Atherosclerosis and hypertension, both of which are profoundly influenced by diet and that can be approached, at least in part, from a nutritional point of view, as well as the rising “epidemic” of obesity, are at the core of the major cardiovascular diseases affecting the developed world. Diet is a complex amalgamation of numerous nutrients, some of which may interact with each other. It can be challenging to analyze nutrients and their effects on cardiovascular disease thoroughly. These diseases are affected by numerous dietary risk factors in a variety of environmental and racial contexts.
Because these risk factors are frequently present in young people, early prevention must be practiced. Although studies in the developed world provide the majority of the knowledge about nutritional risk factors & cardiovascular disease, the situation is quickly escalating to epidemic levels in the developing world, placing a significant burden on the economy & health services.
Diet has a major impact on a number of cardiovascular disease risk factors. Although studies in the developed world account for the majority of knowledge about nutritional risk factors & cardiovascular disease, the situation is quickly escalating to epidemic levels in the developing world, posing impending economic and health service burdens.
A large portion of cardiovascular disease in the developed world is caused by atherosclerosis. It can be evaluated on two different levels. First, autopsy studies or high-resolution imaging of lesion size in the living subject can be used to monitor the lesion itself most directly at the preclinical level. The second occurs when the condition has advanced to the point where clinical cardiovascular disease, such as angina, coronary thrombosis, and sudden death, each of which is frequently used as a proxy for the underlying atherosclerosis, is manifested as a result of atherosclerosis and its complications. These latter measurements might not be reliable indicators of the severity of underlying vascular disease because numerous changes influence lesion evolution late in its progression.
Chronic inflammation, known as atherosclerosis, occurs at hemodynamically defined locations in large and medium-sized arteries. It is characterized by the buildup of cholesterol and its esters in the vessel walls, either as extracellular lipids like free cholesterol crystals or as large lipid droplets in macrophage foam cells. Therefore, it is reasonable to assume that cholesterol will take center stage in studies of atherogenesis. Hypercholesterolemia and lipoprotein dysfunction are necessary for the onset of atherosclerosis, at least in experimental animals.
The PDAY studies show that by age 15, one frequently sees early lesions at sites where more advanced lesions are later observed, proving that atherosclerosis starts quite early in life. Therefore, regardless of the recommended preventive measures, they must ultimately be started early in life.
The aforementioned studies highlight the significance of reducing the diet’s saturated-to-unsaturated fat ratio. Oils high in saturated fats may play a significant role in the diets of many developing nations, but it is important to note that the average daily intake of fat in these nations is much lower than that of industrialized nations.
Monounsaturated fatty acids, which are primarily present in olive oil, n-6 polyunsaturated fatty acids, n-3 polyunsaturated fatty acids, & trans fatty acids are just a few of the different types of unsaturated fatty acids. With regard to hypercholesterolemia & cardiovascular disease, each is functionally distinct.
Many plant oils, most notably corn oil or safflower oil, contain linoleic acid, the diet’s most common n-6 polyunsaturated fatty acid. The Kinsell and Ahrens15,16 liquid formula diet experiments, which did not involve altering the rest of the diet, provided the most convincing evidence of the effects of n-6 polyunsaturated fatty acids on lowering blood cholesterol. In contrast, blood cholesterol increased when saturated fat was included in the liquid formula diet.
The two main sources of body cholesterol are endogenous synthesis and dietary absorption. Although there is a lot of individual variation in absorption rates, intestinal cholesterol is only partially absorbed, in contrast to triacylglycerol, the main dietary fat, which is almost entirely absorbed. 35 Dietary cholesterol and cholesterol that the liver excretes into the bile are the two main sources of the cholesterol pool in the intestinal lumen (about 800 to 1300 mg per day).
These two sources of cholesterol are not distinguished by their absorptive mechanisms. There is epidemiological, experimental, & clinical evidence for the significance of cholesterol absorption in regulating plasma & body cholesterol homeostasis, much like the role of dietary fat in controlling cholesterol levels.
