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P. G. Nair et al.

[51]. A randomized clinical trial (RCT) that administered E. ofcinalis extract to newly diagnosed DM patients with dyslipidaemia reported its anti- diabetic and lipid-lowering potentials. Fruit extract at a dose of 2g/day exhibited superior activity to Metformin [52].

6.3 Cinnamomum verum J.Presl

C. verum, commonly called true cinnamon, is a small tree belonging to the Lauracea family. The tree’s inner bark is the useful part traditionally used in treating many conditions like DM.It is also used as a spice in culinary practices to add colour and avour to food [53]. Much research has been carried out on the biological activity of C. verum extract and its phytocompounds. A bioactive compound extracted from the aqueous extract has been reported to increase insulin signalling by decreasing the activity of insulin receptor kinase inhibitors in rat epididymal fat cells. Cinnamon compounds are supposed to regulate protein phosphorylation and dephosphorylation in intact adipocytes, thereby regulating IR [54]. Oral administration of cinnamon improved glucose infusion rate by upregulating the insulin signalling pathway in the skeletal muscles of Wistar rats. In the study, it was seen that the cinnamon extract did not affect insulin secretion. However, it signicantly increased the tyrosine phosphorylation level of the insulin receptor β subunit (IR-β) and insulin receptor substrate-1 (IRS-1) [55]. In HFD-induced models of IR, cinnamon extract (CE) signicantly reduced hyperinsulinemia, dyslipidaemia, and plasma adiponectin. IR has been strongly associated with the overexpression of lipid metabolism- related biomarkers. CE regulated lipid metabolism by reducing the chylomicron-apolipoprotein (apo) B48, VLDL-apoB100 particles, sCD36, plasma FABP4, and RBP4 levels. At the molecular level, CE increased the IRS 1, IRS 2, and adipose mRNA expression in adipose tissue. CE also suppressed the overexpression of Lpl, Fas, and Fabp4 genes, which are usually the early markers of metabolic syndrome [56]. CD36, a complex multifunctional protein, is another essential macrophage activation marker in IR conditions. The soluble form of CD36 (sCD36) is elevated in metabolic syndrome and is a surrogate marker in conditions like atherosclerosis [57]. CE reduced the increased levels of sCD36in adipose tissue, highlighting the protective role of cinnamon [55]. Clinically cinnamon administration decreased serum glucose, total cholesterol, triglycerides, and LDL in individuals with type 2 DM [58]. In another pilot study, oral administration of cinnamon for 8weeks to 15 non-diabetic women with PCOS improved insulin sensitivity and reduced IR signicantly compared to the placebo group. Large sample prospective RCTs are required to validate the ndings of such studies [59].

6.4 Momordica charantia L.

M. charantia (MC), also called bitter gourd, is a medicinal plant with a long history of usage in traditional medicine. The unripe fruit of the plant is bitter and is a commonly used vegetable. Cucurbitane-type triterpenoids isolated from MC are extensively studied for their anti-diabetic activities [60]. Many biologically effective novel proteins and enzymes have been isolated from MC fruit. These have been reported to be effective in various metabolic dysfunctions and exhibit cytotoxic activity against various cancer cells [61]. In diabetic animal models, MC extract reduced serum glucose levels by increasing glucose utilization in the liver. The study also reported that the extract showed no insulin secretagogue activity [62]. In another study, MC aqueous extract signicantly lowered blood glucose levels compared to insulin in KK-Ay mice with IR.It increased the GLUT 4 protein content in mouse muscles and signicantly reduced hyperinsulinemia by increasing the peripheral utilization of glucose. However, in normal mice, repeated administration of MC did not affect the blood glucose levels. This suggests that MC may directly activate insulin receptors in peripheral muscles to increase glucose uptake [63]. The adenosine monophosphate- activated protein kinase (AMPK) is a metabolic sensor that is involved in activities that regulate lipid, glucose, and energy imbalances. It controls various key molecules of metabolic pathways and is recognized as a potential drug target for treating metabolic dysfunctions [64]. Terpenoid fractions extracted from the stem of MC has shown to activate AMPK in cells. This further increased the tyrosine phosphorylation of IRS-1 and triggered the insulin signalling pathway [65]. Peroxisome proliferator-activated receptor (PPAR γ) in the adipose tissue plays a crucial role in glucose homeostasis and differentiation of fat cells. Synthetic PPAR γ ligands are usually employed to activate PPAR γ, increasing insulin sensitivity. Administration of MC extracts to HFD-fed C57BL/6J mice increased the PPARγ mRNA expressions in adipose tissues. It also acted as a ligand of PPAR γ and increased insulin sensitivity. MC extracts also regulated the PPAR α-mediated pathway to upregulate the genes responsible for fatty acid oxidation and cellular uptake of free fatty acids [66]. Leptins are a group of proteins secreted by the white adipose tissue that regulate metabolic activities, energy expenditure in the body. Serum leptin levels are usually elevated in conditions like obesity and act as a predictive marker of metabolic syndrome [67]. MC extracts could signicantly reduce S. leptin levels and thus may be effectively used to manage metabolic syndrome triggered by visceral obesity [66]. In a preliminary open-label uncontrolled clinical study, MC supplementation for 3months signicantly reduced the incidence of metabolic syndrome. The results remained consistent after 1month of drug cessation.

