Validated nutrition assessment tools: comparison guide [45].
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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:{caption:"IntechOpen Maintains",originalUrl:"/media/original/113"}},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
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Increasing cancer incidence and improved survival rates have seen the number of cancer survivor’s increase exponentially throughout the last few decades. As a consequence of this, cancer survivors may experience a number of permanent side effects from their cancer or the treatment [1]. Traditionally, patient follow-up has been undertaken by oncological specialists with a major focus on possible cancer reoccurrence; however, this fails to identify or adequately address many patients’ concerns regarding post-cancer treatment. For a majority of patients, nutrition during treatment and post-cancer diagnosis and treatment is an area they can control and change for their own health and well-being.
\nHowever, Zhang (2015) [2] published a study indicating that cancer survivors are usually motivated to improve their health but were found to have suboptimal diets. She examined the dietary intake of 1533 cancer survivors and 3075 individuals who had never had cancer. The researcher estimated the quality of the diets using the Health Eating Index, which is based on the United States government’s 2010 Dietary Guidelines for Americans. The scores ranged from 0 to 100, with 0 indicating no adherence to 100 which is total adherence. After adjusting for age, sex and ethnicity, Zhang found that the group who had not had cancer had an average index of 48.3 and the cancer survivors on average indexed 47.2. It was found that cancer survivors in general from this population ate less fibre, more empty calories and more refined sugars and fats. In addition, they examined patients who had different types of cancer and found that those who had breast cancer had the healthier diets and those who had lung cancer had the worst diets. It was also identified that cancer treatment may cause people to have specific food cravings, or change the way food tastes. This may influence the food choices they make post treatment.
\nNutritional deficiencies in people with cancer who are undergoing traditional oncology treatment are a critical component for the health and survival of patients with or after cancer diagnosis. To date, a majority of research and nutritional screening has focused on malnutrition and weight loss in relation to nutritional deficiencies. This nutritional assessment is essential for the diagnosis of nutritional compromise as nutritional deterioration has been found to be associated with adverse outcomes in terms of cancer prognosis such as response rate and survival [3]. The nutritional screening and identification for malnutrition has been well documented. However, this screening omits the general patient undergoing treatment for cancer who is not elderly, malnourished or losing weight. Patients who have lung, oesophagus, stomach, colon, rectum, liver and pancreas cancer have been found to be at greatest risk of weight loss and malnutrition [3].
\nHowever, breast and prostate cancer, which are two of the most common cancers, have been found to be associated with weight gain, not weight loss [4]. To date, nutritional screening of patients undergoing adjuvant or neo-adjuvant chemotherapy has not been conducted to ascertain nutritional status. Research into possible nutritional insufficiencies may provide an insight to assist clinicians in aiding patients to thrive with or after cancer. Moreover, individual research has identified a number of nutritional deficiencies that can occur from certain chemotherapeutic agents, radiation and surgery. Combining the research that has been conducted for people with cancer or post cancer may provide the information necessary for clinicians and patients post diagnosis and treatment to live a healthy, balanced life based on nutrient sufficiency, not deficiency.
\nNutritional therapy for cancer requires a greater understanding of nutritional biochemistry, interactions as well as patients’ expectations and disease impact. Nutritional analysis and early nutritional interventions (diet counselling, oral supplementation, enteral or total parenteral nutrition) may reduce, prevent or even reverse poor nutritional status, improve performance status and consequently affect their quality of life (QoL) [5]. The nutritional intervention may also depend on the type of cancer treatment, either curative or palliative. A nutritional intervention for a curative cancer treatment can have an additional role which is to increase the tolerance and response to the oncology treatment, decrease complications, reduce morbidity by optimizing the balance between energy expenditure and food intake, and decrease the possible risk of metastasis, whereas nutritional interventions for palliative care is aimed at improving the patients’ QoL, controlling symptoms including vomiting, nausea, constipation and pain related to food intake [5].
\nUnderstanding the biochemistry associated with a patient who has a solid tumour versus a patient who is tumour-free post surgery/treatment is important for nutritional assessment. Cancer can have a major impact on a patient’s physicality and psychological well-being. For example, proteolysis and lipolysis are accelerated while muscle protein synthesis is depressed in a person with a solid tumour. In addition, carbohydrate metabolism is modified by tumour growth such as an increased hepatic glucose production and Cori cycle activity and a reduction in insulin sensitivity in peripheral tissues. This results in a loss of lean body mass and fat tissue, causing an increase in energy expenditure and resulting in wasting [6, 7]. This type of cancer-related weight loss is different from simple starvation whereby normal refeeding can restore normal nutritional status. These tumour-associated metabolic abnormalities can frequently prevent the restoration of muscle mass and lead to cachexia due to complex interactions between pro-inflammatory cytokines and the host metabolism [8–10].
\nIn addition to the effects of having a tumour, oncological treatments such as surgery, chemotherapy and radiotherapy can cause side effects and physiological changes that can affect food intake and nutritional status [11–14]. Moreover, the stress response from the treatment can have an effect on nutritional status and body composition. The changes in glucose metabolism, loss of muscle mass and increased fat distribution during chemotherapy also affect energy expenditure [15, 16]. In addition, the fatigue and nutritional status will vary depending on the patient who is assigned curative or palliative treatment.
\nA study conducted in 2015 on breast cancer patients analysed weight gain during adjuvant chemotherapy and survival. It was found that weight gain (between 1 and 12 kg) had a negative impact on both disease-free and overall survival rates [17]. Currently, the cause of weight gain during chemotherapy has not been revealed.
\nIndividual nutrient deficiencies or insufficiencies can also occur during treatment. An example of this is vitamin D3. A systematic review published in 2013 found that 31% of cancer patients undergoing treatment were vitamin D3 deficient and 61% had insufficient levels [18]. The following chapter will investigate evidence-based research on nutrient deficiencies and insufficiencies during different phases of cancer treatment, stages and side effects of treatment.
\nThe majority of research on tumour-induced effects on nutritional status is focused on cachexia or weight loss. Research has found that the progressive nutritional deterioration displayed in cachexia is different from starvation and is the result of the tumour burden on the body. The increased proteolysis and lipolysis is due to possible biochemical reactions in the body such as pro-inflammatory cytokine activation or specific molecules released by the tumour itself [19]. The proteolysis that is found in cachexia has also been found in cancer growth and can occur in individuals with a solid tumour who are not cachexic. The neoplasm or cancer growth can compromise the normal biochemical mechanisms that regulate muscle homeostasis, which results in the loss of muscle mass, functional impairment and compromised metabolism. The end result of this tumour-induced condition is enhanced muscle protein breakdown and amino acid release that sustains liver gluconeogenesis and tissue protein synthesis [20].
\nResearch on individual nutrient deficiencies or insufficiencies has not been completed to date. It is uncertain at this stage if solid tumours cause nutrient deficiencies or nutrient insufficiencies. Further research is required to ascertain individual nutrient status of patients with cancer.
\nPatients undergoing cancer treatment have been found to frequently experience malnutrition. The nutritional status of cancer patients varies depending on the treatment, the type of cancer and the ability to eat. A study on Indian patients published in 2015 investigated 57 cancer patients and evaluated them during treatment using a Patient-Generated Subjective Global Assessment (PG-SGA). The results found that 15.8% (9/57) were well nourished, 31.6% (18/57) were moderately or suspected of being malnourished and 52.6% (30/56) were found to be severely malnourished [21]. The researchers found that the highest malnutrition was in lip/oral cancer patients (33.3%) and that the prevalence of malnutrition was highest in patients during treatment (84.2%) [21].
\nTherefore, although not all nutrients have been researched to identify specific nutritional deficiencies or insufficiencies, it is highly likely that patients undergoing cancer treatment would have certain nutrient deficiencies or insufficiencies. These would vary just as patient responses to treatment vary as well.
