Coronary artery disease and stroke account for over 20% of deaths worldwide1 but there are striking variations in age-adjusted
cardiovascular disease (CVD) mortality rates among countries. These international variations are not due to genetic differences among populations. This is evident from trends in rates within countries and changes in rates among migrants moving from low-risk to high-risk countries.
The United States has one of the highest rates of CVD in the world.2 In the most recent year for which data are available, an estimated 15.5 million Americans were affected by coronary heart disease (CHD) alone, which includes myocardial infarction and angina pectoris.
Heart disease strikes someone in the United States every 42 seconds and kills more than 370,000 Americans each year.3

  • Approximately one in seven deaths in the United States is from CHD, which makes it the number-one killer of Americans.3
  • 550,000 Americans have a new coronary attack (defined as first hospitalized myocardial infarction or coronary heart disease death) each year.3
  • 200,000 people have a recurrent coronary attack.3
  • 160,000 people experience silent first myocardial infarctions each year.3

The number of coronary deaths divides approximately evenly between men and women, although the average age of a first heart attack is approximately 64 for men and 70 for women. On the other hand, risk factors such as high blood pressure and diabetes increase heart attack risk in women more severely than in men.4

In 2013, the American Heart Association (AHA) issued new guidelines for the assessment of CVD risk.5 According to the AHA, in addition to age and gender, risk is primarily determined by total cholesterol level, HDL-cholesterol, systolic blood pressure, and whether one smokes and has diabetes.
Evidence indicates that adjusted population attributable fractions for CHD mortality are as follows:
• 34.7% for high blood pressure
• 16.7% for smoking
• 20.6% for poor diet
• 7.8% for insufficient physical activity
• 7.5% for abnormal glucose levels
From the information above, it is clear that dietary choices can significantly impact the risk of developing CHD. While markedly reducing CHD risk via dietary modification requires a comprehensive approach, there is no doubt that soyfoods can play an important role in heart-healthy diets.


Soyfoods have been recognized by nutritionists for decades as rich sources of high-quality protein, but over the past 20 years the effect of soy protein on blood cholesterol levels has attracted attention from the nutrition and medical communities. The first rodent studies6,7 showing that soy protein lowered cholesterol levels were published more than 60 years ago, and the first clinical trial demonstrating this effect was published in 1967.8 Throughout the 1970s and 1980s,
Italian researchers were instrumental in showing that soy protein directly lowered blood cholesterol levels in very hyper-cholesterolemic patients.9-11 Nevertheless, it wasn’t until 1995 that the cholesterollowering effects of soy protein received widespread recognition.

In that year, a meta-analysis of the clinical data, which included 38 different comparisons, found that soy protein reduced low-density lipoprotein cholesterol (LDLC) by approximately 13 percent.12 This reduction was independent of the fatty acid content of soyfoods and, because statins were not yet widely used in clinical practice, the effect of soy protein was similar to that of the available cholesterol-lowering medications.

The results of the 1995 meta-analysis prompted much investigation into the cholesterol-lowering effects of soy protein. Some of this research has been directed at identifying the specific soybean components and mechanisms responsible for cholesterol reduction, whereas other research explored the responses to soy protein in different subpopulations such as hypercholesterolemic individuals and pre and postmenopausal women. In regard to mechanism, some data suggest that cholesterol reduction is a result of the upregulation of hepatic LDL receptors by the peptides formed upon digestion of soy protein.13, 14 Researchers also continue to explore whether isoflavones in soybeans impact the cholesterol-lowering effects of soy protein.15 Soyfoods are uniquely rich sources of these diphenolic compounds.16

In 1999, the U.S. Food and Drug Administration (FDA) approved a health claim for soyfoods and CHD based on the cholesterol-lowering effects of soy protein.17 Claims similar to the FDA claim have been approved in >10 other countries,18 including most recently Canada, which did so in 2014.19 However, despite the large amount of  research upon which the FDA health claim was based, the cholesterollowering ability of soy protein has been challenged in recent years. Some inconsistency in the literature is expected given that many trials involved relatively small sample sizes and that in general about 20% of individuals whose cholesterol levels are elevated do not respond to dietary changes.20