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Waist circumference was also considerably reduced in the study population following MC supplementation [68]. A few clinical trials have reported MC to be effective in DM, dyslipidaemia, and obesity [69].

6.5 Trigonellum foenum-graecum L.

T. foenum-graecum (fenugreek) is a small plant belonging to the Fabaceae family. Fenugreek leaves are used as a vegetable in culinary practices, whereas seeds are used as a spice or condiment. Traditional medicinal practices have recorded much therapeutic activity of the plant, especially as a digestive aid. Many recent studies have found it helpful in treating DM, dyslipidaemia, cancer, and obesity. It is rich in dietary bre and contains bio constituents such as saponins, alkaloids, steroidal compounds, avonoids, and amino acids that exhibit diverse pharmacological activity [70]. In animal models of IR, fenugreek extract (FE) lowered serum insulin, glucose, and triglyceride levels [71]. Adiponectin, a biologically active protein produced by adipose tissues, plays a pivotal role in regulating energy metabolism, cell proliferation, and insulin sensitivity in the body. It also exhibits antiinammatory and anti-atherogenic activities. In conditions like obesity, excessive fat accumulation decreases adiponectin production, causing different metabolic complications [72]. FE enhanced adiponectin levels and caused considerable weight reduction in experimental animals. It also increased PPAR γ expression at molecular levels to increase fatty acid uptake and insulin sensitivity [71]. Three polyphenolic stilbenes rhaponticin (RHAc), desoxyrhaponticin (dRHAc), and rhapontigenin (RHAg) isolated from FE have been reported to improve insulin sensitivity and mitochondrial function in IR 3T3-L1 adipocytes. Lipid drop accumulation is a common phenomenon during the differentiation of preadipocyte 3T3-L1 cells into adipocytes. This is usually presented as increased triglyceride levels. FE stilbenes treatment reduced triglyceride levels during cell differentiation suggesting its role in reducing lipid accumulation. They also increased glucose uptake by activating protein kinase B (AKT) and AMPK signalling pathways. IR causes mitochondrial dysfunction and decreases ATP production. Stilbenes improved mitochondrial membrane potential and increased ATP in adipocytes. The free radical scavenging potential of the compounds was highlighted as one of the reasons which promoted the biological activities of these compounds. Among the three compounds, RHAc showed maximum activity [73]. In mice, intragastric administration of FE reduced hyperglyacemia in HFD and STZ-induced type 2 DM.Reactive oxygen species (ROS) play a signicant role in developing IR and related complications. In the study, FE increased the superoxide dismutase (SOD) activity for clearing excessive ROS production and inhibiting lipid peroxida-

tion [74]. Aqueous FE was administered orally to HFD-fed C57BL/6J, type 2 DM models to study its preventive and curative effects. HFD models with and without DM decreased serum insulin and glucose by reducing IR. Elevated lipid parameters were also signicantly reduced [75]. In HFD and fat emulsion-administered models of hyperlipidaemia, fenugreek- controlled lipid prole by inhibiting cholesterol absorption and enhancing its excretion. Fenugreek contains polysaccharides like galactomannan which increases the viscosity of the small intestine and thereby inhibits the reabsorption of cholesterol and bile salt [76]. A double-blind placebo-controlled clinical study that administered FE to 25 newly diagnosed DM patients with fasting sugar less than 200 mg/dL showed considerable hypoglycaemic activity with improved insulin sensitivity. Serum triglyceride levels were decreased in the study population [77]. Another RCT that administered fenugreek as adjuvant therapy to Metformin in 12 patients with type 2 DM reduced blood glucose levels. It signicantly increased HDL/LDL ratio compared to Glibenclamide treated group. Although it reduced IR, HbA1c, LDL, and triglycerides, the results were nonsignicant compared to the standard drug. Rich dietary bre and polysaccharides in fenugreek delay gastric emptying and inhibit glucose absorption. It was also found helpful in reducing body weight. Nevertheless, the study’s sample size seems signicantly smaller, and a large prospective RCT is required to validate the ndings [78].

