Surfer Dies of Heart Disease at Age 32
A preliminary release of the autopsy and toxicology report for pro surfer Andy Irons indicates the 32-year old surfer died in 2011 of severe coronary artery disease caused by atherosclerosis.
Pathology consultant J.M. Di Maio, M.D. commented that Mr. Irons’ arteries were narrowed by as much as 70-80%. This narrowing and hardening of the arteries restricts blood flow that feeds the heart muscle, causing heart attack.
The cause of death was announced as ischemic heart disease: In other words, Mr. Irons died of a heart attack.
A press release from the Tarrant County (Florida) Medical Examiner’s office also indicated that Mr. Irons had, in addition to heart disease, traces of both recreational and prescribed drugs in his bloodstream. Controversy has thus arisen regarding the role of these drugs in his death.
What causes coronary artery disease and atherosclerosis, and how can it kill someone so young and active?
Atherosclerosis and heart disease
Atherosclerosis is linked to elevated cholesterol, hypertension, and lipid peroxidation. The narrowing and hardening of artery walls has been shown in research to be caused by artery wall damage from oxidized LDL and other oxidative radicals. This artery damage stimulates an inflammatory response resulting in plaque build-up, fibrin and thickened lumen – often called hardening of the arteries. With increased plaque build-up comes the deadly risk of thrombosis events – the release of patches of the plaque that clog what little opening there is left in the arteries.
Repeated epidemiological studies sponsored by the CDC, the Heart Association and the World Health Organization have found that artery damage and plaque build-up is linked to obesity, diabetes, a sedentary lifestyle, and a diet high in saturated fats and/or fried foods. High blood pressure and fast or irregular heart rate, especially in persons over 40 years old, are strong markers.
Any of these can exist even for a surfer like Andy Irons.
Cholesterol and lipid peroxidation
Higher levels of total cholesterol, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol, and total triglycerides are also key markers. The exception appears to be in the case of the elderly, where recent studies have illustrated that moderately high total cholesterol among the elderly may be linked with lower mortality (Onder et al. 2003; Miller 2004). Nonetheless, a link between small LDL particle size and atherosclerosis has been made (Gardner et al. 2996), and the oxidation of LDL particles – lipid peroxidation – appears to be one of the most significant mechanisms.
Hyperperoxides readily form oxidative radicals. These directly damage the artery walls, causing the damage associated with atherosclerosis.
The pathway towards LDL peroxidation is accelerated by lipooxygenases (LOX) and cyclooxygenases (COX). These in turn are stimulated by an overload of consumed toxins in the body.
Consumed toxins come from ethanol (alcohol), air pollutants, food additives, formaldehyde and chemical metabolites from pharmaceuticals and processed recreational drugs such as methamphetamine. Smoking also adds significant toxins.
Even a pro surfer can be afflicted by diet
For even a young, active person, the combination of a diet with lots of fried fats rich in red meats and saturated fats, air and water pollutants, drinking, smoking, chemical exposures and drugs all come together to produce LDL peroxidation, which in turn damages the artery walls and produces atherosclerosis.
It might be added that increased exposure to toxins related to surfboard manufacturing – as experienced surfers often spend time with their shapers and board makers – can also increase toxicity and oxidative radicals within the bloodstream. In addition, many sunscreens are made with chemical toxins that are absorbed into the skin, and the oceans are becoming extremely toxic due to waste water dumping.
Diet or Genetics?
Most heart conditions can be linked to the lifestyle choices we make. There also appears to be genetic predispositions. Yet it is debatable how many genetic factors are actually lifestyle and dietary habits being passed down through families (Jensen 2002; Vauthier et al. 1996). Poor diet and lifestyle choices passed down through families include smoking and second-hand smoking; diets high in red meats and saturated fats; sedentary lifestyle; heightened stress; and/or drug and alcohol consumption.
Diets high in saturated fats and fried foods are the most significant, as they directly reduce LDL particle size and increase oxidized LDL (Keogh et al. 2005; Nestel 2005). This increases triacylglycerol-rich lipoproteins – a central player in lipid peroxidation. Foods high in saturated fats include animal meats, eggs, and butter. Other dairy such as milk, cheese and yogurt, especially skim versions, contain less saturated fat. Dairy foods can also supply various vascular benefits. A 2002 study of 51 healthy adults confirmed this, as dairy-derived conjugated linoleic acid significantly improved VLDL-cholesterol and triacylglycerol-rich lipoprotein levels (Noone et al. 2002).
Trans-fats are also known to cause lipid peroxidation and atherosclerosis. Increased consumption of hydrogenated or partially hydrogenated oils; or foods fried or grilled for too long, can contain high levels of trans-fats. These trans-fats lead to oxidative LDL, inflammation and subsequent plaque build-up (Lopez-Garcia et al. 2005; Stachowska et al. 2004; Naruszewicz et al. 2003).
The Mediterranean diet and vegetarian diets have both been shown in multiple studies to help prevent lipid peroxidation and atherosclerosis. It could also improve surfer performance – if you are a surfer like I am.
The Healthy Fats
A healthy fat that actually decreases lipid peroxidation is coconut oil. Coconut oil, historically considered a harmful saturated fat, actually contains medium chain fatty acids. Medium chain fatty acids from coconut oil have been shown in human studies to lower lipoprotein-A concentrations in the blood while having fibrinolytic (plaque and clot reducing) effects (Muller et al. 2003).