\r\n\tThis book will aim at serving as a complete and updated reference for a broad audience, including, students, orthotics, optometrist and ophthalmologist. The book will describe in detail general myopia features as well the most recent diagnostic techniques (e.g. OCT and visual field) which occupy a more and more relevant position in early myopia complications detection. It will explore the connection between myopia and other, popular disorders such as glaucoma, choroidal neovascularization, and retinal detachment: highly myopic eyes tend to have a retina and choroid thinner than normal and, then, the assessment of myopic eyes is far from being a simple task even with the most advanced imaging techniques. In the light of such observations, the book will give a special mention to pharmacological and surgical treatments currently available along with rehabilitation procedures and optical devices.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"41ca0f616bfa2745783b652b87ebedc3",bookSignature:"Prof. Felicia M. Ferreri",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/8705.jpg",keywords:"Myopia of prematurity, Retinal detachment, Intraocular pressure, Myopia and glaucoma, Myopic macular degeneration, Ocular motility,Visual rehabilitation, Clinical treatment, Retinal sensitivity, Visual Electrophysiology response, Visual Field, Ultrasonic Biometry",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 3rd 2018",dateEndSecondStepPublish:"December 24th 2018",dateEndThirdStepPublish:"February 22nd 2019",dateEndFourthStepPublish:"May 13th 2019",dateEndFifthStepPublish:"July 12th 2019",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"32442",title:"Prof.",name:"Felicia M.",middleName:null,surname:"Ferreri",slug:"felicia-m.-ferreri",fullName:"Felicia M. Ferreri",profilePictureURL:"https://mts.intechopen.com/storage/users/32442/images/system/32442.png",biography:"Felicia M. Ferreri graduated summa cum laude from University of Messina, Italy in 1998 and completed her ophthalmology residency at the Policlinico Universitario, Messina in 2002. She was interned at San Raffaele Hospital in Milan (Corneal Section) and at Hospital Careggi in Florence (pediatric ophthalmology diseases). She spent research periods in Seville ('Virginio del Rocio' hospital), Madrid ('San Carlos' hospital), Manchester ('The 'Bolton Hospital') and Rio de Janiero (Universidade Fluminense).\r\nShe served as co-investigator for many national and international clinical trials. Since 2002, she is an Assistant Professor in Ophthalmology at the University of Messina. Her research interests are in the areas of glaucoma, neuro-ophthalmology, pediatric ophthalmology, and cataract. She authored more than 50 scientific papers.",institutionString:"University of Messina",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"2",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"University of Messina",institutionURL:null,country:{name:"Italy"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"191",title:"Ophthalmology",slug:"medicine-ophthalmology"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"280415",firstName:"Josip",lastName:"Knapic",middleName:null,title:"Mr.",imageUrl:"https://mts.intechopen.com/storage/users/280415/images/8050_n.jpg",email:"josip@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copy-editing and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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It is either acute or chronic, and has many underlying causes which can be diagnosed and classified histologically where endoscopic appearances such as redness are often misleading. Gastritis is seldom if ever symptomatic, but usually have important clinical sequelae, principally duodenal and gastric ulceration, gastric adenocarcinoma and primary gastric lymphoma (El-Zimaity, 2007; Thirumurthi & Lanza 2010). The three most important causes of gastritis are categorized as Helicobacter pylori infection, prolonged use of aspirin, non-steroidal anti inflammatory drugs (NSAIDs) and autoimmunity (Dohil & Hassall, 2011).
Acute gastritis, is usually a diffuse and intense mucosal alteration, mostly is characterized by a sudden onset of symptoms and rapid resolution after the underlying aetiological mechanisms or agents (either chemical or physical) have been corrected. The patients can present with an acute gastroenteritis-like illness, or other symptoms which may be overshadowed by their general physical condition. Broadly speaking, acute gastritis arises when there is an acute imbalance between mucosal injury and repair mechanisms (Fig. 1) and can be organized in three groups based on the aetiologies: (i) infectious gastritis (ii) secondary to caustic injury; and (iii) ulcero-haemorrhagic (Srivastava & Lauwers, 2007).
Acute gastritis. Erosion and complete effacement of the epithelium is observed. The residual glands, on the left, display regenerative changes with basophilic epithelium.
No correlation may be exist between microscopic inflammation (histologic gastritis) and the presence of gastric symptoms (eg, abdominal pain, nausea, vomiting). In fact, most patients with histologic evidence of acute gastritis (inflammation) are asymptomatic. The diagnosis is usually obtained during endoscopy performed for other reasons. Acute gastritis may present with an array of symptoms, the most common being nondescript epigastric discomfort. Other symptoms include nausea, vomiting, loss of appetite, belching, and bloating. Fever, chills may be present. The diagnosis of acute gastritis may be clarified from the patient\'s history and can be confirmed histologically by biopsy specimens taken at endoscopy. Epidemiologic studies reflect the widespread incidence of gastritis (Ford et al., 2010).
Acute gastritis has a number of causes, including certain drugs; alcohol; bile; ischemia; bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy food poisoning; and direct trauma. The common mechanism of injury is an imbalance between the aggressive and the defensive factors that maintain the integrity of the gastric mucosal lining (mucosa) (Kasper et al., 2006).
Acute erosive gastritis can result from the exposure to a variety of agents or factors, referred to as reactive gastritis. These agents/factors include nonsteroidal anti-inflammatory medications (NSAIDs), alcohol, cocaine, stress, radiation, bile reflux, and ischemia. The gastric mucosa exhibits hemorrhages, erosions, and ulcers. NSAIDs, such as aspirin, ibuprofen, and naproxen, are the most common agents associated with acute erosive gastritis, mostly attributed to therapeutic. Major injury is attributed to reduced prostaglandin synthesis. Prostaglandins are chemicals responsible for maintaining mechanisms that result in the protection of the mucosa from the injurious effects of the gastric acid.
Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium called H. pylori is the most common cause of gastritis. Complications result from a chronic infection rather than from an acute infection. The prevalence of H. pylori in otherwise healthy individuals varies depending on age, socioeconomic class, country of origin where the infection is usually acquired in childhood. In the Western world, the number of people infected with H pylori increases with age. Evidence of H. pylori infection can be found in 20% of individuals younger than 40 years and in 50% of individuals older than 60 years. Transmission is likely from person to person through the oral-fecal route or through the ingestion of contaminated water or food. This is why the prevalence is higher in lower socioeconomic classes and in developing countries. H pylori is associated with 60% of gastric ulcers and 80% of duodenalulcers (Andersen, 2007).
H. pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in chronic gastritis. The acute gastritis encountered with H. pylori is usually asymptomatic. The bacterium imbeds itself in the mucous layer, a protective layer that coats the gastric mucosa. It protects itself from the acidity of the stomach through the production of large amounts of urease, an enzyme that catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide. The alkaline ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium conferring protection. H. pylori also has flagella that enable it to move and help it to penetrate the mucous layer so that it comes into contact with gastric epithelial cells. It also has several adhesions that help it to adhere to these cells. It produces inflammation by activating a number of toxins and enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that cause acute gastritis (Fig. 2) (Das & Paul, 2007).
Proposed interaction between host, environment and H. pylori infection in the development of gastric and doudenal ulcers.
Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to chronic superficial gastritis. The infection is established within a few weeks after the primary exposure to H. pylori. The intense inflammation can result in the loss of gastric glands responsible for the production of acid and mostly referred to as atrophic gastritis consequently production of gastric acid drops. The virulence genotype of the microbe is an important determinant for the severity of the gastritis of intestinal metaplasia, transformation of gastric epithelium which can lead to gastric cancer (Soltermann et al., 2007).
Reactive gastropathy is the second most common diagnosis made on gastric biopsy specimens after H. pylori gastritis. It is now considered to represent a nonspecific response to a variety of other gastric irritants (Owen, 2003).
Tuberculosis is a rare cause of gastritis and generally associated with generally associated pulmonary or disseminated disease (Marshall, 1993) where secondary syphilis of the stomach is a rare cause of gastritis (Chen et al., 2006).
Phlegmonous gastritis is an uncommon form of gastritis (rare) caused by numerous bacterial agents, including streptococci, staphylococci, Proteus species, Clostridium species, and Escherichia coli. Phlegmonous gastritis usually occurs in individuals who are debilitated. It is associated with a recent large intake of alcohol, a concomitant upper respiratory tract infection, and AIDS. Phlegmonous means a diffuse spreading inflammation of or within connective tissue. In the stomach, it implies infection of the deeper layers of the stomach (submucosa and muscularis).
Viral infections can cause gastritis either localized or diffuse and cytomegalovirus (CMV) is a common viral cause. It is usually encountered in individuals who are immunocompromised, including those with cancer, immunosuppression, transplants, AIDS with a localized or diffuse involvement to the gastric tissuesand AIDS (Bonnet et al., 2001; Sepulveda & Patil, 2008).
Fungal infections that cause gastritis include Candida albicans and histoplasmosis. Gastric phycomycosis is another rare lethal fungal infection. The common predisposing factor is immunosuppression. C albicans rarely involves the gastric mucosa and when isolated in the stomach, the most common locations tend to be within a gastric ulcer or an erosion bed and it is generally of little consequence. Disseminated histoplasmosis can involve the stomach. The usual presenting clinical feature is bleeding from gastric ulcers or erosions on giant gastric folds (Lauwers et al., 2010).
