Shorts

By Jule Klotter

Electromagnetic Radiation Impact on Cardiovascular Health

In their 2017 invited editorial for the European Journal of Preventive Cardiology, Priyanka Bandara and Steven Weller argue for the need to include exposure to microwave radio frequency electromagnetic radiation as an environmental risk factor for cardiovascular illness. They begin by citing a 2017 study by Vernon et al that showed an increase in serious heart attacks among people without recognized, modifiable risk factors (high cholesterol, hypertension, diabetes and smoking). In that single-center retrospective study of consecutive ST elevation myocardial infarction patients, the incidence among people without risk factors increased from 11 percent in 2006 to 27 percent in 2014. Bandara and Weller reviewed medical literature and found ample evidence that “rapid and widespread deployment of wireless communication and surveillance infrastructure and the use of personal wireless devices” could be a significant factor in this unexplained increase.

Bandara and Weller report that 216 of 242 studies (89%) found increased oxidative stress and/or reduced antioxidant levels with radio frequency electromagnetic radiation (RF-EMR) exposure. Oxidative stress, which damages tissue and can alter signal transduction pathways, is a recognized contributor to cardiovascular disease (CVD). In addition, RF-EMR affects the autonomic system, increasing the sympathetic response. Healthy men (under age 50) exposed to RF-EMR during work showed autonomic dysregulation compared to unexposed controls. In lab experiments, RF-EMR exposure to cordless and mobile phones altered heart rate variability, a measure of autonomic balance. Moreover, RF-EMR disrupts voltage-gated calcium ion channels (VGCC). “The downstream effects of VGCC disruption may involve alteration of important functions of Ca2+/calmodulin-dependent enzymes (such as nitric oxide synthase and protein kinase II), influencing the pathophysiology of CVD,” say Bandara and Weller. Some animal studies have also found multiple histopathological changes in the heart muscles of animals exposed to RF-EMR (Azab and Ebrahim).

RF-EMR exposure increases blood pressure and heart rate. For example, a 2015 study, led by Linda Saili, exposed Albino rabbits to WiFi signals (2.45 GHz) for one hour. This exposure increased the animals’ heart rate (+22%) and arterial blood pressure (+14%). In addition, the researchers found that the WiFi exposure changed the action of epinephrine and dopamine. Bandara and Weller report that chronic occupational RF-EMR exposure is associated with increased CVD risk and change in the diurnal rhythms of blood pressure and heart rate.

Bandara and Weller refer to epidemiological evidence from chronically exposed populations near radio frequency transmitters (radio/TV/radar towers) before the explosion of cell towers and other man-made RF-EMR sources. Soviet research, according to a 1976 US Army medical intelligence document, found “a significantly higher incidence of coronary disease, hypertension, and disturbances of lipid metabolism” in engineers and officials exposed to microwaves compared to unexposed controls—even though family history of heart disease was about the same in the two groups. The US document also stated that being “more stringent in the enforcement of stringent exposure standards…could be unfavorable…on industrial output and military functions.” Apparently, public health is less of a concern than industry and the military.

The World Health Organization linked the high incidence of heart attacks and cancers among people living in North Karelia, Finland, to a nearby Soviet early warning radar station. The North Karelian lifestyle intervention program, which increased consumption of antioxidant-rich fruits and vegetables and decreased smoking rates, brought improved health. “The success of the North Karelia project…supports our hypothesis that chronic exposure to RF-EMR causes CVD via redox mechanisms of [oxidative stress],” write Bandara and Weller, “which can be countered, albeit not fully, with increased dietary intake of antioxidants.” Because oxidative stress affects inflammation, neutrophil infiltration, platelet aggregation, and endothelial integrity, Bandara and Weller say that reducing RF-EMR exposure would be prudent for patients recovering from a heart attack—although no studies have been conducted yet.

“It is clearly time to investigate the potential role of RF-EMR exposure from common wireless device use on CVD,” say Bandara and Weller. “Noting that existing research findings are influenced by the funding source, fresh directives are necessary for objective high quality research to expand current primary and secondary prevention strategies.” Perhaps, new research can find strategies for mitigating the harmful effects—if industry and enabling government agencies stop trying to obscure the problems.

Azab AE, Ebrahim SA. Exposure to Electromagnetic Fields Induces Oxidative Stress and Pathophysiological Changes in the Cardiovascular System (abstract). Journal of Applied Biotechnology & Bioengineering. 2017;4(2).

Bandara P, Weller S. Cardiovascular disease: Time to identify emerging environmental risk factors. European Journal of Preventive Cardiology. 2017: 24(17): 1819-1823.