6.6 Eugenia jambolana Lam.

E. jambolana, called black plum or Jamun, is an evergreen tree from the Myrtacea family. Indian traditional medicine practices use all plant parts to treat various diseases. Jamun fruits are advised to be ideal for inclusion in the diet of diabetic patients, and seeds are used explicitly by traditional practitioners in the treatment of DM [79]. Interestingly before the discovery of insulin, E. jambolana preparations were frequently used as an antidiabetic drug in European countries [80]. In HFD-induced obese mice models, jamun extract (JE) reduced IR, body weight, and white adipose mass. It also prevented liver steatosis by reducing the expression of genes related to lipogenesis. Cholesterol, triglyceride, and free fatty acid levels were also signicantly reduced. Gut microbial dysbiosis is a major causative factor of metabolic disorders. Studies suggest that in obese individuals, dysbiosis is seen in the bacterial ora with an increased proportion of Firmicutes and a decrease in Bacteroidetes. This derangement alters intestinal permeability to cause increased absorption of lipopolysaccharides and activate inammatory pathways. JE administration helped to restore the ratio of Firmicutes to Bacteroidetes. Prevotella, Bacteroides, and Alloprevotella, which are typically short-chain fatty acid

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P. G. Nair et al.

producers, were also enhanced in experimental models. These help to improve glucose metabolism and reduce obesity and liver steatosis [81]. Administration of JE to HFD-fed IR albino rat models reversed hyperinsulinemia, hyperlipidaemia, and hyperglycaemia. It could signicantly reduce the IR compared to the control group [82]. In the long-term and short-term models of DM, the ethyl acetate fraction of JE showed good antihyperglycemic activity. The gallic acid and other polyphenolic compounds present in the fraction contributed to its antidiabetic activity. It was also noticed that the apoptotic cells in pancreatic islets were signicantly reduced in the study group due to the potent antioxidant activity of JE.Hexokinase (Hex-1), an enzyme crucial to carbohydrate metabolism, is diminished in diabetic patients. After 35days of administration, JE improved the expression of Hex-1in experimental animals and restored carbohydrate metabolism [83]. Patients usually take JE as an adjuvant, along with other oral antihyperglycemic medications. Drugs reducing hyperinsulinemia can signicantly treat conditions such as DM, obesity, hypertension, and coronary heart diseases. In high fructose diet-fed animal models, an aqueous extract combination of E. jambolana and M. charantia prevented hyperinsulinemia and hyperglycaemia. However, alcoholic extracts were found to be ineffective [84]. An herbdrug interaction study reported that the administration of JE along with Sitagliptin reduced the systemic exposure of Sitagliptin. It helped reduce Sitagliptin’s side effects without compromising its therapeutic efcacy [85]. An open-label RCT administered E. jambolana seed powder to 30 newly diagnosed cases of type 2 DM signicantly reduced blood glucose levels and IR.It also reduced HDL cholesterol in the study population and thus may be considered a suitable choice for preventing atherosclerosis and other cardiovascular complications associated with DM [86].

6.7 Gymnema sylvestre (Retz.) R.Br.

G. sylvestre (GS) is an essential medicinal plant in the Asclepiadaceae family. It is an effective herb used in Ayurvedic medicine to treat DM.Leaves are the foremost useful part. Triterpene saponins isolated from leaves are