Parasitic infections are rare causes of gastritis. Anisakidosis is caused by a nematode that embeds itself in the gastric mucosa along the greater curvature. Anisakidosis is acquired by eating contaminated sushi and other types of contaminated raw fish. It often causes severe abdominal pain that subsides within a few days and this nematode infection is associated with gastric fold swelling, erosions, and ulcers (Kim et al., 2003).
Ulcero-hemorrhagic gastritis is most commonly seen in patients who are critically ill. and it is believed to be secondary to ischemia related to hypotension and shock or to the release of vaso constrictive substances, but the etiology is often unknown. The gastric mucosa reveals multiple petechiae, mostly in the fundus and body, or exhibits a diffusely hemorrhagic pattern. The gross pathology may resemble that of NSAID- or other ingestion-induced gastritis, except that the location of injury is different. This form of gastritis can be life-threatening if the patient experiences hemorrhaging and may even require emergency gastrectomy (Chamberlain, 1993).
Microscopic evidence of acute gastritis can be seen in patients with Crohn disease, though clinical manifestations are rare (occurring in only about 2-7% of patients with Crohn disease). Focally enhancing gastritis is now recognized as a condition seen in both Crohn disease and ulcerative colitis (Xin & Greenson, 2004).
Eosinophilic gastritis is often seen in conjunction with eosinophilic gastroenteritis but can be associated with various disorders, including food allergies (eg, cow milk, soy protein), collagen vascular diseases, parasitic infections, gastric cancer, lymphoma, Crohn disease, vasculitis, drug allergies, and H. pylori infections. An eosinophilic infiltrate is seen involving the gastric wall or epithelium (Rothenberg, 2004).
Chronic gastritis is caused mainly by Helicobacter pylori infection, and nonatrophic gastritis progresses to atrophic gastritis for a long period. It is characterized by the presence of chronic inflammatory infiltrate in the gastric mucosa (Fig. 4). H. pylori-atrophic gastritis is strongly associated with gastric cancers, and its diagnosis is very important. It is diagnosed histologically according to the Updated Sydney System, which is now widely used in the world (Satoh et al., 2008). Chronic gastritis can be classified on the base of the underlying etiologic agent (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the histopathologic pattern, which may suggest the etiologic agent and clinical course (eg, H pylori –associated multifocal atrophic gastritis). Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis) (Rugge & Genta, 2005).
The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or another infection, is described in the relevant disease (Boulton et al., 2011). The pathogenesis of the most common forms of gastritis is described as follows.
Chronic gatritis showing inflammation of mucosa linning
The host response to H. pylori and bacterial products is composed of T- and B-cell lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes that eventually phagocytize the bacteria. The presence of polymorphonuclear leukocytes in the gastric mucosa is diagnostic of active gastritis. The interaction of H pylori with the surface mucosa results in the release of proinflammatory cytokine interleukin (IL)-8, which leads to recruitment of polymorphonuclear cells and may begin the entire inflammatory process. Gastric epithelial cells express class II molecules, which may increase the inflammatory response by presenting H pylori antigens, leading to further cytokine release and more inflammation. High levels of cytokines, particularly tumor necrosis factor-a (TNF-α) and multiple interleukins (eg, IL-6, IL-8, IL-10), are detected in the gastric mucosa of patients with H. pylori gastritis (Zalewska-Ziob et al., 2009).
In subsequent or joining such inflammation pattern is an increase in oxidative damage due to high level of ROS and increased apoptosis level in human gastric mucosa (Obst et al., 2000; Cover et al., 2003). Infection also leads to the expression of inducible nitric oxide synthase ( iNOS) in host macrophage and polymorphnuclear leukocytes (Tari et al., 2003). NO produced by these cells infiltrating the gastric mucosa may damage DNA. Interaction between NO and superoxide anion can form peroxinitrite, potent nitrating agent leading to apoptosis in a variety of cell types (Yue et al., 2001).
Prostaglandins especially PGE2 in the stomach play an important role in the maintenance of gastric mucosal integrity via several mechanism including regulation of gastric mucosal blood flow, kinetic of epithelial cells, synthesis of mucous, inhibition of gastric acid secretion and referring to its protective potential to gastric mucosa (Takeeda et al., 2004).
Patients having Hpylori infection demonstrate significant gastremia which is mostly attributed to intragastric increase of H pylori inducing corpus atrophy and G cells damage in the antrum part. It may be also depends on alkalinization in G cells environment caused by H pylori urease (Walsh et al., 1976; Shacter et al., 2002).
Serum pepsinogens (1&11) are higher also and specifically in patient category having IgM positive as compared to others (IgM-ve). This may be attributed to a polypeptides secreted by HP during earlier infection which stimulates chief cells directly and promote pepsinogen synthesis (Takeeda et al., 2004; Kist, 1991; Elseweidy et al., 2010a;2010b).
This led certain study (Kekki et al., 1991) to consider serum pepsinogen level-as a non endoscopic blood test in the diagnosis of atrophic gastritis, HP eradication and, a screening tool for high risk subjects having atrophic gastritis rather than a test for cancer itself.
Generally known Hp infection is associated with special local and systemic immune response. Early after 18 days of infection IgM response is detectable while IgG, IgA response occurs later after 60 days of infection at which time IgG titers decline. IgG, IgA serology is widely used as an accurate test for the diagnosis of Hp infection but those 2 immunoglobulins remains detectable after eradication of HP and d\'not demonstrate the infection status (acute, chronic or previously treated infection). Therefore the use of IgM test would allow for direct screening of the sample and serve as a diagnostic tool for establishing active or recent infection (Alem et al., 2002, Elseweidy et al 2010).
Accordingly many authors concluded that diagnosis of atrophic gastritis using test panel of seum gastrin 17, pepsinogen 1, HP antibodies were in good agreement with endoscopic and biopsy findings, considering such panel a non endoscopic diagnostic and screening tool (Vaananen et al., 2003).
Histological section of human fundic gland of patient suffering from gastritis with anti H. pylori IgM positive group showing (a) x100 irregular short fundic gland (FG), wide gastric pit (GP), multiple inflammatory cells (arrows) and blood vessels (double arrows) filling lamina propria (LP), (b) x400 showing irregular simple columnar epithelium (E), small pyknotic nuclei (arrows) of cells lyning fundic gland (FG) and multiple inflammatory cells (double arrows) filling lamina propria (LP) (Elseweidy et al., 2010 a).
Phenolic compounds, which include tannins and flavonoids, are apparently related to the interesting anti-inflammatory, woundhealing, antioxidant and antiulcerogenic properties to several medicinal plants (Moleiro et al., 2009).
Tannins are potent scavengers of peroxyl radicals and can also interact with mucus proteins, improving their cytoprotective effect by forming a protein lining over the gastrointestinal mucosa (Okuda, 2005; Moleiro et al., 2009).
Fresh fruit and vegetables have been reported to exert multiple biological effects on the mucosa of the gastrointestinal tract due to their antioxidant contents (La Vecchia & Tavani, 1998). In particular, a diet rich in vegetable is associated with a lower incidence of gastric tumours (Roukos et al., 2003).
Apart from their action as radical scavengers, phenolic compounds also have several indirect effects; they can inhibit lipoxygenase (Laughton et al., 1991), reduce platelet aggregation (Ferro-Luzzi & Ghiselli, 1993) and reduce the bioavailability of food carcinogens (Stavric, 1994). Certain flavonoids or compounds with flavonoid-like properties have antiulcer activity and can prevent gastric mucosal lining lesions brought about by a number of ulcerogens (Alarcon de la Lastra et al., 2002).
Certain polyphenolics can exert a preventive action on gastric injury in rats. Research topics her have focussed on the antiulcer activity of polyphenol from grape seed (Saito et al., 1998), cacao liquor (Osakabe et al., 1998), curcuminoids and Black seed oil (Elseweidy et al., 2008) or from Opuntia ficus indica (Galati et al., 2003). This activity was mainly explained by the strong antioxidant power and/or by some other factors, such as strong protein-binding capacity (Saito et al., 1998), modulation of leukocyte function (Osakabe et al., 1998), mucus production and restoration (Galati et al., 2003). It is believed that the antioxidant activity of polyphenols is an important factor to combat the potential of free radicals.
Morinda citrifolia L. (Rubiaceae), commonly known worldwide as “Noni” or so called in Thai as “Yor” is regularly consumed as food, additionally as medicinal plants used in primary health care. The decoction or infusion of roasted mature unripe fruits is recommended to relieve the symptoms of nausea and vomiting, if it is not too severe. According to the claimed efficacies in Thai traditional textbooks, the fruit is also used for treatment of various gastrointestinal disorders as a carminative, appetite stimulant, and reliever of gum diseases, heartburn or stomachache. Nevertheless, experimental studies demonstrated the preventive activity of an ethyl acetate extract of the fruit against acute gastric lesions induced by ethanol, aspirin and pyloric ligation; and acute duodenal ulcer induced by cysteamine in rats (Muralidharan & Srikanth, 2009). This extract was claimed to exhibit potent antioxidant properties and the active components are thought to be non-polar lignans (Kamiya et al., 2004). Previous studies of the effect of an aqueous fruit extract on gastrointestinal motility reported controversial results with increase (Chuthaputti et al., 1996) and delay (Pu et al., 2004) gastric emptying action.
