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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
\n\n\n\n\n'}],latestNews:[{slug:"intechopen-signs-new-contract-with-cepiec-china-for-distribution-of-open-access-books-20210319",title:"IntechOpen Signs New Contract with CEPIEC, China for Distribution of Open Access Books"},{slug:"150-million-downloads-and-counting-20210316",title:"150 Million Downloads and Counting"},{slug:"intechopen-secures-indefinite-content-preservation-with-clockss-20210309",title:"IntechOpen Secures Indefinite Content Preservation with CLOCKSS"},{slug:"intechopen-expands-to-all-global-amazon-channels-with-full-catalog-of-books-20210308",title:"IntechOpen Expands to All Global Amazon Channels with Full Catalog of Books"},{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"}]},book:{item:{type:"book",id:"7003",leadTitle:null,fullTitle:"Herbs and Spices",title:"Herbs and Spices",subtitle:null,reviewType:"peer-reviewed",abstract:"This edited volume, “Herbs and Spices”, is a collection of reviewed and relevant research chapters, offering a comprehensive overview of recent developments in the field of agricultural and biological sciences. 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His research interests include computer graphics, computer vision, image processing, machine learning, pattern recognition, soft computing, data science, intelligent systems, information technology and information systems. Prof. Sarfraz has been a keynote/invited speaker at various platforms around the globe. He has advised more than 85 students for their MSc and Ph.D. theses. He has published more than 400 publications as books, journal articles, and conference papers. Prof. Sarfraz is a member of various professional societies. He is the Chair and member of the International Advisory Committees and Organizing Committees of various international conferences. 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From coronary air embolism to paradoxical venous thromboembolism, CEPs represent an etiologically heterogeneous group of events [4, 5, 6, 7]. It has been postulated that CEPs are the underlying cause of up to 3% of acute coronary syndromes (ACS) [6]. Given their rarity, CEPs require a high index of suspicion by the treating clinician [8, 9, 10]. In this chapter, we will aim to cover the various processes and pathophysiology underlying this cause of acute coronary syndrome. Our focus will be on the more commonly seen forms of coronary embolism, with an abbreviated overview provided of the less common etiologies.
A thorough literature search was conducted using PubMed, Google™ Scholar, and Bioline International. The following search terms were utilized, in various combinations/derivations/iterations, listed alphabetically: “cardiac,” “coronary,” “emboli,” “embolism,” “embolus,” “heart,” “infarction,” “myocardial,” “myocardium,” “paradoxical,” “phenomenon,” “vascular,” “vasculature,” and “vessel”. Secondary identification of additional literature sources was performed using articles referenced by our primary sources.
Coronary emboli may be classified based on etiology (i.e., thrombotic, septic, neoplastic, valvular heart disease-related, iatrogenic), although other classifications (i.e., direct, paradoxical and/or iatrogenic) have been proposed and/or described [6, 11, 12, 13]. A list of all previously reported types/causes of coronary emboli is provided in Table 1.
Thrombotic | Paradoxical thrombus/embolus |
Left atrial appendage thrombus | |
Left atrial thrombus | |
Left ventricular mural thrombus | |
Autoimmune | Inherited coagulation factor deficiencies (prothrombin deficiency, protein C/S deficiency) |
System lupus erythematosus | |
Antiphospholipid syndrome | |
Infectious | Infective endocarditis |
Rheumatic heart disease | |
Valve-related | Fibroelastoma |
Mitral valve calcifications | |
Blood cysts | |
Neoplastic | Malignancy |
Iatrogenic | Post-cardiac procedure |
Miscellaneous causes | Pregnancy |
Air embolism |
Causes of coronary embolism.
Coronary emboli may originate in the left or right side of the heart [14, 15]. Of course, for emboli originating in the right heart to lodge in the coronary arteries, they would need to be somehow “shunted” to the left-sided system, possibly through a patent foramen ovale [16, 17, 18]. An angiographic example of paradoxical coronary artery embolism is show in Figure 1 [19].
Angiographic example of a large coronary artery embolus located in the mid-left anterior descending artery. Source: Zhang et al. [
It must be mentioned here that systemic emboli finding their way to the left heart are still more likely to embolize to the carotid or intracranial vasculature, primarily due to two particular considerations. Firstly, the coronary anatomy and coronary artery takeoff is typically such that emboli are less likely to specifically dislodge and enter into their ostia [13, 20, 21]. Secondly, it is hypothesized that coronary vessels may be protected to some degree, mainly due to them receiving flow primarily during diastole [22, 23, 24, 25, 26]. For similar reasons, one might extrapolate that most reported cases of coronary embolism occur in the left coronary circulation due to the anatomy of the right coronary artery takeoff making it potentially less conducive to emboli [22, 23, 24, 25, 26, 27, 28].
