the innate immune response

A study conducted in Norway enrolled 563 elderly men with a high risk of atherosclerosis who received n-3 PUFA supplementation or placebo for 3 years [18]. The authors found that the levels of interleukin-18 were significantly reduced by n-3 PUFA and were significantly negatively correlated with the content of EPA and DHA. Interleukin-18 is one of the two early pro-inflammatory mediators produced by a protein complex called inflammasome, which is activated, among many other stimuli, by oxidized low-density lipoprotein and cholesterol crystals and has been implicated in the development of atherosclerosis [19]. Therefore, the findings by Troseid and colleagues suggest one of the possible mechanisms of the ability of n-3 PUFAs to counteract the development of atherosclerosis [18]. 

 

Effects of n-3 PUFAs on stability of atherosclerotic plaques

Plaque ruptures followed by thrombus formation are immediate causes of heart attack and strokes [6]. A number of studies have been devoted to understanding the factors affecting plaque stability [20]. Some of them have found that increased PUFA consumption is associated with improved plaque stability.

 

 A study conducted in the UK enrolled 162 patients who were awaiting carotid endarterectomy [21]. Before surgery, patients were given capsules of fish oil (as a source of n-3 PUFAs), sunflower oil (as a source of n-6 PUFAs), or did not receive any supplement; supplementation lasted for 1.5 months on average. The authors found increased EPA and DHA content in carotid plaques and fewer plaques with signs of inflammation in patients taking n-3 PUFAs in comparison with the control group, whereas n-6 PUFAs had no such effects [21]. The authors concluded that n-3 PUFA intake increased plaque stability, which might underlie the reduced incidence of cardiovascular events associated with n-3 PUFA intake.

 

In line with these results, a later study found that serum content of EPA and DPA was significantly inversely associated with the number of lipid-rich plaques in coronary arteries of patients suspected of having coronary artery disease, and significantly lower n-3 PUFA levels were found in patients diagnosed with acute coronary syndrome [22].

 

Although fish is a good source of PUFAs, it also contains pollutants from seawater, such as mercury, which makes the health benefits of regularly consuming large amounts of fish questionable [3]. In particular, mercury exposure, at least in young adults, is known to increase the risk of diabetes later in life [23]. Although overall the benefits of fish consumption are considered to outweigh the risks, the authors of a study devoted to evaluating the balance between the benefits and risks of high fish consumption advised to avoid certain fish species [3]. Therefore, PUFA–containing supplements such as Cavsor are a good alternative to fish as a source of these essential fatty acids; such supplements are particularly recommended for people with documented coronary artery disease [24].

 

References

  1. Ander, B.P., Dupasquier, C.M., Prociuk, M.A. & Pierce, G.N. Polyunsaturated fatty acids and their effects on cardiovascular disease. Exp Clin Cardiol 8, 164-172 (2003).
  2. Jakobsen, M.U. et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 89, 1425-1432 (2009).
  3. Mozaffarian, D. & Rimm, E.B. Fish intake, contaminants, and human health: evaluating the risks and the benefits. JAMA 296, 1885-1899 (2006).
  4. Mozaffarian, D., Micha, R. & Wallace, S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 7, e1000252 (2010).
  5. Food and Agriculture Organization of the United Nations. Fats and fatty acids in human nutrition. http://www.fao.org/3/a-i1953e.pdf (2008).
  6. National Health Service, U.K. Atherosclerosis. http://www.nhs.uk/conditions/atherosclerosis/Pages/Introduction.aspx (2014).
  7. National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health & Human Services. What is atherosclerosis? http://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis (2015).
  8. Inaba, Y., Chen, J.A. & Bergmann, S.R. Carotid plaque, compared with carotid intima-media thickness, more accurately predicts coronary artery disease events: a meta-analysis. Atherosclerosis220, 128-133 (2012).
  9. Grenon, S.M., Hughes-Fulford, M., Rapp, J. & Conte, M.S. Polyunsaturated fatty acids and peripheral artery disease. Vasc Med 17, 51-63 (2012).
  10. Seneviratne, A.N. & Monaco, C. Role of inflammatory cells and toll-like receptors in atherosclerosis. Curr Vasc Pharmacol 13, 146-160 (2015).
  11. Stoll, G. & Bendszus, M. Inflammation and atherosclerosis: novel insights into plaque formation and destabilization. Stroke 37, 1923-1932 (2006).
  12. Monaco, C. Inflammation in atherosclerosis. University of Oxford http://www.kennedy.ox.ac.uk/research/inflammation-in-atherosclerosis (2015).
  13. Strandberg, T.E., Vanhanen, H. & Tikkanen, M.J. Effect of statins on C-reactive protein in patients with coronary artery disease. Lancet 353, 118-119 (1999).
  14. Ridker, P.M. et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England J Med 359, 2195-2207 (2008).
  15. Madsen, T., Schmidt, E.B. & Christensen, J.H. The effect of n-3 fatty acids on C-reactive protein levels in patients with chronic renal failure. J Renal Nutr 17, 258-263 (2007).
  16. Poudel-Tandukar, K. et al. Dietary intakes of alpha-linolenic and linoleic acids are inversely associated with serum C-reactive protein levels among Japanese men. Nutr Res 29, 363-370 (2009).
  17. Julia, C. et al. Intakes of PUFAs were inversely associated with plasma C-reactive protein 12 years later in a middle-aged population with vitamin E intake as an effect modifier. J Nutr 143, 1760-1766 (2013).
  18. Troseid, M., Arnesen, H., Hjerkinn, E.M. & Seljeflot, I. Serum levels of interleukin-18 are reduced by diet and n-3 fatty acid intervention in elderly high-risk men. Metab Clin Exp 58, 1543-1549 (2009).
  19. Ozaki, E., Campbell, M. & Doyle, S.L. Targeting the NLRP3 inflammasome in chronic inflammatory diseases: current perspectives. J Inflamm Res 8, 15-27 (2015).
  20. van der Wal, A.C. & Becker, A.E. Atherosclerotic plaque rupture--pathologic basis of plaque stability and instability. Cardiovasc Res 41, 334-344 (1999).
  21. Thies, F. et al. Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomised controlled trial. Lancet 361, 477-485 (2003).
  22. Amano, T. et al. Impact of omega-3 polyunsaturated fatty acids on coronary plaque instability: an integrated backscatter intravascular ultrasound study. Atherosclerosis 218, 110-116 (2011).
  23. He, K. et al. Mercury exposure in young adulthood and incidence of diabetes later in life: the CARDIA Trace Element Study. Diabetes Care 36, 1584-1589 (2013).
  24. Saita, E., Kondo, K. & Momiyama, Y. Anti-Inflammatory Diet for Atherosclerosis and Coronary Artery Disease: Antioxidant Foods. Clin Med Insights Cardiol 8, 61-65 (2015).