It has been claimed also that aqueous extract have anti-inflammatory (McKoy et al., 2002) and antioxidative activities (Ikeda et al., 2009) in several in vitro test systems. Among a number of major components identified in the aqueous fruit juice, scopoletin, a coumarin derivative, as one of the main compounds that has known pharmacological activities especially an ability to control the serotonin level in the body (Levand and Larson, 1979), together with anti-inflammatory (Deng et al., 2007; Moon et al., 2007) and antioxidative activities (Ikeda et al., 2009). Scopoletin is also recommended as a marker constituent for the quality control and pharmacokinetic study of Noni products (Samoylenko et al., 2006).
This aqueous fruit extract as well as its biomarker: scopoletin, may be beneficial as a potential preventive and therapeutic agent for gastro-esophageal inflammation. This is mainly through its antisecretory and prokinetic activities including its ability to enhance the mucosal defensive mechanisms. Their efficacy was compared with a standard potent antisecretory proton pump inhibitor (lansoprazole) and referring to its stronger prokinetic efficacy in accelerating gastric emptying and intestinal transit in rats. These observed beneficial effects of AFE may be accounted for by one of its major active biological components scopoletin (Mahattanadul et al., 2011).
It is well known that flavonoids which have anti-inflammatory, antioxidant, antiallergic, hepatoprotective, antithrombotic, antiviral, and anticarcinogenic activities. As reported before the anti-inflammatory activities of flavonoids demonstrate their candidacy as therapeutic agents (Lewis, 1989). The flavonoids are typical phenolic compounds that act as potent metal chelators, antioxidants and free radical scavengers, which modulate intracellular signaling caused by upstream binding partners, such as, regulatory kinases and receptors (Williams et al., 2004a).
Such flavonoid is a natural flavone with various bioactivities and was found to be highly efficient to scavenge free radicals in cell-free systems (Rice-Evans et al., 1996), as compared to traditional antioxidants like vitamin C and E (Geetha et al., 2005). Gerritsen et al., (1995) found that flavonoids, especially an apigenin, blocked the cytokine-induced expressions of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin on human endothelial cells.
Regarding gastric secretion, the oral administration of QGC reduced gastric content significantly, dose-dependently, and prevented the development of reflux esophagitis. These results suggest that QGC has inhibitory effects on reflux esophagitis and gastritis in rats. Furthermore, in feline esophageal epithelial cells, QGC was found to have a protective effect on ethanol induced cell damage by inhibiting ROS generation, activation downstream of ERK (Min et al., 2009), and downstream signal transduction induced by interleukin-1 beta (Lee et al., 2009a).
Mangifera indica L. (Anacardiaceae) is a large tree that grows in tropical and subtropical regions. The Caribbean population used aqueous decoction from M. indica flowers for the treatment of gastritis and gastric ulcer. Phytochemical research from different parts of M. indica has demonstrated the presence of phenolics, triterpenes, flavonoids, phytosterols and polyphenols (Selles et al., 2002; Singh et al., 2004).
Garrido et al., (2004) reported the antinociceptive and anti-inflammatory activities of Vimang®, an aqueous extract obtained from M. indica. They attributed these activities to their inhibitory influence on the prostaglandin synthesis through arachidonic acid metabolism additionally production of reactive oxygen species. Tordera et al., (1994) demonstrated the influence of several anti-inflammatory flavonoids present in M. indica on mast cell degranulation and arachidonic acid release in rats.
M. indica is also described as an antioxidant agent (Sanchez et al., 2003). Oxygen-derived free radicals have been postulated to play an important role in the pathogenesis of acute gastric mucosal injuries such as those induced by stress (Hariganesh & Prathiba, 2000), ethanol (Salim, 1990) and NSAIDs (Pihan et al., 1987) and scavenging of these radicals can stimulate the healing process. This was illustrated before in experimental model induced by acetic acid and attributed mainly to their high content of flavonoids (Naito et al., 1995).
Several medicinal plants including species of the Brazilian Cerrado biome as well as plants of the “Caatinga” biome contain phenolic compounds like tannins and flavonoids that have anti-inflammatory, antioxidant and antiulcerogenic properties (Almeida et al., 2005; Moleiro et al., 2009).
Catechins (flavan-3-ols) such as catechin, epicatechin, epigallocatechin, epicatechin gallate and epigallocatechin gallate, are particularly abundant in the bark of the species of Mimosaceae family (Santos et al., 2002). These compounds has anti-inflammatory and anti cholesterolemic effects additionally protective agent against cytotoxicity owing to their antioxidant properties (Williams et al., 2004b).
Araujo et al. (2008) studied plants with elevated levels of phenolic compounds within specific groups of plants for further therapeutic applications. They concluded that Caatinga medicinal plants, which are known and/or used for their wound-healing or anti-inflammatory properties, tend to have high tannin contents. Moreover, these compounds appear markedly elevated in some species, such as Abarema cochliacarpos, that are intensively used by the local communities (Monteiro et al., 2006).
Abarema cochliacarpos is a plant native to Brazil, occurring mainly in the Atlantic Forest and in the Caatinga biomes. It is a tree species of the legume family Mimosaceae (International Union for Conservation of Nature "IUCN", 2009), which is popularly known as “barbatimao”. In this community, the decoction of the bark is utilized to wash external ulcers while its tincture, (bark immersed in white wine) “cachaca”, or ingested form is used against inflammation and gastric ulcers, among other uses (Silva et al., 2006). Other authors also observed similar applications in different traditional communities (Agra et al., 2008).
As to pharmacologic effects, the hydroalcoholic extract from the bark of Abarema cochliacarpos showed antimicrobial activity. Both crude aqueous and methanol extracts also showed antinociceptive effects (Silva et al., 2009). Butanolic fraction of the methanolic extract was tested recently in a model of acute experimental trinitrobenzene sulfonic acid (TNBS)-induced colitis and showed anti-inflammatory effects (Silva et al., 2010a).
It has been suggested that Abarema cochliacarpos (Gomes) Barneby & Grimes extracts exerts gastroprotective effects and wound healing properties in the ethanol-induced ulcer model. The safety and efficacy in the healing of gastric ulcers is based on its ability to activate the expression of COX-2, vascular-endothelial growth factor (VEGF) and stimulate proliferative factors like HSP-70 that re-establish the gastric mucosa integrity (Silva et al., 2010b).
Eberhardt and colleagues (2000) illustrated the antiproliferative effect of apple extract in vitro using tumor cells and attributed such effect to the presence of phytochemicals (phenolic acids and flavonoids) other than ascorbic acid. Therefore, dietary antioxidants play a crucial role in the maintenance of gastric homeostasis by counteracting the potentially mucosal damage exerted by ROS. This may explain the role of dietary antioxidants as scavenger of oxygen, nitrogen free radicals and breaking lipid peroxisdation reactions. Phenolic compounds are one of the major classes of dietary antioxidants and apple phenolic compounds represent 22 percent of such total (Le Marchand et al., 2000).
In vitro and in vivo studies demonstrated the protective effect of apple juice regarding gastric mucosa of rat. This was markedly observed in gastric injury model induced by aspirin and independently of its inhibition to gastric acid. Therefore it might be of therapeutic benefit in prophylaxis of aspirin- related gastropathy (D\' argenio et al., 2008). Accordingly a diet rich in apple antioxidants might exert a beneficial effect in gastric diseases associated with generation of reactive oxygen species (Graziani et al., 2005).
Foeniculum vulgare (FVE) is a well-known umbelliferous plant. For centuries, FVE fruits have been used as traditional herbal medicine in Europe and China. It is native to southern Europe and the Mediterranean area. The seeds of this plant have been used to regulate menstruation, alleviate the symptoms of female climacteric syndrome, and increase libido (Albert-Puleo, 1980). FVE also possesses emnenagague, galactagogue and antispasmodic properties additionally in folk remedies for treatment of dysmenorrheal, also as diuretic and wound dressing in Turkish traditional medicine (Savino et al., 2005).
It contains 1%-3% of a volatile oil, which is composed of 50%-85% of anethole and about 20% of d-fenchone (Dadalioglu & Evrendilek, 2004). Other compunds present in FVE are d-a-pinene, d-a-phellandrene, dipentene, methyl chavicol, feniculun, anisaldehyde, and anisic acid (Mimica-Dukic et al., 2003).
Previous studies proved that anethole possesses significant antioxidant, anti-inflammatory and ulcer healing activity in experimental models (Freire et al., 2005). Additionally, flavonoids, sterols, tannins and coumarins of some plants are also known to possess antiulcer activity (Khalil, 2006). Therefore, the presence of flavonoids content and other bioactive compounds in FVE may be beneficial in ulcer therapy. Its gastro protective effect has been also observed before in certain gastric mucosal lesion induced by ethanol, attributed mostly to its antioxidant activity and reduction of lipid peroxidation cascade.
Therefore it may be a new alternative for clinical management of gastric ulcer diseases and/or an antioxidant against oxidative stress (Birdane et al., 2007).
The leaves of Piper carpunya Ruiz & Pav. (syn Piper lenticellosum C.D.C.) (Piperaceae), known with the popular name of “guaviduca” in Ecuador are widely used in folk medicine in tropical and subtropical countries of South America, as an anti-inflammatory, anti-ulcer, anti-diarrheal and anti-parasitical remedy as well as an ailment for skin irritations. The antiinflammatory activity has been confirmed in rat models like the carrageenan-induced paw edema and the results obtained can support its use in the traditional medicine of Ecuador (De las Heras et al., 1998). Recently, this plant has been shown to protect against gastric ulcers induced by non-steroidal anti-inflammatory drugs (NSAID) in rats (Trabadela et al., 2009).