Coronary emboli may become lodged in major epicardial arteries supplying a sizable area of myocardium, and smaller emboli may even embolize distally so as to affect small arterioles which do not supply a large area [29, 30, 31]. These events may or may not be clinically symptomatic or readily diagnosable, but evidence in this generally poorly understood area of cardiac pathophysiology continues to be lacking. It is important to note, however, that coronary emboli may occur in the setting of concomitant atherosclerosis, where even a small embolus could lodge at the site of atherosclerotic lesion and result in significant epicardial coronary occlusion, thus exposing potentially significant area of myocardium at risk for a subsequent secondary ischemic event [31, 32, 33, 34, 35]. An association with infectious etiology may be present as well in this context [32].
Due to various mechanisms being responsible for coronary embolic phenomena leading to acute coronary syndromes, we will address them one by one in the subsequent discussion. The authors’ goal is not to provide an exhaustive description of each mechanism, but rather to point the reader to other definitive sources for further details.
Coronary emboli may be formed due to thromboembolic causes involving different etiologies and pathways (Table 1). As with all thromboembolic phenomena, predisposing conditions of the Virchow’s triad (hypercoagulability, stasis, endothelial injury) will need to be present for thrombi to form [36, 37].
For venous thromboemboli to “transform” into coronary emboli, the presence of a patent foramen ovale is required [6, 38]. This enables the embolus to cross from “right to left” side of the heart and thus develop the potential to lodge in the coronary circulation [18, 38]. A thrombus may originate in the left atrial appendage, as seen among patients with atrial fibrillation [39, 40], or it may originate in the left atrium/ventricle itself, as in patients with severely reduced ejection fraction or those who have had an anterior/apical myocardial infarction in the past [6, 41]. The former is of particular clinical importance, as patients diagnosed with coronary embolus may benefit from ambulatory monitoring to look for atrial fibrillation as a possible underlying cause.
Arterial emboli are more likely to be reported in the setting of hypercoagulable states including autoimmune diseases, inherited coagulation factor deficiencies, hyperviscosity syndromes, and acquired hypercoagulabe states (e.g., pregnancy, malignancy, previous heparin exposure, Table 1) [42, 43, 44]. As coronary emboli are a rarely reported phenomenon, no randomized trials or guidelines exist regarding diagnostic workup for these, although it would not be unreasonable to initiate workup for thrombophilia whenever appropriate diagnosis or suspicion exists [37, 42, 43, 44, 45].
Infective endocarditis is one of the most dreaded infectious etiologies associated with significant morbidity and mortality [46, 47]. Coronary septic arterial emboli (CSAE) secondary to infectious endocarditis have been reported and according to one source such events may carry a mortality of up to 50% [48]. CSAE appear to be more likely to occur in patients having vegetations of the mitral valve or fungal infections, as fungal vegetations are known to reach larger overall dimensions, thus increasing the cumulative possibility of embolization [49, 50]. Rheumatic heart disease, though more common in low-income countries, is another possible etiology that can be associated with CSAE and must be kept in mind when evaluating patients from high-incidence geographic areas [51, 52].
Tumors originating in the heart such as atrial myxomas, or on valves such as papillary fibroelastomas, are well known to cause cryptogenic brain infarctions [14, 53]. There are also reports of embolization to the coronary circulation [54, 55, 56]. Given that end-organ damage, including cerebrovascular accidents may constitute the initial clinical presentation of such neoplasms, it would not be unreasonable to propose that an embolic myocardial infarction may occur in this setting [56, 57]. It is also likely that such occurrences are under-recognized and probably more common than generally thought, thus requiring high index of clinical suspicion and prompt diagnosis [56, 57]. The overall urgency is highlighted by the possibility that subsequent presentations in cases of “missed diagnosis” may manifest as unexplained/sudden death [57, 58]. Appropriate high-quality imaging may include but is not limited to transthoracic and/or transesophageal echocardiography [56, 59, 60, 61].
Stenotic heart valves resulting from progressive calcification process also pose the possibility of calcific embolization to distal locations, including the coronary circulation [48, 62, 63]. Rheumatic valvular heart disease could be another possible risk factor for coronary embolization [48]. Long-term valvular heart disease leads to structural changes in the myocardium, eventually increasing the risk of atrial fibrillation, which in itself may be a contributor to both systemic and coronary embolization [39, 64]. Of note, coronary embolism has been reported following aortic and mitral valve replacement, with successful management reported to involve abciximab and urokinase [65]. Another report describes acute myocardial infarction due to coronary embolism in a patient with mitral valve prosthesis. That particular case was successfully managed using angioplasty [66]. An example of a left coronary embolism associated with subtherapeutic oral anticoagulation in a patient with mitral and aortic mechanical valve prostheses is shown in Figure 2 [67].
An example of a left coronary artery coronary embolism associated with subtherapeutic anticoagulation in the setting of mitral and aortic mechanical valve prostheses. [A, left] Note the filling defect present upon initial diagnosis. [B, right] Following thrombectomy, the left coronary artery is seen to be patent. Source: Protasiewicz et al. [
Ruptured atherosclerotic plaques in the coronary arteries may lead to acute thrombotic occlusions and are the frequent pathophysiologic factor behind acute ST-elevation myocardial infarctions [68, 69]. Vessels affected by such processes may be characterized by a high thrombotic burden. For example, saphenous venous grafts in post-coronary artery bypass graft patients seem particularly vulnerable [70, 71], with various pathophysiologic mechanisms proposed including immune-mediated process [71, 72].
