High Risk of Metabolic Complications Due to High Consumption of Processed Foods

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Abstract:

The lack of knowledge among adolescents makes them more sensitive to engage in unhealthy habits which might harm health and nutritional status. A high caloric diet and lack of physical activity are responsible for the generation of reactive oxygen species leading to neurological diseases. The gap in knowledge about Junk food and its complications poses a significant threat to public health policy. Metabolic Syndrome develops due to high fat-induced chronic inflammation and leads to cognition disturbances, stroke, and neurological diseases such as Alzheimer's disease. Adolescent age is the most devastating one where several Lifestyle associated diseases (Sophisticated and cozy lifestyle) occur and is linked with chronic diseases viz., Alzheimer, Non-Alcoholic Steatohepatitis, Type 2 Diabetes Mellitus, Non-Alcoholic Fatty liver disease, Obesity, Hypertension, etc. The unstructured eating behaviors should be prevented at the earliest to overcome the "Fast food Genocide" from eating Processed foods to obesity and nutritional deficiencies leading to neurological complications and destructing the brain cell. As we age, memory begins to decline, and thus by lowering our intake of high calorific foods and salt intake, we could reduce metabolic syndrome-related and age-related issues like blood pressure, T2DM, obesity, etc. Thus, to curb diseases linked with Junk foods, awareness about nutritional values of foods among adolescents and higher tax slabs of junks foods should be made to reduce the purchase of such products.

Related collections

Most cited references 119

Record: found
Abstract: found
Article: found

Is Open Access

Health effects of dietary risks in 195 countries, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017

Ashkan Afshin, Patrick John Sur, Kairsten A. Fay … (2019)

Summary Background Suboptimal diet is an important preventable risk factor for non-communicable diseases (NCDs); however, its impact on the burden of NCDs has not been systematically evaluated. This study aimed to evaluate the consumption of major foods and nutrients across 195 countries and to quantify the impact of their suboptimal intake on NCD mortality and morbidity. Methods By use of a comparative risk assessment approach, we estimated the proportion of disease-specific burden attributable to each dietary risk factor (also referred to as population attributable fraction) among adults aged 25 years or older. The main inputs to this analysis included the intake of each dietary factor, the effect size of the dietary factor on disease endpoint, and the level of intake associated with the lowest risk of mortality. Then, by use of disease-specific population attributable fractions, mortality, and disability-adjusted life-years (DALYs), we calculated the number of deaths and DALYs attributable to diet for each disease outcome. Findings In 2017, 11 million (95% uncertainty interval [UI] 10–12) deaths and 255 million (234–274) DALYs were attributable to dietary risk factors. High intake of sodium (3 million [1–5] deaths and 70 million [34–118] DALYs), low intake of whole grains (3 million [2–4] deaths and 82 million [59–109] DALYs), and low intake of fruits (2 million [1–4] deaths and 65 million [41–92] DALYs) were the leading dietary risk factors for deaths and DALYs globally and in many countries. Dietary data were from mixed sources and were not available for all countries, increasing the statistical uncertainty of our estimates. Interpretation This study provides a comprehensive picture of the potential impact of suboptimal diet on NCD mortality and morbidity, highlighting the need for improving diet across nations. Our findings will inform implementation of evidence-based dietary interventions and provide a platform for evaluation of their impact on human health annually. Funding Bill & Melinda Gates Foundation.

0 comments Cited 1843 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: found

Is Open Access

The Global Epidemic of the Metabolic Syndrome

Mohammad G. Saklayen (2018)