\nSurgery for head and neck cancers includes tumours inside the sinuses, nose, mouth, salivary glands and down the throat including oesophageal cancer (Australian Cancer Research Foundation (ACRF)). The greatest impact on nutritional status from surgery for head and neck cancers is dysphasia (difficulty swallowing, approximately 14.7%) [22]. This impacts the patient’s ability to eat and therefore nutrient intake. Research on specific nutrient deficiencies due to dysphasia has not occurred to date. Further research in this area is required.
\nThe gastrointestinal cancers involve surgery for stomach (gastric), bowel (colorectal), liver, oesophageal in some cases, pancreatic, anal, bile duct, gastrointestinal carcinoid, gallbladder and small intestinal cancers (ACRF). Depending on the cancer, location, staging and possible metastasis will depend on the implications on nutritional status.
\nA study published in 2016 investigated lean body mass after gastrointestinal surgery [23]. The loss of lean body mass has been found to decrease the compliance of adjuvant chemotherapy particularly in patients undergoing gastrectomy for gastric cancer. The researchers examined 485 patients. They found that the median loss of lean body mass was 4.7%. In 225 patients (46.4%), a lean body mass of 5% or more occurred. A statistical significance was found using both uni- and multivariate logistic analysis for severe lean body mass loss due to surgical complications including infection or fasting (odds ratio (OR) = 3.576;
Hence, the identification of nutritional intervention requirements of patients undergoing surgery for gastrointestinal cancer is required. This is an important factor and could impact on patient adjuvant treatment compliance and possible survival post surgery.
\nAll surgical interventions for cancer will have some form of nutritional impact on patients. Individual assessment of patients prior to and post surgery is important for patient health, compliance and health/well-being through treatment and post treatment.
\nConsidering that a large percentage of cancer patients undergo surgery for a biopsy or to remove tumours, lymph nodes or de-bulking a neoplasm, the human body requires support for both minor and major surgeries. The body is an amazing machine when supported correctly. The main nutritional support required is based on decreasing inflammation, supporting the immune system and the body to fight infection.
\nTraditionally, it is suggested to avoid alcohol, tobacco, simple sugars, processed foods and recreational drugs prior to and post surgery [24, 25]. Smoking and hazardous drinking have been found to be the most common lifestyle risk factors that influence surgery complications [25]. In addition, avoiding nutrient supplementation that could increase the risk of bleeding such as fish oils, vitamin E, turmeric and herbs such as ginkgo should be stopped before 1 week.
\nAntibiotic use is common in surgery pre- or postoperatively [26, 27]. Prophylactic use of antibiotics has been to prevent the potential risk of infection postoperatively as pre- and perioperative antibiotics have been found to lower the infection rate [26]. To assist the recolonization of the microbiota, it is recommended to use pre- and probiotics [28].
\nPossible nutrient deficiencies pre- and postoperatively such as iron [29] need to be taken into consideration in addition to possible insufficiencies and nutrients to assist in healing such as vitamin C, zinc and amino acids such as proline and glycine [30, 31]. The prevalence of nutrient deficiencies postoperatively has been mainly focused on bariatric patients rather than on cancer patients [32]. However, nutrients found to be deficient in these patients may be correlated to some cancer patients as a high percentage of patients with cancer have been found to have a higher body mass index (BMI) [33]. Therefore, nutrients such as vitamin D, which has been found to be deficient in approximately 57% of patients, vitamin B12, iron and folate, are best to be monitored pre- and postoperatively [32].
\nHence, nutritional screening, management and support pre- and postoperatively assist the patient in chance for compliance through further interventional treatments in addition to survival.
\nThere are a large number of chemotherapy agents now on the market and are all divided into groups depending on their mechanism of action. Chemotherapy is often an effective treatment; however, each agent can cause particular side effects that can affect the person’s health and well-being. Many of the new drugs now available do not cause the same severity of side effects and the new development in conventional medicine has helped to manage and reduce the main side effects of nausea, vomiting and leucopenia [34, 35].
\nNutrient deficiencies that can occur from chemotherapy have limited research. A common side effect is chemotherapy-induced anaemia; however, this is not caused by low iron levels or deficiency. This side effect is due to the chemotherapy agent’s mechanism of action on the development of red blood cells. Supplemental iron has been effective for an iron deficiency but not for chemotherapy-induced anaemia. Too much iron may promote tumour growth or worsen chemotherapy side effects. Therefore, iron supplementation should only be recommended if there is a diagnosed iron deficiency confirmed by pathology tests.
\nVitamin B12 has been found to be deficient in certain individuals after chemotherapy [36]. A case study was presented in which a patient in a clinical trial for chemotherapy-induced peripheral neuropathy was found to be deficient in vitamin B12 post chemotherapy. This woman had normal vitamin B12 blood parameters pre-chemotherapy administration and again upon intramuscular vitamin B12 injection and supplemental vitamin B12 and 6 months after supplementation. Although this represents only one individual, it is possible that certain individuals may develop vitamin B12 deficiencies during chemotherapy, which may induce more severe presentation of other chemotherapy-induced side effects.
\nHereditary disorders that cause haemolytic anaemias have also been found to induce a vitamin B12 deficiency, which require lifelong vitamin B12 administration [37]. These conditions need to be identified prior to chemotherapy administration to ensure that the patient is not in a deficient state. Another consideration is the use of protein pump inhibitors (PPI) and histamine H2-receptor antagonists as an association has been found with their use and a vitamin B12 deficiency [38]. PPIs are used during chemotherapy to assist with reflux and could have an impact on vitamin B12 absorption. In addition, metformin is another drug that has been found to decrease vitamin B12 and in combination with either histamine H2-receptor antagonists or PPIs, neuropathy due to vitamin B12 depletion has been found [39].
\nAnother vitamin that has been found to be deficient during chemotherapy is vitamin D3. Teleni et al. in 2013 conducted a meta-analysis on vitamin D3 status in cancer patients [18]. They found that 31% of patients undergoing active treatment were deficient in vitamin D3 and 67% had insufficient levels. These findings and the awareness, impact and importance of vitamin D3 in the medical fraternity have now seen it being one nutrient that has been commonly prescribed to cancer patients undergoing treatment.
\n\nThe main mineral that has been found to be deficient in patients undergoing chemotherapy such as cetuximab is magnesium [40]. Hypomagnesaemia has also been found in patients on PPIs particularly in combination with diuretics [41], which are common medications used in conjunction with chemotherapy agents. It is important to monitor magnesium levels in patients and potential oral supplementation may be required.
\nResearch on nutrients to assist side effects from chemotherapy has continued; however, nutrients that are depleted during chemotherapy are still required. Potential nutrient deficiencies rather than macronutrient depletion may play an important role in patient mortality or morbidity. Further research is required to ascertain possible insufficiencies and deficiencies that could contribute to poor health and well-being of patients diagnosed with cancer and undergoing chemotherapy.
\nRadiation, similar to chemotherapy, is considered to be an effective treatment against actively dividing cells. According to the American Cancer Society, more than 50% of all cancer patients undergo radiotherapy (www.cancer.org). Nutritional impact from radiation depends on where the person is receiving radiation. Head and neck cancers, lung cancer and gastrointestinal cancers have been found to have the greatest nutritional impact on cancer patients. The nutritional status of patients undergoing radiation therapy has been assessed, with specific nutritional indicators measured. One particular study focused on chemoradiotherapy on nasopharyngeal cancer. They found that after radiotherapy, 20.2% of patients had more than 10% weight loss. Statistically significant (
Individual nutrient screening of patients undergoing radiation is extremely limited. The main nutritional research on radiation is based on the prevention of malnutrition and weight loss, particularly for head and neck cancers. The importance of early nutritional management and intervention has been stipulated and implementation in hospitals has been encouraged [43]. Further research into individual nutrient deficiencies and insufficiencies during radiotherapy may also contribute to the health and outcome of cancer patients.
