\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{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"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"},{slug:"intechopen-s-chapter-awarded-the-guenther-von-pannewitz-preis-2020-20200715",title:"IntechOpen's Chapter Awarded the Günther-von-Pannewitz-Preis 2020"},{slug:"suf-and-intechopen-announce-collaboration-20200331",title:"SUF and IntechOpen Announce Collaboration"}]},book:{item:{type:"book",id:"932",leadTitle:null,fullTitle:"Acute Pancreatitis",title:"Acute Pancreatitis",subtitle:null,reviewType:"peer-reviewed",abstract:"Acute Pancreatitis (AP) in approximately 80% of cases, occurs as a secondary complication related to gallstone disease and alcohol misuse. However there are several other different causes that produce it such as metabolism, genetics, autoimmunity, post-ERCP, and trauma for example... This disease is commonly associated with the sudden onset of upper abdominal pain that is usually severe enough to warrant the patient seeking urgent medical attention. Overall, 10-25% of AP episodes are classified as severe. This leads to an associated mortality rate of 7-30% that has not changed in recent years. Treatment is conservative and generally performed by experienced teams often in ICUs. Although most cases of acute pancreatitis are uncomplicated and resolve spontaneously, the presence of complications has a significant prognostic importance. Necrosis, hemorrhage, and infection convey up to 25%, 50%, and 80% mortality, respectively. Other complications such as pseudocyst formation, pseudo-aneurysm formation, or venous thrombosis, increase morbidity and mortality to a lesser degree. 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The Republic of Suriname is located on the northeast coast of South America, just north of the Amazon delta, and borders the Atlantic Ocean to the north, French Guiana to the east, Brazil to the south, and Guyana to the west (Figure 1) [1]. Despite its location in South America, Suriname is culturally considered a Caribbean rather than a Latin American country and is a member of the Caribbean Community (CARICOM) [1]. The climate is tropical with abundant rainfall, a uniform temperature of on average 27°C, and a relative high humidity of 81% in the capital city of Paramaribo [2]. There are four seasons, namely the long rainy season (April–July), the long dry season (August–November), the short rainy season (December–January), and the short dry season (February–March) [2].
Map of Suriname depicting the 10 administrative districts. The insert indicates the location of Suriname in South America.
Suriname’s land area of roughly 165,000 km2 can be distinguished into a northern urban-coastal and a rural-coastal area as well as a southern rural interior (Figure 1) [2]. The urban-coastal area comprises Paramaribo and the Wanica district (Figure 1) and harbors approximately 80% of the population of almost 570,000 [2, 3]. The rural-coastal area comprises the districts of Marowijne, Commewijne, Saramacca, Coronie, and Nickerie (Figure 1) and is, together with the southern-rural districts of Para, Brokopondo, and Sipaliwini (Figure 1), home to the remaining 20% of Suriname’s inhabitants [2, 3]. The latter part of the country is referred to as the hinterland, encompasses more than three-quarters of its land surface, and consists largely of sparsely inhabited savanna and dense, pristine, and highly biodiverse tropical rain forest [2]. This makes Suriname comparatively one of the most forested countries in the world [2, 4].
\nThe urban areas are characterized by a “western” lifestyle, modern health-care facilities, and an economy that is mainly based on commerce, services, and industry [5]. The rural societies have a more traditional way of living, lack comprehensive public health services, and have agriculture, forestry, crude oil drilling, bauxite and gold mining, as well as ecotourism as major economic activities [5]. These activities have been growing in scale and economic importance in recent years and are, together with agriculture and fisheries, the country’s most important means of support, contributing substantially to the gross domestic income in 2014 of U$ 5.297 billion and an average per-capita income of U$ 9583 [5, 6]. This positions Suriname on the World Bank’s list of upper-middle income economies [5, 6].
Suriname’s population is among the most varied in the world, comprising the Indigenous Amerindians, the original inhabitants; descendants from enslaved Africans imported between the seventeenth and the nineteenth century (called Maroons and Creoles); descendants from contract workers from China, India (called Hindustanis), and the island of Java, Indonesia (called Javanese) attracted between the second half of the nineteenth century and the first half of the twentieth century; descendants from settlers from a number of European and Middle Eastern countries; and more recently, immigrants from various Latin American and Caribbean countries including Brazil, Guyana, French Guiana, Haiti, and Cuba [1, 3]. The largest ethnic groups are the Maroons and Creoles, as well as the Hindustanis and Javanese, comprising approximately 22 and 16%, and 27 and 14%, respectively, of the total population [3].
\nAlthough members of all ethnic groups are encountered throughout the country—particularly in Paramaribo—certain ethnic groups are clustered in relatively large numbers in certain areas of the country [2, 3]. For example, the district of Nickerie harbors predominantly Hindustanis, that of Para mostly Creoles, that of Commewijne mainly Javanese, while the Maroons and Indigenous peoples primarily populate the interior, living in villages along the major rivers [2, 3]. More importantly, the various ethnic groups have largely preserved their culture and identity, still practicing their original religion and speaking their original language in addition to Dutch, the official language of government, business, media, and education, as well as Surinamese or Sranan Tongo, the widely used English- and Portuguese-based lingua franca [1, 3].
\nThe same holds true for their specific perceptions of health and disease and their ethnopharmacological traditions [7]. However, throughout time, considerable intercultural exchange has taken place about the knowledge and use of medicinal plants [7]. This paper first presents a brief historical overview of Suriname, then addresses the ethnopharmacological practices of the largest ethnic groups (the Maroons and the Creoles, as well as the Hindustanis and the Javanese), and concludes with a few remarks on the previsions provided by the various plant-based traditional medicinal practices.
Petroglyphs found at archeological sites in the western Corantijn basin and the eastern Marowijne basin of Suriname demonstrate that this region was inhabited by Indigenous peoples since at least 3000 BC, long before contact with Europeans [8]. The collection of 313 pre-Columbian pottery and charcoal fragments found in several caves at the Werephai site in the deep southwest of Suriname even dates human presence in Suriname as far back as 5000 before present [8]. It is possible that these peoples were nomadic tribes who roamed the Amazon area, and represent the ancestors of the present-day Akurio, Trio, Warrau, and Wayana, Indigenous tribes who still mainly populate the rainforest inland, but there is no documentation to support this assumption.
\nThe Arawaks, a nomadic Indigenous tribe that lived at the coast from hunting and fishing, are generally believed to be Suriname’s original inhabitants [9], but there are also no written documents to sustain this supposition. Around 1200 AD, the Caribs sailed to Suriname from their territory extending from the mouth of the Orinoco River in contemporary Venezuela to that of the Amazon River in present-day Brazil, and drove the Arawaks away from their lands [9]. The Arawaks moved to the savannas further land inward and the Caribs settled at the mouth of the Marowijne River in northeastern Suriname where they established, among others, the village of Galibi (from “Kupali Yumï,” meaning “tree of the forefathers” in the Carib language) [9].
The first Europeans arrived in Suriname in the early 1600s. They were Spanish, English, French, and Dutch fortune hunters who were attracted by tales of a fantastical city of gold called El Dorado somewhere at South America\'s “Wild Coast” [10]. However, it were English settlers led by Captain John Marshall who first colonized the area in 1630 [10, 11]. They called the colony “Surinam” after the Surinen indigenous people who then inhabited the “land of many waters” in the fertile Guiana plains [11]. Encouraged by the successes in their colonies in Virginia and Barbados, the English established tobacco plantations at Marshall’s Creek along the Suriname River, but this venture failed because of plummeting prices on the European market [11]. By 1645, Marshall’s colony was abandoned [11], but “Marchallkreek” is marked on maps until today.
\nAbout 20 years later, in 1651, English troops commanded by Major Anthony Rowse succeeded in establishing the first permanent plantations in Suriname as well as a fort to defend the newly acquired asset [11]. The colony was named Willoughbyland in honor of their patron Lord Francis Willoughby, the then governor of Barbados [11]. Willoughby’s intention was to establish a settlement for cultivating sugarcane, a cash crop that was fetching much higher prices in Europe than tobacco [11]. The much needed experience with sugarcane cultivation came from Dutch Jews who lived in Brazil and French Guiana but had to flee persecution by the Portuguese—the then owners of both regions—who were hostile to Protestantism and Judaism [12]. The Jews mainly established sugarcane plantations in the savanna region which is still known today as the Jodensavanna (the “Jew’s savanna”) [12].
Cheap labor was initially—in the 1650s—provided for by indentured servants from England, some Indigenous tribes people from the interior who had been captured by the coastal tribes and sold to the English colonists, as well as the relatively few black slaves who had directly been brought from Barbados by their owners or had been bought from the Dutch [11, 12]. However, because of the growing need of laborers on the sugarcane plantations, the British Royal Company of Adventurers occupied Dutch assets in Western Africa including centers for slave trading, initiating structured and government-sanctioned trans-Atlantic slave trade [11]. As a result, by 1663, most of the work on the approximately 50 plantations was done by over 3000 African slaves [11].
\nThe victorious days of the British did not last long. In February 1667, Dutch ships from Zeeland led by Abraham Crijnssen invaded Willoughbyland, captured Fort Willoughby, and renamed it Fort Zeelandia [11, 13, 14]. Five months later, the English and Dutch signed the Treaty of Breda that assigned Suriname to The Netherlands in exchange for New Amsterdam, the main city of the former Dutch colony of New Netherlands in North America [11, 13, 14]. This arrangement was made official in the Treaty of Westminster of 1674, after the British had recaptured and again lost Suriname in 1667 and the Dutch regained the colony in 1668 [11, 13]. The Dutch renamed Willoughbyland Dutch Guiana and the English renamed New Amsterdam New York after the Duke of York [11, 13, 14].
In 1683, the newly acquired colony was managed by the city of Amsterdam, the family Van Aerssen van Sommelsdijck, and the Dutch West Indies Company united in the Society of Suriname [13, 14]. In order to obtain maximum profits, the Society relied ever more on slave labor, dominating the trans-Atlantic slave trade for a long time [13–15]. All and all, around 300,000 Africans have been shipped to Suriname. In addition to sugar, the plantations produced cocoa, cotton, and indigo, which were exported to Amsterdam and returned enormous revenues [15]. However, treatment of the enslaved Africans was notoriously brutal, and many escaped to the interior from the start where they formed large communities—collectively called Maroons—with independent settlements and preservation of their culture that would last until today [15, 16].
\nThe British again ruled Suriname from 1799 through 1816 during the occupation of The Netherlands by France and put an end to slave trade in 1807 [11], but it took the Dutch until 1863 to abolish slavery [13, 14]. However, the slaves who had remained on the plantations were obliged to conduct ill-paid work and were only fully released in 1873 [13, 14]. As soon as they became truly free, the majority abandoned the plantations and settled in Paramaribo [17]. Many of them mixed with other races, particularly Dutch, becoming a separate ethnic group from the Maroons called Creoles [17]. This is an important reason for the somewhat looser ties of Creoles with African traditions when compared to Maroons despite their common heritage [17]. Still, African-based traditional medicinal practices are deeply rooted in most Creoles [17].
\nIn the meantime, as a plantation colony, Suriname still heavily depended on manual labor. To make up for the shortage after 1873, the Dutch arranged with the British to bring in indentured laborers from India [18, 19]. Around the turn of the twentieth century, in 1916, many workers were again imported, this time from the Dutch East Indies (modern Indonesia), especially from the island of Java [19, 20]. As mentioned above, these contract workers were the predecessors of the Hindustanis and Javanese, respectively, in Suriname. In addition, between 1850 and 1860, small numbers of (mostly male) laborers had been brought in from China and the Middle East [1, 21, 22].
