Our Number One Killer

Written By Jessica Zabow

What is Cardiovascular Disease?

Cardiovascular disease (CVD) encompasses four conditions, one of which is coronary artery disease (1). Coronary artery disease (CAD) represents one-third to one-half of CVD incidence, and involves insufficient blood circulating through the heart, which can lead to angina or chest pain. Unfortunately, heart attack and/or heart failure may also ensue.

While cardiovascular mortality has recently declined due to medical and pharmaceutical interventions, it remains a leading cause of death, with over 17 million deaths globally in 2013 (4). In Australia, one in five people aged 45-74 are at high risk of a CVD event within five years, and in 2010 there were almost half a million hospitalisations primarily related to CVD (4).

The underlying pathophysiology for CVD is atherosclerosis (2). This is a narrowing of the arteries. The disease process involves a build up of cholesterol into the artery wall, and subsequent immune responses that lead to inflammation, cellular accumulation, and plaque formation (3). Plaques can rupture leading to a clot, also known as thrombosis (5). When this occurs in the heart it causes a heart attack, and when it occurs in the brain it causes is a stroke.

The primary risk factors include age, male sex, high blood pressure, high cholesterol, obesity, and high blood sugar (18). Age is associated with increased risk likely due to a greater exposure to other risk factors, especially high cholesterol and blood pressure.

Unfortunately for many people, the first symptom of CVD is a fatal heart attack (2). However, atherosclerosis develops decades prior to such an acute event (2).

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Atherosclerosis: The Beginnings

It may surprise you to learn that fatty streaks on arteries, the initial stages of atherosclerosis, actually occur in utero (6). While these fatty streaks disappear later in childhood they do, however, come back in adolescence (5).

This idea was first brought to light in a 1993 study that looked at autopsies of American soldiers who had died in the Korean War from non-cardiac trauma. The average age of the cohort was only 26 years. Amazingly, they found coronary atherosclerosis (plaque build up in the primary arteries of the heart) in 78.3% of subjects. Of these cases, over 50% narrowing was seen in 20.7% and over 75% narrowing in 9% of subjects (7). This means that advanced CAD was present within a group of seemingly healthy young men.

A 1998 study analysed the hearts of 204 people between 2 and 39 years of age who had passed away (8). They found that fatty streaks on the coronary arteries were present in 50% of 2-15 year olds, and in 85% of 21-39 year olds. More developed atherosclerosis in the form of fibrous plaques was seen in 8% of 2-15 year olds, and 69% of 26-39 year olds. If CAD appears to be prevalent in young people, perhaps this is just normal? Comparative epidemiological (population) studies will help us answer this question!

Epidemiological studies indicate that this process of atherosclerosis does not occur universally. A 1977 study investigated the incidence of coronary heart disease deaths in Japanese people living in Japan, Hawaii, and California (9). They found the incidence rate to be lowest in Japan, with half that rate of Hawaii, and that California had the highest incidence, with 50% more cases than Hawaii. They credited these differences to Westernised lifestyle, which has been described elsewhere involving high-fat diets (particularly saturated fat) and sedentary lifestyles (10).

This evidence highlights that the development of heart disease begins long before a heart attack, but what actually causes atherosclerosis?

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LDL Cholesterol: A Key Driver

There is a very clear link between LDL cholesterol (LDL-C) levels and risk of heart disease. The study I mentioned earlier that investigated fatty streaks in foetal arteries actually found that the babies with the largest fatty streaks had mothers with high LDL-C (6). Similarly, the study looking at the 204 deceased young people found LDL-C levels were positively associated with fatty streak and fibrous plaque presentation - the higher the LDL-C, the more severe the atherosclerosis (8).

LDL-C is the key deliverer of cholesterol into the artery wall, the beginning stage of atherosclerosis and heart disease (11). LDL-Cholesterol is synthesised in the liver, however there are certain dietary factors that increase it. These are saturated fats, trans fats, cholesterol, and refined sugar (specifically fructose) (12, 13, 14, 15). Top sources of these foods are listed below:

  • Saturated fat: dairy fat, meat, coconut & palm oil (found in processed foods)

  • Trans fats: margarine, shortening, & processed foods (beware of hydrogenated oils!)