\nEffective nutritional screening, implementation of nutritional care plans and support are essential components for cancer patients. The screening and early detection of malnutrition is considered crucial in identifying patients at nutritional risk. A high prevalence of malnutrition has been identified in hospitalized cancer patients undergoing treatment, for example, colorectal cancer [44].
\nCurrently, there are a number of nutritional assessment tools used in clinical practice for cancer patients. The accuracy of diagnostic tools is based on sensitivity, specificity and positive- and negative-predictive values calculated on the likelihood that a given test result would be expected when the target condition is present compared with the likelihood of the same result if the condition was absent [44].
\nTables 1 and 2 evaluate the nutritional tools available. The information has been obtained from the Queensland Government of Australia who conducted and published a malnutrition screening and assessment tool comparison in addition to a validated nutrition assessment tool comparison [45]. The screening tools evaluated used the parameters such as recent weight loss, poor intake/appetite and body weight measurements. It was found that all tools evaluated generally performed well. Choosing the correct nutritional screening tool will depend on various aspects such as complexity, sensitivity to that population group, who will be performing the screening, what actions will be undertaken and how the outcomes will be incorporated into the current facility procedures [45].
\nName author, year | \nSetting and patient population | \nNutrition assessment parameters | \nRationale/clarification | \n
---|---|---|---|
Subjective Global Assessment (SGA) 1987 [46] | \nSetting: Acute [47–49] Rehab [50] community [51] Residential aged care [52] Patient group: Surgery [47] Geriatric [50–53] Oncology [48] Renal [49] | \nMedical history (weight, intake, GI symptoms, functional capacity) and physical examination Categories: 1. SGA A (well nourished) 2. SGA B (mild-moderate malnutrition) 3. SGA C (severe malnutrition | \nRequires training Easy to administer Good intra- and inter-rater reliability Patent-Generated | \n
Subjective Global Assessment (PG-SGA) Ottery, F. 2005 [54] http://pt-global.org/ | \nSetting: Acute [55–57] Patient group: Oncology [55] Renal [56] Stroke [57] | \nMedical history (weight, intake, symptoms, functional capacity, metabolic demand) and physical examination Categories: SGA categories (A, B or C) as well as providing a numerical score for triaging. Global categories should be assessed as per SGA. | \nNumerical score assists in monitoring changes in nutritional status Easy to administer Scoring can be confusing requires training Patients can complete the first half of the tool by themselves | \n
Mini-Nutritional Assessment (MNA) Guigoz Y et al. 1994 [58] http://www.mna-elderly.com/ | \nSetting: Acute [58] Community [58] Rehab [58] Long-term care [58] Patient group: Geriatric [58] | \nScreening and assessment component includes diet history, anthropometry (weight history, height, MAC, CC), medical and functional status. Assessed based on numerical score as: - no nutritional risk - at risk of malnutrition or - malnourished | \nLengthy Low specificity for screening section of tool in acute populations Can be difficult to obtain anthropometric data in this patient group | \n
Validated nutrition assessment tools: comparison guide [45].
Name author, year, country | \nPatient population | \nNutrition screening parameters | \nCriteria for risk of malnutrition | \nWhen/by whom | \nReliability established | \nValidity established | \n
---|---|---|---|---|---|---|
Malnutrition Screening Tool (MST) [59] Ferguson et al. (1999) Australia | \nAcute adults: inpatients and outpatients [59, 60] Elderly [61] Residential aged-care facilities [61] | \nRecent weight loss Recent poor intake | \nScore 0–1 for recent intake Score 0–4 for recent weight loss Total score: > 2 = at risk of malnutrition | \nWithin 24 h of admission and weekly during admission. Medical, nursing, dietetic, admin staff; family, friends, patients themselves | \nAgreement by 2 Dieticians in 22/23 (96%) cases Kappa = 0.88 Agreement by a Dietician and Nutrition Assistant in 27/29 (93%) of cases Kappa = 0.84; and 31/32 (97%) of cases Kappa = 0.93 | \nCompared with SGA and objective measures of nutrition assessment. Patients classified at high risk had longer length of stay. Sensitivity = 93% Specificity = 93% | \n
Mini-Nutritional Assessment – Short Form (MNA-SF) [62] Rubenstein et al. (2001) United States | \nElderly Best used in community, subacute or residential aged-care settings, rather than acute care [63] | \nRecent intake Recent weight loss Mobility Recent acute disease or psychological stress Neuropsychological problems BMI | \nScore 0–3 for each parameter Total score: <11 = at risk, continue with MNA | \nOn admission and regularly not stated | \nNot reported | \nCompared to MNA and clinical nutritional status. Sensitivity = 97.9% Specificity = 100% Diagnostic accuracy = 98.7% Compared with SGA in older inpatients Sensitivity = 100% Specificity = 52%2 | \n
Malnutrition Universal Screening Tool (MUST) [64] Malnutrition Advisory Group, BAPEN (2003) UK | \nAdults – acute and community | \nBMI Weight loss (%) Acute disease effect score | \nScore 0–3 for each parameter Total score: >2 = high risk 1 = medium risk 0 = low risk | \nInitial assessment and repeated regularly Able to be used by all staff | \nInternally consistent and reliable. Very good to excellent reproducibility Kappa = 0.8–1.0 | \nFace validity, content validity, concurrent validity with other screening tools (MST and NRS) [65] Predicts mortality risk and increased length of stay and discharge destination in acute patients [66] | \n
Nutrition Risk Screening (NRS-2002) [67] Kondrup et al. (2003) Denmark | \nAcute adult | \n% of recent weight loss % of recent poor intake BMI Severity of disease Elderly | \nScore 0–3 for each parameter Total score: >3 = start nutritional support | \nAt admission and regularly during admission Medical and nursing staff | \nGood agreement between a Nurse, Dietician and Physician Kappa = 0.67 | \nRetrospective and prospective analysis. Tool predicts higher likelihood of positive outcome from nutrition support and reduced length of stay among patients selected at risk by the screening tool and provided nutrition support. | \n
Comparison of malnutrition assessment and screening tools [45].
Breast cancer has been found to be the most frequently diagnosed cancer in women worldwide. It is estimated that 1.7 million cases and 521,000 deaths in 2012 were attributed to breast cancer and breast cancer alone accounts for 25% of all cancer cases and 15% of all cancer deaths among females [68]. There have been a number of different nutrient deficiencies or insufficiencies that have been attributed to an increased risk of breast cancer development. These include vitamin D3, iodine, folate, zinc, betacarotene and coenzyme Q10. Table 3 shows the association of these nutrients and the risk of breast cancer.
\nNutrient | \nOutcome | \n
---|---|
Coenzyme Q10 | \nOne study in 1998 investigated the role of coenzyme Q10 or ubiquinone in 200 women hospitalized for a biopsy and/or ablation of a breast tumour. They found that 80 patients (40%) with carcinomas and 120 patients (60%) with a non-malignant lesion had a coenzyme Q10 deficiency. There was also a correlation between the intensity of the deficiency and the prognosis of the breast cancer severity [69]. | \n
Folate | \nA lot of focus has been placed on the methylenetetrahydrofolate reductase (MTHFR) polymorphisms of late. A case-controlled study and pooled meta-analysis conducted in 2007 found that peri-menopausal ladies with the C677T polymorphism did have an increased risk of developing breast cancer [70]. | \n
Folate, zinc, betacarotene | \nA recent study in 2014 found that multiple genetic polymorphisms and/or deficiencies in folate, zinc and betacarotenes were associated with the triple negative breast cancer development, particularly in combination [71]. | \n
Iodine | \nIodine was presented as a possible anti-proliferative agent for mammary glands in 2005 [72]. It has been found in both animal and human studies to exert a suppressive effect on the development and size of benign and cancer neoplasms [72]. As iodine stores in the thyroid and breast tissue, it exerts a protective action on the development of breast cancer. As hypothyroidism has been found to be high in breast cancer patients, it is proposed that low iodine levels may be considered a risk factor for breast cancer [73]. | \n
Selenium | \nIn a meta-analysis conducted in 2014, an inverse relationship was found between selenium serum levels and the risk of breast cancer [74]. Therefore, maintaining selenium levels may decrease the risk of breast cancer for some women. | \n
Vitamin D3 | \nA vitamin D deficiency is highly prevalent among breast cancer females [75]. A vitamin D deficiency has been found in 99% of breast cancer females at diagnosis and approximately in 90% in healthy females [76]. Alcohol status and weight have an impact on vitamin D status and breast cancer risk [77]. | \n
Nutrient deficiencies and breast cancer risk.