This history makes Suriname, notwithstanding its relatively small population, one of the ethnically most diverse countries in the world. It also provides an explanation for the large variety of traditional forms of medicine practiced in the country. Suriname received in 1954 the status of an autonomous constituent country of the Kingdom of The Netherlands, along with The Netherlands and the Netherlands Antilles [22]. In this construction, Suriname could elect its own government and manage its own administration, but The Netherlands retained control of its defense and foreign affairs [22]. Approximately 20 years later, in November 1975, the country became completely independent from The Netherlands [22].
\nHowever, fear of ethnic violence and disappointment about economic development led to massive migration of Surinamese to The Netherlands just before and after 1975, resulting in a Surinamese diaspora in that country of roughly 350,000 in 2008 [22]. To make matters worse, a group of soldiers led by Suriname’s current president Desi Bouterse perpetrated a coup and took control of the country from February 25, 1980, on [22]. Absolute lows in that period were the execution on December 8, 1982, of 15 adversaries who were allegedly plotting a counter-coup, and the Interior War between a group of mostly Maroon anti-government insurgents led by Ronnie Brunswijk and Bouterse’s army between 1986 and 1992 [22].
\nFortunately, since then, peace and democracy have been restored [22]. Currently, Suriname is a constitutional democracy with a president elected by the unicameral National Assembly or by the larger United People\'s Assembly [22]. Despite many economic and political problems, this young democracy continues to serve as a unique example of genuine unity in diversity.
The Maroons (from the Spanish expression “cimarrón” for “runaway”) are the descendants from enslaved Africans who escaped from the plantations in coastal Suriname to the hinterland between the mid-seventeenth and the late eighteenth centuries [14, 15, 23, 24]. The slaves had mostly been imported from present-day Ghana, Benin, and Loango, but also from many other parts of West Africa such as Gambia, Guinea, Senegal, and Ivory Coast [14, 15]. The runaway slaves regrouped into small bands, settled in the forest, and established various small communities [23, 24]. Finding themselves in new and unfamiliar environments and in constant danger of recapture, they relied on the Indigenous peoples living in the adjoining rain forests to gradually develop means of subsistence and defense [25, 26].
\nThey soon formed resistance groups in the interior and often raided the plantations to recruit new members and capture women as well as to acquire weapons, food, and supplies [16, 23, 24, 27]. The authorities retaliated, often with the help of militia consisting of the colonial army, mercenaries, and groups of urban slaves called Redi Musus (“those wearing red hats”) and had occasional victories [16, 23, 24, 27]. However, accustomed to open-field army-to-army battle in Europe, they were no match for the Maroon guerilla warfare in the treacherous tropical jungle [16, 27]. After more than half a century of vicious combat, the Maroons’ independence was recognized by the signing of a peace treaty with the Dutch colonial administration in the 1760s [16]. This allowed them to occupy a large part of the interior where they preserved much of their cultural concepts of health and illness and much of their traditional medicinal practices [28].
\nThe new and unique Maroon culture was highly successful and several independent tribes developed [23, 24]. These currently include the Saramaka, the Paramaka, the Aukan, the Kwinti, the Aluku or Boni, and the Matawai, each with its own language and cultural characteristics [23, 24]. However, all groups maintain a strict hierarchical authority system organized along matriarchal lines, and all are headed by a paramount chief (the granman) who is chosen by a combination of descent and divination [23, 24]. The granman is assisted by several village captains (the kapitens) who are locally appointed. Important decisions about issues affecting the entire village are taken during lengthy gatherings called krutus [23, 24]. This system is acknowledged and respected by the central government in Paramaribo [23, 24].
\nThe enslaved Africans who did not join the Maroons and continued to work on the plantations were granted their formal freedom on July 1, 1863, and their actual freedom on July 1, 1973 [13, 14, 17]. Many remained in Suriname’s coastal area and mixed with Europeans, particularly Dutch but also members from other ethnic groups [17]. These Creoles were economically and politically highly successful and were the first non-Whites to hold public offices in Suriname from 1954 on, when the country received partial autonomy from The Netherlands [1, 17]. They widely adopted Christianity and Catholicism, but retained their affiliation with their African heritage and still adhere to various African traditions [17]. For instance, the generally appreciated call-and-response Creole kaseko and kawina songs supported by percussion can directly be traced to age-old African forms of music [1, 17]. This also holds true for many Creole perceptions of health and disease as well as the use of various plant-based medications which they refer to as oso dresis (“home-made medicines”) [1, 17, 29].
Many of the Maroon and Creole traditions have their roots in the early period of African dominance and Egyptian leadership before 3200 BC, when North Africa was home to many skilled practitioners who had developed a comprehensive medicinal system [30]. This holistic discipline was—and still is—mostly based on a large variety of medicinal plants and spirituality, spread throughout the continent, and was carried to Suriname by the enslaved Africans [28]. Traditional African medicine assumes that disease results from imbalances in social circumstances and spiritual perceptions. This would hold true for “physiological” diseases ranging from venereal diseases to cancer and even Ebola, but also for psychiatric disorders such as depression and anxiety [28]. The diagnosis is often reached through spiritual means, and the treatment is usually derived from the comprehensive herbal pharmacopeia and would accomplish both physical and spiritual healing [28]. Due to the relatively small number of university-trained physicians and the relatively high costs of allopathic medicines, as much as 86% of the inhabitants of Sub-Saharan Africa rely on traditional African medications [31]. For this reason, many African countries have expressed the commitment to develop safe, efficacious, quality, and affordable traditional medicines accessible to the majority of their inhabitants [32].
\nBased on these ancient African medicinal concepts, Afro-Surinamese have developed Winti (“wind” or “spirit”), a nature-oriented religion in which the spiritual world is consulted by music, singing, trances, and rituals in order to create and maintain a harmonious balance between humans and the visible and invisible powers of nature [29, 33, 34]. Winti is one of the most distinctive characteristics of Maroon and Creole culture and is mainly based on the abovementioned beliefs and magical rituals, the enslaved Africans had brought along [29, 33, 34] but has also been influenced by Indigenous traditions [25, 35]. The invisible powers are several gods called wintis, as well as the spirits of ancestors [29, 33, 34].
\nSpecialized practitioners called Winti priests—either males or females—serve as intermediaries between man, specific wintis, and the spirits of ancestors, and can evoke the spirits by special rituals to solve physical, psychological, or social problems [29, 33, 34]. The condition may be diagnosed during a special Winti ritual and is treated by medicinal and spiritual therapies consisting of specific herbs, special rituals, or both [29, 33, 34]. The Winti priests are referred to as lukuman (“the one who looks”, i.e., performs the diagnosis), dresiman (“the one who cures”, i.e., prepares and administers the medication), or duman (“the one who accomplishes”, i.e., treats and cures), to distinguish them from obiaman, bonuman, and wisiman who are in general associated with black magic practices [29, 33, 34].
\nWinti priests have a profound knowledge of the medicinal plants and the diseases and conditions they treat [29, 33, 34]. Some plants—such as the African rice Oryza glaberrima Steud. (Poaceae) and the Bambara groundnut Vigna subterranea (L.) Verdc. (Fabaceae), but also crops that originated from Asia such as the taro Colocasia esculenta (L.) Schott (Araceae) and the banana Musa sp. L. (Musaceae)—were grown in Suriname from leftovers of the food provided to the slaves or from seeds they had smuggled during their trans-Atlantic journey [35]. Others such as the cassava Manihot esculenta Crantz (Euphorbiaceae) and several yam species (Dioscorea spp.) have been adopted from the Indigenous [25, 26, 36]. And still others—particularly members of the plant families Fabaceae, Euphorbiaceae, and Asteraceae—were deemed useful because of their resemblance with species known from Africa or by trial and error [35].
One of the first traditional medicinal healers of Suriname was the freedman Quassie van Timotibo, also known as Kwasi, who popularized one of the earliest and most popular Surinamese traditional medicines, kwasibita (“Kwasi’s bitter”) [37]. Suspected to be a member of the Redi Musus and held responsible for the fall of Fort Buku headed by Boni—one of the most revered Maroon rebel generals [16, 24, 27]—Kwasi was considered a traitor among a large part of the slave population [37]. However, he was respected by many Whites as the most proficient dresi- and lukuman of eighteenth-century Suriname [37]. Kwasi had obtained much of his medicinal knowledge from the Indigenous peoples and discovered around 1730 the remarkable qualities of the bitterwood or kwasibita Quassia amara L. (Simaroubaceae) for treating malaria fevers and stomach troubles [37, 38]. This owed him the reputation of “the most honorable and most learned gentleman, master Phillipus of Quassy, professor of Herbology in Surinam” [37]. Today, kwasibita preparations are among the most consumed oso dresis for promoting general health [38].
\nMaroons and Creoles use many other plants for treating a variety of disease conditions including, among others, parasitic infections, hypertension, diabetes mellitus, bone fractures, and psychological conditions [33, 34, 38–44]. Spiritual herbal baths and ritual washing are often part of the treatment, as they would have a medicinal and magical effect on the body, calming the nervous system [33, 34, 38, 39]. The washings would also provide spiritual purification, protect against injury, repair broken relationships, and exorcise evil forces [33, 34, 38–44]. A few popular plant-based medicinal applications are the so-called kowru dresis, genital steam baths for females, and remedies for children’s ailments [35, 38].
\nKowru dresis (“medicines against a cold”) are prepared from several plants including the leaves from Senna spp. (Fabaceae), the seeds from the aniseed Pimpinella anisum L. (Apiaceae), the aerial parts from the stonebreaker Phyllanthus niruri L. (Phyllanthaceae), the leaves from the birthwort Aristolochia spp. L. (Aristolochiaceae), the roots from the liquorice Glycyrrhiza glabra L. (Fabaceae), and/or the roots from the Chinese rhubarb Rheum palmatum L. (Polygonaceae) [28, 33, 34, 38]. These preparations are used to remove obstructions in bowels, airways, blood circulation, and genitourinary system, but also for mental well-being [28, 33, 34, 38]. The latter use is presumably based on the ancient African belief that even psychological conditions result from an imbalance between “hot” and “cold” and can be reversed by removing the “cold” [30]. Notably, in various communities Senna spp. and R. palmatum are traditionally used as a laxative and a purgative, respectively [45, 46]; P. anisum as a carminative and for colics [47]; P. niruri for stomach, genitourinary, liver, and spleen problems [48]; Aristolochia spp. for their antihelminthic activity [49]; and G. glabra for rejuvenation [50].
\nGenital steam baths are abundantly used by females for their personal hygiene [28, 33–35, 38] but also—as indicated by their suggestive vernacular names—to improve the appearance of the vagina in order to enhance sensation during intercourse, securing the relationship with and economic support by the male partner [28, 33–35, 38]. A few of the dozens of plants used in genital steam baths are the broko pipi (“broken penis”) Bellucia grossularioides (L.) Triana 1871 (Melastomataceae); the Paranamklem (“Paranam grip”) Ludwigia nervosa (Poir.) H. Hare (Onagraceae); the musude baasa (“early-morning hug”) Miconia tomentosa (Rich.) D. Don ex DC. (Melastomataceae); and the kunami (“come to me”) Clibadium surinamense L. (Asteraceae). Leaves from the shy plant Mimosa pudica L. (Fabaceae) that fold inward and droop when touched, and aromatic plants such as the pêpë uwíi Guatteria schomburgkiana Mart. (Annonaceae) may be added to the bath [28, 33–35, 38].
