Journal: Progress in cardiovascular diseases
Running is a popular and convenient leisure-time physical activity (PA) with a significant impact on longevity. In general, runners have a 25-40% reduced risk of premature mortality and live approximately 3years longer than non-runners. Recently, specific questions have emerged regarding the extent of the health benefits of running versus other types of PA, and perhaps more critically, whether there are diminishing returns on health and mortality outcomes with higher amounts of running. This review details the findings surrounding the impact of running on various health outcomes and premature mortality, highlights plausible underlying mechanisms linking running with chronic disease prevention and longevity, identifies the estimated additional life expectancy among runners and other active individuals, and discusses whether there is adequate evidence to suggest that longevity benefits are attenuated with higher doses of running.
The evidence for the Portfolio dietary pattern, a plant-based dietary pattern that combines recognized cholesterol-lowering foods (nuts, plant protein, viscous fibre, plant sterols), has not been summarized.
Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD). However, TC is only modestly associated with CHD, and more important than the total level of cholesterol in the blood may be the number and size of low-density lipoprotein (LDL) particles that contain it. As for saturated fats, these fats are a diverse class of compounds; different fats may have different effects on LDL and on broader CHD risk based on the specific saturated fatty acids (SFAs) they contain. Importantly, though, people eat foods, not isolated fatty acids. Some food sources of SFAs may pose no risk for CHD or possibly even be protective. Thus, advice to reduce saturated fat in the diet without regard to such nuance could actually increase people’s risk of CHD. When saturated fats are replaced with refined carbohydrates, and specifically with added sugars (like sucrose or high fructose corn syrup), the end result is not favorable for heart health. Such replacement leads to changes in LDL, high-density lipoprotein (HDL), and triglycerides that may increase the risk of CHD. Additionally, diets high in sugar may induce many other abnormalities associated with elevated CHD risk, including elevated levels of glucose, insulin, and uric acid, impaired glucose tolerance, insulin and leptin resistance, non-alcoholic fatty liver disease, and altered platelet function. A diet high in added sugars has been found to cause a 3-fold increased risk of death due to cardiovascular disease. But sugars, like saturated fats, are a diverse class of compounds. The monosaccharide, fructose, and fructose-containing sweeteners (e.g., sucrose) result in greater degrees of metabolic abnormalities than seen with glucose (either isolated as a monomer or in chains as starch) and may present greater risk for CHD. This paper reviews the evidence linking saturated fats and sugars to CHD, and concludes that the latter is more of a problem than the former. Dietary guidelines should shift focus away from reducing saturated fat, and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined. To reduce the burden of CHD, guidelines should focus particularly on reducing intake of concentrated sugars, specifically the fructose-containing sugars like sucrose and high-fructose corn syrup in the form of ultra-processed foods and beverages.
Failure to change risk behaviors following myocardial infarction (MI) increases the likelihood of recurrent MI and death. Lower-socioeconomic status (SES) patients are more likely to engage in high-risk behaviors prior to MI. Less well known is whether propensity to change risk behaviors after MI also varies inversely with SES.
Pericardial heart disease includes pericarditis, (an acute, subacute, or chronic fibrinous, noneffusive, or exudative process), and its complications, constriction, (an acute, subacute, or chronic adhesive or fibrocalcific response), and cardiac tamponade. The pathophysiology of cardiac tamponade and constrictive pericarditis readily explains their respective findings on clinical examination, Doppler echocardiography, and at cardiac catheterization. The primary abnormality of cardiac tamponade is pan-cyclic compression of the cardiac chambers by increased pericardial fluid requiring that cardiac chambers compete for a fixed intrapericardial volume. Features responsible for the pathophysiology include transmission of thoracic pressure through the pericardium and heightened ventricular interdependence. Constrictive pericarditis is a condition in which the pericardium limits diastolic filling, causes dissociation of intracardiac and intrathoracic pressures, and heightened ventricular interdependence. Both conditions result in diastolic dysfunction, elevated and equal venous and ventricular diastolic pressure, respiratory variation in ventricular filling, and ultimately, reduced cardiac output.
Ninety-five percent of the World’s populations have a mean salt intake between 6-12 g, which is much lower than the tolerated daily level of up to 55 g/d. In spite of this, the recommended upper level by many health institutions is as low as 5.8 g/day. When reviewing the evidence for an upper level of 5.8g/day, it becomes apparent that neither the supporting studies selected by the health institutions, nor randomized controlled trials and prospective observational studies disregarded by the health institutions, document that a salt intake below this 5.8 g, has beneficial health effects. Although there is an association between salt intake and blood pressure, both in randomized controlled trials and in observational studies, this association is weak, especially in non-obese individuals with normal blood pressure. Furthermore a salt intake below 5.8 g is associated with the activation of the renin-angiotensin-aldosteron system, an increase in plasma lipids and increased mortality. A redesign of the salt dietary guidelines, therefore, seems to be needed.