Nutrient | \nOutcome | \n
---|---|
Selenium | \nA systematic review and meta-analysis of selenium and prostate cancer found that the relationship between plasma/serum selenium and prostate cancer showed that the risk of developing prostate cancer decreased with increasing plasma/serum selenium levels (170 ng/mL) [78]. Further studies are required but there is a link between low selenium levels and prostate cancer risk. | \n
Vitamin D3 | \nVitamin D3 (25(OH)D concentrations have been found to be inversely correlated with prostate cancer risk but not vitamin D–related polymorphisms or parathyroid hormone. This indicates that there is a possibility that low vitamin D3 blood pathology may pose a risk of prostate cancer risk [79]. No association has been found to vitamin D levels or vitamin D supplementation on prostate-specific antigen (PSA) levels [80]. It has been suggested that adding vitamin D supplementation might be an economical and safe way to possibly reduce the prostate cancer incidence and improve the cancer prognosis and outcome [81]. | \n
Vitamin E and trace minerals | \nAs mentioned, a study on Nigerian prostate cancer males was conducted. This study showed that the levels of whole blood superoxide dismutase (SOD), vitamin E, serum selenium and zinc were significantly lower in prostate cancer patients. Therefore, the authors conclude that deficiencies in vitamin E, zinc and selenium may be risk factors for the development of prostate cancer [82]. | \n
Zinc | \nHuman studies on zinc deficiencies and prostate cancer are limited. In vitro studies have found that a zinc deficiency does impact prostate cells and can compromise DNA integrity by impairing the function of zinc-containing proteins [83, 84]. One study conducted on Nigerian prostate cancer patients did find an association with a zinc deficiency and prostate cancer in addition to selenium and vitamin E deficiencies [82]. | \n
Nutrient deficiencies linked with prostate cancer.
A majority of the population feel that prostate cancer is the most frequently diagnosed cancer in men worldwide, but in fact it is the second with 1.1 million new cases estimated to have occurred in 2012. However, it is the most frequently diagnosed cancer in men in developed countries. The incidence rates vary with the highest rates found in Australia/New Zealand, Northern America, Northern and Western Europe and some Caribbean nations. The lowest incidence rates are found in the Asian countries [68]. Nutrient deficiencies that have been studied and identified as potential risk factors include vitamin D3, selenium, zinc and vitamin E (Table 4).
\nColon or colorectal cancer is the third most commonly diagnosed cancer in males and second in females. It is estimated that 1.4 million cases and 693,000 deaths occurred in 2012 due to colorectal cancer. The highest incidence rates have been found in Australia/New Zealand, Europe and North America. The lowest incidence rates are found in Africa and South-Central Asia [68]. Nutrients that have been associated with an increased colon cancer risk include vitamin D3 and folate. Folic acid is controversial with a deficiency and if excess is linked with colorectal cancer risk. In addition to specific nutrients, dietary factors are linked with colorectal cancer development as seen in Table 5.
\nNutrient | \nOutcome | \n
---|---|
Fibre, low-fruit and -vegetable, high red and processed meat intake | \nAlthough not a specific nutrient, it has been well established that a diet low in fruits and vegetables, fibre and high in red and processed meat intake is a risk factor for colorectal cancer development [85–87]. | \n
Folic acid | \nFolic acid is a controversial nutrient for colorectal cancer. High levels have been associated with a reduced colorectal cancer risk; however, excessive folate levels may promote tumour progression [88]. These facts have prevented countries fortifying foods with folate due to the risk of colorectal cancer. Preventing a deficiency in folic acid is recommended as it is a risk factor for cancer development but monitoring levels to prevent excess is also recommended. | \n
Selenium | \nAnimal studies have found that a selenium deficiency can acerbate colitis and promote tumour development and progression in inflammatory carcinogenesis [89]. | \n
Vitamin D3 | \nVitamin D may protect and treat inflammatory bowel disease and assist colon cancer [90]. Vitamin D3 deficiency and insufficiency has been linked as a risk factor for colorectal cancer as found in observational studies in both human and experimental studies (animal and cell lines). The protection from vitamin D3 has been attributed its influence on cell proliferation, differentiation, apoptosis, DNA repair mechanism, inflammation and immune function [91]. A high prevalence of a vitamin D3 deficiency and insufficiency has been found in colorectal cancer patients [75]. | \n
Nutrient deficiencies linked with colorectal cancer.
Nutrient | \nOutcome | \n
---|---|
Selenium | \nSeveral epidemiological studies have shown an increased risk of lung cancer among adults with low blood levels of selenium; however, the results are inconsistent. One study conducted in the south-eastern United States found that there was a risk of lung cancer development in lower income and black Americans [92]. | \n
Vitamin A | \nCigarette smoking has been directly associated with the development of lung cancer. It has been demonstrated that cigarette smoke significantly reduces retinoic acid in the lungs of rats and increases the formation of precancerous and cancerous lesions [93]. It has been found that this is attributed to two independent pathways, RARα- and RARβ-mediated pathways. Human studies are limited if a vitamin A deficiency increases the risk of lung cancer development if exposed to cigarette smoke. | \n
Vitamin D3 | \nA high prevalence of low vitamin D3 has been found in lung cancer patients ranging from a mild deficiency to severe deficiencies [75]. | \n
Zinc | \nHuman studies on zinc deficiency and lung cancer are limited. Cell culture work on human lung fibroblasts has found that a zinc deficiency can cause DNA instability and compromise its integrity and therefore may be important in the prevention of DNA damage and cancer [94]. | \n
Nutrient deficiencies linked with lung cancer.
The popularity of breast and prostate cancer override the one cancer that is the most frequent cause of death among males in 2012 and is the leading cause of death in females in developed countries and second in less developed countries, lung cancer. The highest lung cancer incidence rates include Europe, Eastern Asia and Northern America and the lowest rates are in sub-Saharan Africa. Although smoking has high correlation with lung cancer development, a high prevalence of non-smoking individuals has been diagnosed with lung cancer. This high prevalence has been thought to reflect indoor air pollution, cooking fumes, exposure to occupational and environmental carcinogens such as asbestos, arsenic, radon and polycyclic aromatic hydrocarbons. Recently, outdoor pollution as also been attributed as a cause of lung cancer [68]. In addition, certain nutrients may also play a role in the development of lung cancer. These include vitamin D3, zinc, vitamin A and selenium as seen in Table 6.
\nCondition | \nPossible nutrient deficiency or insufficiency | \n
---|---|
Alteration of taste and smell | \nZinc | \n
Cachexia | \nMultiple nutrient deficiencies, protein, essential fats | \n
Chemotherapy-induced peripheral neuropathy | \nVitamin B12, vitamin B6, vitamin E, omega 3 fatty acid (DHA) | \n
Dehydration | \nWater, electrolytes | \n
Diarrhoea | \nWater, electrolytes, gut bacteria (lactobacillus, bifidus etc.) | \n
Eczema/dermatitis | \nEssential fats, omega 3 fatty acids, vitamin E, vitamin D3, zinc, vitamin A | \n
Hand and foot syndrome | \nVitamin B6 | \n
Mucositis | \nGlutamine, vitamin A, zinc, glucosamine, vitamin C | \n
Radiation-induced enteritis | \nGlutamine, vitamin A, zinc, glucosamine, vitamin C | \n
Potential nutritional deficiencies or insufficiencies for conditions linked with cancer treatment.