In 2008, the American Heart Association (AHA) formally expressed their opposition to the existing soy health claim. In their 2006 position paper, the AHA acknowledged the important role soyfoods can have in heart-healthful diets because they are low in saturated fat and high in polyunsaturated fat (PUFA).21 However, the decrease in LDLC in 3 response to soy protein, which they estimated to be approximately 3%, based on the results of 22 studies, was insufficient in their view to warrant a health claim.21 The AHA endorsed the health claim in 2000 shortly after it was first issued.22

Importantly, however, the AHA did not conduct a formal statistical meta-analysis of the 22 studies upon which they based their estimate of the potency of soy protein. When such an analysis was conducted, Jenkins et al.23 found that the AHA had considerably underestimated the hypocholesterolemic effects of soy protein since the analysis showed that soy protein lowered LDLC by 4.3 percent. Furthermore, when the analysis was limited to the 11 studies that provided evidence that the control and soy diets were matched for nutrient content, soy protein was found to lower LDLC by 5.2 percent. Over the past decade or so, all of the meta-analyses of the clinical data have found soy protein statistically significantly lowers LDLC.19, 23-26 A conservative  estimate based on the results of these analyses is that soy protein lowers LDLC approximately 4%, which is similar to the effects of soluble fiber, which also has a health claim.27 Since each 1% decrease in LDLC lowers CHD risk by 1-3%, incorporating soy protein into the diet can substantially reduce CHD morbidity and mortality.28, 29 Finally, research shows that soy protein modestly raises high density
lipoprotein cholesterol and lowers circulating triglyceride levels. In addition, soy protein was found to decrease postprandial triglyceride levels, elevated levels of which are increasingly viewed as important for reducing CHD risk.30


In contrast to other legumes which are nearly fat-free, approximately 40% of the calories from soybeans are comprised of fat.31 The fatty acid composition of soy is very heart-healthy as it is comprised of only 12% saturated fat, 29% monounsaturated fat and 59% PUFA (53% linoleic acid and 6% α-linolenic acid).32 The soybean is one of the few good sources of both essential fatty acids and, because of its widespread use in the United States, soy oil accounts for over 40% of the intake of both essential fatty acids.33 Although the omega-3 fatty acid α-linolenic acid (ALA) does not possess the same properties as the long-chain omega-3 fatty acids found in cold-water fish, evidence suggests that ALA has direct coronary benefits; the degree is a matter of some debate.34-36

In 2010, using National Health and Nutrition Examination Survey III population data, Jenkins et al.,23 estimated that as a result of differences in fatty acid intake, when soyfoods replace more traditional sources of protein in the Western diet, LDLC is reduced by 3 to 6 percent. There was a 4% reduction in LDLC when 24g soy protein –
an amount similar to the 25g/day established by FDA as the threshold intake for cholesterol reduction – replaced a comparable amount of the more commonly consumed protein sources. Thus, as a result of the displacement of traditional sources of protein in Western diets (which tend to be high in saturated fat) by soyfoods and the direct effects of soy protein, soyfoods can be expected to decrease LDLC by approximately 8 percent.