  • Cholesterol: eggs, liver, shellfish, & meat

  • Fructose: sugar sweetened beverages & processed foods

You may have heard that it doesn’t matter if your LDL “bad” cholesterol is high if your HDL “good” cholesterol is also high. Unfortunately this is not the case. Cardiovascular outcomes are not improved when HDL levels are increased medically, nor do people with genetically high HDL see lower CVD risk (16). HDL can remove cholesterol built up in arteries and return it to the liver to be removed from the body through the digestive system. However, this only occurs when it is functioning properly. HDL levels do not indicate the degree to which this process is occurring adequately. One study found that a high saturated fat meal reduced the anti-inflammatory properties of HDL, whereas a high polyunsaturated fat meal enhanced it - further highlighting the importance of our dietary choices on our cardiovascular health (17).

Polyunsaturated fats are found in fish, nuts, seeds, avocado, and soy foods in varying amounts. High intakes of both cholesterol and saturated fat together have actually been found to significantly increase LDL-C (19). This means that pairing eggs (high in cholesterol) with dairy or meat (high in saturated fat) is really not heart healthy. Plus, meat and dairy contain BOTH saturated fat and cholesterol together.

But what is a healthy LDL-C level?

Victoria Health suggests people who have risk factors like high blood pressure should get their LDL-C below 2 mmol/L (~77 mg/dl) (22). However, one study investigated the level of atherosclerosis in several main arteries using an imaging technique. The 4,184 participants had no cardiovascular risk factors (18). A clear relationship was found between LDL-C and severity of atherosclerosis. Those with under 80 mg/dl (2.07 mmol/L) had significantly less plaque build up. BUT, only those with 50-60 mg/dl (1.3-1.6 mmol/L) had NONE! But 1.3-1.6 mmol/L is a lot less than the 2 mmol/L recommendation for at-risk people. And this study’s participants were low risk!

What do we learn from this? The recommendations for LDL-C are too high. We need to get our cholesterol lower.

The good news … we can do it through diet.

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Nutrients & Food Groups - Put to the Test

The most important question to ask when investigating the overall healthfulness, or specific health effect, of a food is COMPARED TO WHAT? This question is often left out of the conversation, leading people to the wrong conclusion. This is fodder for tantalising nutrition claims and headlines that capture attention, sell products, and confuse the masses. The truth is: anything can be made to appear healthy in a scientific investigation if you are comparing it to something that is less healthy. There is always a spectrum: more healthy doesn’t necessarily mean healthy in general.

When it comes to heart disease risk, the message is clear as day. There have been several studies that swap nutrients or food groups for others and observe the effects on heart disease risk.

One study looked at the effects of swapping dairy fat for other sources of fat or food groups. It included over 220,000 people and encompassed over 5 MILLION person-years - allowing great scope for data analysis to determine relationships between dietary patterns and CVD occurrence (20).

This is what they found when 5% of energy from dairy fat was replaced by the same amount of calories of different nutrients/foods:


  • Carbohydrates (refined starches & added sugars): reduced CVD risk by 3%

  • Carbohydrates (whole grains): reduced CVD risk by 28%

  • Polyunsaturated fats: reduced CVD risk by 24%

  • Vegetable fats: reduced CVD risk by 10%

  • Other animal fat (meat): increased CVD risk by 6%


Notice here that there was a whopping 25% difference in reduced CVD risk between refined and whole carbohydrates. This is why it is so important to have a dialogue around specific foods rather than nutrients. Whole food carbohydrates are completely different from refined carbohydrates in so many ways. It is clear looking at this data that grouping them in together and omitting whole carbohydrates like whole grains just because they inherently are carbohydrates is not a good idea. The same can be said for “fat”. Saturated fats (high in meat and dairy) should clearly be kept low, but polyunsaturated fats definitely have been shown to be healthy!

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An Holistic Clinical Intervention

Dr Dean Ornish delivered an integrative intervention to patients with moderate to severe coronary heart disease (21). Twenty patients completed five years of the experimental program, which included a low-fat vegetarian diet (low in saturated fat and cholesterol and high in fibre), aerobic exercise, stress management, smoking cessation, and group social support. A control group applied only moderate diet and lifestyle change. Imaging techniques were used to measure percentage of artery blockages (severity of atherosclerosis).

The group who applied rigorous diet and lifestyle change saw a 4.5% improvement in atherosclerosis after one year, and 7.9% improvement after five years. The control group, after one year, had a 5.4% worsening in their artery blockage and after five years a 27.7% worsening. Within the five years of the study, those in the control group were almost 2.5 times more likely to experience a cardiac event. These remarkable differences in arterial stenosis (blockage) and cardiac events occurred even though half the control group were actually using statins (cholesterol-lowering medication) by the end for the five year study. The experimental group did not use ANY medications.