Cardiac catheterization procedures may also cause distal embolization of intravascular particles [73]. Depending upon where, and how far, any dislodged thrombi or microthrombi travel, periprocedural myocardial infarction can become a very real risk [74]. Various procedural techniques including specialized “wire filter” protection devices [74, 75] and thrombus extraction catheters [76] can be utilized during coronary interventions to prevent or reduce distal embolization. Finally, distal coronary embolization involving cholesterol particles is also a possibility in patients undergoing diagnostic coronary angiography or thrombolysis [77, 78].
A careful history and physical examination is necessary, with specific focus on finding any systemic signs of emboli in septic patients, as well as the possibility of an autoimmune disease in the subset of non-septic patients [79, 80, 81]. As with suspected coronary artery disease, patients suffering from coronary embolism may present with typical or atypical chest pain or with “angina equivalents” such as dyspnea [79, 81, 82]. As with all acute coronary syndromes, electrocardiography will be very important in determining the diagnosis and may dictate the urgency for cardiac catheterization (e.g., the presence of ST-elevation myocardial infarction). The presence of Q-waves in contiguous leads may be indicative of a “silent” myocardial infarction. Troponin and other cardiac enzyme testing certainly plays an important role in determining the extent and the progression of myocardial ischemia [83, 84]. Subsequent workup should include transthoracic and transesophageal echocardiography, advanced high-resolution imaging (e.g., CT or MRI), and coronary angiography [18, 85, 86, 87]. In addition, miscellaneous adjunctive diagnostic tools, such as Holter/event monitoring, can also be helpful in cases where etiology of the event(s) in question may be uncertain [88, 89].
Coronary angiography remains the mainstay of CEP diagnostics [87]. As outlined previously, patients affected by this condition may have “silent” myocardial infarction or may present with an acute ST segment elevation myocardial infarction. When performing angiography, associated thrombi have a distinct hazy angiographic appearance [87, 90, 91]. Moreover, angiography can help document the evolution and resolution of coronary embolism [92]. Finally, diagnostic angiography can be converted into a therapeutic procedure if indicated [87, 93].
The angiographer should keep in mind that the presence of multiple acute thromboembolic lesions in various vessels increases the suspicion for embolic coronary phenomena [94]. As mentioned above, these emboli may also acutely occlude parts of vessels with pre-existing atherosclerosis, further complicating the diagnosis. Intravascular ultrasound following aspiration atherectomy may be useful when assessing for underlying atherosclerosis versus purely acute thromboembolic phenomena. Optical coherence tomography of these vessels may also be useful but has not yet been studied sufficiently in this particular setting [95, 96]. A patient with angiographic evidence of coronary embolism but with no traditional risk factors for coronary artery disease should raise the suspicion for some of the less common causes (e.g., autoimmune, infectious, inflammatory, or neoplastic) [6, 94, 97].
After diagnostic confirmation, coronary thrombi are often removed using aspiration catheters, as outlined in previous paragraphs. Biopsy of these specimens would aid in differentiating between thrombotic, septic, and neoplastic causes of embolism, particularly due to the fact that these may be the presenting events in some neoplasms. Autoimmune disease may also need to be ruled out [6, 94, 97].
Transthoracic echocardiography should be a part of the routine workup for patients with suspected CEP. Diagnostically, it will be critically important to demonstrate or rule out the presence of patent foramen ovale [98, 99, 100] and identify any thrombi in left-sided cardiac chambers, particularly with the help of ultrasonic contrast [33, 59]. Any suspicion should be further supplemented with transesophageal echocardiography to ascertain any transthoracic echocardiography findings, especially those of uncertain significance or insufficiently granular detail(s) [59, 101]. In addition, this would also be helpful to visualize the left atrial appendage when looking for evidence of either stasis or thrombus formation there [102, 103]. Such findings can be present in the setting of atrial fibrillation [102].
As outlined earlier in this manuscript, Holter/event monitoring to look for atrial fibrillation would also be reasonable in patients being seen for embolic phenomena [88, 89]. As for all thromboembolic diseases, thrombophilia workup would also be useful in ascertaining the etiology of coronary embolism in appropriately selected at-risk patients [104].
Coronary embolic syndromes are quite heterogeneous, and lack randomized controlled trial data or specific guidelines on their management. The initial approach including timing of cardiac catheterization for coronary embolism should be the same as for routine acute coronary syndrome (with classification of available evidence quality provided in parentheses) [106].
Oxygen (Class 1), nitrates (Class 1), and beta blockers (Class 1) are the mainstay of the initial medical management [106] in addition to parenteral anticoagulation (Enoxaparin/unfractionated heparin [UHF]/Bivalirudin) [109].