\nImportant childhood conditions requiring traditional treatment include atita and evil eye. Atita, commonly known in Suriname as zuurte or suri (“sourness”), is an ill-described condition in newborns that is characterized by stomach ache, cramps, diaper rash, yellow, sour-smelling feces, and diarrhea with small grains resembling okra seeds [28, 33–35, 38]. Atita may be caused by the baby’s intestinal flora which must adapt to the uptake of proteins from breast milk [35]. This condition is treated by bathing the baby with a decoction of the leaves and/or flowers from the ingiwiri (“Indian herb”) Nepsera aquatica (Aubl.) Naudin. (Melastomataceae), the yorkapesi (“demon pea”) S. occidentalis (L.) Link. (Fabaceae), or the busipesi (“bush pea”) S. chrysocarpa (Desv.) H.S. Irwin & Barneby and having the baby drink some of the decoction [28, 33–35, 38].
\nA baby is at risk to get evil eye or ogri ai (“bad eye”) by an envious or a malevolent glare that can inflict harm, suffering, or even death [28, 33–35, 38]. This condition is commonly treated by bathing the infant with Reckitt’s Blue, which presumably has its origin in its whitening (i.e., cleansing) effect on laundry [28, 33–35, 38]. Ogri ai can presumably be prevented by rubbing asafetida or didibri kaka (“devil’s feces”)—the foul smelling dried latex from the rhizomes of the stinking gum Ferula assafoetida L. (Apiaceae)—in the baby’s hair, and placing a gold bracelet with three black beads on its clothes [28, 33–35, 38].
The first indentured laborers from (then British) India arrived on June 5, 1873, in Paramaribo with the sailing ship Lalla Rookh that had departed more than 3 months earlier from central depots in Calcutta [18, 19]. The 452 passengers—called “Hindustanis” by the Dutch—were mostly recruited from the modern-day states of Uttar Pradesh and Bihar in northern and eastern India, respectively [18, 19]. Important reasons to leave their homeland were the high unemployment and the substantial loss of traditional jobs due to the rapid industrialization of India [18, 19]. However, at least some of them might have been misled into believing that they were taken to a place of pilgrimage called Sri Ram which turned out to be Suriname [18, 19]. Sixty-three more shiploads with laborers arrived in Suriname, taking as many as 34,304 Hindustani to the Dutch colony until 1916, when this practice was discouraged by Mahatma Gandhi’s movement for an independent India [18, 19].
\nAlthough formally considered laborers on a 5-year contract rather than slaves [18, 19], working conditions on the sugar and coffee plantations were more or less equal to slavery [18, 19]. Working hours were long, payment was low, housing was in former slave accommodations, and not completing assigned tasks was severely punished [18, 19]. This regularly led to bloody uprisings, the largest one of which occurred in 1902 at the Marienburg sugar factory in Commewijne, then the center of sugarcane processing in Suriname [18, 19]. Angry workers killed the Scottish supervisor James Mavor, and in retaliation the Dutch colonial forces killed 24 workers and wounded over 39 [18, 19]. The Hindustani fatalities were buried in a mass grave that has remained unidentified until today [18, 19].
\nNevertheless, only one-third of the workers returned to India after the completion of their contract [18, 19]. The remaining two-thirds accepted the offer of free settlement rights on plantations plus a bonus of a 100 Dutch guilders for abandoning their right to a return passage [18, 19]. Several of them used their bonus money and their savings to grow rice on their small plots of land, particularly in the western district of Nickerie yielding them appreciable incomes [18, 19]. Even today, a number of Hindustanis own sizable rice farms in Suriname [51].
All and all, the Hindustani community has economically and politically been very successful in the Surinamese society but has managed to keep their culture and traditions alive, strengthening the group identity [51]. This holds true for their religion, marriage rituals, customs in raising children, family and communal life, burial rites, as well as celebrations as Holi Phagwah, the festival of colors that celebrates the victory of good over evil and the arrival of spring, and Diwali, the festival of lights that rejoices the triumph of light over darkness [51]. Notably, Surinamese Hindi or Sarnami—a dialect based on Bhojpuri, the main language spoken in the parts of India, the Hindustani originated from—is the third-most spoken language in Suriname after Surinamese and Dutch [51].
\nThe Hindustanis have also largely preserved their cultural and traditional medicinal practices which are strongly linked to Ayurvedic medicine or Ayurveda (Sanskrit for “knowledge of life”) [52–54]. Ayurveda is probably one of the oldest forms of medicine [52–54]. It originates from India and dates back more than 3000 years ago, and is still one of the country’s most important traditional health-care systems [52–54]. Up to 80% of Indians use Ayurvedic medications for a variety of conditions including complex ailments such as angina pectoris and diabetes mellitus [52–54]. Ayurvedic practitioners are educated in 180 training centers [52–54], and the huge intellectual property and economic interest are managed by the prominent Department of Ayurveda, Yoga and Naturopathy, Unani, Siddha, and Homeopathy [52–54]. India’s government also supports laboratory and clinical research on Ayurvedic preparations [52–54].
\nAyurvedic medicinal concepts are based on the belief that health and wellness depend on a delicate balance between mind, body, and spirit, and that imbalance results in disease [52–54]. This holistic approach is a fundamental aspect of Ayurveda [52–54]. Today, Ayurveda is widely practiced throughout the world and in many countries recognized as a form of complementary and alternative medicine [52–54]. The principal ingredients of Ayurvedic medications are preparations derived from leaves, fruits, seeds, bark, or roots from certain plants [52–54]. Hundreds of plant species are used for such preparations [52–54]. In addition, Ayurvedic medications may be prepared from animal products such as milk, bones, or fats, and/or minerals such as sulfur, lead, arsenic, copper sulfate, and gold [52–54].
The Hindustanis in Suriname also use a large variety of plants for their Ayurveda-based cultural and medicinal customs [55–57]. Several of these plants have been brought over from India but others have been discovered in Suriname or adopted from other cultures [55–57]. Examples of long known and very popular Ayurvedic medicinal plants are the neem Azadirachta indica A. Juss., 1830 (Meliaceae), the ashoka tree Saraca asoca (Roxb.) Willd. (Fabaceae), the Indian bael tree Aegle marmelos (L.) Corrêa (Rutaceae), the bitter melon Momordica charantia Linn (Cucurbitaceae), the jambolan Syzygium cumini (L.) Skeels (Myrtaceae), the turmeric Curcuma longa L. (1753) (Zingiberaceae), and the holy basil or tulsi Ocimum tenuiflorum L. (Lamiaceae) [55–57].
\nThe bitter-tasting constituents of parts of A. indica are believed to boost the immune system and to treat many diseases, among others, colds, fevers, respiratory conditions, stomach ailments, high blood pressure, and/or diabetes mellitus [58]. Volatile substances emanating from A. indica leaves placed under the bed sheets would also treat chicken pox [59], and a tea from these parts of the plant is typically used as an internal cleanse [58]. These beneficial effects may be related to the anthelmintic, antifungal, antibacterial, and antiviral activities of nimbinin, one of the main bioactive compounds of A. indica [60].
\nThe stem bark, flowers, and seeds from S. asoca are used against postmenopausal syndrome and gynecological disorders [61]. And preparations from various parts of A. marmelos, M. charantia, and S. cumini are extensively used for treating diabetes mellitus but so far without convincing scientific evidence [62–64]. However, a few studies suggest that the presumed blood glucose-lowering activity of M. charantia may depend on the way the medication is prepared: preparations from fresh leaves seem to elicit a better effect when compared to the widely available tablets or capsules [65].
\nC. longa and O. tenuiflorum are among the most popular Ayurvedic herbs. The powdered rhizomes from C. longa are an essential part of curry which is used as a spice in many Hindustani dishes [51]. C. longa preparations are furthermore used, among others, as a diuretic; to stimulate blood flow in the pelvic area; to treat fevers with jaundice, hepatitis, and malaria; to prevent excessive menstrual pain; to enhance mental functioning and well-being; and externally for herpes, bruises, wounds, and rheumatism [66]. The leaves from the aromatic plant O. tenuiflorum—either fresh, dried, powdered, or as a tea—would treat a similar variety of diseases including stress and a disturbed homeostasis [67].
\nMany of these plants are also considered sacred and are used in various Hindu rituals [51]. For instance, preparations from A. indica leaves, bark, and fruits are consumed during certain ceremonies, festivals, and commemorations; the fruits from A. marmelos are offered to Shiva, the god of yoga, meditation, and arts during religious rituals; a paste of turmeric in coconut oil is applied on the skin of the bride and the groom during pre-marriage rituals to make their skin bright and glowing; the flowers from O. tenuiflorum are used as a holy cleanser for food offerings during prayers; and S. asoca is worshipped during Chaitra, the first month of the Hindu calendar, marking the arrival of Spring.
The first group of Javanese indentured laborers arrived in Paramaribo on August 9, 1890 [19, 20]. It consisted of 94 small farmers from villages in Central and East Java in the former Dutch East Indies [19, 20]. They had been recruited by the very influential Netherlands Trading Society established by the Dutch King Willem I, either by force, bribery, or manipulation [19, 20]. The approximately 40-day journey was hard, and many Javanese died on the ship, in-transit in The Netherlands, or upon arrival in Paramaribo [19, 20]. Those who survived were mainly set to work on sugarcane plantations in the district of Commewijne [19, 20].
\nThis was deemed so successful that many more followed from 1894 on. In 1904, Javanese laborers were even specifically recruited to construct the Colonial Railways for the transport of sugarcane from surrounding plantations to the sugarcane factory in Marienburg [19, 20]. Contracts were signed for 5 years, but life in Suriname’s countryside was brutal and wages were minimal [19, 20]. For this reason, thousands of Javanese returned to Indonesia or to The Netherlands, particularly after Indonesia’s independence in 1954 [19, 20].
\nThe influx of indentured workers from Java ceased in 1939 with the advent of the Second World War, and had brought a total of 32,956 Javanese in Suriname [19, 20]. Those who settled in Suriname received a plot of land and a reimbursement of 100 guilders repatriation money [19, 20]. They were initially kept isolated in the countryside, particularly after Governor Johannes C. Kielstra’s (1933–1943) consent of Javanese farm villages with their own village head (the lurah) and chief committee [19, 20]. On the other hand, this secluded lifestyle strengthened the group identity, as they maintained the rich culture they had brought with them from Java [19, 20].
\nNowadays, the Javanese community has been well integrated in the Surinamese society, but many of their traditions and rituals have been preserved [68–70]. This holds true not only for their language but also for their types of entertainment such as the wayang shadow puppet show accompanied by distinctive orchestral gamelan music, and Javanese ludruk theater that includes the centuries old tradition of storytelling through slow, graceful, and expressive dances [70]. An important ritual that has been preserved is the preparation of the sacrificial slamatan meal at seven specific time periods to commemorate the departed, including the day of passing and 1000 after his/her death [70].