Numerous plant remedies have shown to be active against Helicobacter pylori infection, such as the oil extract of Chamomilla recutita (Shikov et al., 2008), the ethanolic extract of Cuminum cyminum L., Propolis (Nostro et al., 2005) as well as the methanolic extract of Alchornea triplinervia (Spreng.) Mull. Arg., which exhibited anti-secretory, anti-Helicobacter pylori and gastroprotective effects (Lima et al., 2008).
Several mechanisms of action have been proposed to illustrate its anti-inflammatory effects. This may be explained through other properties such as anti-oxidant activity, inhibition of eicosanoid generating enzymes or as modulator for proinflammatory molecules. Recent studies have also shown that some flavonoids are modulators of proinflammatory gene expression (Garcia-Lafuente et al., 2009). Gastro protective activity of flavonoids may be through reducing gastric acid secretion and inhibition of gastric H+, K+-ATPase. One example is Baccharis illinita D.C., which is also used in folk medicine, and whose anti-secretory activity is attributable to the flavonoid luteolin (Freitas et al., 2008).
Furthermore, some flavonoids have also demonstrated inhibitory effects on Helicobacter pylori growth and vacuolation. Helicobacter pylori induces gastric epithelial cell apoptosis via secreted mediators such as the VacA cytotoxin and lipopolysacccharides which damage epithelial acid-secreting parietal cells (Neu et al., 2002). Several flavonoids have inhibitory influence on the apoptotic signaling induced by Helicobacter pylori VacA toxin (Xiao et al., 2007). Antimicrobial compounds from plants may inhibit bacterial growth by different mechanisms and could therefore be useful in case of resistance state to antibiotics. In this way, Castillo-Juarez et al., (2007) found that the petroleum ether fraction from Amphipterygium adstringens (Schltdl.) Standl. had significant anti-microbial activity against Helicobacter pylori. From this fraction, the authors isolated a mixture of anacardic acids and three known triterpenes: masticadienonic acid, 3-alpha-hydroxymasticadienonic acid, 3-epi-oleanolic as well as the sterol ß-sitosterol.
Previous study suggested that the flavonoids (vitexin, isovitexin, rhamnopyranosylvitexin and isoembigenin), nervogenic acid and geranylbenzoate isolated from the ethanolic extract of Piper carpunya may contribute to the anti-myeloperoxidase activity, as well as to their anti-Helicobacter pylori effect. These flavonoids may also be responsible for the important inhibition of H+, K+-ATPase pathway, additionally the obtained phytosterols and phytol could be involved in these gastroprotective activities (Quilez et al., 2010).
Quassia is a plant that grows typically in the American tropical regions (from Mexico to the Brazilian Amazona) below 500 m altitude, especially in the Caribbean side of Central America and the Pacific coast of Costa Rica and Panama. The plant prefers very humid environments, but it can be found in the dry forest next to a riverbank (López and Pérez, 2008).
Quassia amara L. is one of the most mentioned plants in ethnomedicine for the treatment of malaria, mainly in Surinam, Guyana and French Guyana, where tea cups are carved from the wood and the addition of hot water forms an infusion in them (Odonnea et al., 2007). There only exist a few studies on the gastrointestinal, digestive and secretagogue activity of Quassia amara L. extracts. The results point to an increase of bile secretion with a standardized extract, inhibition of ulcer induction with crude extracts, accompanied by a slight decrease in pH and peptic activity of gastric juice additionally an enhancement of cytoprotective factors like gastric mucus (Toma et al., 2002).
The biological activity of Quassia amara L. has been attributed mainly to its high content of quassinoids. These metabolites are oxygenated triterpenes derived from euphol and are exclusive to the Simaroubaceae family. The most important quassinoids in Quassia amara L. are quassin and neoquassin. Quassin is one of the most bitter substances known, it represents 0.1% of the dried weight of wood and bark, and it is present in larger quantities when the plant is grown in the shade (Guo et al., 2005).
Quassia amara L. bark standardized extracts, Lipro® and Ligas®, which were standardized to its quassinoid content, showed an important anti-ulcerogenic and gastroprotective potential in acute ulcer induction models. Their effect was related to an increase in gastric barrier mucus and non protein sulfhydril groups (Garcia-Barrantes & Badilla, 2011). Gastric barrier mucus is an important factor in gastroprotection (Kaunitz, 1999). Animals treated with Ligas® showed substantial mucus production. Prostaglandins I2, E2 and F2 are some of the main stimuli for the production of gastric and duodenal mucus (Dharmani et al., 2005). The increase in mucus could be a signal of the role of prostaglandins in the anti-ulcerogenic properties of the extracts.
Gardenia jasminoides Ellis (GJE), has been used in traditional oriental medicine for the treatment of jaundice, fever, hypertension, and ulcers of a skin (Tseng et al., 1995). It has been reported that the crude extract of GJE fruit has biological and pharmacological activities. In the phytochemical studies of GJE, genipin, chlorogenic acid, rutin, and ursolic acid were detected in GJE extracts (He et al., 2006). Genipin is an aglycone derived from an iridoid glycoside called geniposide present in fruit of GJE, and is an excellent natural cross-linker for proteins, collagen, gelatin, and chitosan cross-linking. It has been also used for pharmaceutical purposes, such as choleretic action for liver diseases control, and the relief of type 2 diabetes symptoms. Ursolic acid is a pentacyclic triterpene acid, used in cosmetics (Shishodia et al., 2003), and as inhibitor for various types of cancer cells by inhibiting the STAT3 activation pathway (Pathak et al., 2007) and human fibrosarcoma cells by reducing the expression of matrix metalloproteinase-9 by the glucocorticoid receptor.
Gastric cancer is the second commonest cause of death from malignant disease worldwide (Neugut et al., 1996). Antioxidant compounds, such as vitamin C and E, have a key role for prevention and termination of development of gastric cancer (Block, 1991). It has been recognized that chronic infections of the gastric mucosa by Helicobater pylori (H. pylori) plays a pivotal role in gastric carcinogenesis. Such infection usually causes acute and chronic inflammation cell infiltrate, leading to an increase of reactive oxygen species (ROS), which are highly reactive compounds. The latter may combine with DNA in a number of potentially genotoxic ways, subsequently accumulated in H. pylori gastritis. Therefore it may be possible to prevent carcinogenesis through reduction of ROS damage to cellular constituents, especially DNA, additionally the eradication of H. pylori can lead to a reduction in ROS activity in the gastric mucosa (Drake et al., 1998).
Lee et al., (2009b) in confirm indicated that the ethanolic extracts of GJE exerted protective activities against potential gastritic diseases like gastritis and gastric cancer. This action might be due to antioxidant activity, anti-H. pylori activity of ursolic acid and genipin that counteract free radicals exerting anti-ulcer activity.
Curcumin, the polyphenolic yellowish pigment of the rhizome Curcuma longa Linn, is known to possess anti-inflammatory, antioxidant, wound-healing, and antiallergic activities (Das& Das, 2002). Several investigators have also reported the antiulcerogenic activity of the ethanolic extract of the rhizome of C. longa in acute gastric mucosal lesion (Rafatullah et., 1990), but not in chronic ulcer models. More recently, it has been considered that curcumin exerts a variety of pharmacological actions through inhibition of inducible nitric oxide synthase (iNOS) as well as its potential as radical scavenger (Elseweidy et al., 2008) Thus, the previously proposed mechanisms for antiulcerogenic effect of curcumin (Yano et al., 2000), such as inhibitory effect on gastric secretion, cytoprotection, antioxidant activity and inhibition of mast-cell degranulation, need to be evaluated again.
Curcumin, exerted its preventive effect on gastric lesion formation, although it possesses anti-inflammatory activity resulting from a blockade of all branches of the arachidonic acid pathway (Ammon et al., 1993). This effect is consistent with the findings reported by several authors that the inhibition of prostaglandins synthesis is unlikely to be the mechanism responsible for the inflammatory ulceration formation. Curcumin therefore may exert this through its antioxidant activity and its inhibition of nuclear factor kappa B activation which up-regulates many genes involved in inflammation and immunity, including its potent suppressive effect on mast-cell degranulation (Jobin et al., 1999). Although there is a potential increase of gastric acid secretion with a high dose of curcumin, gastric acid secretion has been found to play little role in the pathogenesis of this model (Ohta et al., 1999).
Apparent healing – promoting effect of curcumin was also observed in gastric ulcer model, induced by acetic acid with an enhancement of mucosal layer regeneration. This effect was not seen in a dose-related fashion, presumably through some curative mechanisms differently modified by curcumin dosage. Accordingly, it is conceivable that the effect of curcumin occurs at least partly through its inhibition of the cytokine-mediated inflammatory mechanism, suppression of iNOS activity and antioxidant activity as mentioned above. In addition, the curative properties and ulcer healing might result from the elevation of epidermal growth factor and transforming growth factor-beta-1, as shown in acceleration of cutaneous wound healing in rats, guinea pigs and mice (Sidhu et al., 1998).
Another study attributed such preventive and curative effects of curcumin to an increase in the mucosal defensive mechanism through its antioxidant property, increase in mucin secretion and inhibition of NO or cytokine-mediated inflammation (Mahattanadul et al., 2006).