In recent years there has been considerable controversy about the impact of saturated fat on CHD risk with some analyses finding no relationship.37 Certainly, it is recognized that not all dietary saturated fatty acids exert the same effect on serum LDLC.38 In addition, the impact of dietary saturated fatty acids on serum LDLC depends upon the type and composition of food in which the saturated fat is consumed. For example, saturated fat in butter raises LDLC to a much greater extent than saturated fat in cheese.39 This finding has been attributed to the high calcium content of cheese, which can form insoluble salts with the saturated fatty acids, preventing them from being absorbed.40

While it is far beyond the scope of this review to examine the relationship between dietary fatty acid intake and CHD risk in depth, data indicate that the impact of saturated fat is dependent upon that which replaces it. To this point, a combined analysis of the Nurses’ Health Study (1980 to 2010, n=84,628) and the Health Professionals Follow-up Study (1986 to 2010, n= 42,908 men) found that replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFA, monounsaturated fat, or carbohydrates from whole grains was associated with a 25%,
15%, and 9% lower risk of CHD, respectively, whereas replacing saturated fat with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk.41 Interestingly, a recent analysis found that in many countries around the world inadequate intake of PUFA contributes much more to CHD mortality than an excess intake of saturated fat.42 Thus, full-fat soyfoods and soybean oil can markedly help to reduce risk of developing CHD.

Nevertheless, despite soy’s cholesterol-lowering effect, some concerns have arisen that too much omega-6 PUFA and, in particular, linoleic acid, may increase CHD risk by increasing inflammation. However, the AHA has rejected concerns about the pro-inflammatory properties of linoleic acid and concluded that omega-6 PUFA plays a critically important role in heart-healthful diets.43 This position is supported by a comprehensive review by Johnson and Fritsche,44 published in 2012, which concluded that “virtually no evidence is available from randomized, controlled intervention studies among healthy, non-infant human beings to show that addition of LA [linoleic acid] to the diet increases the concentration of inflammatory markers.”

One reason for this lack of effect may be because, although linoleic acid is converted to arachidonic acid (AA) from which a number of proinflammatory eicosanoids are produced, tissue levels of AA don’t substantially increase because they are tightly regulated.45 Also, it is now recognized that not all of the eicosanoids produced from AA are pro-inflammatory; some in fact may be anti-inflammatory.46 Interestingly, in eightweek-old male C57Bl/6 mice, diets high in saturated and monounsaturated fat increased pro-inflammatory markers in the liver and adipose tissue whereas no such effects were noted in animals fed diets high in linoleic acid.4


There is epidemiologic evidence that soyfoods exert coronary benefits independent of their effect on blood cholesterol levels. For example, • In Shanghai, a prospective study involving nearly 65,000 postmenopausal women found after controlling for a variety of factors that soy protein intake was associated with an 86%
reduction in the risk of non-fatal myocardial infarction.48

• In China, a cross-sectional study involving 406 adults ages 40 to 65 years old (134 males, 272 females) without confirmed relevant diseases, found that soyfood intake was inversely related to bifurcation intima-media thickness, although the association was more apparent in men than women.49

• In Japan, a prospective study involving 40,462 participants, ages 40 to 59 years old without cardiovascular disease or cancer at baseline, found that when comparing women with frequent (≥5x/week) versus infrequent (≤2x/week) soy consumption, the
multivariable hazard ratios were 0.64, 0.55 and 0.31 for risk of the incidence of cerebral infarction, myocardial infarction and CHD mortality, respectively.50 However, there was only a nonsignificant trend toward a protective effect of soy among men. In contrast to the above studies, in Singapore, a prospective study
involving 63,257 Chinese adults aged 45-74 years, found soy intake was unrelated to mortality in either men or women after 890,473


person-years of follow-up.51 Also, a large prospective study from Shanghai found that over the 5.4-year follow-up period, soy intake was associated with an increased risk of CHD among men.52 This finding comes from a study that was published as a letter to the editor and is inconsistent with the prospective studies from Japan50 and Singapore;51 nevertheless, this result warrants additional investigation.

For at least two reasons, it is highly unlikely that the cholesterollowering effects of soyfoods were primarily responsible for the protective effects observed in the prospective studies from Japan50 and Shanghai48 and the cross-sectional study from China.49 First, soy protein consumption in the upper intake categories was between eight and 16g/day, which, based on the results from the clinical studies, is likely too little to lower cholesterol. Second, the protective effects were far greater than could be expected from the cholesterol reduction typically associated with soy protein. Perhaps the explanation is a “healthy user effect,” i.e., that soyfood consumption is associated with an overall healthier lifestyle. This explanation is unlikely, however, because most of the studies controlled for a wide range of potentially confounding variables. Also, soy consumption in Asia is much less reflective of an overall lifestyle than it is in countries where soyfoods have not been part of the traditional diet.