The Javanese have also maintained their traditional medicinal practices which are mainly based on medicinal plants and are referred to as Jamu [70]. Jamu is the widely practiced form of traditional medicine in Indonesia that probably has its origin in the Mataram Kingdom era in ancient Java, some 1300 years ago [71, 72]. Jamu is mostly based on plants, but materials from animals such as honey, royal jelly, bee larvae, milk, and chicken eggs are also used [71, 72]. Jamu products called jamus are in Indonesia traditionally available from (particularly female) peddlers and street-side vendors, but are nowadays also produced and retailed by large companies in dried form in sachet packaging or as tablets, capsules, and liquid drinks [71, 72]. The manufacturers of jamus are united in Gabungan Pengusaha Jamu, an Indonesian Herbal and Traditional Medicine Association [71, 72]. Together, they employ roughly 15 million workers, produce over 1200 different jamu products, and bring in annual revenues of more than US$ 73 million [71, 72].
\nJamu is practiced in both Indonesia and Suriname by highly respected medicinal practitioners known as dukuns or tabibs [70, 71, 73]. The dukun is very influential and holds extensive knowledge about the preparation of the large variety of sometimes rather complicated jamus [70, 71]. An example is the very popular jamu galian consisting of different parts of eight plants that is widely used in Suriname as a general health-promoting tonic [70, 71, 73]. The dukun also plays an important role during, for instance, nyuwuk, a ritual to bring a person at ease by praying over and blowing three times over a glass of water that then must be drunk by the client [70, 71, 73]. Nyuwuk is often performed prior to examinations, circumcisions, or giving birth [70, 71].
Many plants incorporated in jamus belong to the family Zingiberaceae which have been brought from Java and are now cultivated in Suriname [74]. A few examples are the laos Alpinia galanga (L.) Willd., the pink and blue ginger C. aeruginosa Roxb., (1810), the temu giring C. heyneana Valeton & Zijp, the earlier mentioned C. longa that has its origin in Indian Ayurveda, the yellow ginger C. xanthorrhiza Roxb., the aromatic ginger Kaempferia galanga L., the bengle Zingiber cassumunar Roxb., and the bitter ginger Z. zerumbet (L.) Roscoe ex. Sm. [74]. For medicinal purposes, the macerated and/or decocted rhizomes are used, either from a certain species or from combinations of several species [74].
\nAs the majority of Javanese is Muslim [2], jamus are usually prepared on Mondays and Thursdays which are assigned for fasting in Islam. They are used for treating a wide variety of conditions. For instance, the rhizomes from A. galanga would treat the fungal skin infection “lota” (pityriasis alba), stomach cramps, and dysentery [74]. And those from C. xanthorriza would help against liver ailments, eczema, constipation, and gallstones, and for cleansing the uterus after giving birth [74]. The mother is also advised to drink on a daily basis a decoction of C. xanthorriza, C. aeruginosa, and Z. zerumbet rhizomes together with leaves from P. anisum [73]. These apparent health benefits may be attributed, at least in part, to the anti-parasitic activity of A. galanga preparations and one of its bioactive constituents galangin [75, 76], and the anti-inflammatory and hepatoprotective effects of curcumin in C. xanthorriza products [77].
\nJamus prepared from C. longa are used for treating, among others, inflamed gums, abscesses, menstrual pains, and skin rash, partially because of their antiseptic activity and refreshing effect [74]. The latter action may also help explain the application of a C. longa-based ointment called bobok for alleviating the discomfort of sprains, insect bites, and toothache [74]. Furthermore, the juice collected from C. longa rhizomes is, together with that from Z. zerumbet rhizomes, used for treating stomach ache, and together with the macerated rhizomes of C. aeruginosa, and Z. zerumbet, a grated onion, sugar, and a packet of cooked Glycine max soybeans, for treating pinworm infections in children [74]. The potential health benefits of C. longa may be ascribed to the antimicrobial and anti-inflammatory properties of curcuminoids in the plant [66].
\nMedicinal plants belonging to families other than the Zingiberaceae that are incorporated in popular jamus are the cat’s whiskers Orthosiphon grandiflorus Bold. (Lamiaceae), the betel Piper betle L. (Piperaceae), the ketyi beling Strobilanthes crispa Blume (Acanthaceae), and the gambir Uncaria gambir (W. Hunter) Roxb., 1824 (Rubiaceae) [74]. An infusion of the leaves from O. grandiflorus and S. crispa, either separately or in combination, can be used against kidney stones and renal colics [74]. And rolled-up or macerated leaves from P. betle are placed in the nostrils to stop nose bleeding. P. betle leaves are also chewed together with those from U. gambir to heal inflamed gums [74]. There is at least some preclinical evidence to support these applications [78–81].
As a result of its fascinating and tumultuous history, Suriname has become a treasure chest of traditional medicinal approaches and rituals based on plants. Traditions and rituals from every continent on Earth have found their way in the country and have largely been preserved. This is illustrated by the various examples given in this overview about Maroons and Creoles as well as Hindustanis and Javanese. However, the same applies to the rich Indigenous South American cultures, traditional Chinese medicine, and the cultures brought over by many other ethnicities in the country. Gradually, many of these traditions are finding their way to other ethnicities. This is likely to result in a unique and even richer traditional medical culture in the country.
\nFor instance, the use of kowru dresis as well as many remedies and rituals against evil eye has its origin in Africa but is not anymore restricted to Maroons and Creoles and has become common practice in all ethnic groups in Suriname. The neem plant A. indica, the turmeric C. longa, and the bitter melon M. charantia have presumably been introduced in Suriname by Hindustanis but are now widely used throughout the country against a variety of conditions. And the broad use of the cat’s whiskers O. aristatus for treating kidney stones and renal colics is attributable to the Javanese. This ethnic group is also responsible for the presence of many medicinal Zingiberaceae species in Suriname and the general use of the laos A. galanga against the skin disease lota.
\nContributing to this pool are the traditional medicinal customs of the Indigenous which already had a profound influence on Maroon culture, and traditional Chinese medicine that has become, similarly to Indian Ayurveda, a form of complementary and alternative medicine that is worldwide respected. It is foreseeable that these cultural fusions—meetings of the mind—will lead to the development of a distinct form of herbalism in Suriname that will generate a unique array of medicines.
The purpose of this chapter is to provide a review of the pathophysiology of metabolic syndrome (MS) and the relationship between its different components. Because this is a very broad subject, not all aspects will be discussed. Throughout the chapter, a bibliographic reference is left for each topic so that this can be looked into more deeply. This is a non-systematic review of the literature through research on PubMed and Google.
At an epidemiologic study conducted by Armindo Sousa Ribeiro et al, in a Portuguese population, was found that 23.8% of the population has MS more prevalent in 24 males, no smoking, no significant alcohol consumption, sedentary life style, with a high body mass index (BMI) and its prevalence increases with age [1]. Each CVRF has different importance in the metabolic syndrome [2].
In Western societies, cardiovascular diseases (CVD) are the main cause of mortality and morbidity for both sexes. This fact entails very high social and economic costs [3].
CVDs are the biggest cause of mortality worldwide. In the 2010 Global Burden of Disease Study, CVD is estimated to cause 15.6 million deaths per year worldwide, corresponding to 29.6% of all deaths [4]. Although the tendency is to reduce the number of deaths in Europe due to CVD, this remains the main cause of death, corresponding to more than 4 million deaths per year, that is to say 45% of all deaths recorded in Europe [4]. Of the CVD, coronary heart disease remains the most important cause of death in both genders, which corresponds to 19% in the male sex and 20% in the female sex.
There are several definitions of MS. MS groups a constellation of pathophysiological factors that increase the risk of developing diabetes mellitus (DM) type 2 and CVD [5, 6, 7, 8, 9, 10]. At present, attempts have been made to unify criteria to have a consensus on its diagnosis [11].
The World Health Organization (WHO), International Diabetes Federation (IDF), National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III), and the American Association of Clinical Endocrinologists (AACE) have proposed their diagnostic criteria or components of MS (Figure 1) [11].
Components of the metabolic syndrome considering its definition: according to the National Cholesterol Education Program Adult Treatment Panel III (ATP III), World Health Organization (WHO), American Association of Clinical Endocrinologists (AACE), and International Diabetes Federation (IDF).
In 2009, representatives of the IDF and the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI)-ATP III Guidelines discussed resolving differences between definitions of MS, unifying criteria [6, 11]. The definition of MS according to the unification of criteria (harmonizing the metabolic syndrome) is used for many international works and publications and requires the presence of three of the following five criteria:
Elevation of fasting blood glucose (≥100 mg/dl) or receiving antidiabetic treatment with insulin or oral antidiabetics
Elevation of systolic blood pressure (SBP) ≥ 130 mmHg or diastolic blood pressure (PAD) ≥ 85 mmHg or receiving antihypertensive drug treatment
High-density lipoprotein (HDL) cholesterol values <40 mg/dl (men) or <50 mg/dl (women)
Triglycerides ≥150 mg/dl or under treatment with specific lipid lowering agents
Abdominal perimeter ≥102 cm (men) or ≥88 cm (women) [6, 12]
The concept of MS was carried out in a progressive manner. Its clinical importance is enormous due to the fact that it can identify patients with high risk of suffering some CVD and/or DM, allowing a preventive intervention [6, 13, 14].
The notion that CVRF has a tendency to aggregation allows an earlier diagnosis of MS, thus also leading to the early introduction of therapeutic, pharmacological, or non-pharmacological measures.
The interest in the MS is not something recent. Its nomenclature has evolved over the years.
About 260 years ago, before the description of MS, the Italian anatomist and doctor, Morgagni, identified the association between visceral obesity, arterial hypertension (AHT), atherosclerosis, hyperuricemia, and frequent episodes of sleep apnea. In the mid-twentieth century, French physicist Vague first identified the relationship between android obesity and the increased prevalence of DM and CVD. In the 1960s Avogaro and Crepaldi attributed the name “plurimetabolic syndrome” to the simultaneous presence of obesity, AHT, and DM. They verified that all these abnormalities were frequent among the population and contributed to an increase in cardiovascular risk [15]. A decade later, Haller related this set of risk factors with atherosclerosis [15].
In 1980, Vague suggested that adipose tissue alone had little effect on the onset of DM in obese individuals. It is currently known that central or android obesity is a predisposing factor for DM and atherosclerosis and affects insulin secretion unlike gynoid obesity [15].
In 1988, Reaven described this phenomenon as syndrome X, the set of hyperglycemia and insulin resistance, obesity, dyslipidemia, and hypertension. Reaven also suggested that insulin resistance and the consequent increase in blood insulin levels were the central pathophysiological features in syndrome X which in itself was a risk factor for CVD [15, 16].
In 1991, Ferrannini and his colleagues referred to this as insulin resistance syndrome [15, 17].
In 1993, Van Gaal attributed for the first time the name MS to all comorbidities associated with visceral obesity and currently this nomenclature is being used [15].
The concept of MS has evolved significantly in the last decade, which resulted in the presentation of multiple clinical definitions by different scientific societies. In general terms as it was widely treated, MS is defined as an aggregation of several CVRF in the same individual. The nuclear elements for the classification and diagnosis of MS are basically obesity, abnormal glycemic metabolism, iatrogenic dyslipidemia, and hypertension.
The metabolic syndrome was defined by the World Health Organization (WHO) in 1998 [13, 15]. In 2001, there was a new revision of the definition through the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III), where glycemia is not considered an essential factor; in this way it only becomes one of the diagnostic components of MS [18].
With the verification of evidence of the relationship between central obesity and cardiovascular risk, there was a tendency to value this diagnostic component for MS more. Thus, in 2004, the International Diabetes Federation (IDF) created a new definition of MS, where central obesity, defined by the value of the abdominal circumference, would be essential for diagnosis [7, 19]. With the adoption of this definition, an increase in the prevalence of MS was observed in a large part of the populations studied, particularly in the elderly [20].