Research into nutrient deficiencies linked with certain conditions is limited. Certain nutrients have been found to be insufficient or deficient for certain conditions and may assist the patient in managing the situation. Table 7 lists some conditions and possible nutrients, which could be found to be deficient or insufficient. It may be beneficial to consider the replacement of these nutrients for patients, or at least pathological or physical assessment to check the status.
\nCurative cancer treatment normally occurs after surgery and can be intense. The impact on the nutritional status of the patient strongly depends on the tumour site, stage and progression of the cancer, the risks of the active treatment and the base nutritional status of the patient. For example, a patient undergoing concurrent chemotherapy and radiation for head and neck or lung cancer has a higher risk of malnutrition and impact on nutritional status than a patient undergoing adjunct chemotherapy for breast cancer.
\nNutritional assessment and management should be started at the time of diagnosis and monitored throughout active treatment and afterwards. An ideal nutritional intervention and management commences with the initial evaluation of the patient’s nutritional status through preliminary assessment tools and blood pathology tests. Regular re-evaluation is required throughout the treatment and post treatment until a good nutritional status is restored.
\nAdvanced cancer or palliative treatment is defined as patients who have metastatic cancer or are not responsive to curative treatment [5]. The life expectancy for these patients can vary from 1 month to many years. Therefore, nutritional assessment and intervention will depend on the stage of the cancer, the individual’s current state, controlling the symptoms, maintaining an adequate hydration state and maintaining or restoring the patients ‘well-being’.
\nBody weight will vary depending on the person as weight gain can occur due to lack of mobility and fatigue or weight loss/cachexia towards the end of life. Oedema and ascites from the tumour sites can also cause discomfort and impact digestive ability. Nutritional intake can also influence the QoL of the patient [5]. Constant re-evaluation and nutritional options are required as the patient’s physical state changes. Consideration of nutrient intake, supplementation and nutritional fluid replacements are all important for each stage. Optimal nutritional status may not be restored in some cases; however, maintaining nutritional status for as long as possible has been found to be beneficial for the patient’s well-being and QoL [5].
\nCurrent treatment for cancer is focused on survival, cure or pain management of the patient through active treatments such as surgery, chemotherapy, immunotherapy, radiation or hormone treatment. The nutritional status of patients generally is not a major consideration of primary health professionals unless malnutrition or weight loss is present, or the treatment may induce malnutrition. However, with the increasing number of cancer survivors, base nutritional status, nutritional assessment and support need to be extended to all cancer patients prior, during and post active cancer treatment. Nutritional screening and assessment needs to be considered an essential component of all aspects of cancer treatment.
\nThis increased likelihood of individuals with cancer living longer after treatment has seen ‘cancer survivorship’ become a popular concept amongst organizations, hospitals, institutions and researchers within the field of oncology. A cancer ‘survivor’ is commonly defined as any person who has been diagnosed with cancer from the time of diagnosis through the balance of their life [95], although, many parties advocate for use of the term to relate to individuals who have had a previous cancer diagnosis and are now pursing life ‘after active treatment’ [95]. There are three distinct phases of cancer survivorship:
One of the main focuses of cancer survivorships is diet, nutrition, exercise and long-term side-effect management. From definition, this starts from cancer diagnosis. Potential nutrient deficiencies or insufficiencies are areas that need further attention as well as their possible impact on side effects experienced by patients. Integration of nutritional assessment and intervention can be achieved through the current medical system and should be an important component of cancer patient-centred care.
\nInvestigation into nutrient deficiencies in newly diagnosed cancer patients with emphasis on the type of cancer, social and economic status, gender and culture.
Future trials and/or nutritional monitoring, assessment and intervention throughout cancer patient’s active treatment and post treatment.
Research into how nutritional deficiencies or insufficiencies may affect patient side effects to treatment.
Research into potential nutrient deficiencies and insufficiencies as risk factors for cancer development and their mechanisms of action in cell impairment and cancer initiation and progression.
Proprietary or “paywall” publishing mode dominated the scholarly world throughout the late 20th and early 21st centuries. This is for-profit commercial publishing where publishers make their returns by the collection of research of scholars, application of peer-review, offering of editorial and formatting services, the collation of this research into subject-specific journals, and then selling subscription-based access of these works to academic libraries, scholarly societies and individual researchers. Access to individual articles on a short-term basis (typically 24 hours) is also supplied on a pay-for-use model. Commercial publishers also provide publishing facilities for books and monographs, although these have been on the decline [1]. The advent and wide use of the internet have strongly affected the process of scholarly publishing worldwide. A new mode of publication has emerged and widely employed by scholars and researchers. This new mode is Open Access (OA) publishing of scholarly work. This chapter will discuss OA focusing on its benefits to all the stakeholders and presenting other aspects of this new way of scholarly communication including its definition, types, development, its pros and cons and the myths and misconceptions surrounding it.
Open access refers to free, unrestricted online access to research outputs such as journal articles and books. OA content is open to all, with no access fees. Open access is more than free access. When people think about open access (OA), they immediately relate it with free access. Providing reuse rights is another important asset of open access. Open access in its purest form is “digital, online, free of charge, and free of most copyright and licensing restrictions”. Open access entails a new model of publishing wherein the author, supported by an institution or funding agency, pays the publishing costs and owns the copyright. The publisher manages the peer review process and publishes directly to the Internet, where content is accessible free of charge to the public. Open access publishers take full advantage of available computing technology to streamline the publishing process [2]. Open Access aims to provide users with information that is unconstrained by the motive of financial gain or profits [3]. Furthermore, Open access implies that “users must be able to copy, use, distribute, transmit and display the work publicly and to make and distribute derivative works, in any digital medium for any responsible purpose, subject to proper attribution of authorship” [4, 5].
In subscription-based publishing, authors are required to transfer the copyright of their works to the publisher who makes profits via the dissemination and reproduction of the works. Contrary to this, with OA publishing, authors can retain copyright to their work and license its reproduction to the publisher. The most commons licenses used in open access publishing are the Creative Commons (CC) licenses. The widely used Creative Commons By Attribution (CC BY) license is one of the most permissive, only requiring attribution to be allowed to use the material (and allowing derivations and commercial use). A range of more restrictive creative commons licenses are also used. More rarely, some of the smaller academic journals use custom open access licenses. Some publishers (e.g. Elsevier) use “author nominal copyright” for OA articles, where the author retains copyright in name only and all rights are transferred to the publisher [6].
The OA movement can be said to have started in the year 1971 with Project Gutenburg Founded by Michael Hart [7]. This project is now providing free public domain text files with more than 60,000 eBooks. However, the modern open access movement began in the 1990s with the wide availability and access to the World Wide Web and online publishing became the norm. Starting in the early years of the 21st century there was a significant momentum towards making access to published research free of charge to scholars and universities through the Open Access movement. Three pioneering initiatives laid the foundation for the ideas and principles of OA movement. These are The Budapest Open Access Initiative on Feb. 14, 2002, The Bethesda Statement on Open Access Publishing on Apr. 11, 2003, and The Berlin Declaration on Open Access on Oct. 22, 2002 [8]. The Budapest Open Access Initiative was worked out during the human rights proponents gathering for the Open Society Institute meeting in December 2001. During the meetings a number of participants suggested that a global support is needed to create open information access within the scientific community. A draft was created during that meeting, and formalized two months later, in February 2002 as the Budapest Initiative. In April 2003, the United States and the United Kingdom based biomedical community convened and drafted a set of publishing principles guiding scientific dissemination. These principles were finalized and published in June 2003 as the Bethesda Statement. In October 2003, the European scientific community called for support by European researchers to engage in Open Access, with the Berlin Declaration [9].