In support of the epidemiologic studies, which found inverse relationships between CHD risk and soy intake, are various clinical studies that show soyfoods, soy protein or soybean isoflavones favorably affect a number of biological measures that impact heart disease risk. For example, four recently published meta-analyses concluded that soy modestly lowers blood pressure.53-56 In the largest of these, which included 27 studies, soy lowered systolic and diastolic blood pressure by 2.21 and 1.44 mgHg, respectively.54 Reducing systolic blood pressure by just 2-5mmHg may reduce stroke and CHD disease by 6-14% and 5-9%, respectively.57


Two meta-analyses have found that soybean isoflavones improved endothelial function in postmenopausal women.58, 59 Endothelial cells line the blood vessels and their functioning can impact CHD risk. When the data from one of these meta-analyses were sub-analyzed, the improvement was only found in those women who had impaired endothelial function at baseline.58 Of course, these women are at greater risk of having or developing CHD. This finding provides an explanation for the inconsistent literature in that some studies included women with both impaired endothelial function and others with normal endothelial function. It may also be that some of the observed anti-inflammatory effects of isoflavones occur only in people at
risk of CHD who have elevated levels of inflammatory markers.60


Unlike endothelial-mediated vasodilation (primarily nitric oxidedependent), arterial compliance relates to the constriction and dilation of arteries associated with systole and diastole. Arterial compliance is determined by components of the artery wall, such as elastin, proteoglycans and smooth muscle cell function. The most straightforward, valid, and reliable measure of arterial stiffness is pulse wave velocity (PWV), which is predictive of future cardiovascular events.61

In 2011, a systematic review by Pase et al.62 concluded on the basis of five studies63-67 that isoflavones reduce arterial stiffness, although one of the four that reported benefit intervened with an isoflavone metabolite.67 Three additional studies not reviewed by Pase et al.62 are supportive of the ability of isoflavones to improve arterial compliance in postmenopausal women.68-70 Conversely, no differences in arterial compliance were noted in a small group of hypercholesterolemic men and women when comparing a soymilk/soy yogurt intervention with a dairy milk/yogurt intervention.71


Subclinical atherosclerosis can be assessed using ultrasound to measure the thickness of the carotid arteries, which are located on both sides of the neck beneath the jawline and provide the main blood supply to the brain. The thickness of the carotid artery is referred to as carotid intima-media thickness or CIMT. Typically, CIMT increases or progresses over time; the extent of progression reflects risk of future coronary events.
An important clinical trial to evaluate the impact of soy on CIMT is the Women’s Isoflavone Soy Health (WISH) study, a 3-year study involving 350 healthy postmenopausal women ages 45 to 92. Based on changes in CIMT, this study found that isoflavone-rich soy protein inhibited the progression of subclinical atherosclerosis.72 Participants in the WISH study were randomly assigned to groups consuming either 25g of isolated soy protein or 25g of milk protein per day. The soy protein provided 91mg of isoflavones (expressed in aglycone equivalent weight).

At study termination, progression among the women consuming soy was 16% lower than in the milk group. Furthermore, the difference between groups increased steadily over the 3-year study period. This suggests that after a longer period of soy exposure, progression would have been reduced to an even greater extent, and with it, risk of coronary events. Additionally, subanalysis of the results revealed that among women who were fewer than five years, five to 10 years, and more than 10 years post-menopause, CIMT progression was reduced by 68 (p=0.05), 17 (p=0.51) and 9% (p=0.77), respectively. That progression was reduced so significantly in early postmenopausal women is notable for two reasons.