extensively studied for their broad therapeutic activity. Leaves on intake numb the taste buds on the tongue and interfere with the perception of sweet taste. This helps to limit the consumption of sweet food later. Various studies have reported that G. sylvestre extracts and their isolated compounds possess antidiabetic, antihyperlipidemic, anticancerous, and anti-obesity properties. It is also consumed as herbal supplements, beverages, and teas to regulate DM and related complications [87, 88]. In animal models of metabolic syndrome, deacyl gymnemic acid isolated from GS decreased systolic blood pressure, hyperglycaemia, hyperinsulinemia, and IR [89]. In an afnity ultraltration method coupled with liquid chromatography-mass spectrometry, nine sapogenin compounds in GS extract inhibited α-glucosidase [90]. Apart from antihyperglycemic activity, GS has shown anticancerous activity in human skin melanoma cells. It was found that GS treatment increased the mortality of melanoma cells dose-dependent. It also increased the expression of cytochrome c, caspase 3, PARP, Bax genes responsible for apoptosis. On the other hand, the expression of anti-apoptotic mRNAs of the Bcl2 gene was considerably decreased. This study suggested that GS may be a drug of choice for inclusion in the palliative care of DM patients with cancer [91]. Another STZ-induced type 2 DM study showed that GS extract increased insulin secretion in rat pancreas by increasing insulin mRNA expression. It also promoted endogenous β-cell regeneration by upregulating pancreatic regenerative markers such as Pdx1, Neurogenin 3, MafA, and NeuroD1. E-cadherin (ECAD) is a critical adhesion molecule found in islets of Langerhans which can inuence insulin production. GS administration upregulated ECAD, inuencing pancreas structure and stimulating insulin secretion [92]. A double-blind placebo-controlled RCT that supplemented GS to 24 patients with metabolic syndrome reduced body weight, body mass index (BMI), and VLDL cholesterol. It showed no signicant changes in insulin sensitivity and secretion in those patients [93]. Another RCT reported that GS supplementation to 30 patients with impaired glucose tolerance reduced HbA1c and increased insulin sensitivity. Improvements were noted in the anthropometric measures after treatment and reduced LDL cholesterol [94] (Table2).

The Importance and Scope of Medicinal Plants Suggested in Traditional Medicine in the Holistic Care of Occupational Lifestyle…

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Table 2 The reported activity of medicinal plants and their monomers in IR and associated occupational lifestyle disorders

Study drug Dose/duration Curcumin 4g/kg, 2days a week for

Turmeric extract

Curcumin C3 complex Curcuminoids (500mg/day) with

Indian gooseberry extract 100mg/kg of body weight In vivo Decreased dyslipidemia, IR and prevented metabolic

EmbliQur (E. ofcinalis fruit and C. longa rhizome extract in proportion 2:1)

Sabbery Amla fruit extract with 100/kg

E. ofcinalis extract with 10% β-glucogallin

Cinnamon (puried fraction)

Cinnamon extract 30/300mg/kg BW for 3weeks In vivo Increased glucose uptake in skeletal muscles by

Cinnamon extract 50mg/kg for 8weeks In vivo

Cinnamon 1,3,6 gm/day for 40days Clinical Reduced serum glucose, total cholesterol, LDL, and

Cinnamon capsule 333mg, three times a day for

M. charantia fruit alcoholic extract

M. charantia aqueous extract

Triterpenoid compounds puried from the stem extract of M. charantia

M. charantia aqueous P extract and methanolic G extract

Wild bitter gourd powder 4.8gm daily for 3months Clinical Decreased metabolic syndrome incidence rate.

Fenugreek extract Intragastric injection of 1000mg/

Stilbenes isolated from fenugreek seed extract

28weeks 3% by weight admixture with a

standardized diet

60mg/kg suspension for 14days In vivo Neuroprotective activity by upregulation of

Bio-enhanced extracts (BTE30mg/kg and 60mg/kg) and regular (RTE-30mg/kg) for 30days

piperine (5mg/day) for 3months

500/1000mg/kg for 28days In vivo Both doses signicantly reduced IR, blood glucose

β-glucogallin

1g/2g for 90days Clinical Signicant reduction in FBS, PPBS, HbA1c, and

1:30/1:300 nal dilution fraction In vitro Inhibit protein tyrosine phosphatases-1 activity and

8weeks 500mg/kg of BW In vivo Hypoglycaemic activity by increasing the glycogen

100mg/kg BW for 3weeks In vivo Decreased IR by increasing GLUT 4 content in

Diluted fractions from 5mg/mL compound dissolved in dimethylsulfoxide

P extract—0.5g, 1gm/kg of BW G extract—0.2g, 1gm/kg of BW

kg/day for 2weeks

0–100μmol/L

Type of study Key ndings Reference

In vivo

In vivo and invitro

In vivo BTE showed signicant anti-diabetic activity and

Clinical Reduction in the serum concentration of insulin,

In vitro Antidiabetic activity by inhibiting pancreatic

and invitro

Clinical Improved insulin sensitivity in non-diabetic women

In vitro Activated AMPK to increase the IRS-1-linked

In vivo

In vivo Signicantly increased insulin sensitivity and

In vitro Reduced lipid accumulation during differentiation of

Reduced IR by potent antioxidant and antiinammatory activity

Improved insulin sensitivity by increasing serum adiponectin levels

cholinergic, Glut 3, insulin receptors in the cerebellum of STZ-induced DM rats

weight reduction by decreasing IR and increasing beta cell function

HOMA-IR and HbA1c

alterations in ovariectomized high fructose-fed rat models

levels, and insulin. A dose of 1000mg/kg was more effective than 500mg/kg in reducing IR