Artichoke (Cynara Scolymus L.) is a plant that is widely grown in Mediterranean countries, including southern France and California in the United States. In general, the dried extract consisting of leaves and not flowering heads of artichoke has been eluted with water in European countries and the main components are caffeoylquinic acid derivatives (cynarin and chlorogenic acid), flavonoids (luteolin and apigenin) and bitters (cynaropicrin) (Joy & Haber, 2007). Artichoke leaf extract has been used for hepatoprotective and cholesterol reducing (Aktay et al., 2000) purposes. Based on in vitro (Perez-Garcia et al., 2000) and in vivo (Speroni et al., 2003) studies, it is believed that artichoke leaf extract is very effective as an antioxidant and its leaf extract contains cynaropicrin and chlorogenic acid as the main components. It is currently used in Germany and Switzerland as a remedy for indigestion. And its better compounds such as cynariopicrin as inflammatory agents due to its inhibitory influence on inflammatory mediators (Holtmann et al., 2003).
Previous results indicated that artichoke leaf extract is effective against acute hemorrhagic gastritis and its beneficial effect is due to that of cynaropicrin. The gastric mucus-increasing action of artichoke leaf extract may be, at least in part, related to the anti-gastritic action of the extract (Ishida et al., 2010).
Some European pear (Pyrus communis L.) cultivars have been reported to contain significant amounts of polyphenols, such as chlorogenic acid, flavan-3-ols and arbutin. procyanidins are reported to have many beneficial properties, such as potent antioxidant activity (Zhu et al., 2002), free radical scavenging activity (Arteel & Sies, 1999), antiinflammatory activity and anti-influenza viral activity (Hamauzu et al., 2005).
It has been shown that procyanidins extracted from pear (Winter Nelis) fruit had a very high mean degree of polymerization (mDP), indicating that these compounds may interact with mucosa proteins. Accordingly the mechanism of mucosa protection by pear procyanidins may be both physical and chemical. By binding strongly to the mucosa, procyanidins build a protective layer against injury, reducing leukocyte migration, and then exerting its local antioxidant protection against free radicals (Hamauzu et al., 2007).
Sesamol (3,4-methylenedioxyphenol), the lignan of sesame oil, is a potent antioxidant and anti-inflammatory agent in various oxidative systems, including endotoxin and iron intoxication (Hsu et al., 2007). Recent study has confirmed its effect in gastric haemorrhage model and mucosal ulcer induced in rats by aspirin. Sesamol her significantly reduced gastric mucosal lipid peroxidation, nitric oxide production, gastric mucosal proinflammatory cytokines (tumor necrosis factor-a and interleukin 1-ß levels), and the activity of gastric mucosal myeloperoxidase. This was attributed to an inhibition of neutrophil infiltration, subsequent gastric mucosal inflammation and oxidative stress in rats (Hsu et al., 2009a). It seems likely that sesamol protective influence on gastric mucosal injury may be at least partially through an inhibition of mucosal reactive nitrogen species and subsequent lipid peroxidation.
Inhibition of neutrophils activation and their infiltration into gastric mucosa may be sesamol’s anti-inflammatory and antioxidative mechanism. Neutrophil activation and infiltration are crucial in the pathogenesis of NSAID-induced gastric inflammation and oxidative stress (Souza et al., 2008). Activating neutrophils results in the expression of proinflammatory genes and the overproduction of proinflammatory mediators, including TNF-α and IL-1ß, which initiates an inflammatory response (Jaeschke & Hasegawa, 2006). Overproduction of proinflammatory mediators can upregulate nitric oxide production leading to an increase of reactive nitrogen species, lipid peroxidation, and cell damage (Hayes and McLellan, 1999). Similar effect for Sesamol was also observed in the gastric mucosa of aspirin-treated rats preventing inturn gastric injury. This may be attributed to certain combination between sesamol and aspirin, inhibiting inturn neutrophil infiltration, mucosal inflammation and oxidative stress (Hsu et al., 2009a).
Daily consumption of sesame or sesame oil may be beneficial in protecting against gastric mucosal damage induced by long-term use of NSAID. Sesame lignan sesamol is one of the important antioxidative components in sesame in addition to some other antioxidants such as sesamin, sesamolin, and gamma-tocopheral (Tokusoglu et al., 2003). All of them could attenuate NSAID initiated gastric mucosal oxidative stress. Therefore, we suggested that daily consumption of sesame or sesame oil could protect against NSAID-induced gastric mucosal damage. However, more investigations will be needed to confirm this.
Also, pretreatment of sesame oil, significantly decreased acidified ethanol-induced mucosal ulcer formation and luminal hemorrhage. Sesame oil her reduced mucosal lipid peroxidation, as well as glutathione and nitric oxide production in experimental rats model attenuating in turn oxidative stress and gastric mucosal injury (Hsu et al., 2009b).
Gastritis represents an inflammation of the stomach lining in response to injury.It is either acute or chronic and has many underlying causes,however the most important of them are Helicobacter pylori (HP) infection, Autoimmunity additionally prolonged uptake of certain drugs,specifically aspirin and nonsteroidal antiinfilammatory drugs (NSAIDs).The common mechanism of an injury is an imbalance between the aggressive and defensive factors that maintain the integrity of the gastric lining (mucosa). In subsequent or joining such inflammation pattern an increase in oxidative damage due to high level of reactive oxygen species (ROS), higher gastrin, pepsinogen, expression of inducible nitric oxide synthase (iNOS) leading to corpus atrophy and G cells damage. Interaction of NO and can form peroxynitrite, leading finally to apoptosis in a variety of cell types.
Tannins and flavonoids (phenolic compounds) are commonly found in several medicinal plants. Certain therapeutic properties mainly anti-inflammatory, wound healing, antioxidant and anti ulcerogenic are mostly attributed to these plant constituents.
Tannins are potent scavengers of per oxi radicals and can interact with mucus proteins, improving their cytoprotective effect by forming a protein lining over the gastrointestinal mucosa, additionally involved in wounds treatment. Fresh fruits and vegetables have been reported to exert multiple biological effects on the mucosa of gastrointestinal tract due to their antioxidants content. Certain flavonoids or compounds with flavonoid-like properties have antiulcer activity, prevent gastric mucosal lesions brought about by a number of ulcerogens. This had been illustrated before on polyphenol from grape seed, aqueous fruit extract of morinda citrifolia, Quarcetin, apple extract, curcumin, black seed oil, quassin, artichoke and others. It is conceivable that some of these plant constituents exerted their effects through the inhibition of cytokine-mediated inflammatory mechanism, suppression of iNOS, antioxidant activities and healing of the produced ulcer.
We acknowledge the work of Dr. Hebatallah H. Atteia, and Dr. Mona M. Taha for their technical help and Assistance.
One of the most common symptoms of autism spectrum disorder (ASD) affecting children is problems related with nutrition and eating habits (46–89%) compared to healthy children (25%) [1]. Children with ASD usually prefer consuming products of one type and one color, with a specific texture and smell, or having the same or similar packaging. They also refuse to try new foods and have specific nutritional behaviors, for example, they eat in a ritualistic way [2, 3]. Children with ASD have also problems with their digestive system, such as constipation, diarrhea, bloating, esophagitis, and reflux [4]. Due to the fact that gastrointestinal disorders may affect the incidence and severity of other symptoms in children with ASD, adequate nutrition should play an important role in treatment of mental symptoms. This can improve their life comfort and overall health.
In order to explain the etiology of autism, many hypotheses have been created that combine the occurrence of this disorder with genetic determinants, environmental influences, autoimmunity, viral infections, and drugs. One theory links the ASD symptoms with the gastrointestinal disorders and the composition of the intestinal flora [5]. It is based on the concept of the gut-brain axis, that is, the interaction between the gastrointestinal tract and the nervous system. This axis is a two-way communication between the central nervous system (CNS) and the gastrointestinal tract controlled with autonomic nervous system (with sympathetic and parasympathetic nerves). Mechanisms of this association include the action of neurological, immunological, and hormonal mediators [5, 6]. The increased permeability of the intestinal membrane, which commonly occurs in autistic children, can lead to excessive penetration of the blood exogenous peptides incompletely hydrolysed due to impaired digestion of casein and glutamine in the intestinal lumen. These peptides are transported to the brain, where they pass through the blood-brain barrier and as neuro- and immunoactive substances interfere with the neurological mechanisms of brain development [3, 7]. The biological activity of these compounds comes from their structural similarity to the endogenous opioid peptides [8]. The intestinal microflora can also affect the functioning of the CNS through the ability to synthesize identical or similar neuroactive molecules such as, inter alia, acetylcholine, catecholamine, histamine, or melatonin. On the other hand, the composition of intestinal bacterial flora may also depend on the level of stress or intensity of emotions; thus the digestive and nervous systems interact with each other [7].
Parents of children with ASD most frequently observe the selectivity of food and a very narrow range of consumer products [3, 9]. Eating disorders in children with ASD can be divided into the three following categories: (1) refusing to eat, (2) limited range of food consumed, and (3) frequent consumption of one product [10]. It was shown that children with ASD choose food based on its texture (69%), occurrence (55%), taste (45%), smell (36%), and temperature (22%). There was also a reluctance to try new food products in 69% of respondents [11].
