Coronary heart disease (CHD), the leading cause of death worldwide, is ideally managed through a combination of lifestyle change, optimum medical care, and interventional therapies, including surgery [1]. These three modalities are partners, rather than competitors, from which cardiologists and patients may chose, according to evidence, patient needs, and preferences. While genetic predisposition is important, diet, lifestyle choices, and other modifiable factors account for about 70% to 90% of CHD pathology [2-5], and are reviewed elsewhere [6-8]. This commentary reflects upon the need for better diet studies, the continuing high burden of cardiovascular risk, particularly obesity and type 2 diabetes (T2D), and the concept that atherosclerosis is a systemic disease.

The relationship of diet and lifestyle to heart disease has been appreciated for over 40 years, and yet despite a cohesive basic core of nutrition fundamentals, significant advances, and a tsunami of literature, achieving the potential of cardiovascular prevention remains elusive [9-11]. Major barriers do not include lack of knowledge, but involve adoption, implementation, the environment, and social determinants [12-14].

Counterproductive controversy about some issues has become fashionable, but it is not necessary to cite debated issues when recommending smaller portions, more fresh produce, additional fiber, fewer processed foods (especially meats), controlled salt and sugar intake, and greater physical activity (especially avoidance of prolonged sitting) to the public. Most concerning is the minimal improvement in the U. S. diet, which is still considered poor [12,13]. All told, despite all intermediary and putative explanations, the prevalence of ideal cardiovascular health has not meaningfully changed in the past decade, and remains so even when using self-reported data [15,16]. With respect to the six aforementioned items, individual behavior remains the most important factor, rather than guideline failure [17]. Therefore it is not surprising that background cardiovascular risk and subclinical CHD in asymptomatic individuals remains relatively high, as evidenced by positive calcium artery scores in over half of ostensibly healthy rural U. S. adults younger than 65 years [18]. Since this score is associated with the number, duration, and intensity of risk factors present, including obesity and T2D, behavioral/lifestyle modification as part of prevention programs needs much more attention, as outlined in recent ESC Guidelines (Figure 1) [19].

Figure 1: Potential pitfalls in published dietary interventions included in this.

At times, and in combination, these have generally led to a high proportion of both false positive and false negative findings, accompanied by correspondingly poor evaluations [20]. A few of these challenges are discussed, in a number of different forums, by several investigators [11-13,21-24].

In the low-fat vs low-carbohydrate debate, program designs did not succeed in elimination of potential barriers over a period of three decades and considerable investment of resources, despite the call for a large, sufficiently powered study of sufficient duration. Unfortunately, the associated mêlée diminished the value of science and objectivity, lowered probability of definitive work, and allowed commercial interests, media pieces, and agendas to prevail. The implausibility and absurdity of repeating the same errors over and over in interventions is expertly discussed by Ioannidis [20] and in the citations to his editorial.

To remove many of the confounding variables, Hall et al. [25] conducted a “metabolic intervention” While this effort was small and of short duration, it was meticulously controlled. Calorie for calorie, dietary fat restriction resulted in more body fat loss than carbohydrate restriction in people with obesity. This type of information provides a basis for future work as part of an objective, rigorous approach to nutrition studies [26].

The saturated fat-cardiovascular disease risk (CVD) association is another “controversy” characterized by misinformation and confusing dialogue. A panoramic analysis was provided by Stamler [27], where essential references appear. The evidence was evaluated by the U. S. Dietary Guidelines Advisory Committee [22] whose recommendations —in a transient triumph of the scientific method—were later modified. Reframing the question by replacing 5% of saturated fat intake isocalorically from polyunsaturated- and monounsaturated-fatty acids reduced mortality risk by 27% and 13% respectively [28]. Dietary saturated fat does in fact contribute to CV risk, and replacement with polyunsaturated fat or whole-grain carbohydrates improves risk [29]. No advantage in outcomes is achieved by replacing with mixed carbohydrates, or for that matter, butter [30].

As mentioned, it is possible to offer sound dietary advice while avoiding issues that distract or impede patient motivation for behavior change. Even though improvement in dietary studies is desirable, existing information, which can eliminate most of clinical arteriosclerosis right now, continues to be disregarded. Most assuredly, the rate of decrease in CHD mortality has leveled from 2011-2014, and the likely culprits are the dual epidemics of obesity and T2D [31]. Advances made in controlling prevalence of smoking, dyslipidemia and hypertension are being offset by rises in corpulence and dysglycemia, amply justifying innovative and intensive prevention through diet and lifestyle.

In summary, arteriosclerosis occurs in multiple vessels concomitantly, and in the coronary tree, plaque occurs diffusely and in various stages of maturation and resolution. New mechanistic data regarding the prolonged pathogenesis and ubiquity of coronary lesions lends support to systemic therapies. Diet and lifestyle improvements offer a simple, safe, thorough, cost-effective solution, and are recommended in all guidelines as first-line therapy. This approach also promotes plaque regression and stabilization due to both antiinflammatory and lipid-lowering mechanisms [41], and simultaneously improves weight, blood pressure, and hyperglycemia. The effectiveness of lifestyle programs is well-accepted, is reflected in risk scores and dietary indices, and is supported by a burgeoning literature [9,42,43].

Despite the need for improvement, there is an accepted core of dietary knowledge that, together with other lifestyle measures, effectively prevents and treats obesity, T2D, and related CVD. Unfortunately, prevention is underutilized for a number of reasons. Unless the present trajectory is reversed, past gains in CHD mortality will be eroded, and successes in controlling other risk factors will be threatened. In addition, newer techniques indicate that CHD is a diffuse, systemic disease, in which systemic therapies play a key role. Soft, fatty uncalcified lesions in asymptomatic individuals constitute the substrate from which most CV events eventually arise. Since primordial prevention offers more complete protection than optimum therapies after risk factors appear, nutritional and lifestyle medicine have become even more important.