Many stakeholders contributed to building institutions and resources for shaping up the global OA movements. Some of the institutions emerged during the first two decades of the third millennium are namely, Public Library of Science (PLOS), BioMed Central (BMC) – publishers of peer-reviewed OA journals, the Scholarly Publishing and Academic Resources Coalition (SPARC), and Open Access Scholarly Publishers Association (OASPA) [10]. In addition to the previously mentioned (BBB); the Budapest, Berlin and Bethesda OA declarations or statements got signed by the scholarly communities, particularly by the funding agencies, research councils, learned societies, institutions, universities, and scientists for the OA dissemination of public funded research.
The latest strong support for the OA movement is represented by what is known as PLAN S where the s could stand for “science, or shock” but “speed” is the most relevant where it refers to speed with the transition to direct and open access [11]. Plan S is an initiative for Open Access publishing that was launched in September 2018. The plan is supported by cOAlition S, an international consortium of research funders. Plan S requires that, from 2021, scientific publications that result from research funded by public grants must be published in compliance with Open Access journals or platforms.
There are three basic types of open access publishing. These are Green Open Access, Gold Open Access, and Hybrid Open Access [12].
Green Open access publishing refers to the self-archiving of published or pre-publication works for free public use. Authors provide access to preprints or post-prints of their works with publisher permission in an institutional or disciplinary digital repository. Thus, Green open access refers to the practice of republishing a publication in an open access institutional or disciplinary repository. In this case the publication is first published in a traditional, closed-access journal. These materials are then made available to all via the internet, without restrictions or pay walls. In the “Green Route” of open access, institutions create repositories for their own research which is made open after an appropriate embargo period agreed upon with commercial publishers. As such Green Open Access generally refers to the post-print of an article [1]. In this context, there are three basic version types that can be self-archived in repositories: These are:
Pre-Prints – The author’s copy of article before it has been reviewed by the publisher, or pre-reviewed.
Post-Prints – The author’s copy of article after it has been reviewed and corrected, but before the publisher has formatted it for publication, or post-reviewed.
Publisher’s Version – The version that is formatted and appears in print or online.
Gold open access publishing refers to works published in an open access journal and accessed via the journal or publisher’s website. The Gold Route involves publishing in an open access journal, which then provides the dissemination and curation services in the same way as current proprietary publishers. This form of publishing is funded through government, society or institutional grants, and sometimes through charging authors a fee for deposit, known as an article processing charge (APC). However, the latter practice is implemented by a minority of open access journals and most journals do not charge any fees at all [13].
Hybrid open access publishing is mostly associated with gold open access. It takes place in journals that offer authors the option of making their articles open access, for a fee. Hybrid journals are subscription-based journals that make individual articles openly available in return for a fee. The hybrid route has been suggested as a means for traditional publishers to make a transition to open access publishing without significantly decreasing revenue, by charging fees for open access articles equal to the average subscription revenue per article. In the Hybrid Open Access publishing type, sometimes called Paid Open Access, the fee is paid to the publisher or journal by the author, the author’s organization, or the research funder [14, 15].
There are a number of other variations of these major types of open access publishing types. These include the Diamond Open access and the Platinum Open Access. The Diamond Open access journals provide scholarly publishing free of fees and access charges. They have direct or indirect subsidies from institutions like universities, research centres, government agencies etc. Whereas the Platinum model of open access publishing refers to the situation in which journals are published directly by the research or funding institutions themselves.
In Gold and Hybrid OA models, publishers usually publish articles with Creative Commons (CC) licenses. Open Access does not imply there is no copyright attached to the open document; rather, in most cases the Creative Commons Attribution License (CCAL) model is used. Founded in 2001, the CCAL states that users are free to share, adapt, or use the work as long as they give attribution in the manner specified by the author or licensor [16]. The Attribution License is one of six codes under the Creative Commons License. Thus Open Access journals do not charge subscription or pay-per-view fees compared to traditional journals. The authors, their institutions, or the research funders pay the “open access” fee to make it free to readers; authors retain copyright for the article and most permission barriers are removed [17, 18].
There is a controversial type of open access called the Bronze Open Access. In the Bronze model no open access Fee is paid but the publisher chooses to make a publication freely available to read. Many Open Access advocates and research funders would not regard Bronze as truly Open Access because the publisher can stop the publications being freely available at any time, whereas genuinely Open Access publications have a specific licence that means the publication is irrevocably open access and the terms of use and reuse are clearly stated [19].
Although bronze OA lacks a license, it is temporarily free to read only on the publisher’s website, and Publishers can deny access to the majority of open-access articles at their discretion [20].
These two terms are interlinked to the basic three types of open access. But in contrast to Gold, Green and Hybrid OA, they do not describe forms of publication, but define the attributes of an article published in OA. Therefore an article might be described jointly as Gratis Open Access, or Gratis Gold or Green Open Access, etc. [21]. Gratis Open Access means free of charge Open Access. This means that price barriers alone are removed from access to the publication. It allows no uses beyond what is considered legitimate under copyright and fair use. Libre Open Access, on the other hand, means free of charge and free of at least some permission barriers. This means that the article is free for some kinds of further use and reuse, and presupposes some kind of open licence that allows types of uses that are not permitted by default [22].
Open access publishing has a plethora of advantages for authors, institutions and readers across all sections of society. These advantages can be summarised as follows [8, 23]:
Increased accessibility of research work by users and other researchers. This leads to the enhancement and acceleration of the research cycle when results are available on an Open Access basis, where work is published, read, cited and then built upon by other researchers.
Increased visibility for authors and institutions, resulting in a higher impact of the research. There are no financial or copyright barriers so the readership continues to increase, enhancing the visibility and impact of the author’s Work. There is a greater chance of research results being seen when scientific journals are free to read and use, thus influencing the thinking of others. This state of affairs results in the increase of the academic’s impact factor.
Immediacy and Shorter publication times compared to non-open access publishing. Open access publishing takes shorter period of time from the date of submission of an article to a journal to its publication date.
Increased citations. A number of studies revealed that open access publishing leads to a greater number of citations. There is accumulating evidence showing that open access research articles are cited more often than those closed access articles. The studies reveal that across most subject areas there is at least a twofold increase in citation rate and that in some subject areas it is even higher [24].
Removing of price barriers. Open access removes price barriers and that openly accessible works are often full-text indexed, helping potential readers easily locate a work using a search engine, and access the work without being turned away by pay walls.
Contribution to author royalties. Some authors found that widespread dissemination of their openly accessible works stimulates demand for print copies of their works, contributing to royalties for these authors [23].
Those seeking wider visibility of their research work, higher impact for their research, less publication cost, and a shorter period of time from the date of submission to the publication date, should opt for publication in an OA journal [25].
The most prominent and prevalent disadvantage of OA publishing is the emergence of predatory publishers and predatory journals. A predatory journal will not maintain the academic standards that are expected of a reputable scientific journal. The objective of the predatory journal is to make money for the owners without concern for the quality of the research published. A predatory journal will pretend to follow the essential editorial processes required for authentic academic publishing, but will not so do. Thus the quality of the research published in a predatory journal is likely to be low. Predatory journals can be identified by a number of characteristics, the most important of which may be the fact that they tend to market themselves through intensive e-mailing to invite selective victims who might otherwise have difficulty in having their research published in reputable journals. This lead to the development of what has become known as the predatory journal, which for a fee paid by the author delivers an un-scrutinised and unedited piece of writing purporting to be a high quality report on a piece of rigorously conducted scientific research. These journals are then presented to the public as Open Access journals [8, 26, 27].