Decision regarding the use of percutaneous coronary intervention versus balloon angioplasty would be up to the clinician’s judgment given plaque morphology as assessed by intravascular ultrasound as well as on optical coherence tomography.
Following the initial management, dual antiplatelet inhibition would be recommended for these patients [107] for a duration of 6–12 months as per the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines [108].
As no randomized controlled data are available on lipid management for the particular subset of patients suffering from coronary embolism, we would recommend following current society guidelines for lipid management in these patients.
For patients with reduced ejection fraction on echocardiography, angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers in addition to aldosterone antagonists are recommended (Class 1) [106, 109].
Long-term anticoagulation in patients diagnosed with embolic coronary disease remains a question to be answered. As with other embolic phenomena, 3–6 months of anticoagulation with warfarin or with direct anticoagulants would be reasonable, with further therapy to be decided upon ascertaining the underlying etiology.
Workup to determine the etiology is essential, and treatment of the cause of embolism is of course necessary. As mentioned above, remote cardiac monitoring to look for atrial fibrillation is essential as it may necessitate lifelong anticoagulation particularly in patients with high CHADS2VASC scores.
Lastly, in patients possibly requiring triple antithrombotic therapy, data are limited, with current management approaches based on consensus recommendations with only a brief mention in the 2016 ACC Guidelines [108]. The decision regarding the duration or discontinuation of triple therapy versus P2Y12 inhibitor plus vitamin K antagonists (VKA)/direct oral anticoagulants (DOAC) would be based on the individualized bleeding risk versus the potential risk of discontinuing these medicines [108].
It has been reported that air embolism can complicate a variety of invasive procedures involving the vasculature, from central venous access placement to coronary artery bypass grafting [105, 106]. In the context of CEPs, the presence of patent foramen ovale (PFO) plays an important contributory role [107]. Though rarely reported, air embolism due to decompression illnesses or due to iatrogenic causes may also cause coronary embolism. Finally, iatrogenic CEPs are fortunately uncommon, yet they are dreaded events that may occur in the cardiac catheterization lab or during coronary artery bypass graft (CABG) surgery [103, 104].
Amniotic fluid embolism (AFE) in pregnant women can also lead to coronary embolization [105, 108]. Of note, for amniotic fluid to embolize to the coronary arteries, the patient must also have a PFO which helps facilitate the right-to-left transit of causative particles, which then lodge in the systemic arterial system and, potentially, the coronary arteries. It has been noted that the appearance of amniotic fluid emboli in the coronary circulation may be associated with elevated mortality when compared with cases not involving the coronary vessels [108]. Marked constriction of coronary arteries has also been described in the setting of AFE, although it is not known if that is a direct or an indirect effect [109, 110].
Coronary embolic phenomena are a heterogeneous group of clinicopathologic entities attributable to a variety of etiologic factors. Due to their rarity and the tendency to clinically mimic other coronary syndromes, CEPs are often underdiagnosed. Timely diagnosis using an elevated index of suspicion in high-risk patients is important to improving the associated morbidity and mortality. Scarcity of high quality data regarding CEPs necessitates further studies and dedicated consensus guidelines. Progress in diagnosis and treatment of CEPs will require concerted efforts by clinicians, educators, and researchers.
Tea is produced from
\n | Green tea (mg/g-km) | \nBlack tea (mg/g-km) | \nOolong tea (mg/g-km) | \n
---|---|---|---|
Total phenolic substance | \n208.80–236.78 | \n221.75–248.31 | \n87.70–195.6 | \n
Total catechin | \n221.94–234.71 | \n187.84–279.43 | \n16.64–282.75 | \n
Total flavone and flavonoid glycosides | \n4.53–5.43 | \n3.03–5.01 | \n4.09–4.68 | \n
EGCG (epigallocatechin agallate) | \n53.14–126.20 | \n2.42–81.93 | \n16.53–132.54 | \n
GC (catechin gallate) | \n5.05–10.52 | \n0.20–10.82 | \n7.5–8.93 | \n
EGC (epigallocatechin) | \n4.40–97.79 | \n0.71–78.82 | \n12.96–19.94 | \n
ECG (epicatechin gallate) | \n14.19–27.80 | \n0.42–13.02 | \n2.09–46.28 | \n
EC (epicatechin) | \n0.20–28.30 | \n0.10–3.59 | \n2.68–2.77 | \n
GCG (gallocatechin gallate) | \n2.60–48.02 | \n0.09–58.89 | \n49.54–60.92 | \n
Gallic acid | \n0.59–5.20 | \n0.57–5.80 | \n1.30–1.37 | \n
Caffeine | \n15.66–77.30 | \n3.14–83.20 | \n2.58–40.84 | \n
Theophylline | \n0.60–0.80 | \n0.10–0.20 | \n— | \n
Theobromine | \n0.27–6.0 | \n0.41–4.70 | \n0.72–0.99 | \n
Phenolic compounds of different types of tea [10].