α-amylase and salivary α-amylase enzymes. Exhibited signicant antioxidant potential

lipid prole

increase insulin receptor activity

IR- β and IRS phosphorylation in a dose-dependent manner

Decreased the level of various biomarkers related to IR.Increased mRNA levels of components involved in the insulin signalling pathway

triglycerides in a dose-dependent manner

with PCOS

synthesis in liver

muscles

tyrosine phosphorylation

Regulation of PPAR γ/PPAR α pathways to improve insulin sensitivity and plasma lipid prole, respectively

Reduction in waist circumference

adiponectin levels. Decreased weight gain and triglycerides

preadipocyte cell lines into adipocytes. Increased glucose uptake by AKT and AMPK phosphorylation. Improved mitochondrial function

[37]

[40]

[41]

[42]

[43]

[47]

[48]

[50]

[52]

[54]

[55]

[56]

[58]

[59]

[62]

[63]

[65]

[66]

[68]

[71]

[73]

(continued)

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Table 2 (continued)

Study drug Dose/duration Fenugreek seed extracts

(E1, avonoid and E2, stilbene glycoside)

Fenugreek seed hydroalcoholic extract

Fenugreek 2g/day for 12weeks Clinical Signicant increase in HDL/LDL ratio [78] Jamun fruit extract 100mg/kg for 8weeks In vivo Reduced IR, cholesterol, free fatty acids, and

E. jambolana aqueous and alcoholic extract

Ethyl acetate fraction of E. jambolana seeds

Combined extract of M.

charantia fruit and E. jambolana kernel

E. jambolana powder 5gm twice daily for 6months Clinical Reduced IR and hyperglycaemia. Elevated HDL

Deacyl gymnemic acid 50/100/200mg/kg for 20days In vivo Decreased systolic blood pressure, S. glucose,

Ethanolic extract of G.

sylvestre

Gymnema extract 150mg/kg for 30days In vivo

G. sylvestre 600mg/day for 12weeks Clinical Decreased BMI, VLDL, and body weight. Insulin

Intragastric administration of 80mg/kg/day for 4weeks

2g/kg/day In vivo Decreased IR and lipid parameters [75]

1gm/day Clinical Decreased IR and triglycerides [77]

1000mg/kg for 14days In vivo Reversed hyperglycaemia, hyperinsulinemia, and

200mg/2mL distilled water/kg of body weight/day for 35days

100, 200, and 400mg/day for 15days

0–300μg/mL

300mg two times a day for 12weeks

Type of study Key ndings Reference

In vivo Exhibited anti-diabetic and antioxidant activities [74]

triglycerides. Restoring gut microbial dysbiosis

hyperlipidemia

In vivo Decreased degeneration of pancreatic beta cell DNA

and increased glucose tolerance

In vivo Aqueous extract prevented hyperglycaemia and

hyperinsulinemia. Alcoholic extract was ineffective

levels

insulin, and IR

In vitro Anticancerous activity by increasing the expression

of apoptotic genes cytochrome c, caspase 3, PARP, Bax, and downregulation of anti-apoptotic gene Bcl2

Promoted endogenous pancreatic β-cell regeneration by upregulating markers Pdx1, Neurogenin 3, MafA, and NeuroD1

sensitivity and secretion remained unaffected

Clinical Reduced HbA1c, body weight, BMI, and LDL [94]

P. G. Nair et al.

[81]

[82]

[83]

[84]

[86]

[89]

[91]

[92]

[93]

7 Conclusion

The world has witnessed an irrefutable transition of disease burden from infectious diseases and infant-maternal mortality to lifestyle disorders. Considering universal health coverage, an inclusive approach in integrative medicine accommodating herbal drugs has much scope in lifestyle disorders. There is rising evidence regarding the possibilities of herbal medicines in different states of IR and associated clinical syndromes commonly found in lifestyle disorders. In addition to standard care medicines that focus on the patient’s routine biochemical parameters, herbal drugs that target multiple pathways, as in IR and associated autophagy, autoimmunity–autoinammation, gut dysbiosis, and glucose intolerance, shall be a breakthrough in lifestyle disorder management. However, this approach demands safety- efcacy proling of herb-standard drug interactions. Hence pre-clinical and clinical trials that judiciously highlight the objective of integrative medicine in IR and related clinical states should be systematically planned and executed.

