International Journal of Advance Innovations, Thoughts & Ideas
Open Access

Overnutrition is a bad eating habit that has been linked to increased health risks, particularly in wealthy countries. As a result, there is a discrepancy between energy storage and energy breakdown. Many biochemical mechanisms including hormones are implicated in the transmission of surplus energy into pathological states, including atherosclerosis, hypertension, cardiovascular disease, and diabetes. Various forms of regular exercise have been demonstrated to be useful in resolving the over nutrition comorbidities to varying degrees. Hormesis, or cellular workouts, are induced by dietary programmes and may underpin the cellular processes that modulate the harmful consequences of over nutrition by activating certain cellular signal pathways.[1] The oxidative stress signalling pathway, Nuclear factor erythroid-2, Insulin-like growth factor-1, AMP-activated protein kinase, Sirtuins, and Nuclear factor Kappa N are all of interest.[2] As a result, the efficacy of intermittent fasting diets and other hormesis-inducing eating regimens is assessed in terms of their health and lifespan benefits. Simultaneously, the importance of meals on the immune system is investigated as critical components that might jeopardies overall health outcomes. In addition, the influence of the subtle but important relationship between nutrition and sleep on the cardiovascular system and quality of life is explored.ccNuclear factor erythroid-2, Insulin-like growth factor-1, AMP-activated protein kinase, Sirtuins, and Nuclear factor Kappa N are all of relevance in the oxidative stress signalling pathway. As a consequence, the health and longevity advantages of intermittent fasting diets and other hormesis-inducing eating regimens are evaluated. Simultaneously, the impact of food on the immune system is being explored as crucial factors that might jeopardise overall health results. The impact of the modest but significant interaction between diet and sleep on the cardiovascular system and quality of life is also investigatedHypertension, hyperlipidemia, diabetes mellitus, poor diet and physical inactivity, overweight and obesity, and smoking are the main modifiable risk factors for heart disease and stroke, according to the Framingham Heart Study. It's worth noting that genetics has a role in illness progression as a non-modifiable risk factor. According to the Centers for Disease Treatment and Prevention ), big improvements in diet and physical activity, control of high blood pressure and cholesterol, and smoking cessation would significantly lower the risk of Americans developing and dying from cardiovascular disease. Except for cigarette smoking, all of these risk factors – hypertension, hyperlipidemia, obesity, and Diabetes may be brought on by one thing: overeating.[3]What possibilities do we have? Consume fewer calories and engage in greater physical exercise. Atherosclerosis can also be caused by consuming too many calories. Lipid deposition in the arterial wall of large and medium-sized arteries is caused by persistently elevated amounts of particular lipids in the blood. Lowdensity lipoprotein and other apo B-containing lipoproteins, which include smaller triglyceride-rich very low-density lipoproteins that become modified by aggregation, acetylation, or oxidation while freely fluxing across the endothelial barrier, interacting with proteoglycans, and can retain in the extracellular matr, are the lipids in the blood that can cause deposition The influx of macrophages to remove the lipid deposit Toll-like receptors (TLR) and scavenger receptors like CD36 are used by macrophages to initiate proinflammatory responses . TLR activation results in increased generation of reactive oxygen species (ROS), upregulation of protein kinases C and Syk, and activation of NADPH oxidase. Previous mouse studies found a Mox kind of macrophage that uses Nuclear erythroid factor 2 (Nrf2) to convert macrophage phenotypes into pro- or anti-inflammatory macrophages. Mox converts macrophages to a proatherogenic type in the presence of hyperlipidemia, leading in the phagocytosis of cholesterol crystals that can harm the lysosomal system. According to the graph below, cholesterol esters in lipid plaques can excite macrophages and promote foam cell production via nuclear factor-B (NF-B) and Mitogenactivated protein kinase (MAPK) signalling this thrombus-forming atheromatous plaque may rupture. Following the rupture of the plaque, the wounded artery goes through a healing phase that includes increased calcium and fibrous material deposition, which contributes to lumen stenosis and vascular remodelling that is constrictive and inward. The pathogenesis of hypertension related to atherosclerosis involves stenosis and eventual non-compliant stiffness of the artery. According to the Merck Manual, atherosclerotic alterations cause 80 percent of hypertension. The thrombus formed by lipid deposition can sometimes induce full blockage or dislodge and produce thromboembolism in the coronary arteries or the neurovascular system, resulting in heart disease, arterial dissection, and/or stroke. [4-5] the goal of this study is to look at how caloric restriction activates several molecular pathways that contribute to hormetic effects and cell lifespan, as well as resistance to cardiovascular disease, stroke, and cancer. Many great sources in the literature indicate to a variety of chemical processes, each strongly pointing to a distinct pathway via which this hormetic effect is delivered. The cumulative influence on health is proven in this review by combining the outcomes of research across all minute molecular pathways, resulting in cell longevity and life longevity. By presenting a biological rationale for the tremendous effect of calorie restriction and physical exercise, this review intends to increase the motivation and growth of the cultural movement toward change and the establishment of healthy habits.

Acknowledgement

The National Institute on Minority Health and Health Disparities of the National Institutes of Health financed this investigation (in part) under Award Number G12MD007597. The authors are entirely responsible for the material, which does not necessarily reflect the views of the National Institutes of Health..

Acknowledgement

I would like to thank my Professor for his support and encouragement.

Conflict of Interest

The authors declare that they are no conflict of interest

1. Barnett, M. R., Keshavarz, Z., Ma, X. (2006) A semianalytical Sachs model for the flow stress of a magnesium alloy. Metall Mater Trans A Phys.Metall. Mater Sci 37 2283–2293.

Indexed at, Google Scholar, Crossref

2. Bartos DC, Grandi E, C.M. (2015) Ion channels in the heart. Compr  Physiol 5: 1423-1464.

Indexed at, Google Scholar, Crossref

3. Hort N,  Mathaudhu N,  Neelameggham X The Minerals, Metals & Materials Society (TMS)]. eds 17–20.

Indexed at, Google Scholar, Crossref

4. Abaspour S (2014)  Thermodynamics-based design of creep resistant mg solid solutions using the miedema scheme. Queensland: The University of Queensland, Australia 46 (12):5972-5988.

Indexed at, Google Scholar, Crossref

5. Abe E, Kawamura, Hayashi Y K (2002) Long-period ordered structure in a high-strength nanocrystalline Mg-1 at% Zn-2 at% Y alloy studied by atomic-resolution Z-contrast STEM. Acta Mater 50: 3845-3857.

Indexed at, Google Scholar, Crossref