Children with ASD aged 2–12 years are characterized by poorer skills of independent eating, more frequent occurrence of avoidance, and neophobia of food in comparison to the healthy peers [3]. These children also prefer energy-rich products such as hotdogs, peanut butter, cakes, fries, and pasta, while they eat a few vegetables and fresh fruit [12, 13]. It was also found that obesity in children with ASD can occur more likely than in healthy children [3]. The prevalence of eating disorders such as selectivity and refusal to eat reaches almost 90% in children with ASD [1, 2, 14]. A UK study found that 59% of children who had ASDs were eating less than 20 different foods [9].
The most common gastrointestinal complaints are constipation, diarrhea, abdominal pain, and reflux. It has been also found that they may suffer gastric acid hypochlorhydria, intestinal motility disorders, decreased activity of disaccharidases, and primarily lactase in intestinal juice [4, 8]. It has been also observed that 70% of children with ASD suffer from gastrointestinal disorders, where in healthy children this frequency was only 28% [5, 15]. In accordance with the other studies, gastrointestinal complaints are five times more frequent in children with ASD; abdominal pain occurs twice as often; and constipation and diarrhea are four times more often than in healthy controls [16]. However, the higher incidence of gastrointestinal complaints in children with ASD is not clearly stated, as not all studies show such dependence [3, 15]. It is often also suggested that gastrointestinal symptoms may be related to the medication being taken and the side effects they may cause [3].
Studies in which intestinal biopsy was performed among children with ASD suffering from food disorders showed a deficiency of disaccharidases and hexose transporters. This may indicate that the digestive system carries incorrect digestion of carbohydrates and their transport through enterocytes. Decreased digestion and absorption of these compounds may result in the accumulation of sugars in the intestinal lumen, and this can lead to the occurrence of osmotic diarrhea and bloating [5].
People suffering from ASD frequently have increased intestinal mucosal permeability, which may be due to their chronic inflammation. One of the studies carried out among children with ASD showed a significant increase in CD3 + and CD8 + lymphocytes in the intestinal epithelium and increased expression of proinflammatory cytokines in their mucosa. Elevated levels of cytokines were associated with the occurrence of behavioral and communication disorders [5].
Children with ASD can be characterized with a different composition of the bacterial flora of the stomach and intestines. Studies have shown in children with ASD a reduced amount of Bifidobacteria and more frequent occurrence of Bacteroides vulgatus and Desulfovibrio than in healthy ones [5, 7]. Higher amounts of Clostridia were found in their stool, which may be associated with a more frequent occurrence of problems from the digestive system [5].
Due to the selectivity of food and a little varied diet, the intake of vitamins and minerals in children with ASD may be insufficient and lead to malnutrition. This applies in particular to vitamins A, D, K, and B12 as well as calcium and zinc [3, 9, 10, 17]. Research in which nutritional diaries were used, covering 3 days in the group of children aged 8–11 years, showed that insufficient intake of vitamin D, calcium, and vitamin A occurred more frequently in children with ASD than in the group of healthy ones. There was also an increase in protein intake in children with ASD, higher than the recommended norm by 111%. Children with ASD were also characterized by a higher intake of vitamin B6 and vitamin E [3].
It was found that in people with ASD, the intake of vitamin E and B6 is higher than in healthy people, while the intake of iron, calcium, and vitamin D is significantly lower. It was also found that children characterized by food selectivity are more exposed to calcium, zinc, and vitamin D deficiency. Examining the amount of nutrients consumed in children with ASD with a narrow range of eaten products, they confirmed an increased risk of deficiency not only of vitamin D, calcium, and zinc but also vitamin B12 compared to healthy ones [17, 18]. Based on a study in which a 3-day nutritional interview was used, it was shown that in the group of children with ASD aged 4–8 years, the intake of calories and protein is too low and the intake of carbohydrates higher than recommended. Insufficient intake of vitamin D was diagnosed in 87% of children under the age of 4, in 89% of children between 4 and 8 years of age, and in 79% of children between 9 and 11 years of age [19]. Studies indicate a higher incidence of folic acid; vitamins B6, A, C; zinc; and calcium deficiency in children with ASD than in healthy ones [20]. Other studies show that the intake of protein in the children with ASD exceeded the norm by more than 171%, and the supply of animal protein was exceeded by 200%. The excessive consumption of sodium, phosphorus, magnesium, and vitamins A, C, and B and insufficient supply in the diet of vitamin D, calcium, iron, potassium, fiber, and cholesterol were also indicated [8]. However, the majority of people with ASD are characterized by excessive intake of vitamin C and low carotenoid intake [19, 21]. In another group of children with ASD examined for nutritional deficiencies, insufficient calcium intake and excessive supply of vitamin B6 and E were found. Too little intake of iron, calcium, vitamin D, and fiber was found in both children with ASD and in the group of children developing properly [9].
The diet of a pregnant woman affects the growth and development of the fetus, including the maturation of his brain. It can therefore be assumed that there is a probability of dependence between maternal nutrition and an increased risk of ASD in a child. It has been shown that the risk of ASD is about 40% lower among those children whose mothers took folic acid before conception 6 weeks and 6 weeks after conception. Women who had healthy children consumed 123.9 ± 46.4 μg more folic acid than mothers of children with ASD. Schmidt et al. found lower intake of folic acid in the first month of pregnancy in women who had children with ASD than mothers of healthy children. The relationship between the increase in folate intake and the decrease in the risk of ASD was demonstrated [22]. There was also a higher intake of polyunsaturated fatty acids (PUFA), before and during pregnancy, among women whose children developed normally than mothers of children with ASD. According to the study, women whose intake of omega-3 acids in the study group was the lowest had a 53% higher risk of giving birth to a child who had ASD than women with a middle range of consumption of these acids [23]. In other studies, there was no evidence of a decrease in the risk of ASD with an increase in the intake of omega-3 acids above the norm, but it has been proven that the risk increases with a very low intake of these acids [24]. It may also be important for pregnant mothers to eat fish, which is a rich source of unsaturated fatty acids and vitamin D. However, no study has linked the amount of fish consumed by pregnant women to the occurrence of ASD in their children. It was suggested that a small intake of vitamin D, by a pregnant woman, may be a risk of ASD in a child, but this relationship was not confirmed by any study [22].
Obesity of the mother and eating a diet full of fat during pregnancy can also increase the risk of ASD in the child. The increase in the prevalence of ASD was associated with a higher rate of obesity [25]. The offspring of obese women are more exposed to the appearance of behavioral disorders such as depression, anxiety, ADHD, and ASD. It is related to the influence on the fetal development of factors related to maternal obesity, among others, hyperlipidemia, hyperglycemia, and insulin resistance [25]. Compared to children of women with normal body mass, in obese children (II and III classes) ASD was diagnosed more frequently [26]. A relationship between the occurrence of ASD and excessive weight gain in women during pregnancy has been demonstrated. There was also an increased risk of developing ASD in children whose mothers were obese prior to pregnancy [26]. One of the theories explaining the association of obesity in children with ASD is the occurrence of higher levels of leptin. This causes placental dysfunctions, which may disrupt the normal, neurological development of the child [25]. People with autism have more leptin in plasma than healthy subjects [11]. Obesity is considered to be an inflammatory disease; it causes an increase in inflammatory cytokines in the body that reach many organs, including the brain. Therefore, excessive body weight and maternal diabetes can activate the inflammatory response in the placenta [25]. Diet high in fat in pregnant women stimulates inflammatory cytokines, including interleukin (IL-4, IL-5) and monocyte chemoattractant protein-1 (MCP-1). These cytokines have been associated with the occurrence of ASD. In addition, these compounds transmitted by obese or mothers with diabetes to the fetus can initiate physiological and behavioral responses observed in children with ASD whose mothers during pregnancy have developed infections [25].