First, it adds substantially to the biologically plausibility of the findings and second, it provides clear insight into the soy component responsible for the beneficial effects. The pronounced effect in early menopausal women suggests isoflavones were primarily responsible for the reduced CIMT progression because over the past 15 years
a hypothesis has emerged, referred to as the “estrogen timing hypothesis,” which maintains that exposure to estrogen-like compounds leads to dramatic coronary benefits when begun soon after menopause, but has less effect in later years.72


In summary, soyfoods can make important contributions to hearthealthful diets through several different mechanisms. They provide high-quality protein but minimal amounts of saturated fat. They provide ample amounts of omega-6 and omega-3 essential fatty acids. Soy protein directly lowers blood LDLC levels, modestly elevates high density lipoprotein cholesterol levels and decreases triglyceride levels. Furthermore, soyfoods appear to favorably affect CHD risk factors independent of lipid levels; for example, improving endothelial function and systematic arterial compliance and lowering blood pressure.

1. Mathers, C.D. and D. Loncar, Projections of global mortality and burden of disease from 2002 to 2030. PLoS
Med, 2006. 3(11): p. e442.
2. MacMahon, S., et al., Blood pressure, stroke, and coronary heart disease. Part 1, Prolonged differences in blood
pressure: prospective observational studies corrected for the regression dilution bias. Lancet, 1990. 335(8692):
p. 765-74.
3. Mozaffarian, D., et al., Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart
Association. Circulation, 2016. 133(4): p. e38-e360.
4. Mehta, L.S., et al., Acute myocardial infarction in women: A scientific statement from the American Heart
Association. Circulation, 2016.
5. Pan, W.H., et al., Diet and health trends in Taiwan: comparison of two nutrition and health surveys from 1993-
1996 and 2005-2008. Asia Pac J Clin Nutr, 2011. 20(2): p. 238-50.
6. Meeker, D.R. and D. Kesten, Effect of high protein diets on experimental atherosclerosis of rabbits. Arch Pathol,
1941. 31: p. 147-162.
7. Meeker, D.R. and H.D. Kesten, Experimental atherosclerosis and high protein diets. Proc Soc Exp Biol Med,
1940. 45: p. 543-545.
8. Hodges, R.E., et al., Dietary carbohydrates and low cholesterol diets: effects on serum lipids on man. Am J Clin
Nutr, 1967. 20(2): p. 198-208.
9. Sirtori, C.R., et al., Soybean-protein diet in the treatment of type-II hyperlipoproteinaemia. Lancet, 1977. 1(8006):
p. 275-7.
10. Sirtori, C.R., et al., Clinical experience with the soybean protein diet in the treatment of hypercholesterolemia. Am
J Clin Nutr, 1979. 32(8): p. 1645-58.
11. Sirtori, C.R., et al., Cholesterol-lowering and HDL-raising properties of lecithinated soy proteins in type II
hyperlipidemic patients. Ann Nutr Metab, 1985. 29(6): p. 348-57.
12. Anderson, J.W., B.M. Johnstone, and M.E. Cook-Newell, Meta-analysis of the effects of soy protein intake on
serum lipids. N Engl J Med, 1995. 333(5): p. 276-82.
13. Cho, S.J., M.A. Juillerat, and C.H. Lee, Cholesterol lowering mechanism of soybean protein hydrolysate. J Agric
Food Chem, 2007. 55(26): p. 10599-604.
14. Manzoni, C., et al., Subcellular Localization of Soybean 7S Globulin in HepG2 Cells and LDL Receptor Up-
Regulation by Its alpha’ Constituent Subunit. J Nutr, 2003. 133(7): p. 2149-55.
15. Zhuo, X.G., M.K. Melby, and S. Watanabe, Soy Isoflavone Intake Lowers Serum LDL Cholesterol: A Meta-