Acknowledgments The authors are thankful to Prof. Rabinarayan Acharya, Director General, Central Council for Research in Ayurvedic Sciences, Ministry of AYUSH, Government of India, G. Babu. Director, Central Ayurveda Research Institute, Kolkata and Dr. D. Sudhakar, Director, National Ayurveda Research Institute for Panchakarma, Kerala for their support, motivations and encouragement.

Conict of Interest None declare.

Consent for Publication All authors have given consent

for publication.

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Extraction ofPhytoconstituents

https://t.me/medicina_free

forLifestyle Diseases

JosephTchamgoue, YvanAndersonT.Ngandjui, RostanM.Talla, BrunoDuponA.Ambamba, JeanClaudeTchouankeu, andSimeonF.Kouam

Abstract

Diseases whose occurrence is mainly related to an individual's daily living habits are referred to as lifestyle diseases. Some of these diseases require treatment for several years, and others require lifelong treatment. These diseases attack men, women, and children in developed, middle-income, and poor countries and are ranked as one of the primary causes of morbidity and mortality worldwide. For centuries, several plants have been used for their curative and preventive abilities against human ailments including lifestyle diseases. In the past years, the therapeutic benets of a good number of medicinal and edible plants have been studied underlining their role in preventing and managing lifestyle diseases, thanks to their bioactive compounds. In the present chapter, an overview of thirty-ve frequently used plants for the management of different lifestyle diseases, their mechanism of action and their bioactive constituents are provided. Moreover, the suitable techniques for the extraction of phytoconstituents from these plants are detailed.

J. Tchamgoue (*) Department of Organic Chemistry, Faculty of Science, University of Yaoundé I, Yaoundé, Cameroon

Department of Chemistry, Higher Teacher Training College, University of Yaoundé I, Yaoundé, Cameroon

Y. A. T. Ngandjui Department of Chemistry, Higher Teacher Training College, University of Yaoundé I, Yaoundé, Cameroon

Institute for Nanotechnology and Water Sustainability, College of Science, Engineering and Technology, University of South Africa, Florida Science Campus, Johannesburg, South Africa

R. M. Talla · J. C. Tchouankeu Department of Organic Chemistry, Faculty of Science, University of Yaoundé I, Yaoundé, Cameroon

B. D. A. Ambamba Department of Biochemistry, Faculty of Science, University of Yaoundé I, Yaoundé, Cameroon

S. F. Kouam Department of Chemistry, Higher Teacher Training College, University of Yaoundé I, Yaoundé, Cameroon

Keywords

Lifestyle diseases · Medicinal and edible plants · Mechanism of action · Phytoconstituents · Extraction techniques

1 Introduction

Lifestyle diseases (LSD) are diseases associated with daily habits and signies adopting detrimental habits that detract from a healthy lifestyle [1]. Atherosclerosis, heart disease, stroke, obesity, hypertension, diabetes mellitus, hyperglycemia, asthma, and cancer are just a few LSD which can have long duration, slow progression and are likely to cause death. They result from the combination of physiological, behavioral, environmental, and genetic factors [2, 3]. The symptoms associated with these illnesses are not seen in the early stages due to the fact that they take a considerable number of times to develop. Some of these diseases have to be treated for several years, while others need everlasting management. These diseases attack men, women, and children in developed, middle-income, and poor countries. Consumption of tobacco and excessive use of alcohol are key risk factors, but there are many others such poor diets (consumption of foods high in fat, salt, and sugar), physical inactivity, poverty, and stress [4]. Worldwide, approximately 41million people are killed by LSD each year, including 14million early deaths between the ages of 30 and 70 [1]. Of these, cardiovascular diseases were responsible for

17.9million deaths, and the number of deaths from cancers,

chronic respiratory diseases, and diabetes mellitus were 9million, 3.9million, and 1.6million, respectively. These four diseases account for 80% of deaths due to LSD.According to the World Health Organization (WHO), Europe has the highest LSD-related morbidity and mortality rate among the six regions of the world, with approximately 90% of all deaths. In the European Region, obesity and overweight are the most important risk factor for LSD, affecting more than 59% of adults and 29% of children.

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