In 2005, a new review of the criteria by the American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) maintained the criteria of the NCEP-ATP III [21]. The justification was the fact that in that criterion a single etiology for MS does not stand out and is of simpler application. They modified only the cutoff point of fasting blood glucose from 110 to 100 mg/dl, an adjustment promoted by the American Diabetes Association (ADA) in the diagnosis of DM. However, the first Brazilian Guideline for the Diagnosis of Treatment of MS, of 2005, uses the criteria of the NCEP-ATP III, of 2001, for diagnosis [22, 23]. In the criteria of the IDF, the component of the abdominal circumference becomes essential, using a smaller waist circumference, and categorized more people as having the MS than the ATP III definition. However, higher values of abdominal circumference in older people have been related to lower values of body mass index (BMI), in relation to younger adults [24, 25, 26, 27, 28].
The prevalence of MS varies according to geographic area, with age, race, sex, and classification used for diagnosis [29].
The DARIOS study performs a pooled analysis of 11 studies in 24,670 Spanish individuals aged 35–74, using the criteria of the IDF/NHLBI/AHA-2009, and shows a prevalence of 32% in men and 29% in women [12, 30].
The West of Scotland Coronary Prevention Study (WOSCOPS), one of the largest in Europe, reports a general prevalence of 26.2% [31].
The Third National Health and Nutrition Examination Survey (NHANES III), in the USA showed that 7% of individuals between the ages of 20 and 29, 42% of individuals with ages between 60 and 69 years, and 44% of individuals with ages over 70 years presented MS. The overall prevalence was 23.7% in the 8814 adults who entered the study. This study showed that the incidence increased with age, mainly after 40 years, with significant variations consistent with ethnicity, being the most frequent MS in Hispanics (31.9%) compared with Caucasians (23.8%) and African-Americans (21.6%). A similar prevalence was recorded in both sexes, although it was more prevalent in males in Caucasians and in females in African-Americans and Hispanics [32].
Based on the Diabetes Epidemiology Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) study of Europe in 2004, the prevalence of MS was 15.7% in male and 14.2% in the female [33]. Epidemiological studies on MS have suggested that the prevalence of MS in Western societies is high and is increasing due to the increase in obesity, especially in younger individuals [34].
In Portugal there are few studies on the prevalence of MS. In 2004, an epidemiological study was carried out in Porto where the prevalence of MS was 23.9%, being more prevalent in females (27%) than in males (19.1%) [35].
In 2008, the first study was conducted on the prevalence of MS and its cardiovascular complications in the Portuguese adult population at the primary care level in continental Portugal, Azores, and Madeira—VALSIM study (epidemiological study of the prevalence of metabolic syndrome in the Portuguese population). In this study, 719 family doctors participated. The study was carried out between April 2006 and November 2007. A total of 16,856 individuals were evaluated between the ages of 18 and 96, with averages of 58.1 ± 15.1 years. This study showed a high prevalence of MS in adults affecting 27.5% of the population analyzed, being more prevalent in females (28.7%) compared with males (26%). This study revealed an increase in the prevalence of MS related to age, body mass index, and abdominal perimeter. This study also demonstrated the association between metabolic risk factors, including MS and the occurrence of cardiac events, stroke, and DM [34]. The prevalence of MS exhibited a regional variation, being more prevalent in Alentejo (30.99%), Madeira (29.38%), Central Region (28.79%), and North Region (28.17%) and less prevalent in Algarve (24.42%), Lisbon and Tagus Valley (25.71%), and Azores (26.05%) [34].
The pathophysiology of MS is not yet fully understood, but the most accepted hypothesis is insulin resistance, so MS is also known as insulin resistance syndrome. Insulin resistance is defined as a defect in its action at the peripheral level that results in hyperinsulinemia, required to maintain normal blood glucose [36, 37]. Predisposing factors for insulin resistance are central obesity and the release of large concentrations of free fatty acids from adipose tissue. Free fatty acids in the liver will determine the increase in glycogenesis and gluconeogenesis, increased triglyceride production, and the secretion of very low-density lipoproteins (VLDL).
Insulin is a hormone with anti-lipolytic action that is produced in pancreatic beta cells and is released into the bloodstream starting its metabolic effects after binding to its receptor. The insulin receptor is a transmembrane glycoprotein composed of four subunits linked by disulfide bridges, that is, two extracellular alpha subunits that contain the insulin binding domain and two β subunits, which contain an extracellular domain, a transmembrane domain, and a intracellular domain insulin binding to the α subunit and β subunit, and tyrosine kinase activation in the β subunit is the first stage of insulin action on glucose metabolism [38, 39]. The activation of tyrosine kinase, and phosphorylation of the β subunit of the insulin receptor, catalyzes the phosphorylation reaction of several tyrosine residues in a family of proteins called insulin receptor substrate (IRS), which include IRS-1, IRS-2, IRS-3, and IRS-4, which are the most specific in the insulin signaling cascade. Other isoforms are growth factor receptor-bound protein 2 (GRB2)-associated binding protein 1 (Gab-1), Shc, and p62 [40, 41].
Structurally, the four IRS proteins have many similarities, in particular, the phosphotyrosine-binding domain (PTB), whose function is the recognition sequence of asparagine-proline glutamic phosphotyrosine acid (NPEpY) located in the juxta membrane region of the β receptor of insulin. It is involved in the interaction of IRS proteins with the insulin receptor and with the COOH-terminal domain of the proteins, capable of binding to the SH2 domains [39]. In addition to their similarities, the four IRS proteins differ in tissue distribution [39]. The SH2 domain consists of 100 amino acids, and it is the phosphotyrosine binding site [41]. The activation of proteins that contain the SH2 domain is important for the transmission of the insulin signal and thus carry out its functions [39].
The IRS-1 gene located on chromosome 2q36–37 was the first substrate that was identified. IRS-1 is involved in many of the actions of insulin, in the activation of nitric oxide (NO) synthetase, in the activation of the activity of the iN + pump, and in vascular relaxation through activated protein kinases by mitogens (MAP kinase) [39, 42].
The IRS-2 gene is found on chromosome 13q34 [43]. The IRS-2 protein and the IRS-1 are very similar in structure and functions, and the main difference lies in the region between amino acids 591 and 789 of the IRS-2. IRS-2, unlike IRS-1, is more in the cellular cytosol [44].
IRS-3 does not appear to be expressed in human cells [39].
IRS-4 is a protein that consists of 1257 amino acids located in the cell membrane of various organs in which it is expressed. It was discovered initially in embryonic kidney cells. The IRS-4 gene is found on the X chromosome [39].
Insulin causes vascular relaxation through stimulation of NO production in the endothelial cells of blood vessels and by reducing the concentration of intracellular calcium in muscle and smooth muscle cells by decreasing sensitization of the light chains of calcium (Ca2+)-myosin. These effects are mediated by the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, as well as the stimulation of glucose transport in skeletal muscle and vascular adipose tissue [45]. In the case of insulin resistance, the increase in lipolysis produces greater amounts of fatty acids, promoting greater inhibition of the lipolytic effect of insulin, causing an increase in lipolysis [46, 47].
Insulin resistance is defined as the inability of glucose uptake by skeletal muscle and adipose tissue and the inability of the liver to inhibit gluconeogenesis in response to an increase in insulin [38, 43].
The evidence of the causal relationships between insulin resistance and hypertension is increasing [48]. There are still many uncertainties about the mechanisms that link the two conditions, but in addition to the common genetic predisposition between insulin resistance and AHT, there are several other possible mechanisms that can explain it [48, 49].
The renin-angiotensin-aldosterone system (RAAS) is a therapeutic target for AHT. Changes in the RAAS are also important in insulin resistance, and the common molecular mechanisms of insulin resistance and AHT are not well understood [50, 51].
The RAAS thus plays an important role in MS. Angiotensinogen is a 58 kDa protein produced primarily in the liver under physiological conditions, but it can be produced in smaller amounts in adipocytes, mesangial cells, and epithelial cells of the proximal contoured tubule and in the brain (neurons and glial cells). Angiotensinogen by the action of the renin enzyme produced in the glomerular juxta cells in the kidney is subjected to cleavage in the amino-terminal acid of 10 NH2 to form angiotensin I. Angiotensin I is an inactive peptide that is hydroxylated by the enzyme angiotensin converter, forming an octapeptide designated angiotensin II [50].
The RAAS has autocrine/paracrine activity in various tissues, especially in the skeletal muscle, smooth muscle of blood vessels, kidneys, heart, and pancreas [52]. The angiotensin (AT) II receptor is a transmembrane protein that belongs to the family of receptors coupled to the G protein which is divided into type I (AT1) and type II (AT2) [40, 42, 53]. The genes encoding the AT1 receptor were cloned in 1992, and the genes encoding the AT2 receptor were cloned in 1994 [54]. The binding of angiotensin II to the AT1 receptor leads to the phosphorylation of various proteins such as IRS-1 and IRS-2, making the P110/PI3K subunit the common activation mechanism for the insulin signaling pathway. Resistance to insulin is caused by the inhibition of insulin through the inhibition of the mechanisms involved in glucose transport and vasodilation [42, 45].
Skeletal muscle is important in the development of insulin resistance, which is responsible for 75–95% glucose metabolism [55, 56]. Skeletal muscle constitutes the largest insulin-sensitive tissue in the body and is the primary site for insulin-stimulated glucose utilization [55]. Skeletal muscle resistance to insulin is fundamental to the metabolic dysregulation associated with obesity and physical inactivity and contributes to the development of the MS [55]. Potential mechanisms contributing to reduced insulin signaling and action in skeletal muscle include adipose tissue expansion and increased inflammatory adipokines, increased RAAS activity, decreases in muscle mitochondrial oxidative capacity, increased intramuscular lipid accumulation, and increased reactive oxygen species (ROS) [55].
Angiotensin II has prooxidant and pro-inflammatory effects that regulate apoptosis, inflammation, cell growth, fibrosis, and insulin sensitivity by inducing the formation of oxygen free radicals through the enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase [56]. ROS are formed by the electron transport chain in the mitochondria, and it increases in situations that require the oxidation of substrates such as glucose [56]. Multiple ROS activate transcription factors such as factor nuclear kappa B (NF-KB) protein-1 and hypoxia-inducible factor-1 HIF-1, which are involved in the mechanism of insulin resistance in skeletal muscle [57].
Hyperinsulinemia can alter some of the components of the RAAS such as pro-fibrotic stimulants and pro-inflammatory actions mediated by angiotensin II and can cause cardiovascular disease development [50].
Obesity is a worldwide epidemic that has generated many scientific publications in recent years. Thus, new paradigms were emerging, while the old challenges are still to be unraveled [58]. Obesity is a chronic disease and has become a major problem in most industrialized countries due to its increased prevalence and association with various diseases and due to its great economic impact [59]. To preserve the energy reserves of body fat during periods of negative energy balance, the body has developed various regulatory mechanisms [60]. This control is achieved by balancing the intestinal absorption of glucose, the production of glucose by the liver, and the absorption and metabolism of glucose by peripheral tissues [61]. Insulin regulates blood glucose due to its action in stimulating glucose uptake in the muscle and liver and inhibiting hepatic gluconeogenesis [61]. Despite the change in tolerance to the action of insulin initially, blood glucose is normal because pancreatic β cells have the ability to increase the ability of insulin secretion to overcome existing insulin resistance [9]. Excess nutrients induce hypertrophy of adipocytes that promote the development of various chronic morbidities such as type 2 DM and insulin resistance, glucose intolerance, and dyslipidemia with the consequent development of cardiovascular diseases [60]. There is also strong evidence to suggest that cell hypoxia may be an important factor in the pathophysiology of adipocytes and may be one of the causes of this dysfunction contributing to the metabolic alteration associated with obesity [62].