This study is a testament to how making holistic change can alter your health trajectory - even for those who are already suffering disease. The control group applied “moderate” change, and they saw “moderate” results - 2.5 times the likelihood of a heart attack. Moderation in intervention produces moderation in outcomes.

For our number one killer we don’t need moderation … we need a complete overhaul.

I hope upon reading this article on CVD that you have improved your understanding about what heart disease is, how it develops, and that it is possible reduce our risk through diet and lifestyle changes. There is a lot of misinformation out there about this topic - especially the role of cholesterol and saturated fat. But the science is clear: a diet that is low in saturated fat, trans fat, cholesterol and refined sugars, and high in dietary fibre and polyunsaturated fats is the best dietary pattern we can follow for heart health.

According to two other successful intervention studies (23, 24), the best foods for heart health are:

  • Whole grains (e.g. brown rice, barley, steel cut/rolled oats)

  • Soy (e.g. edamame, tofu, tempeh, whole soy beans)

  • Unsalted and raw nuts & seeds (e.g. walnuts, flax seeds, chia seeds, almonds)

  • Legumes (e.g. lentils, chickpeas, beans)

  • And of course antioxidant-rich fruits & vegetables


If you would like advice to assist you in reducing your risk of CVD or in assisting management of your CVD in a comprehensive and holistic way, I am available for consultations. I also help with many other health and lifestyle concerns. Click here for more information.

 

By Jessica Zabow
Clinical Nutritionist (BHSc)
& Yoga Teacher (RYT500)

 
 
 

References:

  1. Lopez, E.O., Ballard, B.D., & Jan, A. (2021). Cardiovascular disease. StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK535419/

  2. Ambrose, J.A., & Singh, M. (2015). Pathophysiology of coronary artery disease leading to acute coronary syndromes. F1000Prime Reports, 7(1), 1-5. https://doi.org/10.12703/P7-08

  3. Bergheanu, S.C., Bodde, M.C., & Jukema, J.W. (2017). Pathophysiology and treatment of atherosclerosis. Netherland Heart Journal, 25(1), 231-242. https://doi.org/10.1007/s12471-017-0959-2

  4. Peng, Y., & Wang, Z. (2018). Cardiovascular health status among Australian adults. Clinical Epidemiology, 10(1), 167-178. https://doi.org/10.2147/CLEP.S155783

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  6. Napoli, C., D’Armiento, F.P., Mancini, F.P., Postiglione, A., Witztum, J.L., Palumbo, G., & Palinski, W. (1997). Fatty streak formation occurs in human foetal aortas and is greatly enhanced by maternal hypercholesterolaemia. Journal of Clinical Investigation, 100(11), 2680-2690. https://doi.org/10.1172/JCI119813

  7. Joseph, A., Ackerman, D., Johnstone, J., & Kupersmith, J. (1993). Manifestations of coronary atherosclerosis in young trauma victims - An autopsy study. Journal of the American College of Cardiology, 22(2), 459-467. https://doi.org/10.1016/0735-1097(93)90050-B

  8. Brenson, G.S., Srinivasan, S.R., Bao, W., Newman, W.P., Tracy, R.E., & Wattigney, W.A. (1998). Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The New England Journal of Medicine, 338(23), 1650-1656. https://doi.org/10.1056/NEJM199806043382302

  9. Robertson, T.L., Kato, H., Rhoads, G.G., Kagan, A., Marmot, M., Syme, S.L., … Kawamoto, S., (1977). Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California. The American Journal of Cardiology, 39(2), 239-243. https://doi.org/10.1016/s0002-9149(77)80197-5

  10. Iso, H. (2008). Changes in coronary heart disease risk among Japanese. Circulation, 118(25), 2725-2729. https://doi.org/10.1161/CIRCULATIONAHA.107.750117

  11. Boren, J., Chapman, M.J., Krauss, R.M., Packard, C.J., Bentzon, J.F., Binder, C.J., … Ginsberg, H.N. (2020). Low-density lipoproteins cause atherosclerotic cardiovascular disease: Pathophysiological, genetic, and therapeutic insights. European Heart Journal, 41(24), 2313-2330. https://doi.org/10.1093/eurheartj/ehz962