Tea is also an important source of caffeine which is found naturally in coffee, cola, chocolate, cocoa or added as an additive to various energy drinks, medicine and cosmetics [11], is the most consumed drink in the world, whose use is increasing each passing day, and is considered to be a psychoactive substance [12, 13].
\nCaffeine is a member of a group known as purine alkaloids which also contain 3,7-dimethylxanthine (theobromine), 1,7-dimethylxanthine (paraxanthine), and methyluric acids. Its chemical formula is C8H10N4O2 and its systematic name is known as 1,3,7-trimethylxanthine [14].
\nCaffeine is largely absorbed by the stomach and small intestine after being taken into the body, quickly moves into body cells and reaches the highest level in 15 to 60 minutes after crossing the blood-brain barrier. The half-life of caffeine varies depending on factors such as puberty, pregnancy, and disease, but it is considered to be 5–6 hours in a healthy individual [15, 16]. Metabolites such as paraxanthine, theobromine, and theophylline are released as a result of caffeine metabolism. Only 10% of caffeine is excreted from the body without being metabolized [17].
\nCaffeine is available at different levels in many foods that we often consume in our daily lives. Therefore, it can be easily said that individuals consume caffeine regularly every day. However, the prediction that caffeine intake into the body for nutrition and short, medium and long-term exposures can lead to various health problems has led the scientific world to do research in this area. This study aims to examine the studies on the correlation between caffeine intake of individuals and health, and to emphasize the importance of tea for health.
\nToday, individuals consume low or high levels of caffeine, often knowingly and sometimes unknowingly. Since the production and consumption of caffeine-containing foods vary by country, society and individual, it is quite difficult to accurately calculate individuals’ nutritional intake of caffeine. Table 2 shows caffeine levels in certain foods which are frequently consumed by the general population and considered to be important in terms of caffeine content.
\nFood group | \nFood subgroup | \nCaffeine level (mg/L or mg/kg) | \n
---|---|---|
Chocolate | \nChocolate milk or chocolate beverages | \n7–67 | \n
Chocolate snacks | \n62–418 | \n|
Dark chocolate | \n340–525 | \n|
Coffee | \nCoffee drink | \n320–690 | \n
Cappuccino | \n250–315 | \n|
Espresso coffee | \n713–1916 | \n|
Decaffeinated and imitations | \n11–29 | \n|
Instant coffee, ready to drink | \n210–690 | \n|
Turkish coffee | \n620–858 | \n|
Tea | \nBlack tea | \n181–220 | \n
Green tea | \n125–320 | \n|
White tea | \n63 | \n|
Tea (unspecified) | \n158–234 | \n|
Instant | \n47–199 | \n|
Cola beverages (regular) | \n79–130 | \n|
Cola beverages (diet) | \n109–140 | \n|
Energy drinks | \n150–335 | \n
Caffeine is very common in nature, and coffee, tea, energy drinks, chocolate, and cocoa are accepted as sources of nutritional caffeine intake [22]. Caffeine levels in these foods vary according to content, ratio between tea/coffee and water, brewing time and other consumption characteristics [23, 24]. In general, coffee has a higher caffeine level than other foods. As for tea groups, the caffeine level of black tea is higher than other tea types. Caffeine levels are usually at a certain level in soft drinks such as cola and energy drinks as they have standard prescriptions and production techniques. The caffeine level in chocolate varies according to the amount of cocoa it contains. Coffee is also known as the source of nutritional caffeine of adults throughout Europe, especially in Finland, Denmark, Sweden and Switzerland. In all member states of the European Union, there is a “high levels of caffeine” warning on beverage labels containing more than 150 mg/L of caffeine [25].
\nMany institutions and researchers try to estimate nutritional caffeine intake by examining dietary habits of individuals. The number of studies conducted in this area is quite large and the findings of some studies are given below.
\nFDA states that a daily intake of 400 mg of caffeine can be considered safe for healthy adults. On the other hand, it has declared that some individuals may be negatively affected by lower doses of caffeine, and studies will begin to investigate the safety of caffeine added to foods, with particular emphasis on children and adolescents [18]. Health Canada has specified safe daily caffeine intake for healthy adults and pregnant women as ≥400 mg/day and <300 mg/day, respectively. The same institution has reported that daily caffeine intake for children of different age groups is in the range of 45 to 85 mg/day (45 mg/day for 4–6 years, 62.5 mg/day for 7–9 years, and 85 mg/day for 10–12 years) [26].
\nIn a study conducted in America with 24,808 individuals between 2001 and 2010, it was reported that more than 85% of adults (≥19 years of age) regularly consumed caffeine and that their average daily caffeine intake was 180 mg/day. In the same study, highest and lowest intake of caffeine was detected in males between the ages of 31 and 50 and females between the ages of 19 and 30, respectively, the caffeine intake of males (211 mg/day) was more than females (161 mg/day), and 98% of the daily caffeine intake came from beverages. The drinks that cause caffeine intake are as follows: coffee by 64%, carbonated soft drinks by 18%, tea by 16%, and energy drinks by less than 1% [27].