Analysis of 8 Randomized Controlled Trials in Humans. J Nutr, 2004. 134(9): p. 2395-400.
16. Kuiper, G.G., et al., Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta.
Endocrinology, 1998. 139(10): p. 4252-63.
17. Food Labeling: Health Claims; Soy Protein and Coronary Heart Disease, in Federal Register: (Volume 64,
Number 206)]1999. p. 57699-57733.
18. Xiao, C.W., Health effects of soy protein and isoflavones in humans. J Nutr, 2008. 138(6): p. 1244S-9S.
19. Benkhedda, K.B., B, et al., Food Risk Analysis Communication. Issued By Health Canada’s Food Directorate.
Health Canada’s Proposal to Accept a Health Claim about Soy Products and Cholesterol Lowering. Int Food Risk
Anal J, 2014. 4:22 | doi: 10.5772/59411.
20. Denke, M.A., B. Adams-Huet, and A.T. Nguyen, Individual cholesterol variation in response to a margarine- or
butter-based diet: A study in families. JAMA, 2000. 284(21): p. 2740-7.
21. Sacks, F.M., et al., Soy protein, isoflavones, and cardiovascular health: an American Heart Association Science
Advisory for professionals from the Nutrition Committee. Circulation, 2006. 113(7): p. 1034-44.
22. Erdman, J.W., Jr., Soy protein and cardiovascular disease: A statement for healthcare professionals from the
nutrition committee of the AHA. Circulation, 2000. 102(20): p. 2555-9.
23. Jenkins, D.J., et al., Soy protein reduces serum cholesterol by both intrinsic and food displacement mechanisms.
J Nutr, 2010. 140(12): p. 2302S-2311S.
24. Anderson, J.W. and H.M. Bush, Soy protein effects on serum lipoproteins: A quality assessment and metaanalysis
of randomized, controlled studies. J Am Coll Nutr, 2011. 30(2): p. 79-91.
25. Zhan, S. and S.C. Ho, Meta-analysis of the effects of soy protein containing isoflavones on the lipid profile. Am J
Clin Nutr, 2005. 81(2): p. 397-408.
26. Harland, J.I. and T.A. Haffner, Systematic review, meta-analysis and regression of randomised controlled
trials reporting an association between an intake of circa 25 g soya protein per day and blood cholesterol.
Atherosclerosis, 2008. 200(1): p. 13-27.
27. Brown, L., et al., Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr, 1999. 69(1): p.
28. Law, M.R., N.J. Wald, and S.G. Thompson, By how much and how quickly does reduction in serum cholesterol
concentration lower risk of ischaemic heart disease? BMJ, 1994. 308(6925): p. 367-72.
29. Law, M.R., et al., Systematic underestimation of association between serum cholesterol concentration and
ischaemic heart disease in observational studies: data from the BUPA study. BMJ, 1994. 308(6925): p. 363-6.
30. Santo, A.S., et al., Postprandial lipemia detects the effect of soy protein on cardiovascular disease risk compared
with the fasting lipid profile. Lipids, 2010. 45(12): p. 1127-38.
31. Messina, M.J., Legumes and soybeans: overview of their nutritional profiles and health effects. Am J Clin Nutr,
1999. 70(3 Suppl): p. 439S-450S.
32. Hayes, K.C., Dietary fatty acids, cholesterol, and the lipoprotein profile. Br J Nutr, 2000. 84(4): p. 397-9.
33. Blasbalg, T.L., et al., Changes in consumption of omega-3 and omega-6 fatty acids in the United States during
the 20th century. Am J Clin Nutr, 2011. 93(5): p. 950-62.
34. Brouwer, I.A., M.B. Katan, and P.L. Zock, Dietary alpha-linolenic acid is associated with reduced risk of fatal
coronary heart disease, but increased prostate cancer risk: a meta-analysis. J Nutr, 2004. 134(4): p. 919-22.
35. Holguin, F., et al., Cardiac autonomic changes associated with fish oil vs soy oil supplementation in the elderly.
Chest, 2005. 127(4): p. 1102-7.