Saili L, et al. Effects of acute exposure to WIFI signals (2.45 GHz) on heart variability and blood pressure in Albinos rabbit. Environmental Toxicology and Pharmacology. 2015;40:600-605.

Vernon ST, et al. Increasing proportion of ST elevation myocardial infarction patients with coronary atherosclerosis poorly explained by standard modifiable risk factors (abstract). European Journal of Preventive Cardiology. 2017;24(17):1824-1830.

Virgin Coconut Oil and Cardiovascular Disease

Does virgin coconut oil (VCO) contribute to cardiovascular disease (CVD), or is it beneficial? Coconut oil, like butter, palm oil, and animal fat, primarily consists of saturated fat. Although not suitable for deep frying because of its low smoke point, VCO is fine for single-use, shallow frying as it resists oxidation and polymerization during heating, according to a 2016 review by Laurence Eyres and colleagues. Eyres et al urge readers not to conflate coconut oil with medium-chain triglyceride oils. Lauric acid, the predominant fat in coconut oil, behaves more like a long-chain fatty acid in terms of absorption and how it is metabolized.

When compared to unsaturated plant oils, the consumption of coconut oil increases HDL, LDL, and total cholesterol levels, according to the Eyres review: “Overall, the weight of the evidence to date suggests that replacing coconut oil with cis unsaturated fats would reduce CVD risk. Therefore, this review does not support popular claims purporting that coconut oil is a healthy oil in terms of reducing the risk of CVD.” However, Thai researchers report that publicity about the saturated fat-cardiovascular correlation has led to a decline in coconut oil consumption over the past 20 years in Thailand, but the incidence of CVD has increased during the same time period.

Chinwong et al conducted a randomized crossover trial with healthy Thai volunteers that compared dietary coconut oil with a placebo. During the eight-week study, 32 participants added 15 ml of virgin coconut oil or 2% carboxymethylcellulose solution twice a day to their normal diet. Unlike studies that compare coconut oil to unsaturated plant oils, this study found that VCO increased HDL cholesterol but not LDL or total cholesterol. The results only apply to healthy, young (18-25 years) Thais; more research is needed to see if people with CVD, metabolic syndrome, or different ethnic backgrounds have the same response.

Virgin coconut oil is more than a fat; it also has antioxidant properties. A 2016 rat study by Indian researchers compared VCO to copra oil (CO), a common edible oil made from dried coconut and used in south India. While the fatty acid profile of the two are the same, VCO contains more polyphenolic antioxidants, such as caffeic acid, ferulic acid, syringic acid, catechin, and epigallocatechin. For this experiment, rats in the two treatment groups were given a high-fructose diet (60%), known to promote insulin resistance and fatty liver, and either VCO or copra oil. The control group ate a reference diet that included groundnut oil, which is high in unsaturated fatty acids and low in antioxidant polyphenols. After four weeks, blood glucose levels in the control group increased 26 percent, compared to 46 percent for the copra oil group, and just 17 percent for the VCO group. Moreover, the rats fed virgin coconut oil showed less liver damage and steatosis than the CO-fed rats. The authors say, “These results suggest that VCO could be an efficient nutraceutical in preventing the development of diet-induced insulin resistance and associated complications possibly through its antioxidant efficacy.”

In a 2018 study, polyphenols isolated from virgin coconut oil helped protect rats from cadmium-induced dyslipidemia and oxidative stress. Cadmium (Cd), present in cigarettes and contaminated food, inhibits several enzymes involved in lipid metabolism. It significantly increases total cholesterol, low density cholesterol, and triglycerides and decreases HDL cholesterol. For this study, rats were pre-treated with VCO polyphenols for two weeks and then cadmium (5 mg/kg) was added for the next five weeks. The author report, “The co-administration of VCO polyphenol with Cd remarkably restored lipid profile and cardiovascular risk ratios and stabilized antioxidant defense systems comparable to control groups.”

Virtually all research with virgin coconut oil focuses on cardiovascular biomarkers. As Thai researchers Chinwong et al, remark “further research should be conducted in the real-world practice among patients with low HDL-C levels, especially those at high risk of cardiovascular events.”

Chinwong S, Chinwong D, Mangklabruks A. Daily Consumption of Virgin Coconut Oil Increases High-Density Lipoprotein Cholesterol Levels in Healthy Volunteers: A Randomized Crossover Trial. Evidence-Based Complementary and Alternative Medicine. 2017.

Eyres L, et al. Coconut oil consumption and cardiovascular risk factors in humans. Nutrition Reviews. 2016; 74(4):267-280.