\nIn a study examining the daily caffeine intake of adolescents living in the United States between 1999 and 2011, it was reported that more than half of the children at ages ranging from 2.5 to 5 and about 75% of children over the age of 5 consumed caffeine on a daily basis. The mean daily caffeine intakes of children between the ages of 2 and 11 and adolescents between the ages of 12 and 17 were determined as and 50 mg/day, respectively. It was reported that the source of caffeine was carbonated soft drinks for children under the age of 12 and coffee for children that were 12 and older [28].
\nIn another study, daily caffeine intake was calculated as 15, 26, 61, 213, and 135 mg/day for the general population who were 4–8, 9–13, 14–19, and 51–70 years old and those who were 4 years old or younger, respectively. The daily caffeine intake is higher in males (196 mg/day) than females (151 mg/day). Although the distribution of the drinks that cause daily caffeine intake varies by age, the largest contribution is from coffee (64%) and tea (18%) [29].
\nIn another study conducted in the United States, daily caffeine intake was calculated as 120 mg/day (1.73 mg/kg body weight/day) for all age groups. The highest caffeine intake was in individuals in the 35–49 age range (170 mg/day). Daily caffeine intake in pregnant women was estimated to be 58 mg/day. According to the other findings of the study, the daily caffeine intake was calculated as 14 mg/day (0.82 mg/kg body weight/day), 22 mg/day (0.85 mg/kg body weight/day), and 106 mg/day (1.54 mg/kg body weight/day) for ages ranging from 1 to 5, 6 to 9, and 20 to 24, respectively. It was pointed out that the main source of caffeine was coffee in adults and soft drinks in young people. Tea ranked second in both groups [30].
\nAustralian Children’s Nutrition and Physical Activity Survey determined the general daily caffeine intake as 18 mg/day in a study on caffeine consumption of 4487 children and adolescents between the ages of 2 and 16 in 2007. The mean daily caffeine intake by age groups was determined as 3, 8, 19, and 42 mg/day for ages ranging from 2 to 3, 4 to 8, 9 to 13, and 14 to 16, respectively. It was stated that the main source of caffeine was drinks (81%) and that the highest contribution was made by soft drinks (31%), coffee (21%) and tea (17%), respectively [31].
\nIn a study conducted in Italy on 1213 adolescents (12–19 years), it was found that 76% of individuals consumed caffeine on a daily basis and the daily caffeine intake was approximately 125 mg/day (2.1 mg/kg body weight/day) [32] while the daily caffeine intake was calculated as 79 mg/day and coffee, tea, and soft drinks were listed as the beverages with the highest contribution to the daily caffeine intake in a study conducted in England on 2008 individuals of varying ages [33].
\nSince foods and beverages containing caffeine are common and easy to reach, a very large segment of society regularly consumes caffeine from childhood to old age. Just this information once again reveals the importance of caffeine in our lives. Therefore, systematic and comprehensive studies should be carried out on the effects of nutritional caffeine intake on the health of individuals in the short, medium and long term. A lot of research been conducted in this area.
\nThe fatal dose of caffeine in adults is estimated to be 170 mg/kg body weight/day [34] and there have been reports of some deaths due to caffeine overdose [35]. There is no complete consensus about whether caffeine consumption causes various ailments in individuals or whether it has a protective effect against contracting various diseases [36].
\nOne of the areas in which caffeine’s effects on health are most commonly investigated is the cardiovascular system. There are studies showing that caffeine intake by less than 400 mg/day does not have any negative impacts on the cardiovascular system [35], high levels of caffeine consumption leads to an increase in morbidity and mortality in the cardiovascular system by increasing blood pressure and heart rate [37, 38, 39], but, despite all this, caffeine has a protective effect [40, 41, 42].
\nCaffeine intake over 300 mg/day has been reported to cause second trimester miscarriages, low birth weight, and an increase in the likelihood of stillbirth [43, 44, 45]. Furthermore, the risk of developing childhood obesity increases by 87% in fetuses exposed to caffeine in the womb compared to those not exposed to caffeine [46]. However, there are also studies indicating that there is no correlation between caffeine intake in pregnancy and premature birth and fertility [47, 48, 49].
\nPositive impacts of caffeine consumed at low or medium levels on health such as relieving the airways leading to the lungs of individuals, reducing asthma attacks [50], making people feel healthy, reducing the risk of having type 2 diabetes or Parkinson’s disease, and healing liver diseases etc. are also mentioned [51, 52, 53, 54, 55, 56].
\nThere is not enough evidence in current studies to prove that caffeine consumption is associated with any type of cancer in the short, medium and long term, it causes an increase in the number of cancer cases, or that it has a protective effect [57]. It has been reported that caffeine intake by less than 400 mg/day does not cause an increase in the cancer risk [11, 58, 59].