36. Whelan, J., Dietary stearidonic acid is a long chain (n-3) polyunsaturated fatty acid with potential health benefits.
J Nutr, 2009. 139(1): p. 5-10.
37. Chowdhury, R., et al., Association of dietary, circulating, and supplement fatty acids with coronary risk: a
systematic review and meta-analysis. Ann Intern Med, 2014. 160(6): p. 398-406.
38. Kris-Etherton, P.M. and S. Yu, Individual fatty acid effects on plasma lipids and lipoproteins: human studies. Am J
Clin Nutr, 1997. 65(5 Suppl): p. 1628S-1644S.
39. Hjerpsted, J., E. Leedo, and T. Tholstrup, Cheese intake in large amounts lowers LDL-cholesterol concentrations
compared with butter intake of equal fat content. Am J Clin Nutr, 2011. 94(6): p. 1479-84.
40. Soerensen, K.V., et al., Effect of dairy calcium from cheese and milk on fecal fat excretion, blood lipids, and
appetite in young men. Am J Clin Nutr, 2014. 99(5): p. 984-91.
41. Li, Y., et al., Saturated fats compared with unsaturated fats and sources of carbohydrates in relation to risk of
coronary heart Disease: A prospective cohort study. J Am Coll Cardiol, 2015. 66(14): p. 1538-48.
42. Wang, Q., et al., Impact of nonoptimal intakes of saturated, polyunsaturated, and trans fat on global burdens of
coronary heart disease. J Am Heart Assoc, 2016. 5(1).
43. Harris, W.S., et al., Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the
American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and
Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation, 2009.
119(6): p. 902-7.
44. Johnson, G.H. and K. Fritsche, Effect of dietary linoleic acid on markers of inflammation in healthy persons: A
systematic review of randomized controlled trials. J Acad Nutr Diet, 2012. 112: p. 1029-1041.
45. Rett, B.S. and J. Whelan, Increasing dietary linoleic acid does not increase tissue arachidonic acid content in
adults consuming Western-type diets: a systematic review. Nutr Metab (Lond), 2011. 8: p. 36.
46. Harris, W.S. and G.C. Shearer, Omega-6 fatty acids and cardiovascular disease: friend, not foe? Circulation,
2014. 130(18): p. 1562-4.
47. Vaughan, R.A., et al., A high linoleic acid diet does not induce inflammation in mouse liver or adipose tissue.
Lipids, 2015. 50(11): p. 1115-22.
48. Zhang, X., et al., Soy food consumption is associated with lower risk of coronary heart disease in Chinese
women. J Nutr, 2003. 133(9): p. 2874-8.
49. Zhang, B., et al., Greater habitual soyfood consumption is associated with decreased carotid intima-media
thickness and better plasma lipids in Chinese middle-aged adults. Atherosclerosis, 2008. 198(2): p. 403-11.
50. Kokubo, Y., et al., Association of dietary intake of soy, beans, and isoflavones with risk of cerebral and myocardial
infarctions in Japanese populations: the Japan Public Health Center-based (JPHC) study cohort I. Circulation,
2007. 116(22): p. 2553-62.
51. Talaei, M., et al., Dietary soy intake is not associated with risk of cardiovascular disease mortality in Singapore
Chinese adults. J Nutr, 2014. 144(6): p. 921-8.
52. Lewington, S., et al., Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of
individual data for one million adults in 61 prospective studies. Lancet, 2002. 360(9349): p. 1903-13.
53. Hooper, L., et al., Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized
controlled trials. Am J Clin Nutr, 2008. 88(1): p. 38-50.
54. Dong, J.Y., et al., Effect of soya protein on blood pressure: a meta-analysis of randomised controlled trials. Br J
Nutr, 2011. 106(3): p. 317-26.