Famurewa AC, Ejezie FE. Polyphenols isolated from virgin coconut oil attenuate cadmium-induced dyslipidemia and oxidative stress due to their antioxidant properties and potential benefits on cardiovascular risk ratios in rats. Avicenna J Phytomed. 2018;8(1):73-84.

Narayanankutty A, et al. Virgin coconut oil maintains redox status and improves glycemic conditions in high fructose fed rats. J Food Sci Technol. 2016;53(1):895-901.

Mercury and Heart Disease

“As heart rhythm and function are under autonomic nervous system control, it has been hypothesized that the neurotoxic effects of mercury might also impact cardiac autonomic function,” write Giuseppe Genchi and colleagues in their 2017 review article. The researchers performed a literature search in an attempt to uncover the role that mercury exposure might play in cardiovascular disease.

In addition to its neurotoxic effects, mercury increases oxidative stress and decreases antioxidant activity. Mercury latches onto thiol (-SH) and selenium molecules, making these molecules unusable for antioxidant activities performed by the enzymes glutathione peroxidase, catalase, and superoxide dismutase. Mercury also inactivates paraoxonase, an extracellular antioxidative enzyme that supports beneficial HDL activity, and increases LDL oxidation. Mercury also contributes to inflammation, another contributor to CVD, by inducing arachidonic acid metabolite formation (e.g., prostaglandins, thromboxanes, leukotrienes).

Several epidemiological studies have linked mercury exposure, usually via contaminated food, to cardiovascular disease. Mercury, released into the atmosphere by coal-fired power plants and other industrial sources, ends up in soil and waterways—contaminating vegetables, animal products, and especially fish. Populations that rely on contaminated fish as a mainstay, such as those in Brazil’s Amazon basin and Quebec, Canada’s Inuit, have decreased heart rate variability and increased risk of high blood pressure, atherosclerosis, and heart attack.

Even though the mercury content in fish is a problem, fish are also important sources of omega-3 polyunsaturated fatty acids (PUFA) and selenium. Selenium, as mentioned above, is needed by the body’s defensive antioxidant systems; and omega 3s are known to support cardiovascular health. “Many cardiovascular problems related to mercury are mitigated by the concomitant intake of fish, which contains omega-3 PUFA, and by intake of selenium,” the authors explain.

A possible dose-response between mercury exposure and cardiovascular events is still being debated. In the meantime, Genchi and colleagues say, “Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, or other vascular diseases and in patients who have clinical history of exposure or clinical evidence on examination of mercury overload.”

Genchi G, et al. Mercury Exposure and Heart Diseases. International Journal of Environmental Research and Public Health. 2017.

Risk of Stopping Low-Dose Aspirin

Low-dose aspirin reduces the risk of heart attack, particularly in those who have already had one (secondary prevention). Once started, this therapy needs to be continued—unless bleeding or major surgery occurs—as patients who stop taking the aspirin have a >30% increased risk of a cardiovascular event, according to a 2017 Swedish population-based cohort study.

Aspirin is a prescription medication in Sweden, so researchers were able to see which patients over age 40 continued to take the low-dose aspirin (75 to 160 mg) prescribed for prevention of cardiovascular events. They looked for treatment breaks and permanent discontinuation after a year of continuous aspirin treatment from July 1, 2005 to December 31, 2009.

Patients who consistently maintained aspirin therapy had the lowest risk of a cardiovascular event. Those who stopped taking aspiring had a 37% higher risk of an event, an absolute risk of 13.5 events per 1000 person-years: “Put another way, on average, 1 of every 74 patients who discontinued aspirin had an additional cardiovascular event in 1 year.” Those using aspirin for primary prevention had less risk (1 of every 146 primary patients) than those with established CVD (1 of every 36 secondary patients). Treatment with an oral anticoagulant or antiplatelet drug decreased the likelihood of an event when aspirin was discontinued. The authors say, “The risk increased shortly after discontinuation and did not appear to diminish over time.”

This study did not look at possible confounding factors, such as socioeconomic status, lifestyle factors like smoking, or physical measures, including blood pressure. Also, the authors say there is a risk of reverse causation, “that is, patients about to die stop taking aspirin and then die anyway.”

The widespread use of aspirin and the possibility of a rebound effect with discontinuation highlights a need for more research. The authors say, “Experimental studies have suggested a rebound effect after aspirin discontinuation, involving increased thromboxane levels possibly resulting from the pro-thrombotic effects of residual very low levels of aspirin.” Does a rebound effect increase heart attack risk, even if a patient discontinues aspirin therapy for a short time because of surgery or other medical procedure? If so, would discontinuing gradually make a difference?

Sundström J, et al. Low-Dose Aspirin Discontinuation and Risk of Cardiovascular Events. Circulation. 2017;136:1183-1192.