\nOne of the most important features of caffeine is that it is a psychoactive compound. While caffeine less than 400 mg/day is generally considered safe, high doses of caffeine taken for a long time lead to caffeine withdrawal syndromes (caffeinism) such as headache, low concentration, restlessness, insomnia, irritability, decreased learning ability and palpitation [60, 61, 62, 63, 64].
\nThe prevailing view in the literature is that caffeine consumption has a detrimental effect on an individual’s sleep quality. According to current studies, caffeine consumption causes sleep delay, shortening of total sleep time, decreased sleep quality, and, as a result, daytime insomnia. It has also been stated that continued insomnia leads to more caffeine consumption by people [65, 66, 67].
\nIt is stated in a study examining the dose-related effects of caffeine that 85–250 mg caffeine per day increases the feeling of alertness and contributes to increased motivation by decreasing fatigue, higher doses between 250 and 500 mg per day may cause restlessness, irritability, insomnia, and anxiety while 15–30 mg/kg body weight/day caffeine may lead to muscle spasms and severe toxic effects on the cardiovascular and central nervous system in healthy adults [68].
\nIt has been found that caffeine accelerates metabolism by causing thermogenesis and lipid oxidation along with other compounds in food and causes weight loss by enabling people to spend more energy [69, 70, 71, 72].
\nAnother important feature of caffeine is its negative impact on bone health due to its diuretic effect. Excretion of elements such as calcium, magnesium, sodium and potassium from the body with urine increases due to high levels of caffeine intake. This results in decreased bone mineral density especially in females as well as increasing the risk of osteoporosis [73, 74].
\nSince caffeine is present in foods such as tea, coffee, and chocolate included in our daily diet, it is not surprising that the daily caffeine intake recommended for both the general society and specific groups is exceeded. Increased caffeine intake is known to cause various health problems. This is why caffeine free or decaffeinated foods are needed. Significant reduction of caffeine content or removal of caffeine is called decaffeination [75]. The first decaffeination process was carried out in 1903 on coffee beans (coffee beans were moistened with salty water and caffeine was removed with benzene) [76]. There are many different methods of caffeine removal that differ depending on the type of food. These are:
\nCaffeine is a compound that is legal, easy to obtain for the general society, socially acceptable to consume, found in many foods in our daily diet, and generally known for its stimulant properties. Caffeine, whose consumption has increased especially due to the changes in dietary habits in recent years, is a compound that still remains popular today. In this sense, both nutritional caffeine intake and the correlation between caffeine and health have been studied from many different angles. The effects of caffeine consumption on health are still a matter of debate. Although caffeine is generally considered safe except for excessive use in adults, studies on this subject are still insufficient for children and adolescents.
\nIndividuals’ daily caffeine intake varies depending on many factors such as the source of caffeine, age of the individual, breed, dietary habits and culture. In general, it can be said that the level of caffeine intake increases in proportion to age, and males consume more caffeine than females. It is understood that coffee and tea in adults and tea, soft and energy drinks in children and adolescents play an important role in caffeine intake.
\nIn the light of the data given in Table 2 and considering the changes in the consumption patterns regarding foods in recent years, it can be easily said that individuals’ daily caffeine consumption is much more than 400 mg/day which is usually considered to be safe. But it should be noted that caffeine intolerance can vary from person to person. Even very small amounts of caffeine can negatively affect pregnant women, children, the elderly and individuals who are caffeine intolerant. This is why caffeine intake of these individuals should be limited. For this purpose, popularizing caffeine-reduced products on the market can be considered as a strategy for limiting caffeine intake through nutrition. The literature review reveals that tea ranks second in caffeine intake in adults, children and adolescents. Therefore, tea plays a significant role in caffeine intake. But tea has significant differences distinguishing it from coffee, soft drinks and energy drinks that are other sources of caffeine.
\nCoffee is a drink that is generally perceived as healthy. However, it is also rich in acrylamide that was found out to be contained in food in 2002 and identified by the International Agency for Research on Cancer (IARC) as a possible carcinogen for humans. Carbonated soft drinks and chocolate foods contain many additives in addition to high levels of sugar. Many researchers and institutions approach energy drinks with suspicion due to very high caffeine content. Early acquaintance of individuals with carbonated soft drinks and energy drinks also increases the likelihood of addiction. In general, it can be said that the dietary quality of individuals who consume this type of drink frequently decreases.
\nTea is a plant rich in phenolic compounds, especially catechins, and has many benefits on human health due to its antioxidant, antibacterial, anticarcinogen, antimutagenic, and antiallergic effects. Therefore, for conscious consumers, tea is positively different from other foods and drinks due to caffeine and phenolic compounds and is thought to do more good than harm to people. Green tea stands out among tea types with the lowest content of caffeine and high phenolic content.