  12. Li, Y., Hruby, A., Bernstein, A.M., Ley, S.H., Wang, D.D., Chiuve, S.E., … Hu, F.B. (2015). Saturated fats compared with unsaturated fats and sources of carbohydrates in relation to risk of coronary heart disease. Journal of the American College of Cardiology, 66(14), 1538-1548. https://doi.org/10.1016/j.jacc.2015.07.055

  13. Takeuchi, H., & Sugano, M. (2017). Industrial Trans fatty acid and serum cholesterol: The allowable dietary level. Journal of Lipids, 2017(9751756), 1-10. https://doi.org/10.1155/2017/9751756

  14. Sikaroudi, M.K., Soltani, S., Kolahdouz-Mohammadi, R., Clayton, Z.S., Fernandez, M.L., … Shidfar, F. (2020). The responses of different dosages of egg consumption on blood lipid profile: An updated systematic review and meta-analysis of randomised clinical trials. Journal of Food Biochemistry, 44(8), 1-29. https://doi.org/10.1111/jfbc.13263

  15. Stanhope, K.L., Schwarz, J.M., Keim, N.L., Griffen, S.C., Bremer, A.A., Graham, J.L. … Havel, P.J. (2009). Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. The Journal of Clinical Investigations, 119(5), 1322-1334. https://doi.org/10.1172/JCI37385

  16. Rohatgi, A., Khera, A., Berry, J.D., Givens, E.G., Ayers, C.R., Wedin, K.E., … Shaul, P.W. (2014). HDL cholesterol efflux capacity and incident cardiovascular events. The New England Journal of Medicine, 371(25), 2383-2393. https://doi.org/10.1056/NEJMoa1409065

  17. Nicholls, S.J., Lundman, P., Harmer, J.A., Cutri, B., Griffiths, K.A., Rye, K., & Barter, P.J. (2006). Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. Journal of the American College of Cardiology, 48(4), 715.720. https://doi.org/10.1016/j.jacc.2006.04.080

  18. Fernandez-Friera, L., Fuster, V., Lopez-Melgar, B., Oliva, B., Garcia-Ruiz, J.M., Mendiguren, J., … Sanz, J. (2017). Normal LDL-cholesterol levels are associated with subclinical atherosclerosis in the absence of risk factors. Journal of the American College of Cardiology, 70(24), 2979-2991). https://doi.org/10.1016/j.jacc.2017.10.024

  19. Fielding, C.J., Havel, R.J., Todd, K.M., Yeo, K.E., Schloetter, M.C., Weinberg, & Frost, P.H. (1995). Effects of dietary cholesterol and fat saturation on plasma lipoproteins in an ethnically diverse population of healthy young men. Journal of Clinical Investigation, 95(2), 611-618. https://doi.org/10.1172/JCI117705.

  20. Chen, M., Li, Y., Sun, Q., Pan, A., Manson, J.E., Rexrode, K.M., … Hu, F.B. (2016). Dairy fat and risk of cardiovascular disease in 3 cohorts of US adults. American Journal of Clinical Nutrition, 104(5), 1209-1217. https://doi.org/10.3945/ajcn.116.134460

  21. Ornish, D., Schwitz, L.W., Billings, J.H., Gould, L., Merritt, T.A., Sparler, S., … Brand, R.J. (1998). Intensive lifestyle changes for reversal of coronary heart disease. Journal of American Medical Association, 280(23), 2001-2007. https://doi.org/10.1001/jama.280.23.2001

  22. Department of Health Victoria State Government. (2020). Cholesterol. Retrieved from https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/cholesterol#bhc-content

  23. Jenkins, D.J.A., Jones, P.J.H., Lamarche, B., Kendall, C.W.C., Faulkner, D., Cermakova, L. … Frohlich, J. (2011). Effect of a dietary portfolio of cholesterol-lowering foods given at 2 levels of intensity of dietary advice on serum lipids in hyperlipidaemia. Journal of the American Medical Association, 306(8), 831-839. https://doi.org/10.1001/jama.2011.1202

  24. de Lorgeil, M., Renaud, S., Mamelle, N., Salen, P., Martin, J-L., Monjaud, I., … Delaye, J. (1994). Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet, 343(8911), 1454-1459. https://doi.org/10.1016/s0140-6736(94)92580-1

Jessica Zabow
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