THIS is a sequel to “Warfare in defence of palm oil” published last week. The attack on our palm oil industry, spearheaded by the American edible oil industry, has two prongs. The first focuses on deforestation and plays to mass sentiments on the need to protect the environment, and uses its clout to influence international trade governance. The second targets making palm oil unhealthy, citing predominantly one study published in 2006.

Defence on the attack on deforestation should be easy. A concerted PR campaign using all media available telling the facts of our available vast virgin jungle should easily make nonsense of the attack that instigates negative public opinion.

Other than saying palm oil is rich in vitamin E and carotenoids, our Malaysian Palm Oil Council (MPOC) struggles to find answers to attacks criticising palm oil as unhealthy because it is rich in saturated fats and causes raised low-density lipoprotein cholesterol (commonly misunderstood as the “bad” cholesterol) when consumed. MPOC corners itself to decades-old thinking believing saturated fats and LDL are unhealthy, and fail to acknowledge the latest in the cholesterol hypothesis debate. As a result, palm oil is losing its market share even in our own country to the false perception that canola and soybean oils are more superior.

Never before in medical history has there been such a protracted controversy amid shifting paradigm, over a global number one killer where the cure seems imminent, but illusive – the lipid/cholesterol hypothesis of heart disease.

For the last seven decades, the blame started with lipids, and later hypercholesterolemia as the single most important causative factor for coronary heart disease. Starting from the 1950s, it was Ancel Keys who first hypothesised fats as the main causative factor after observing the American diet.

In the 1960s, Keys shifted the blame to saturated fats after observing European diets where there was less prevalence of heart disease even though high in vegetable fats. The scientific field shifted blame to LDL in the 1970s, and then oxidised LDL in the 1980s. Homocysteine was made to be the culprit in the 1990s. It appears what perceived to be the main causative factor for heart disease changed every decade. Scientifically, the cause of heart disease is unknown.

Over the last four years, serious doubts over the cholesterol hypothesis surfaced. Studies published in prominent publications have challenged the cholesterol hypothesis of atherosclerosis. Harcombe and colleagues’ systematic review and meta-analysis published in British Medical Journal Open Heart in 2015 concluded dietary fat guidelines issued worldwide had not been based on available evidence. In the same year the United States Dietary Guidelines Advisory Committee stated there was no scientific evidence of relationship between consumption of dietary cholesterol and serum cholesterol, paving the way to remove food supposedly high in cholesterol, such as butter, eggs, and animal fats from the “naughty” food list.

In 2017 the British Royal Pharmaceutical Society pronounced the cholesterol hypothesis dead. Demasi and colleagues argued that the directive to lower cholesterol for the last few decades had been misguided. They postulated insulin resistance was the most important predictor of cardiovascular disease, and proposed the most effective way to reduce the risk of heart attack and stroke was to consume a high-fat and low glycemic diet.

With respect to Demasi and colleagues’ view on insulin resistance as the most important predictor of cardiovascular disease, our (Wong, Mohamed and Niedzweicki, 2016) views advanced further to close the gap in the cholesterol-heart disease debate. Our paper, “Atherosclerosis and the cholesterol theory: a reappraisal”, built on the work of Matthias Rath and Linus Pauling, made the argument for the significance of vitamin C, lysine, and proline, the nutrients required for the synthesis of collagen molecules; lacking of which may lead to arterial wall weakness and subsequent apolipoprotein cholesterol deposit.

In 1992, Rath and Pauling put forward their unified theory of cardiovascular disease, emphasising the body’s enzymatic degradation of the connective tissue or collagen matrix by the protease, plasmin. Rath and Pauling also proposed that the sticky apoprotein transported by the LDL cholesterol, and lysine, are respectively endogenous and exogenous inhibitors of plasmin-induced proteolysis. A pilot study by Wong, Niedzwiecki and Rath (2016) was conducted and corroborated with the Rath and Pauling hypothesis. In the interest of humanity and for scientific expediency, the scientific field should not ignore published works in this area even though it is not in the realm of mainstream.

Incidentally in 2016, the Nobel Prize for physiology and medicine was awarded to Yoshinori Ohsumi for the discovery of mechanisms for autophagy, the process for degrading and recycling of cellular components. Mainstream researchers have largely ignored Rath and Pauling’s proposed concept of plasmin-induced proteolysis in physiological and pathological conditions. The science could have been widely applied for the benefit of mankind currently engulfed by cardiovascular diseases of all etiology.

The study of Vega-Lopez and colleagues (2006) surmised that the saturated fat-laden palm oil and its consumption led to raised LDL cholesterol, and therefore not a good substitute for use in the food industry. Not only is it flawed in its study design, it is also flawed from the perspective of the latest scientific knowledge pertaining to the lipid and cholesterol hypothesis.

MPOC should take heed of this latest scientific knowledge on the lipid/cholesterol hypothesis debate and use it to promote palm oil as superior to others. – October 24, 2018.

* Captain Dr Wong Ang Peng is a researcher with an interest in economics, politics, and health issues. He has a burning desire to do anything within his means to promote national harmony. Captain Wong is also a member of the National Patriots Association.

* This is the opinion of the writer or publication and does not necessarily represent the views of The Malaysian Insight. Article may be edited for brevity and clarity.