A gluten-free diet relies on elimination from diet products containing wheat, oats, barley, and rye (as well as flour, bread, pasta, cakes, and other products made from these cereals). The casein-free diet (dairy free diet) relies on avoidance of the consumption of milk including breast milk, dairy products, yogurts, cheese, butter, cream, ice cream, and others [27]. Gluten-free and casein-free (GFCF) diets are one of the first nutritional interventions offered to patients with ASD. Many parents have reported improvements in maintaining eye contact and talking to children with ASD who have been on this diet [28]. In the study describing the study conducted on a group of 149 children diagnosed with ASD, it was found that after the introduction of the GFCF diet and its use for 3 months, a significant improvement in 81% of children was observed. However, the authors questioned the significance of the results of this study, because the conclusions on the health status of children and its improvement were drawn by their parents, aware of the conducted nutritional intervention [28]. A blind experiment was carried out among children with ASD regarding the use of the GFCF diet. In both control and research groups, there were 10 children with ASD. In one group, an intervention was introduced relying on elimination of gluten- and casein-containing products from the diet, while the other group continued their previous diet. Observations were made before the beginning of a nutritional intervention and after 1 year from the beginning of its implementation. The tests that were used were based on, inter alia, nonverbal techniques. There was a statistically significant improvement in the ability to learn in a group of children using a diet with the elimination of gluten and casein [14, 20]. In another paper, in one of their presented examples, the GFCF diet began to bear effects after only 2.5 months of its use. An improvement in social communication and in emotional reactivity was recorded [29]. Antibodies of IgG, IgM, and IgA against gliadin, casein, basic myelin protein, maize, eggs, and soy in 50 children with ASD were measured. Analysis of blood samples showed that a large number of children produced antibodies against casein and gliadin. In addition, it was found that these proteins bind to lymphocytes and CD26 enzymes, which can cause inflammation and activate the immune system response [30]. Behavioral changes in ASD patients may result from abnormal activation of the opioid system due to excess receptor antagonists in the brain. It was found that gluten and casein are the source of compounds characterized with the activity of opioid peptides [31]. Fifteen children with ASD who did not show any food intolerance took part in another study. They were divided into two groups and blinded. For 12 weeks, one group was given a diet with the elimination of gluten and casein and the other a diet enriched with these substances. After this time, each group went on an alternative diet for the next 12 weeks. The carers or parents of the examined children were not aware of the kind of food their child was receiving. There was no difference in the behavior and development of the child in any group [15]. The influence of a diet containing gluten and casein on the behavior and complaints from the digestive system in children with ASD, which until then used diet with the elimination of these substances, was investigated. The study was randomized, double blind, and controlled; the experimental group consisted of 38 people and the control group of 36 people. According to the authors’ hypothesis, the introduction of autistic gluten and casein into children’s nutrition was to cause deterioration of their behavior and gastrointestinal complaints. Nutrition interventions were carried out for a week. There were no differences in the health status between the test and control groups. It was suggested that the result of the study could be affected with the short intervention time [32]. Many studies on the GFCF diet focus on the safety of the intervention [31]. In various studies, no differences were observed in the nutrition of children with ASD using the GFCF diet compared to children on the standard diet. However, a significant reduction in the concentration of amino acids was observed, including tryptophan in children using GFCF diets. In addition, patients using a gluten-free diet were found to consume larger amounts of proteins and fats but smaller amounts of carbohydrates, fiber, calcium, and iron [31]. Therefore, it warns against the risk of insufficient supply of micro- and macroelements while using the GFCF diet [29, 32]. The casein-free diet can cause calcium deficiencies. In addition, slower bone development in children using such nutritional intervention was also reported in comparison with children without any dietary restrictions. It was shown that patients with ASD on a non-denaturing diet had lower bone density than the control group. Lower vitamin D intake is also seen in such patients [11, 29, 32].
Another nutritional intervention in children with ASD is a ketogenic diet, which is characterized by an increased fat content, adequate to the amount of protein needed and insufficient for metabolism the amount of carbohydrates, which leads to the body’s use of lipids as the main source of energy. In the original ketogenic diet, the ratio of calories from fat to calories from carbohydrates and proteins was 4:1 (the proportions were 80% of lipids, 15% of proteins, and 5% of carbohydrates). With a standard diet, fatty acids are catabolized to acetyl-coenzyme A (CoA) in the oxidation beta reaction and then oxidized to CO2 and H2O in the Krebs cycle. However, when the amount of fatty acids is too high and exceeds the ability of the Krebs cycle to metabolize CoA (e.g., low carbohydrate or protein diets), in the acetyl-coenzyme A, the liver is converted to ketone bodies (acetoacetate and D-beta-hydroxybutyrate). Ketone bodies produce a similar amount of energy as proteins and carbohydrates; they can also cross the blood-brain barrier, so they can be used by brain cells as a source of energy [33]. Ketogenic diet is an alternative or supportive therapy for patients with drug-resistant epilepsy. It was found that in patients using these diets, it was easier to control epileptic seizures as well as their frequency. The ketogenic diet is also used in other diseases such as Alzheimer’s disease, Parkinson’s disease, migraine, and depression [33, 34]. The ketogenic diet is also used as an option to suppress symptoms accompanying ASD [35]. The study evaluated the effectiveness of the ketogenic diet in a group of 30 children with ASD. Children were evaluated before and after dietary intervention using the Childhood Autism Rating Scale (CARS) scale. It was found that a significant improvement occurred in two patients, the average in eight patients, and a slight improvement in eight patients. Nutritional intervention, in addition to the introduction of a ketogenic diet, also consists of supplementation of vitamins and minerals dosed depending on the age of the subjects. According to the authors, the research on the effectiveness of autistic treatment by ketogenic diet should be extended and continued. The studies showed that in patients who were characterized with a higher CARS score, the improvement in the results of ketogenic diet treatment was lower than in patients with moderate or light ASD [35]. Because the characteristic composition of the ketogenic diet is quite distasteful, often patients decide to interrupt this diet intervention and return to the previous method of nutrition. This diet may additionally lead to nutritional deficiencies [35]. It also has numerous side effects including weight loss, growth inhibition, fatigue, drowsiness, changes in appetite, constipation, diarrhea, nausea, and vomiting [33]. In one of the studies in which the impact of the ketogenic diet on the symptoms of ASD was analyzed, constipation or diarrhea appeared in 12% of children with ASD [35]. Due to the limited number of research results on humans and on animal models stating the reduction in the frequency of behavioral disorders, after using the ketogenic diet, it cannot be unambiguously determined its effectiveness in children with ASD.
Vitamins and minerals play an important role for human health, because they have numerous functions in the body, including enzyme cofactors for many reactions. In particular, attention is paid to the insufficient supply of vitamins and minerals in the diet, as one of the causes leading to many health problems in children, for example, anemia, hypothyroidism, or rickets. Recently, researchers have focused on the relationship between metabolic disorders and developmental disorders, including lack of concentration, learning disabilities, and intellectual development [21]. Children with ASD due to diets, often restrictive, may be exposed to nutrient deficiencies. Dietary supplements are one of the most frequently recommended nutritional interventions for children with ASD, recommended by 49% of physicians [21]. Other studies suggest that 66% of people with ASD are taking supplements—most frequently probiotics, omega-3, vitamin B6, and melatonin [36].
Probiotics are defined as living, nonpathological microorganisms, which have a beneficial effect on the human body, when of course administered in the right dose. They consist mainly of lactic acid producing bacteria, Lactococci and Bifidobacterium or yeast, that is, Saccharomyces boulardii [36]. Probiotics have a beneficial effect especially in gastrointestinal problems such as infectious diarrhea, inflammatory bowel disease, or hypersensitivity syndrome of the large intestine. Their activity in shaping the host’s immune system has also been proved [36]. They can also be effective in the treatment of inflammatory diseases of the gastrointestinal tract and affect the function and permeability of the intestinal epithelium. An important role is also played in restoration of the intestinal microbial balance [37]. It was found that probiotics can be effective in the treatment of children with ASD due to their health-promoting effects on the gastrointestinal tract and the entire body [36]. It has been pointed out that the use of probiotics may help in restoring the proper intestinal microflora and thus eliminate diarrhea and constipation, which are a common problem in people with autism [38]. It was also pointed out that this supplement may play a role in maintaining the continuity of the gut mucosa, activating the immune system and preventing inflammation [39]. A relationship was found between the severity of ASD and gastrointestinal disorders. It can therefore be considered that probiotics contributing to the improvement of this system may also positively affect the behavior of children with ASD. Almost 20% of physicians are encouraged to take probiotics in children with ASD, and 60% of physicians recommend continuing to use probiotics, if parents have decided to apply such supplementation [36]. It is also important to mention that although the US Food and Drug Administration (FDA) considered probiotics to be safe for health, so far no research has been conducted that would address the long-term effects of their supplementation.
In the studies carried out so far, 50% of children and adults with ASD have shown positive effects of vitamin B6 supplementation [40]. According to studies, children with ASD who do not take any supplements are characterized with a higher level of vitamin B6 in plasma than the control group subjects. There are more studies that confirm this phenomenon [40]. One of the explanations is the lower activity of vitamin B6 in people with ASD. It was also found that pyridoxal kinase—an enzyme responsible for the conversion of pyridoxal to the active form of vitamin B6 (PLP, pyridoxal phosphate), in this group of people—is also characterized with a slowed effect [39, 41]. This activity can be lowered by up to 40% compared to people developing properly. PLP is an essential component for the synthesis of mitochondrial components, among others, heme and coenzyme Q10. It has also been shown that this compound protects neurons from excessive oxidative stress by increasing the production of ATP and the use of excess glutamate [42]. People with ASD may notice an improvement in health during supplementation with a high dosage of vitamin B6, which will lead to increased energy production, decreased excitotoxicity, and reduction of oxidative stress. Some of the parents, when using such dietary intervention, observe in children with ASD improvement in the areas of attention, communication, learning, or maintaining eye contact [39, 40]. Often when supplementing vitamin B6, it is also recommended to take magnesium for the purpose of preventing its deficiency and reduction of the level of hyperactivity. In addition, this element blocks excessive irritation of excitotoxic receptors in the brain by means of calcium channel modeling [42]. Supplementation of these two nutrients led to improved behavior in children with ASD [36, 39]. In one of the studies in which the double-blind method was used, it was found that in children supplementing magnesium and vitamin B6, behavioral improvement was noted, while in groups in which only magnesium or vitamin B6 was administered, this improvement was not observed [43]. One of the 9-year-old boys with ASD, who was prescribed supplements with B6, magnesium, and additionally vitamin B12, decreased sleep problems and improved behavior [43]. At present, it is not known what the possible side effects of taking vitamin B6 may be. Older studies show that long-term supplementation of this nutrient may increase the risk of developing peripheral neuropathy [44].