Metabolic syndrome, variously known also as syndrome X, insulin resistance, etc., is defined by WHO as a pathologic condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. Though there is some variation in the definition by other health care organization, the differences are minor. With the successful conquest of communicable infectious diseases in most of the world, this new non-communicable disease (NCD) has become the major health hazard of modern world. Though it started in the Western world, with the spread of the Western lifestyle across the globe, it has become now a truly global problem. The prevalence of the metabolic syndrome is often more in the urban population of some developing countries than in its Western counterparts. The two basic forces spreading this malady are the increase in consumption of high calorie-low fiber fast food and the decrease in physical activity due to mechanized transportations and sedentary form of leisure time activities. The syndrome feeds into the spread of the diseases like type 2 diabetes, coronary diseases, stroke, and other disabilities. The total cost of the malady including the cost of health care and loss of potential economic activity is in trillions. The present trend is not sustainable unless a magic cure is found (unlikely) or concerted global/governmental/societal efforts are made to change the lifestyle that is promoting it. There are certainly some elements in the causation of the metabolic syndrome that cannot be changed but many are amenable for corrections and curtailments. For example, better urban planning to encourage active lifestyle, subsidizing consumption of whole grains and possible taxing high calorie snacks, restricting media advertisement of unhealthy food, etc. Revitalizing old fashion healthier lifestyle, promoting old-fashioned foods using healthy herbs rather than oil and sugar, and educating people about choosing healthy/wholesome food over junks are among the steps that can be considered.

0 comments Cited 1271 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Mechanisms of Insulin Action and Insulin Resistance

Max Petersen, Gerald I. Shulman (2018)

The 1921 discovery of insulin was a Big Bang from which a vast and expanding universe of research into insulin action and resistance has issued. In the intervening century, some discoveries have matured, coalescing into solid and fertile ground for clinical application; others remain incompletely investigated and scientifically controversial. Here, we attempt to synthesize this work to guide further mechanistic investigation and to inform the development of novel therapies for type 2 diabetes (T2D). The rational development of such therapies necessitates detailed knowledge of one of the key pathophysiological processes involved in T2D: insulin resistance. Understanding insulin resistance, in turn, requires knowledge of normal insulin action. In this review, both the physiology of insulin action and the pathophysiology of insulin resistance are described, focusing on three key insulin target tissues: skeletal muscle, liver, and white adipose tissue. We aim to develop an integrated physiological perspective, placing the intricate signaling effectors that carry out the cell-autonomous response to insulin in the context of the tissue-specific functions that generate the coordinated organismal response. First, in section II, the effectors and effects of direct, cell-autonomous insulin action in muscle, liver, and white adipose tissue are reviewed, beginning at the insulin receptor and working downstream. Section III considers the critical and underappreciated role of tissue crosstalk in whole body insulin action, especially the essential interaction between adipose lipolysis and hepatic gluconeogenesis. The pathophysiology of insulin resistance is then described in section IV. Special attention is given to which signaling pathways and functions become insulin resistant in the setting of chronic overnutrition, and an alternative explanation for the phenomenon of ‟selective hepatic insulin resistanceˮ is presented. Sections V, VI, and VII critically examine the evidence for and against several putative mediators of insulin resistance. Section V reviews work linking the bioactive lipids diacylglycerol, ceramide, and acylcarnitine to insulin resistance; section VI considers the impact of nutrient stresses in the endoplasmic reticulum and mitochondria on insulin resistance; and section VII discusses non-cell autonomous factors proposed to induce insulin resistance, including inflammatory mediators, branched-chain amino acids, adipokines, and hepatokines. Finally, in section VIII, we propose an integrated model of insulin resistance that links these mediators to final common pathways of metabolite-driven gluconeogenesis and ectopic lipid accumulation.

0 comments Cited 892 times – based on 0 reviews      Review now

All references

Author and article information

Journal

Title: Current Nutrition & Food Science

Abbreviated Title: CNF

Publisher: Bentham Science Publishers Ltd.

ISSN (Print): 15734013

Publication date Created: February 2023

Publication date (Print): February 2023

Volume: 19

Issue: 3

Pages: 198-208

Affiliations

[1 ]Department of Pharmacology, SRM College of Pharmacy, SRM IST, Kattankulathur, Kancheepuram, Tamil Nadu, India

Article

DOI: 10.2174/1573401318666220622162038

SO-VID: 9978a49c-2fc0-4953-a3b4-ba94b3b77a85

History

Data availability:

Comments

Comment on this article

Cited by 1

A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer’s disease-like animal model
Authors: Singh S. Ankul, Lakshmi Chandran, Singh Anuragh …

See all cited by

Most referenced authors 1,366

See all reference authors