Obesity is defined according to the WHO, as an abnormal or excessive accumulation of fat that can cause imbalances in the health of an individual [63]. Males are more likely to accumulate intra-abdominal adipose tissue compared with females [32, 64]. On average, men have twice the amount of visceral fat than women and have a higher prevalence of metabolic diseases associated with obesity and MS [65].
Obesity is associated with a higher incidence of type 2 DM, insulin resistance, AHT, dyslipidemia, some types of cancer, and CVD [66]. Fat tissue is deposited in two main compartments, subcutaneous and central or visceral [63]. Based on this, obesity can be divided into central and peripheral obesity. Central obesity is characterized by hyperplasia and hypertrophy of adipocytes around the intra-abdominal organs and is associated with greater development of MS [65].
Adipocyte hypertrophy is the main consequence of excess nutrient intake, promoting the development of insulin resistance and glucose intolerance [63]. Triglycerides present in fatty tissue are the body’s largest energy reserve, so adipose tissue is a very effective energy storage mechanism that allows survival of living beings in times of famine [59].
Recent studies have shown that hypoxia in adipose tissue can play an important role in the cellular mechanisms of chronic inflammation, macrophage infiltration, adiponectin reduction, leptin elevation, adipocyte apoptosis, and reticulum endoplasmic and mitochondrial dysfunction in white adipose tissue in obese [67].
Hypoxia inhibits pre-adipocyte differentiation and stimulates the secretion of leptin and vascular epithelial growth factor (VEGF) of mature adipocytes [68].
There are several genes that regulate the action of hypoxia, such as HIF-1α (hypoxia-inducible factor 1α), vascular endothelial growth factor VEGF, glucose transporter-1 (GLUT-1), heme oxygenase-1, and pyruvate dehydrogenase kinase 1 [67]. It was found that, under conditions of hypoxia in adipose tissue, all genes increased their expression except for VEGF messenger ribonucleic acid (mRNA) [67].
Adipose tissue is thus divided into white adipose tissue and brown adipose tissue, which have different functions. Brown adipose tissue has the function of producing heat. The understanding and vision we currently have in white adipose tissue have changed significantly in the last 15 years [69]. Currently, white adipose tissue is considered, not only as a tissue in which energy is stored in the form of triglycerides but also as the main secretory and endocrine organ of the organism [70]. White adipose tissue produces and secretes various proteins. Initially, these proteins were designated adipocytokines [71]. Currently, it is universally adopted the name of adipokines to the set of proteins synthesized and secreted by adipose tissue, since not all proteins are cytokines [71].
In addition to adipokines and fatty acids, adipose tissue produces other lipid substances such as steroid hormones, prostaglandins and prostanoids, cholesterol, and retinol (cholesterol and retinol are not synthesized by adipocytes but are stored and released from them) [71].
In 1994, Friedman and his colleagues discovered leptin, a hormone produced by white adipose tissue. Leptin, also called OB protein, is a hormone composed of 16 kDa and is produced from a protein with molecular weight of 18 kDa. It is cleaved leading to the production of leptin protein. Leptin is expressed in many tissues including the white and brown adipose tissue, stomach, placenta, mammary gland, ovarian follicles, and others [72]. It is expressed primarily in adipose tissue, but it is also expressed in smaller amounts in the brain and in the cerebrospinal fluid [70].
Leptin acts both in the central nervous system (hypothalamus) and in the peripheral organs. This discovery allowed us to realize that adipose tissue is not only a tissue in which energy storage occurs but also an endocrine organ [73].
White adipose tissue produces various adipokines, many of which are inflammatory mediators such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-β, and IL-6. The production of inflammatory interleukins increases with obesity and is involved in the development of insulin resistance and in the metabolic syndrome [62, 74]. Adipokines have various functions, in particular in the energy balance (e.g., leptin) on insulin sensitivity and glucose metabolism (e.g., adiponectin), inflammation (e.g., TNF-α), immunity (e.g., adipsin), lipid metabolism (e.g., cholesterol ester transfer protein), blood pressure control (e.g., angiotensinogen) hemostasis (e.g., plasminogen activation inhibitor-1), and angiogenesis (e.g., vascular epidermal growth factor) [62, 71].
Inflammation is an important process in obesity and in type 2 DM, as it promotes insulin resistance by inhibiting the function of IRS-1 and IRS-2 in the pathway insulin signaling [61, 75].
Obesity is characterized by a state of chronic inflammation with increased inflammatory parameters, for example, haptoglobin, IL-6, C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1), and TNF-α [69]. Large concentrations of cytokines produced by adipose tissue, such as TNF-α, IL-6, and IL-1β, and low concentrations of certain adiponectins cause chronic hyperinsulinemia and insulin resistance [63].
During periods of positive energy balance, there is an increase in white adipose tissue in order to be able to store excess triglycerides. Consequently, adipose tissue becomes hypoxic due to the decrease in vascularization of the same [62]. The role of hypoxia in adipose tissue in obesity and insulin resistance is still unclear [76]. Regulatory responses mediated by HIF-1 depend on its degree and duration [76].
HIF-1 is a heterodimeric transcription factor induced by hypoxia and composed of two subunits, the α subunit consisting of 120 kDa and the β subunit, consisting of 91 to 94 kDa [77]. The α subunit (HIF-1α) determines the transcriptional activity of HIF-1, and its increase occurs in response to hypoxia. The β (HIF-1β) subunit is constitutively expressed and may also be referred to as an aryl hydrocarbon receptor nuclear translocator (tRNA) [78]. Under normoxia conditions, HIF-1α is hydroxylated in proline and asparaginyl residues, catalyzed by the enzyme prolylhydroxylase (PHD), which promotes binding to an ubiquitin ligase complex. This process leads to proteosomal degradation mediated by HIF-1 [76, 78]. Under conditions of hypoxia, hydroxylation and activation of HIF-1 target genes are inhibited [76].
HIF-1α activates fibrosis of adipose tissue, causing an increase in macrophage infiltration into adipose tissue that mediates a greater increase in inflammation and concomitant sensitivity decrease in insulin [79, 80].
VEGF is a target gene of HIF-1. VEGF promotes angiogenesis, a necessary process for the differentiation of adipocytes and the growth of adipose tissue [81].
The endothelium is a layer of cells that lines the inner surface of the blood vessel [82]. Endothelial dysfunction is defined as the interruption of the release of vasodilator factors such as NO and prostacyclin (PGI2) and vasoconstrictor factors such as endothelin-1 (ET-1) and angiotensin II [74]. Alterations in vascular endothelial function at the level of adipose tissue can cause insulin resistance [81]. In insulin resistance, the release rate of free fatty acids from the adipose tissue, which contribute to diabetic dyslipidemia, increased. HDL-cholesterol decreased, increasing low-density lipoprotein (LDL) cholesterol and free fatty acids. This stimulates the inflammatory response, causing the adhesion of monocytes and lymphocytes to the endothelial cells, and increases the flow of glucose and free fatty acids to the cells, causing excessive formation of oxygen free radicals, with an increase in metabolic and hemodynamic degradation. There is an increase in free radicals and nitrites by intramitochondrial enzymatic oxy-reduction which promotes apoptosis and impaired vascular endothelial function [82]. This alteration causes insulin metabolic dysfunction, promoting greater resistance to insulin [74, 82].
Obesity alone is the cause of AHT in 78% of men and 65% of women [83]. Evidence of the causal relationship between insulin resistance and AHT is increasing [40]. Under physiological circumstances, insulin and insulin growth factor-1 (IGF-1) increase vasodilation by stimulating the production of NO and reducing the concentration of intravascular calcium in vascular smooth muscle cells. It also increases the sensitization of myosin-Ca2+ light chains. These actions are mediated through the activation of the PI3K enzyme and the Akt protein. Vascular relaxation in response to activation of PI3K/Akt pathway is mediated by endothelial cells producing NO, which involves phosphorylation of endothelial NO synthetase [41].
Patients with AHT have an increase in fasting and postprandial insulin levels in relation to non-hypertensive patients with the same body mass index [41]. It does not occur with secondary AHT but with essential AHT. This is related in part to the action of insulin that changes at the level of muscle tissue, which is the predominant site of glucose use stimulated by insulin [40].
There is an association between blood pressure and the proportion of type II fibers in skeletal muscle, which are less sensitive to insulin than type I fibers [40]. Under normal physiological conditions, there is a relationship between glucose-mediated insulin availability and increased blood flow in response to insulin. This response decreases in obese people with insulin resistance, which suggests resistance to insulin action in reference to vascular NO production [41]. Due to the difficulty of assimilating the rapid growth of adipose tissue in a hypoxia at an early stage, conditions are created for an increase in the expression of HIF-1α [84, 85, 86, 87].
There is evidence that insulin resistance and hyperinsulinemia predispose patients to the development of AHT due to cellular abnormalities in insulin signaling pathways and are associated with metabolic and hemodynamic alterations [84]. Metabolic abnormalities are linked to hypertension caused by pathophysiological processes that involve the sympathetic-adrenergic system, the imbalance of cell cations, the increase in inflammation, the oxidative stress, and the RAAS [40].
RAAS plays an important role in insulin resistance by being more active in visceral adipose tissue compared to peripheral adipose tissue [83]. Insulin resistance in obese individuals is also associated, in part, with an antagonism to the action of angiotensin II (AT II) [83]. This produces a decrease in NO production with an increase in vasoconstriction and a decrease in GLUT-4 in skeletal muscle. It also reduces glucose uptake and decreases vasodilation in tissues [83]. Under normal conditions, the RAAS system is a mechanism for regulating blood pressure [88]. With the increase in the activity of the RAAS, there is a greater production of ATII, which leads to stimulation of the sympathetic nervous system, insulin resistance, sodium retention, and increased intravascular volume. It also contributes to kidney disease, hypertension, insulin resistance, and left ventricular hypertrophy [83].
There is a common genetic predisposition to insulin resistance and hypertension. Genetic defects have been described in people who had insulin resistance and AHT and mutations found on chromosome 7q, where other genes important for glycemic control, blood pressure, and obesity are also found [49].
Hyperinsulinemia can directly stimulate the reabsorption of sodium and water in the kidney, which increases the volume in the extracellular space, causing AHT. Another mechanism by which insulin can cause hypertension involves stimulation of the sympathetic nervous system (SNS) by increasing the concentration of norepinephrine. This increase is directly related to the increase in pulse and blood pressure by direct effect on the reabsorption of sodium in the kidney, peripheral vasoconstriction, and increased cardiac output [9].
The correlation of CVRF with the metabolic syndrome differs from one another. The notion that CVRF has a tendency to aggregation allows an earlier diagnosis of MS, thus also leading to the early introduction of therapeutic, pharmacological, or non-pharmacological measures. The prevalence of MS increases with age and is present in people of working age, increasing the risk of cardiovascular diseases, work-related absences, and socioeconomic costs. The concept of MS was carried out in a progressive manner. Its clinical importance is enormous due to the fact that it can identify patients with high risk of suffering some CVD and/or DM, allowing a preventive intervention. This may explain the importance of understanding the pathophysiology of the MS, and the author hopes that at the end of the chapter, the reader can understand it. This chapter is the beginning of an explanation of metabolic syndrome that should be complemented by reading other articles.