With regard to their function in cholesterol absorption, 3 intestinal proteins have recently attracted a lot of attention. 38 Sterol export into the intestinal lumen and bile are primarily mediated by the adenosine triphosphate binding cassette transporters G5 & G8 (ABCG5/G8) found in the liver and intestine, respectively.
In so far as it results from an imbalance between energy intake and energy consumption, to which decreased physical activity contributes, obesity is a nutritional disorder. In developed societies, the “epidemic” of obesity is a major cause for concern because it is linked to higher morbidity and mortality rates from various illnesses, including cardiovascular disease, particularly atherosclerosis.
According to the most recent survey, the age-adjusted prevalence of obesity in the United States (defined as a body mass index [BMI] greater than 30 kg/m2) is 30.5%. 46 The 17% overweight rate among American children is particularly alarming. 47 Obesity is linked to a number of cardiovascular risk factors, but the three that stand out the most are hypertension, dyslipidemia (higher triglycerides and lower HDL), & insulin resistance. The metabolic syndrome can be identified by the presence of several of these risk factors. Although not all obese people have metabolic syndrome, it is estimated that 20% to 25% of US adults over the age of 20 have it. 48
Only a portion of the association between obesity & atherosclerosis can be attributed to conventional risk factors, which suggests that other obesity-related factors may also play a role in this proatherogenic effect. This could be the result of the proinflammatory state brought on by the significant visceral adipose tissue mass, as shown, for instance, by plasma levels of serum amyloid A and tumor necrosis factor (TNF)-, interleukin (IL)-6, and IL-6. 53 Obese people may also have higher rates of atherosclerosis because adipokines like leptin & adiponectin, which are released in increased and decreased levels, respectively, from the increased adipose tissue mass,51,53..
Given that adiponectin promotes fatty acid oxidation,54 may influence both the concentration of free fatty acids and insulin resistance. The reader is directed to the excellent reviews cited in this section because it is impossible to discuss the mechanistic details involved in the link between obesity and atherosclerosis in this review.
Numerous cardiovascular diseases, such as atherosclerosis, coronary heart disease, renal disease, & stroke, are impacted by hypertension. It occurs less frequently like an isolated risk factor and more frequently in conjunction with a collection of other risk factors, as in the case of the metabolic syndrome. 56 The impact of hypertension on cardiovascular disease is, in fact, more pronounced in overweight people than in people of normal weight. 57 A significant risk factor for cardiovascular disease caused by atherosclerosis is hypertension. 58 Even at prehypertensive levels, the risk is increased (systolic BP 120 to 139 mm Hg and diastolic 80 to 89 mm Hg). 59 Hypertension is a risk factor for atherosclerosis in young people, just like other causes of atherosclerosis. 60 Adults worldwide have hypertension in about 25% of cases. 61.
Sodium and potassium are the most significant dietary components, and diet is the most significant environmental factor influencing hypertension. High dietary sodium consumption is a relatively recent phenomenon. On average, nearly one-third of Americans suffer from hypertension and take more than 6 g of sodium chloride daily. Only 1% of people with hypertension live in isolated societies, where less sodium is consumed daily than that of industrialised areas.
At the kidney, where the increased sodium load is re-absorbable and causes a loss of potassium, sodium homeostasis is regulated in response to dietary sodium. Nitric oxide (NO) production by endothelial nitric oxide synthase is restricted by an excess of sodium and a deficiency in potassium, which causes vascular wall smooth muscle cells to contract and vasodilation to be reduced (eNOS). 61,63 Individual responses to sodium overload can vary significantly, which frequently leads to the classification of subjects as salt sensitive or insensitive. This variation in salt sensitivity is probably caused by a number of distinct genes, though these have not been identified. Salt sensitivity is dose-dependently inhibited by dietary potassium.