Traditionally, the leading hypothesis regarding the development of obesity involves caloric imbalance, whereby the amount of calories consumed exceeds the amount of calories burned which causes obesity. Another hypothesis for why we get fat has surfaced in the last decade which is the idea that the overconsumption of added sugars and refined carbohydrates induce insulin resistance and high insulin levels causing obesity. While insulin is a fat-storing hormone, this hypothesis does not explain visceral adiposity, or why certain people are found to have fat stored in and around their organs. We propose a new mechanism for body fattening, particular visceral adiposity. This hypothesis involves the overconsumption of fructose, which leads to inflammation in all cells that metabolize it rapidly. When fructose is metabolized in subcutaneous adipocytes, the subsequent inflammation leads to an increase in intracellular cortisol in order to help squelch the inflammation. Unfortunately, the increase in intracellular cortisol leads to an increased flux of fatty acids out of the subcutaneous adipocytes allowing more substrate for fat storage into visceral fat tissue. Moreover fructose-induced inflammation in the liver also leads to increased intracellular cortisol via an upregulation of 11-B hydroxysteroid dehydrogenase type 1 causing increased fat storage in the liver (i.e., fatty liver). In essence, the fructose-induced inflammatory cortisol response causes “thin on the outside, fat on the inside” (TOFI). Furthermore, fructose in the brain, either from fructose uptake via the blood brain barrier or endogenous formation from glucose via the polyol pathway stimulates an increased release of cortisol causing hepatic gluconeogenesis leading to overall insulin resistance and further body fattening. This review paper will discuss in detail the hypothesis that fructose-induced inflammation and cortisol activation causes visceral adiposity.
Cardiovascular (CV) disease (CVD) is the leading global cause of mortality, being responsible for 46% of non-communicable disease deaths. It has been estimated that about 85.6 million Americans are living with some form of CVD, which continues to rise. Healthy lifestyle choices may reduce the risk of myocardial infarction by more than 80%, with nutrition playing a key role. Vegetarian dietary patterns reduce CVD mortality and the risk of coronary heart disease (CHD) by 40%. Plant-based diets are the only dietary pattern to have shown reversal of CHD. Additionally, evidence suggests benefits of vegetarian dietary patterns in both the prevention and the treatment of heart failure and cerebrovascular disease. Plant-based diets are associated with lower blood pressure, lower blood lipids, and reduced platelet aggregation than non-vegetarian diets and are beneficial in weight management, reduce the risk of developing metabolic syndrome, and type 2 diabetes. They have also been shown an effective treatment method in diabetes management. Well planned vegetarian diets provide benefits in preventing and reversing atherosclerosis and in decreasing CVD risk factors and should be promoted through dietary guidelines and recommendations.
There is compelling evidence showing that nut intake confers protection against cardiovascular disease (CVD). We conducted a review of the literature with respect to observational studies and randomized trials completed in the past ≈25 years that examined nut intake and CVD endpoints. We included findings from major cohort studies, a large intervention trial, and numerous smaller nut trials. Collectively, data from observational and intervention studies indicate strong and significant association between nut intake and decreased risk of fatal and non-fatal coronary heart disease , myocardial infarction, and sudden death; and somewhat weak association with stroke. The primary mechanism by which nuts protect against CVD is through the improvement of lipid and apolipoprotein profile. Increasing evidence also indicates that nut consumption may confer protection against CVD via lowering of oxidative stress, inflammation; and improvement in endothelial function. Nut components, such as unsaturated fatty acids, L-arginine, beneficial minerals, phenolic compounds and phytosterols, appear to be of paramount importance for their health effects.
Insulin therapy increased cardiovascular (CV) risk and mortality among type 2 diabetes (T2D) patients in several recently reported clinical outcomes trials. To assess whether this association is causative or coincidental, PubMed searches were used to query the effects of insulin therapy for T2D on CV health and longevity from large-scale outcomes trials, meta-analyses, and patient registry studies, as well as basic research on insulin’s direct and pleiotropic actions. Although several old studies provided conflicting results, the majority of large observational studies show strong dose-dependent associations for injected insulin with increased CV risk and worsened mortality. Insulin clearly causes weight gain, recurrent hypoglycemia, and, other potential adverse effects, including iatrogenic hyperinsulinemia. This over-insulinization with use of injected insulin predisposes to inflammation, atherosclerosis, hypertension, dyslipidemia, heart failure (HF), and arrhythmias. These associations support the findings of large-scale evaluations that strongly suggest that insulin therapy has a poorer short- and long-term safety profile than that found to many other anti-T2D therapies. The potential adverse effects of insulin therapy should be weighed against proven CV benefits noted for select other therapies for T2D as reported in recent large randomized controlled trials.