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\n"}]},successStories:{items:[]},authorsAndEditors:{filterParams:{sort:"featured,name"},profiles:[{id:"105746",title:"Dr.",name:"A.W.M.M.",middleName:null,surname:"Koopman-van Gemert",slug:"a.w.m.m.-koopman-van-gemert",fullName:"A.W.M.M. Koopman-van Gemert",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/105746/images/5803_n.jpg",biography:"Dr. Anna Wilhelmina Margaretha Maria Koopman-van Gemert MD, PhD, became anaesthesiologist-intensivist from the Radboud University Nijmegen (the Netherlands) in 1987. She worked for a couple of years also as a blood bank director in Nijmegen and introduced in the Netherlands the Cell Saver and blood transfusion alternatives. She performed research in perioperative autotransfusion and obtained the degree of PhD in 1993 publishing Peri-operative autotransfusion by means of a blood cell separator.\nBlood transfusion had her special interest being the president of the Haemovigilance Chamber TRIP and performing several tasks in local and national blood bank and anticoagulant-blood transfusion guidelines committees. Currently, she is working as an associate professor and up till recently was the dean at the Albert Schweitzer Hospital Dordrecht. She performed (inter)national tasks as vice-president of the Concilium Anaesthesia and related committees. \nShe performed research in several fields, with over 100 publications in (inter)national journals and numerous papers on scientific conferences. \nShe received several awards and is a member of Honour of the Dutch Society of Anaesthesia.",institutionString:null,institution:{name:"Albert Schweitzer Hospital",country:{name:"Gabon"}}},{id:"83089",title:"Prof.",name:"Aaron",middleName:null,surname:"Ojule",slug:"aaron-ojule",fullName:"Aaron Ojule",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Port Harcourt",country:{name:"Nigeria"}}},{id:"295748",title:"Mr.",name:"Abayomi",middleName:null,surname:"Modupe",slug:"abayomi-modupe",fullName:"Abayomi Modupe",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/no_image.jpg",biography:null,institutionString:null,institution:{name:"Landmark University",country:{name:"Nigeria"}}},{id:"94191",title:"Prof.",name:"Abbas",middleName:null,surname:"Moustafa",slug:"abbas-moustafa",fullName:"Abbas Moustafa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94191/images/96_n.jpg",biography:"Prof. Moustafa got his doctoral degree in earthquake engineering and structural safety from Indian Institute of Science in 2002. He is currently an associate professor at Department of Civil Engineering, Minia University, Egypt and the chairman of Department of Civil Engineering, High Institute of Engineering and Technology, Giza, Egypt. He is also a consultant engineer and head of structural group at Hamza Associates, Giza, Egypt. Dr. Moustafa was a senior research associate at Vanderbilt University and a JSPS fellow at Kyoto and Nagasaki Universities. He has more than 40 research papers published in international journals and conferences. He acts as an editorial board member and a reviewer for several regional and international journals. His research interest includes earthquake engineering, seismic design, nonlinear dynamics, random vibration, structural reliability, structural health monitoring and uncertainty modeling.",institutionString:null,institution:{name:"Minia University",country:{name:"Egypt"}}},{id:"84562",title:"Dr.",name:"Abbyssinia",middleName:null,surname:"Mushunje",slug:"abbyssinia-mushunje",fullName:"Abbyssinia Mushunje",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Fort Hare",country:{name:"South Africa"}}},{id:"202206",title:"Associate Prof.",name:"Abd Elmoniem",middleName:"Ahmed",surname:"Elzain",slug:"abd-elmoniem-elzain",fullName:"Abd Elmoniem Elzain",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Kassala University",country:{name:"Sudan"}}},{id:"98127",title:"Dr.",name:"Abdallah",middleName:null,surname:"Handoura",slug:"abdallah-handoura",fullName:"Abdallah Handoura",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"École Supérieure des Télécommunications",country:{name:"Morocco"}}},{id:"91404",title:"Prof.",name:"Abdecharif",middleName:null,surname:"Boumaza",slug:"abdecharif-boumaza",fullName:"Abdecharif Boumaza",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Abbès Laghrour University of Khenchela",country:{name:"Algeria"}}},{id:"105795",title:"Prof.",name:"Abdel Ghani",middleName:null,surname:"Aissaoui",slug:"abdel-ghani-aissaoui",fullName:"Abdel Ghani Aissaoui",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/105795/images/system/105795.jpeg",biography:"Abdel Ghani AISSAOUI is a Full Professor of electrical engineering at University of Bechar (ALGERIA). He was born in 1969 in Naama, Algeria. He received his BS degree in 1993, the MS degree in 1997, the PhD degree in 2007 from the Electrical Engineering Institute of Djilali Liabes University of Sidi Bel Abbes (ALGERIA). He is an active member of IRECOM (Interaction Réseaux Electriques - COnvertisseurs Machines) Laboratory and IEEE senior member. He is an editor member for many international journals (IJET, RSE, MER, IJECE, etc.), he serves as a reviewer in international journals (IJAC, ECPS, COMPEL, etc.). He serves as member in technical committee (TPC) and reviewer in international conferences (CHUSER 2011, SHUSER 2012, PECON 2012, SAI 2013, SCSE2013, SDM2014, SEB2014, PEMC2014, PEAM2014, SEB (2014, 2015), ICRERA (2015, 2016, 2017, 2018,-2019), etc.). His current research interest includes power electronics, control of electrical machines, artificial intelligence and Renewable energies.",institutionString:"University of Béchar",institution:{name:"University of Béchar",country:{name:"Algeria"}}},{id:"99749",title:"Dr.",name:"Abdel Hafid",middleName:null,surname:"Essadki",slug:"abdel-hafid-essadki",fullName:"Abdel Hafid Essadki",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"École Nationale Supérieure de Technologie",country:{name:"Algeria"}}},{id:"101208",title:"Prof.",name:"Abdel Karim",middleName:"Mohamad",surname:"El Hemaly",slug:"abdel-karim-el-hemaly",fullName:"Abdel Karim El Hemaly",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/101208/images/733_n.jpg",biography:"OBGYN.net Editorial Advisor Urogynecology.\nAbdel Karim M. A. El-Hemaly, MRCOG, FRCS � Egypt.\n \nAbdel Karim M. A. El-Hemaly\nProfessor OB/GYN & Urogynecology\nFaculty of medicine, Al-Azhar University \nPersonal Information: \nMarried with two children\nWife: Professor Laila A. Moussa MD.\nSons: Mohamad A. M. El-Hemaly Jr. MD. Died March 25-2007\nMostafa A. M. El-Hemaly, Computer Scientist working at Microsoft Seatle, USA. \nQualifications: \n1.\tM.B.-Bch Cairo Univ. June 1963. \n2.\tDiploma Ob./Gyn. Cairo Univ. April 1966. \n3.\tDiploma Surgery Cairo Univ. Oct. 1966. \n4.\tMRCOG London Feb. 1975. \n5.\tF.R.C.S. Glasgow June 1976. \n6.\tPopulation Study Johns Hopkins 1981. \n7.\tGyn. Oncology Johns Hopkins 1983. \n8.\tAdvanced Laparoscopic Surgery, with Prof. Paulson, Alexandria, Virginia USA 1993. \nSocieties & Associations: \n1.\t Member of the Royal College of Ob./Gyn. London. \n2.\tFellow of the Royal College of Surgeons Glasgow UK. \n3.\tMember of the advisory board on urogyn. FIGO. \n4.\tMember of the New York Academy of Sciences. \n5.\tMember of the American Association for the Advancement of Science. \n6.\tFeatured in �Who is Who in the World� from the 16th edition to the 20th edition. \n7.\tFeatured in �Who is Who in Science and Engineering� in the 7th edition. \n8.\tMember of the Egyptian Fertility & Sterility Society. \n9.\tMember of the Egyptian Society of Ob./Gyn. \n10.\tMember of the Egyptian Society of Urogyn. \n\nScientific Publications & Communications:\n1- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Asim Kurjak, Ahmad G. Serour, Laila A. S. Mousa, Amr M. Zaied, Khalid Z. El Sheikha. \nImaging the Internal Urethral Sphincter and the Vagina in Normal Women and Women Suffering from Stress Urinary Incontinence and Vaginal Prolapse. Gynaecologia Et Perinatologia, Vol18, No 4; 169-286 October-December 2009.\n2- Abdel Karim M. El Hemaly*, Laila A. S. Mousa Ibrahim M. Kandil, Fatma S. El Sokkary, Ahmad G. Serour, Hossam Hussein.\nFecal Incontinence, A Novel Concept: The Role of the internal Anal sphincter (IAS) in defecation and fecal incontinence. Gynaecologia Et Perinatologia, Vol19, No 2; 79-85 April -June 2010.\n3- Abdel Karim M. El Hemaly*, Laila A. S. Mousa Ibrahim M. Kandil, Fatma S. El Sokkary, Ahmad G. Serour, Hossam Hussein.\nSurgical Treatment of Stress Urinary Incontinence, Fecal Incontinence and Vaginal Prolapse By A Novel Operation \n"Urethro-Ano-Vaginoplasty"\n Gynaecologia Et Perinatologia, Vol19, No 3; 129-188 July-September 2010.\n4- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Laila A. S. Mousa and Mohamad A.K.M.El Hemaly.\nUrethro-vaginoplasty, an innovated operation for the treatment of: Stress Urinary Incontinence (SUI), Detursor Overactivity (DO), Mixed Urinary Incontinence and Anterior Vaginal Wall Descent. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/ urethro-vaginoplasty_01\n\n5- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamed M. Radwan.\n Urethro-raphy a new technique for surgical management of Stress Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/\nnew-tech-urethro\n\n6- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamad A. Rizk, Nabil Abdel Maksoud H., Mohamad M. Radwan, Khalid Z. El Shieka, Mohamad A. K. M. El Hemaly, and Ahmad T. El Saban.\nUrethro-raphy The New Operation for the treatment of stress urinary incontinence, SUI, detrusor instability, DI, and mixed-type of urinary incontinence; short and long term results. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=urogyn/articles/\nurethroraphy-09280\n\n7-Abdel Karim M. El Hemaly, Ibrahim M Kandil, and Bahaa E. El Mohamady. Menopause, and Voiding troubles. \nhttp://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly03/el-hemaly03-ss\n\n8-El Hemaly AKMA, Mousa L.A. Micturition and Urinary\tContinence. Int J Gynecol Obstet 1996; 42: 291-2. \n\n9-Abdel Karim M. El Hemaly.\n Urinary incontinence in gynecology, a review article.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/abs-urinary_incotinence_gyn_ehemaly \n\n10-El Hemaly AKMA. Nocturnal Enuresis: Pathogenesis and Treatment. \nInt Urogynecol J Pelvic Floor Dysfunct 1998;9: 129-31.