\nIntechOpen - where academia and industry create content with global impact
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\\n\\nCo-founded by Alex Lazinica and Vedran Kordic: “We are passionate about the advancement of science. As Ph.D. researchers in Vienna, we found it difficult to access the scholarly research we needed. We created IntechOpen with the specific aim of putting the academic needs of the global research community before the business interests of publishers. Our Team is now a global one and includes highly-renowned scientists and publishers, as well as experts in disseminating your research.”
\\n\\nBut, one thing we have in common is -- we are all scientists at heart!
\\n\\nSara Uhac, COO
\\n\\nSara Uhac was appointed Managing Director of IntechOpen at the beginning of 2014. She directs and controls the company’s operations. Sara joined IntechOpen in 2010 as Head of Journal Publishing, a new strategically underdeveloped department at that time. After obtaining a Master's degree in Media Management, she completed her Ph.D. at the University of Lugano, Switzerland. She holds a BA in Financial Market Management from the Bocconi University in Milan, Italy, where she started her career in the American publishing house Condé Nast and further collaborated with the UK-based publishing company Time Out. Sara was awarded a professional degree in Publishing from Yale University (2012). She is a member of the professional branch association of "Publishers, Designers and Graphic Artists" at the Croatian Chamber of Commerce.
\\n\\nAdrian Assad De Marco
\\n\\nAdrian Assad De Marco joined the company as a Director in 2017. With his extensive experience in management, acquired while working for regional and global leaders, he took over direction and control of all the company's publishing processes. Adrian holds a degree in Economy and Management from the University of Zagreb, School of Economics, Croatia. A former sportsman, he continually strives to develop his skills through professional courses and specializations such as NLP (Neuro-linguistic programming).
\\n\\nDr Alex Lazinica
\\n\\nAlex Lazinica is co-founder and Board member of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his Ph.D. in Robotics at the Vienna University of Technology. There, he worked as a robotics researcher with the university's Intelligent Manufacturing Systems Group, as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and, most importantly, co-founded and built the International Journal of Advanced Robotic Systems, the world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career since it proved to be the pathway to the foundation of IntechOpen with its focus on addressing academic researchers’ needs. Alex personifies many of IntechOpen´s key values, including the commitment to developing mutual trust, openness, and a spirit of entrepreneurialism. Today, his focus is on defining the growth and development strategy for the company.
\\n"}]'},components:[{type:"htmlEditorComponent",content:"Our business values are based on those any scientist applies to their research. We have created a culture of respect and collaboration within a relaxed, friendly and progressive atmosphere, while maintaining academic rigour.
\n\nCo-founded by Alex Lazinica and Vedran Kordic: “We are passionate about the advancement of science. As Ph.D. researchers in Vienna, we found it difficult to access the scholarly research we needed. We created IntechOpen with the specific aim of putting the academic needs of the global research community before the business interests of publishers. Our Team is now a global one and includes highly-renowned scientists and publishers, as well as experts in disseminating your research.”
\n\nBut, one thing we have in common is -- we are all scientists at heart!
\n\nSara Uhac, COO
\n\nSara Uhac was appointed Managing Director of IntechOpen at the beginning of 2014. She directs and controls the company’s operations. Sara joined IntechOpen in 2010 as Head of Journal Publishing, a new strategically underdeveloped department at that time. After obtaining a Master's degree in Media Management, she completed her Ph.D. at the University of Lugano, Switzerland. She holds a BA in Financial Market Management from the Bocconi University in Milan, Italy, where she started her career in the American publishing house Condé Nast and further collaborated with the UK-based publishing company Time Out. Sara was awarded a professional degree in Publishing from Yale University (2012). She is a member of the professional branch association of "Publishers, Designers and Graphic Artists" at the Croatian Chamber of Commerce.
\n\nAdrian Assad De Marco
\n\nAdrian Assad De Marco joined the company as a Director in 2017. With his extensive experience in management, acquired while working for regional and global leaders, he took over direction and control of all the company's publishing processes. Adrian holds a degree in Economy and Management from the University of Zagreb, School of Economics, Croatia. A former sportsman, he continually strives to develop his skills through professional courses and specializations such as NLP (Neuro-linguistic programming).
\n\nDr Alex Lazinica
\n\nAlex Lazinica is co-founder and Board member of IntechOpen. After obtaining a Master's degree in Mechanical Engineering, he continued his Ph.D. in Robotics at the Vienna University of Technology. There, he worked as a robotics researcher with the university's Intelligent Manufacturing Systems Group, as well as a guest researcher at various European universities, including the Swiss Federal Institute of Technology Lausanne (EPFL). During this time he published more than 20 scientific papers, gave presentations, served as a reviewer for major robotic journals and conferences and, most importantly, co-founded and built the International Journal of Advanced Robotic Systems, the world's first Open Access journal in the field of robotics. Starting this journal was a pivotal point in his career since it proved to be the pathway to the foundation of IntechOpen with its focus on addressing academic researchers’ needs. Alex personifies many of IntechOpen´s key values, including the commitment to developing mutual trust, openness, and a spirit of entrepreneurialism. Today, his focus is on defining the growth and development strategy for the company.
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