Another claimed disadvantage of Open Access publishing is that some OA journals do not have high impact factors and this is considered detrimental to a researcher, though this is questionable as many OA journals are new and have not yet received their first impact factor (IF). However, high-IF OA journals are available in a variety of fields [25].
There are a number of myths and misconceptions surrounding open access publishing mode. Some of the most common myths include the following:
Myth 1: “open access journals are not peer reviewed”.
Myth 2: “all open journals charge publication fees”.
Myth 3: “authors must choose between prestigious publication and Open Access publication”.
Myth 4: “post-print archiving violates copyright”.
Myth 5: “OA invites plagiarism.”
Myth 6: “OA helps readers but not authors.”
Myth 7: “All OA is gratis OA.”
Below is a discussion of these myth and misconceptions about open access publishing with points that help dispel them.
Studies show that the majority of OA journals are peer-reviewed with the same or higher standards as traditional scholarly journals. However, it takes time for a new OA journal to build a high impact factor [18, 28]. Indexing of a journal in a major citation database is also considered a reflection of a journal’s quality. Indexing newly established OA journals in major citation databases is complex and time-consuming, furthering existing misconceptions of quality [8]. This myth entails that Open access journals are intrinsically low in quality. But as early as 2004, it was found that in every field of the sciences there was at least one open access title that ranked at or near the top of its field in citation impact. It’s quite normal that open access journals can be of high quality and first-rate: the quality of a scholarly journal depends on its authors, editors, and referees, not its business model or access policy [29, 30].
There are a number of OA journal business models and a number of OA book business models available. The models include the following options and variations:
Charging publication fees in the form of author fees or article processing charges is the best-known business model for open access journals, but it is not the most common. Most peer-reviewed open access journals nowadays charge no fees at all. The Directory of Open Access Journals (DOAJ) [31] provides information about open access journals that do and do not charge fees. It is also well known that most conventional or non-open access journals do charge author-side fees, on top of reader-side subscription fees.
OA is compatible with prestige for two reasons: First, a growing number of OA journals have already earned high levels of prestige, and others are earning it. The second reason is that most pay wall (Toll Access) journals allow OA archiving. When authors retain the right to self-archive, all journals willing to publish their work also allow self-archiving. The current misunderstanding has some negative effects. When scholars know about OA and don’t choose it, they are generally not opposed to it; many support it strongly. They are simply giving higher priority to prestige. But because OA is compatible with prestige, authors rarely have to choose. But they have to choose only when a prestigious journal doesn’t already permit post print archiving and when it rejects the authors’ individualized request for permission. Authors rarely have to choose between them, but to have both at once they will often have to choose to self-archive [32].
Most publishers allow their authors to self-archive their articles in institutional repositories or on their own personal websites. However, conditions and restrictions are frequently imposed. For example, authors are often obliged to observe an embargo period between the publication date and the date on which the document is made openly accessible online. The SHERPA/Romeo Listings provide information on the self-archiving policies of individual publishers. They used to classify publishers in different colours depending on their archiving policies; green publishers let authors archive preprint and post print or publisher’s version/PDF, blue publishers let authors archive post print or publisher’s version/PDF, yellow publishers let authors archive preprint, and white publishers do not formally support archiving. But they recently stated that they have now retired the Romeo colours, as open access policies have become more complicated and the colours no longer gave a clear overview [33]. Many of those authors, whose publishers do not allow self-archiving, supplement their standard publishing agreements with contract addenda which enable them to provide open access to their work in parallel with publication [34].
In the early days of the OA movement some authors worried that OA would increase the incentive to plagiarize their work. On the contrary, OA might make plagiarism easier to commit, for people trolling for text to cut and paste. But for the same reason, OA makes plagiarism more risky to commit. Plagiarism from OA sources is the easiest kind to detect. Some of the misunderstanding here may arise from confusing plagiarism and copyright infringement. Plagiarism and infringement are two separate things although they are overlapping offenses. “Someone can commit plagiarism without infringing copyright (by copying a fair-use excerpt and claiming it as one’s own) and infringe copyright without committing plagiarism (by copying a larger excerpt but with attribution). One can also commit both together (by copying a large excerpt and claiming it as one’s own)” [32].
OA articles are accessible to everyone with an internet connection, a vastly larger audience than any scholarly journal can claim. Not all internet users will care to read your research, of course. But making your work universally accessible to the connected guarantees that it will be accessible to the subset which does care. If there’s an exception for the digital divide, there’s a larger exception for the non-digital or print divide. Moreover, there’s abundant evidence that OA articles are cited more often than non-OA articles, even more than non-OA articles from the same issues of the same journals [35, 36]. Many different studies have tackled this phenomenon, taking on different bodies of literature, using different methods, controlling different variables. They disagree on whether the OA impact advantage is large or small, and whether OA causes the increase in citations or is merely correlated with it. But they agree that OA articles are cited more often than non-OA articles. Authors may hope to earn royalties from their books, but they write journal articles for impact, not for money [37].
Gratis OA removes price barriers but not permission barriers. It makes content free of charge but not free of copyright or licensing restrictions. It gives users no more reuse rights than they already have through fair use or the local equivalent. Libre OA removes price barriers and at least some permission barriers. It loosens copyright and licensing restrictions and permits at least some uses beyond fair use [38]. There is some excuse for the opposite view, that all OA is libre OA. The Budapest, Bethesda, and Berlin definitions of OA all describe forms of libre OA. The current misunderstanding accepts that gratis OA is a kind of OA, but goes one step too far and assumes that gratis OA is the only kind of OA. The misunderstanding is that there is no libre OA, that libre OA adds nothing to gratis OA, or that what libre OA adds isn’t necessary or desirable. In general, OA repositories have good reasons to stick to gratis OA but OA journals don’t. Repositories can’t generate the needed permissions on their own, but journals can [37].
A large-scale study that investigates the prevalence and impact of OA publishing found that almost half of the scholarly papers that people attempt to access online are now freely and legally available [39]. The study tracked 100,000 online requests for journal papers in 2017. It examined reader data from a web-browser extension called
Plan S is the latest initiative to promote and support open access publishing. Below is an excerpt from the Coalition website [40] which is the body responsible for the Plan S, revealing the target of this open access plan:
This chapter presented an overview of the basic principles and common practices of open access publishing as an emerging and expanding mode of scholarly publishing. The chapter started with an introduction to the concept of open access publishing with a brief background of the development of the open access movement. The different types of open access publishing are then highlighted and defined. These types include Gold Open Access, Green Open Access, and Hybrid Open Access, in addition to other variations of these basic types namely, the Diamond Open Access and the Platinum Open Access. The concepts of Gratis vs. Libre Open Access are also defined and explained. The chapter then discussed the advantages and disadvantages of open access focusing on the various advantages of this mode of scholarly publishing to authors and readers as well. The chapter then proceeded to discuss and refute the most common myths and misconceptions about open access publishing. The chapter is concluded with some views on the prevalence and future of open access publishing.
IntechOpen books and journals are available online by accessing all published content on a chapter/article level.