\n \n11-El Hemaly AKMA, Mousa L.A.E. Stress Urinary Incontinence, a New Concept. Eur J Obstet Gynecol Reprod Biol 1996; 68: 129-35. \n\n12- El Hemaly AKMA, Kandil I. M. Stress Urinary Incontinence SUI facts and fiction. Is SUI a puzzle?! http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly/el-hemaly-ss\n\n13-Abdel Karim El Hemaly, Nabil Abdel Maksoud, Laila A. Mousa, Ibrahim M. Kandil, Asem Anwar, M.A.K El Hemaly and Bahaa E. El Mohamady. \nEvidence based Facts on the Pathogenesis and Management of SUI. http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly02/el-hemaly02-ss\n\n14- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Mohamad A. Rizk and Mohamad A.K.M.El Hemaly.\n Urethro-plasty, a Novel Operation based on a New Concept, for the Treatment of Stress Urinary Incontinence, S.U.I., Detrusor Instability, D.I., and Mixed-type of Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/urethro-plasty_01\n\n15-Ibrahim M. Kandil, Abdel Karim M. El Hemaly, Mohamad M. Radwan: Ultrasonic Assessment of the Internal Urethral Sphincter in Stress Urinary Incontinence. The Internet Journal of Gynecology and Obstetrics. 2003. Volume 2 Number 1. \n\n\n16-Abdel Karim M. El Hemaly. Nocturnal Enureses: A Novel Concept on its pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecolgy/?page=articles/nocturnal_enuresis\n\n17- Abdel Karim M. El Hemaly. Nocturnal Enureses: An Update on the pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecology/?page=/ENHLIDH/PUBD/FEATURES/\nPresentations/ Nocturnal_Enuresis/nocturnal_enuresis\n\n18-Maternal Mortality in Egypt, a cry for help and attention. The Second International Conference of the African Society of Organization & Gestosis, 1998, 3rd Annual International Conference of Ob/Gyn Department � Sohag Faculty of Medicine University. Feb. 11-13. Luxor, Egypt. \n19-Postmenopausal Osteprosis. The 2nd annual conference of Health Insurance Organization on Family Planning and its role in primary health care. Zagaziz, Egypt, February 26-27, 1997, Center of Complementary Services for Maternity and childhood care. \n20-Laparoscopic Assisted vaginal hysterectomy. 10th International Annual Congress Modern Trends in Reproductive Techniques 23-24 March 1995. Alexandria, Egypt. \n21-Immunological Studies in Pre-eclamptic Toxaemia. Proceedings of 10th Annual Ain Shams Medical Congress. Cairo, Egypt, March 6-10, 1987. \n22-Socio-demographic factorse affecting acceptability of the long-acting contraceptive injections in a rural Egyptian community. Journal of Biosocial Science 29:305, 1987. \n23-Plasma fibronectin levels hypertension during pregnancy. The Journal of the Egypt. Soc. of Ob./Gyn. 13:1, 17-21, Jan. 1987. \n24-Effect of smoking on pregnancy. Journal of Egypt. Soc. of Ob./Gyn. 12:3, 111-121, Sept 1986. \n25-Socio-demographic aspects of nausea and vomiting in early pregnancy. Journal of the Egypt. Soc. of Ob./Gyn. 12:3, 35-42, Sept. 1986. \n26-Effect of intrapartum oxygen inhalation on maternofetal blood gases and pH. Journal of the Egypt. Soc. of Ob./Gyn. 12:3, 57-64, Sept. 1986. \n27-The effect of severe pre-eclampsia on serum transaminases. The Egypt. J. Med. Sci. 7(2): 479-485, 1986. \n28-A study of placental immunoreceptors in pre-eclampsia. The Egypt. J. Med. Sci. 7(2): 211-216, 1986. \n29-Serum human placental lactogen (hpl) in normal, toxaemic and diabetic pregnant women, during pregnancy and its relation to the outcome of pregnancy. Journal of the Egypt. Soc. of Ob./Gyn. 12:2, 11-23, May 1986. \n30-Pregnancy specific B1 Glycoprotein and free estriol in the serum of normal, toxaemic and diabetic pregnant women during pregnancy and after delivery. Journal of the Egypt. Soc. of Ob./Gyn. 12:1, 63-70, Jan. 1986. Also was accepted and presented at Xith World Congress of Gynecology and Obstetrics, Berlin (West), September 15-20, 1985. \n31-Pregnancy and labor in women over the age of forty years. Accepted and presented at Al-Azhar International Medical Conference, Cairo 28-31 Dec. 1985. \n32-Effect of Copper T intra-uterine device on cervico-vaginal flora. Int. J. Gynaecol. Obstet. 23:2, 153-156, April 1985. \n33-Factors affecting the occurrence of post-Caesarean section febrile morbidity. Population Sciences, 6, 139-149, 1985. \n34-Pre-eclamptic toxaemia and its relation to H.L.A. system. Population Sciences, 6, 131-139, 1985. \n35-The menstrual pattern and occurrence of pregnancy one year after discontinuation of Depo-medroxy progesterone acetate as a postpartum contraceptive. Population Sciences, 6, 105-111, 1985. \n36-The menstrual pattern and side effects of Depo-medroxy progesterone acetate as postpartum contraceptive. Population Sciences, 6, 97-105, 1985. \n37-Actinomyces in the vaginas of women with and without intrauterine contraceptive devices. Population Sciences, 6, 77-85, 1985. \n38-Comparative efficacy of ibuprofen and etamsylate in the treatment of I.U.D. menorrhagia. Population Sciences, 6, 63-77, 1985. \n39-Changes in cervical mucus copper and zinc in women using I.U.D.�s. Population Sciences, 6, 35-41, 1985. \n40-Histochemical study of the endometrium of infertile women. Egypt. J. Histol. 8(1) 63-66, 1985. \n41-Genital flora in pre- and post-menopausal women. Egypt. J. Med. Sci. 4(2), 165-172, 1983. \n42-Evaluation of the vaginal rugae and thickness in 8 different groups. Journal of the Egypt. Soc. of Ob./Gyn. 9:2, 101-114, May 1983. \n43-The effect of menopausal status and conjugated oestrogen therapy on serum cholesterol, triglycerides and electrophoretic lipoprotein patterns. Al-Azhar Medical Journal, 12:2, 113-119, April 1983. \n44-Laparoscopic ventrosuspension: A New Technique. Int. J. Gynaecol. Obstet., 20, 129-31, 1982. \n45-The laparoscope: A useful diagnostic tool in general surgery. Al-Azhar Medical Journal, 11:4, 397-401, Oct. 1982. \n46-The value of the laparoscope in the diagnosis of polycystic ovary. Al-Azhar Medical Journal, 11:2, 153-159, April 1982. \n47-An anaesthetic approach to the management of eclampsia. Ain Shams Medical Journal, accepted for publication 1981. \n48-Laparoscopy on patients with previous lower abdominal surgery. Fertility management edited by E. Osman and M. Wahba 1981. \n49-Heart diseases with pregnancy. Population Sciences, 11, 121-130, 1981. \n50-A study of the biosocial factors affecting perinatal mortality in an Egyptian maternity hospital. Population Sciences, 6, 71-90, 1981. \n51-Pregnancy Wastage. Journal of the Egypt. Soc. of Ob./Gyn. 11:3, 57-67, Sept. 1980. \n52-Analysis of maternal deaths in Egyptian maternity hospitals. Population Sciences, 1, 59-65, 1979. \nArticles published on OBGYN.net: \n1- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Laila A. S. Mousa and Mohamad A.K.M.El Hemaly.\nUrethro-vaginoplasty, an innovated operation for the treatment of: Stress Urinary Incontinence (SUI), Detursor Overactivity (DO), Mixed Urinary Incontinence and Anterior Vaginal Wall Descent. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/ urethro-vaginoplasty_01\n\n2- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamed M. Radwan.\n Urethro-raphy a new technique for surgical management of Stress Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/\nnew-tech-urethro\n\n3- Abdel Karim M. El Hemaly, Ibrahim M Kandil, Mohamad A. Rizk, Nabil Abdel Maksoud H., Mohamad M. Radwan, Khalid Z. El Shieka, Mohamad A. K. M. El Hemaly, and Ahmad T. El Saban.\nUrethro-raphy The New Operation for the treatment of stress urinary incontinence, SUI, detrusor instability, DI, and mixed-type of urinary incontinence; short and long term results. \nhttp://www.obgyn.net/urogyn/urogyn.asp?page=urogyn/articles/\nurethroraphy-09280\n\n4-Abdel Karim M. El Hemaly, Ibrahim M Kandil, and Bahaa E. El Mohamady. Menopause, and Voiding troubles. \nhttp://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly03/el-hemaly03-ss\n\n5-El Hemaly AKMA, Mousa L.A. Micturition and Urinary\tContinence. Int J Gynecol Obstet 1996; 42: 291-2. \n\n6-Abdel Karim M. El Hemaly.\n Urinary incontinence in gynecology, a review article.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/abs-urinary_incotinence_gyn_ehemaly \n\n7-El Hemaly AKMA. Nocturnal Enuresis: Pathogenesis and Treatment. \nInt Urogynecol J Pelvic Floor Dysfunct 1998;9: 129-31.\n \n8-El Hemaly AKMA, Mousa L.A.E. Stress Urinary Incontinence, a New Concept. Eur J Obstet Gynecol Reprod Biol 1996; 68: 129-35. \n\n9- El Hemaly AKMA, Kandil I. M. Stress Urinary Incontinence SUI facts and fiction. Is SUI a puzzle?! http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly/el-hemaly-ss\n\n10-Abdel Karim El Hemaly, Nabil Abdel Maksoud, Laila A. Mousa, Ibrahim M. Kandil, Asem Anwar, M.A.K El Hemaly and Bahaa E. El Mohamady. \nEvidence based Facts on the Pathogenesis and Management of SUI. http://www.obgyn.net/displayppt.asp?page=/English/pubs/features/presentations/El-Hemaly02/el-hemaly02-ss\n\n11- Abdel Karim M. El Hemaly*, Ibrahim M. Kandil, Mohamad A. Rizk and Mohamad A.K.M.El Hemaly.\n Urethro-plasty, a Novel Operation based on a New Concept, for the Treatment of Stress Urinary Incontinence, S.U.I., Detrusor Instability, D.I., and Mixed-type of Urinary Incontinence.\nhttp://www.obgyn.net/urogyn/urogyn.asp?page=/urogyn/articles/urethro-plasty_01\n\n12-Ibrahim M. Kandil, Abdel Karim M. El Hemaly, Mohamad M. Radwan: Ultrasonic Assessment of the Internal Urethral Sphincter in Stress Urinary Incontinence. The Internet Journal of Gynecology and Obstetrics. 2003. Volume 2 Number 1. \n\n13-Abdel Karim M. El Hemaly. Nocturnal Enureses: A Novel Concept on its pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecolgy/?page=articles/nocturnal_enuresis\n\n14- Abdel Karim M. El Hemaly. Nocturnal Enureses: An Update on the pathogenesis and Treatment.\nhttp://www.obgyn.net/urogynecology/?page=/ENHLIDH/PUBD/FEATURES/\nPresentations/ Nocturnal_Enuresis/nocturnal_enuresis",institutionString:null,institution:{name:"Al Azhar University",country:{name:"Egypt"}}},{id:"113313",title:"Dr.",name:"Abdel-Aal",middleName:null,surname:"Mantawy",slug:"abdel-aal-mantawy",fullName:"Abdel-Aal Mantawy",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Ain Shams University",country:{name:"Egypt"}}}],filtersByRegion:[{group:"region",caption:"North America",value:1,count:5681},{group:"region",caption:"Middle and South America",value:2,count:5161},{group:"region",caption:"Africa",value:3,count:1683},{group:"region",caption:"Asia",value:4,count:10200},{group:"region",caption:"Australia and 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