The important vasorelaxant, which is frequently associated with hypercholesterolemia, is less bioavailable due to endothelial dysfunction. Two nitric oxide synthases are present in the endothelium, and iNOS, which is present in smooth muscle cells and macrophages NO in the vessel wall. Numerous atherosclerotic risk factors, including high cholesterol, hypertension, diabetes, and turbulent shear stress, decrease NOS activity, possibly by raising oxidative stress.
67 The administration of arginine can restore the reduced vasorelaxant activity of eNOS because arginine is the substrate for NOS. 68 The intracellular availability of the arginine substrate, which may be influenced by arginine transport by the arginine cation transporter, is a crucial factor in endothelial NO formation. 69 Reduced arginine transport into cells caused by oxidized LDL may be a factor in its pro-atherogenicity. INOS is proatherogenic, whereas eNOS activity is atheroprotective in part due to its vasoreactive characteristics. The latter produces more NO flux than eNOS and, in the presence of ROS, can trigger the production of pro-inflammatory peroxynitrites.
Asymmetrical dimethylarginine, a NOS competitive inhibitor, is more abundant in atherosclerotic lesions as well. Consequently, arginine supplementation’s effects may be quite complex. 72 Tetrahydrobiopterin (BH4), an eNOS cofactor, is decreased by oxidative stress. In these conditions, superoxides are produced by eNOS through a process known as uncoupling, which results in the production of peroxynitrites.
Cardiovascular Disease, Ethnicity, and Socioeconomic Status
With a few exceptions, epidemiological studies have provided the majority of the data on the risk factors for cardiovascular disease in well-fed Western populations. The topic of obesity emphasizes the significance of a favorable energy balance. The increased food availability & larger portion sizes, particularly in fast food restaurants, contribute to the rising prevalence of obesity, even though many endogenous factors may improve this situation.
Although some studies have linked obesity to poverty, Chang and Lauderdale’s review of the evolution of obesity over a three-decade period revealed that among Black women, obesity increased more within the middle-income group than in the poor group, whereas among Black men, obesity increased most in the highest income group.
It’s unclear what separates men and women on a fundamental level. Although socioeconomic status cannot fully account for obesity, it can have an impact on the choice of foods and how healthy they are. Due to cost and availability, the poor frequently choose foods with a high nutritional density, whereas they do not have easy access to fruits and vegetables.
Here, we’ve demonstrated the close connection between diet and cardiovascular disease, which is well known and researched in developed countries but is developing quickly in underdeveloped ones. Both societies are severely burdened by the prevalence of this disease that is influenced by the environment. Many of the root causes & risk factors start when people are young. Therefore, the challenge is to encourage a healthy diet and active lifestyles in children and young adults as early as possible around the world.
How do family history and genetics impact the risk of heart disease?
Heredity is the process by which genes are used to pass traits of one generation to the next. Heart disease, high blood pressure, and other conditions related to these likely have some genetic component. People with a family history of heart disease are also probably to share environments and other elements that could raise their risk. When unhealthy lifestyle choices like smoking and eating poorly are combined with hereditary factors, the risk of heart disease can rise even further.
What role does your metabolism play?
The chemical process by which your body converts the food you eat into the energy that keeps you alive is known as metabolism. Food, or nutrition, is made up of proteins, carbohydrates, & fats. Enzymes in your digestive system break down these substances, which are then transported to your cells, where they can be used as fuel. These substances are either used immediately by your body or stored for future use in the liver, body fat, & muscle tissues.
A specific type of fat that this condition cannot break down builds up in the liver, spleen, and bone marrow. This inability can bring on pain, bone damage, or even death. Treatment for it involves enzyme replacement therapy.
Malabsorptive glucose galactose?
This is a problem with how glucose and galactose are transported across the stomach lining, and it causes severe diarrhea and dehydration. By eliminating lactose, sucrose, & glucose from the diet, symptoms can be managed.