55. Taku, K., et al., Effects of soy isoflavone extract supplements on blood pressure in adult humans: systematic
review and meta-analysis of randomized placebo-controlled trials. J Hypertens, 2010. 28(10): p. 1971-82.
56. Liu, X.X., et al., Effect of soy isoflavones on blood pressure: A meta-analysis of randomized controlled trials. Nutr
Metab Cardiovasc Dis, 2012. 22(6): p. 463-70.
57. Stamler, R., Implications of the INTERSALT study. Hypertension, 1991. 17(1 Suppl): p. I16-20.
58. Li, S.H., et al., Effect of oral isoflavone supplementation on vascular endothelial function in postmenopausal
women: a meta-analysis of randomized placebo-controlled trials. Am J Clin Nutr, 2010. 91(2): p. 480-6.
59. Beavers, D.P., et al., Exposure to isoflavone-containing soy products and endothelial function: A Bayesian metaanalysis
of randomized controlled trials. Nutr Metab Cardiovasc Dis, 2012. 22(3): p. 182-91.
60. Fuchs, D., et al., Proteomic biomarkers of peripheral blood mononuclear cells obtained from postmenopausal
women undergoing an intervention with soy isoflavones. Am J Clin Nutr, 2007. 86(5): p. 1369-75.
61. Vlachopoulos, C., K. Aznaouridis, and C. Stefanadis, Prediction of cardiovascular events and all-cause mortality
with arterial stiffness: a systematic review and meta-analysis. J Am Coll Cardiol, 2010. 55(13): p. 1318-27.
62. Pase, M.P., N.A. Grima, and J. Sarris, The effects of dietary and nutrient interventions on arterial stiffness: a
systematic review. Am J Clin Nutr, 2011. 93(2): p. 446-54.
63. Teede, H.J., et al., Dietary soy has both beneficial and potentially adverse cardiovascular effects: a placebocontrolled
study in men and postmenopausal women. J Clin Endocrinol Metab, 2001. 86(7): p. 3053-60.
64. Teede, H.J., et al., Isoflavones reduce arterial stiffness: a placebo-controlled study in men and postmenopausal
women. Arterioscler Thromb Vasc Biol, 2003. 23(6): p. 1066-71.
65. Tormala, R., et al., Equol production capability is associated with favorable vascular function in postmenopausal
women using tibolone; no effect with soy supplementation. Atherosclerosis, 2008. 198(1): p. 174-8.
66. Nestel, P.J., et al., Soy isoflavones improve systemic arterial compliance but not plasma lipids in menopausal and
perimenopausal women. Arterioscler Thromb Vasc Biol, 1997. 17(12): p. 3392-8.
67. Nestel, P., A. Fujii, and L. Zhang, An isoflavone metabolite reduces arterial stiffness and blood pressure in
overweight men and postmenopausal women. Atherosclerosis, 2007. 192(1): p. 184-9.
68. Nestel, P.J., et al., Isoflavones from red clover improve systemic arterial compliance but not plasma lipids in
menopausal women. J Clin Endocrinol Metab, 1999. 84(3): p. 895-8.
69. Curtis, P.J., et al., Vascular function and atherosclerosis progression after 1 y of flavonoid intake in statin-treated
postmenopausal women with type 2 diabetes: a double-blind randomized controlled trial. Am J Clin Nutr, 2013.
97(5): p. 936-42.
70. Reverri, E.J., et al., Soy provides modest benefits on endothelial function without affecting inflammatory
biomarkers in adults at cardiometabolic risk. Mol Nutr Food Res, 2015. 59(2): p. 323-33.
71. Meyer, B.J., et al., Limited lipid-lowering effects of regular consumption of whole soybean foods. Ann Nutr Metab,
2004. 48(2): p. 67-78.
72. Hodis, H.N. and W.J. Mack, A “window of opportunity:” The reduction of coronary heart disease and total
mortality with menopausal therapies is age- and time-dependent. Brain Res, 2011. 1379: p. 244-52.

Visit : www.sharrets.com/

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s