Omega 3 acids belong to the group of polyunsaturated fatty acids (PUFA). They include alpha-linolenic acid (ALA), docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA). A lot of research confirms that EPA and DHA are important for both the structure and functioning of the brain. Supplementation of these acids is recommended for the treatment of disorders of the nervous system, such as schizophrenia or ADHD [43, 44]. The anti-inflammatory effect of PUFA has also been proven, which may also include a reduction in the number of proinflammatory factors in the body such as Il-6, Il-10, and TNF alpha. The rich sources of EPA and DHA are fish products and seafood while ALA plant products [45]. There are many studies on the role of deficiency of omega 3 in children with ASD. Lower levels of omega 3 were observed in children with ASD compared to the healthy ones. According to the research, the difference in the level of these acids in the research and control group reaches about 10% and nearly 29% of children with ASD supplementing omega 3 [44, 45]. For 6 weeks, 1.5 grams of fish oil was given to 13 children with ASD aged 5–17 years. An improvement in the occurrence of hyperactivity in these children was sought [43, 44]. Similar results were obtained in studies where the supplementation was used for 12 weeks in patients with ASD aged 3–8 years [45]. Thirty children with ASD for 3 months were supplemented with omega 3, omega 6, and vitamin E. An improvement was noted in 20 children, which was confirmed by the Childhood Autism Rating Scale [46]. Omega 3 fatty acid supplements are generally considered safe but their consumption in larger quantities may increase the risk of bleeding and mercury poisoning, which may be contaminated with fish products, which are a good source of fatty acids.
Vitamin D is a fat-soluble vitamin; it occurs in three forms: D1 (calciferol), D2 (ergocalciferol), and D3 (cholecalciferol). The main source of Vitamin D is skin synthesis and food products (marine fish, fish oils, and to a lesser extent meat and dairy products, in which it occurs as a cholecalciferol). For a long time, vitamin D was only known for its positive effect on the skeletal system and mineral metabolism. For several years, numerous studies have been conducted and provided information on other functions of vitamin D, previously unknown to anti-inflammatory effect, protection of mitochondria against oxidation, elevation of glutathione levels, and influence on at least five proteins that regulate DNA repair, increase in seizure threshold, or increase regulatory T lymphocytes. One of the most frequently studied areas in relation to the effects of this vitamin is brain development and mental disorders. It has also been proven that vitamin D can have a positive effect on the treatment of certain autoimmune diseases, for example, multiple sclerosis, because the receptors of this vitamin have been found in lymphocytes and dendritic cells. The research into the possible impact of vitamin D deficiency on the incidence and course of autism has also been intensively developed. Low levels of cholecalciferol in the body and ASD have many similarities with regard to their etiopathogenesis. ASD findings indicate that this disease is more common in urban areas, in a climate with less sunlight, and in areas with higher environmental pollution, which also coincides with the etiology of vitamin D deficiency [47]. A hypothesis was proposed in which the deficiency of vitamin D, both in mothers during pregnancy and in children, is considered as an environmental risk factor for ASD. As a justification, the role of this vitamin in the maintenance of homeostasis of the brain, embryogenesis, and development of the nervous system or modulation of the immune system is given. It was also noticed that the children of women who used antiepileptic drugs with negative effects on the metabolism of vitamin D in the body were more likely to have a deficiency of cholecalciferol and ASD [48]. Vitamin D may also play a role in reducing DNA damage, acting as an intermediary in its repair, and genetic mutations resulting from DNA damage are also involved in the pathogenesis of ASD. T-cell dysfunction in patients with ASD, which is also influenced by vitamin D, is also revealed. Another theory of ASD etiogenesis is insufficient supply of adequate amount of vitamin D during the first 12–24 months of life [49]. It has been shown that children with ASD have a lower level of calcidiol and calcitriol in the body than the control group, consisting of healthy children [50]. The level of vitamin D was compared in the group of 50 children with ASD with a control group including 30 healthy children. Children with ASD had a lower level of vitamin D than the control group, and as many as 48% of them had deficits in vitamin D, although it was found that the amount of time spent in the sun was similar in both groups [49]. One of the studies attempted to reduce the symptoms of ASD in children by supplementing vitamin D. Sixty-seven subjects were given 5000 IU of vitamin D per day. Improvements in behavior such as reduced irritability, drowsiness, social withdrawal, and hyperactivity were observed [51]. One of clinical cases included a 32-month-old child diagnosed with ASD, characterized with severe symptoms including impaired communication; reluctance to social interactions; lack of reaction to other people, to commands from their parents, when their name are called, and to physical contact; avoidance of the eye; and delayed language and communication development. The child also had tantrums. The tomographic examination did not show any changes in the brain, and serum and urine tests did not reveal any metabolic deviations. Diagnostics in the direction of autism was carried out using scales, for example, Autism Behavior Checklist and Childhood Autism Rating Scale. The patient also had low levels of vitamin D at 12.5 ng/ml. It was decided to subject the child to supplementation with vitamin D, intramuscularly at 150,000 IU once a month and orally 400 IU per day. After 2 months, parents noticed a significant improvement in the child’s behavior. The child began to respond to his name, let his parents cuddle, and play with toys. Laboratory tests showed an increase in the concentration of vitamin D to 81.2 ng/ml. The results and assessment made with the aforementioned scales have also improved. This example may suggest that vitamin D plays a large role in improving the basic symptoms of ASD; however, the observations made in this clinical case cannot be transferred to all patients with ASD. It is worth emphasizing, however, that research in this direction should be broadened and continued [52].
One of the most common problems in ASD is eating disorders and gastrointestinal complaints. Nutritional problems occur 2–3 times more frequently in children with ASD than in healthy children [1]. The most common symptoms from the digestive system are constipation, diarrhea, bloating, and reflux. Almost 70% of autistic children suffer from it [2, 53]. Given these reports, the hypothesis combining the symptoms of autism with the functioning of the digestive system and its bacterial microflora based on the concept of the gut-brain axis becomes very interesting and credible [54, 55, 56, 57]. Different types of environmental and situational stressors may contribute to the occurrence of gastrointestinal disorders such as irritable bowel syndrome, enteritis, as well as increase intestinal permeability and change their bacterial flora [58, 59, 60, 61, 62, 63, 64, 65, 66]. Differences were found in intestinal microbiome in children with ASD compared to healthy ones based on the analysis of metabolic products and composition of fecal flora [59, 67]. Gut microbiota-mediated metabolites, such as short-chain fatty acids (SCFAs) and free amino acid (FAA) concentrations, are significantly higher in children with ASD than healthy ones [68, 69]. The SCFAs are mainly produced by Clostridia, Bacteroidetes, and Desulfovibrio, and they can cause symptoms similar to ASD [70]. Fecal samples from children with ASD compared to healthy ones have higher levels of the Clostridium histolyticum that can produce neurotoxins [71]. Children with ASD have less differentiation and lower levels of Bifidobacterium, Coprococcus, Firmicutes, Prevotella, and Veillonellaceae and higher levels of Bacteroidetes, Caloramator Clostridium, Desulfovibrio, Lactobacillus, and Sarcina [59, 72].
One of the most interesting and surprising results in our own research is that children with ASD were characterized by greater intake of offal and red meat than healthy children. As many as 32% of children with ASD eat red meat several times a week. On the other hand, offal is consumed 1–3 times a month by 25% of examined children with ASD [73]. Offal and red meat are a rich source of iron. Perhaps this mineral ingredient can cause frequent consumption of the abovementioned products by children with ASD. Iron plays an important role in the development of cognitive, motor, and behavioral functions. It is also an important mineral component which, as a component of some enzymes, is involved in synthesizing neurotransmitters. Iron deficiency in children with ASD is very common. It has been shown that 24.1% of examined children with ASD have reduced iron levels and 15.5% suffer from anemia due to deficiency. The reason for such frequent iron deficiencies and hence the low level of ferritin present in autism is unknown until now. One of the hypotheses concerns the symptoms of the digestive system and the possible absorption disorders, which makes the iron from food less absorbed. It was found that this hypothesis is erroneous because in their studies, supplementation of this element in children with ASD caused an increase in the level of ferritin and iron, which excludes the problem of absorption deficits [74].
Due to the large interest in this topic, many papers have been made to assess the nutrient intake of children with ASD. The results of these studies often differ from each other, which probably results from the preferences of nutrition of children with ASD. On the basis of numerous studies, it can be concluded that in people with ASD, an inadequate intake of nutrients is more common. These deficiencies may not only lead to an increase in ASD symptoms but may also initiate the development of diet-related diseases. Many pediatricians recommend their patients with ASD to check the level of calcium, iron, and vitamins in the blood and prescribe multivitamin preparations or probiotics [21, 36, 41, 55, 64].
Several studies have reported that the most common diet products chosen by children with ASD are fast food products, that is, French fries, hotdogs, hamburgers, as well as candies, sweets, and products containing preservatives [12, 13]. In the conducted research, 27% of parents answered that the child does not prefer to consume any type of products, and 25% that the child most eats sweets. It is interesting that fast food products, sweets, and other products characterized by the content of artificial food additives are eaten much more often in the group of healthy children than people suffering from autism. Artificial food additives such as preservatives, dyes, flavor enhancers, and sweets can cause hyperactivity in some children as well as impede concentration or learning opportunities. These symptoms are characteristic of such disorders as autism or ADHD. Studies have been carried out in which a change in diet in people with ASD led to an improvement in the functioning of the gastrointestinal tract and to the improvement of the psychological and neurological symptoms of this disorder [55, 58, 63]. This indicates an important role of bacterial microflora, which is based on the concept of the gut-brain axis of etiopathogenesis and ASD therapy in children. The relationship between the digestive and nervous systems is closely related; therefore diet therapy should be an important element in the treatment of autism.
I confirm there are no conflicts of interest. The funding organization played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.
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