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She is an author of about 90 publications (According to Scopus: H-Index: 23; According to WOS: H-Index: 20) on peer-reviewed journals, a member of the “Società Italiana di Biochimica e Biologia Molecolare,“ and a Consultant Reviewer for International Journal of Molecular Science, Journal of Chromatography A, COPD, Plos ONE and Nutritional Neuroscience.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorThree:null}]},overviewPageOFChapters:{paginationCount:50,paginationItems:[{id:"81927",title:"Purinergic System in Immune Response",doi:"10.5772/intechopen.104485",signatures:"Yerly Magnolia Useche Salvador",slug:"purinergic-system-in-immune-response",totalDownloads:3,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"80495",title:"Iron in Cell Metabolism and Disease",doi:"10.5772/intechopen.101908",signatures:"Eeka Prabhakar",slug:"iron-in-cell-metabolism-and-disease",totalDownloads:8,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Iron Metabolism - Iron a Double‐Edged Sword",coverURL:"https://cdn.intechopen.com/books/images_new/10842.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"81799",title:"Cross Talk of Purinergic and Immune Signaling: Implication in Inflammatory and Pathogenic Diseases",doi:"10.5772/intechopen.104978",signatures:"Richa Rai",slug:"cross-talk-of-purinergic-and-immune-signaling-implication-in-inflammatory-and-pathogenic-diseases",totalDownloads:10,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"81764",title:"Involvement of the Purinergic System in Cell Death in Models of Retinopathies",doi:"10.5772/intechopen.103935",signatures:"Douglas Penaforte Cruz, Marinna Garcia Repossi and Lucianne Fragel Madeira",slug:"involvement-of-the-purinergic-system-in-cell-death-in-models-of-retinopathies",totalDownloads:5,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Purinergic System",coverURL:"https://cdn.intechopen.com/books/images_new/10801.jpg",subseries:{id:"17",title:"Metabolism"}}}]},overviewPagePublishedBooks:{paginationCount:27,paginationItems:[{type:"book",id:"7006",title:"Biochemistry and Health Benefits of Fatty Acids",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/7006.jpg",slug:"biochemistry-and-health-benefits-of-fatty-acids",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Viduranga Waisundara",hash:"c93a00abd68b5eba67e5e719f67fd20b",volumeInSeries:1,fullTitle:"Biochemistry and Health Benefits of Fatty Acids",editors:[{id:"194281",title:"Dr.",name:"Viduranga Y.",middleName:null,surname:"Waisundara",slug:"viduranga-y.-waisundara",fullName:"Viduranga Y. 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He has taught at Thompson Rivers University, Canada; University of Paris-Est, France; Osnabruck University of Applied Science, Germany; and Shanghai Institute of Technology and Tianjin University of Technology, China. He has published research in Research Policy, Applied Economics, Review of Economic Philosophy, Strategic Change, International Journal of Logistics, Sustainability, Journal of Environmental Management, Journal of Global Information Management, Journal of Cleaner Production, M@N@GEMENT, and more. He is a member of CEDIMES Institut (France), Academy of International Business (AIB), Strategic Management Society (SMS), Academy of Management (AOM), Administrative Science Association of Canada (ASAC), and Canadian council of small business and entrepreneurship (CCSBE). He is currently the director of the Research Group on Contemporary Asia (GERAC) at Laval University. 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Recently, bioinspired systems have been successfully employing biomechanics to develop and improve assistive technology and rehabilitation devices. The research topic "Bioinspired Technology and Biomechanics" welcomes studies reporting recent advances in bioinspired technologies that contribute to individuals\' health, inclusion, and rehabilitation. Possible contributions can address (but are not limited to) the following research topics: Bioinspired design and control of exoskeletons, orthoses, and prostheses; Experimental evaluation of the effect of assistive devices (e.g., influence on gait, balance, and neuromuscular system); Bioinspired technologies for rehabilitation, including clinical studies reporting evaluations; Application of neuromuscular and biomechanical models to the development of bioinspired technology.',coverUrl:"https://cdn.intechopen.com/series_topics/covers/8.jpg",hasOnlineFirst:!1,hasPublishedBooks:!0,annualVolume:11404,editor:{id:"144937",title:"Prof.",name:"Adriano",middleName:"De Oliveira",surname:"Andrade",slug:"adriano-andrade",fullName:"Adriano Andrade",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRC8QQAW/Profile_Picture_1625219101815",biography:"Dr. Adriano de Oliveira Andrade graduated in Electrical Engineering at the Federal University of Goiás (Brazil) in 1997. He received his MSc and PhD in Biomedical Engineering respectively from the Federal University of Uberlândia (UFU, Brazil) in 2000 and from the University of Reading (UK) in 2005. He completed a one-year Post-Doctoral Fellowship awarded by the DFAIT (Foreign Affairs and International Trade Canada) at the Institute of Biomedical Engineering of the University of New Brunswick (Canada) in 2010. Currently, he is Professor in the Faculty of Electrical Engineering (UFU). He has authored and co-authored more than 200 peer-reviewed publications in Biomedical Engineering. He has been a researcher of The National Council for Scientific and Technological Development (CNPq-Brazil) since 2009. He has served as an ad-hoc consultant for CNPq, CAPES (Coordination for the Improvement of Higher Education Personnel), FINEP (Brazilian Innovation Agency), and other funding bodies on several occasions. He was the Secretary of the Brazilian Society of Biomedical Engineering (SBEB) from 2015 to 2016, President of SBEB (2017-2018) and Vice-President of SBEB (2019-2020). He was the head of the undergraduate program in Biomedical Engineering of the Federal University of Uberlândia (2015 - June/2019) and the head of the Centre for Innovation and Technology Assessment in Health (NIATS/UFU) since 2010. He is the head of the Postgraduate Program in Biomedical Engineering (UFU, July/2019 - to date). He was the secretary of the Parkinson's Disease Association of Uberlândia (2018-2019). Dr. Andrade's primary area of research is focused towards getting information from the neuromuscular system to understand its strategies of organization, adaptation and controlling in the context of motor neuron diseases. 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Biochemistry examines macromolecules - proteins, nucleic acids, carbohydrates, and lipids – and their building blocks, structures, functions, and interactions. Much of biochemistry is devoted to enzymes, proteins that catalyze chemical reactions, enzyme structures, mechanisms of action and their roles within cells. Biochemistry also studies small signaling molecules, coenzymes, inhibitors, vitamins, and hormones, which play roles in life processes. Biochemical experimentation, besides coopting classical chemistry methods, e.g., chromatography, adopted new techniques, e.g., X-ray diffraction, electron microscopy, NMR, radioisotopes, and developed sophisticated microbial genetic tools, e.g., auxotroph mutants and their revertants, fermentation, etc. More recently, biochemistry embraced the ‘big data’ omics systems. Initial biochemical studies have been exclusively analytic: dissecting, purifying, and examining individual components of a biological system; in the apt words of Efraim Racker (1913 –1991), “Don’t waste clean thinking on dirty enzymes.” Today, however, biochemistry is becoming more agglomerative and comprehensive, setting out to integrate and describe entirely particular biological systems. The ‘big data’ metabolomics can define the complement of small molecules, e.g., in a soil or biofilm sample; proteomics can distinguish all the comprising proteins, e.g., serum; metagenomics can identify all the genes in a complex environment, e.g., the bovine rumen. 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Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. 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We encourage the submission of manuscripts that provide novel and mechanistic insights that report significant advances in the fields. 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Behind these definitions are hidden all the aspects of normal and pathological functioning of all processes that the topic ‘Metabolism’ will cover within the Biochemistry Series. 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Thus proteomics, an area of research that detects all protein forms expressed in an organism, including splice isoforms and post-translational modifications, is more suitable than genomics for a comprehensive understanding of the biochemical processes that govern life. The most common proteomics applications are currently in the clinical field for the identification, in a variety of biological matrices, of biomarkers for diagnosis and therapeutic intervention of disorders. From the comparison of proteomic profiles of control and disease or different physiological states, which may emerge, changes in protein expression can provide new insights into the roles played by some proteins in human pathologies. Understanding how proteins function and interact with each other is another goal of proteomics that makes this approach even more intriguing. Specialized technology and expertise are required to assess the proteome of any biological sample. Currently, proteomics relies mainly on mass spectrometry (MS) combined with electrophoretic (1 or 2-DE-MS) and/or chromatographic techniques (LC-MS/MS). MS is an excellent tool that has gained popularity in proteomics because of its ability to gather a complex body of information such as cataloging protein expression, identifying protein modification sites, and defining protein interactions. 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