\r\n\tto cover major health conditions that may benefit from Tai Chi, including neurodegenerative diseases, cardiopulmonary rehabilitation, psychosocial benefits, chronic fatigue and fibromyalgias, osteoporosis ad bone metabolism, and other chronic degenerative conditions that plague modern health. We seek to include reviews of underlying basic science as well as clinical trial data that demonstrate that multiplicity of benefits of this ancient exercise form to advance evidence-based understanding of Tai Chi exercise as an adjunct treatment.
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\n
1. Introduction
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A considerable amount of interest has been placed on the discovery of novel naturally occurring plant-derived compounds for the treatment and prevention of various diseases. Bioactive compounds of plant origin have long been shown to possess strong ameliorative properties against various communicable and noncommunicable diseases [1, 2]. For example, since its traditional use during the 1950s, artemisinin, an antimalarial qinghao derived lactone, has been the leading therapy for the treatment of Plasmodium falciparum malaria worldwide [3]. Similarly, the traditional use of galegine, an alkaloid isolated from Galega officinalis, led to the discovery of biguanide class of antidiabetic medications such as metformin [4]. Agents such as metformin are effective at lowering blood glucose levels and combating complications associated with insulin resistance (IR), the major characteristic of the metabolic syndrome [5]. However, the continued rise in the mortality of diabetic patients warrants an investigation into alternative therapies to reduce the burden of noncommunicable diseases. Naturally derived compounds such as polyphenols are increasingly explored for their therapeutic potential to reverse IR and thus decrease the risk of developing the metabolic syndrome. This may eventually lead to an increased life expectancy of diabetic individuals [6]. Thus, due to its modulatory effect of glucose and lipid metabolism, skeletal muscle has been a target to a growing number of therapeutic interventions in an effort to reverse IR and improve the management of metabolic syndrome [7, 8]. Here, we systematically assessed the available literature on the ameliorative potential of some of the prominent natural products against IR associated complications. A systematic search was conducted on all major databases such as MEDLINE/PubMed, EMBASE, and Google Scholar, for available literature reporting on the ameliorative properties of some of the prominent natural compounds including apigenin, aspalathin, berberine, curcumin, epigallocatechin gallate, hesperidin, luteolin, naringenin, quercetin, resveratrol, rutin, and sulforaphane against IR related to the development of metabolic syndrome. The search was conducted from inception until the end of January 2018, gray literature such as abstract proceedings and pre-prints were also included. There were no language restrictions implemented while review articles were screened for primary findings.
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2. Apigenin
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Apigenin (PubChem CID: 5280443) is a natural flavone (4′,5,7-trihydroxyflavone) with the molecular formula C15H10O5 (MW 270.24 g/mol) that is abundantly present in fruits and vegetables, including parsley, chamomile, and celery (Figure 1) [9]. Apigenin was identified as the main yellow dye compound in the flowers of Delphinium Zalil as early as the 1890s [10], and its bioavailability and metabolism profile has been studied as far back as the 1970s [11]. Although pharmacokinetic studies show that apigenin has low bioavailability [12, 13], this compound has been detected in rat plasma after intravenous bolus administration [14], and it was demonstrated that human intestinal microbiota might contribute to its metabolism [15]. The known metabolites of apigenin detected in the urine of rats consist of p-hydroxyphenylpropionic acid, p-hydroxycinnamic acid, and p-hydroxybenzoic acid metabolites [11] while it is known glucosides include apiin, apigenin, vitexin, isovitexin, and rhoifolin.
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Figure 1.
The chemical structure of apigenin (4′,5,7-trihydroxyflavone).
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In relation to its biological activities, increasing studies have demonstrated that apigenin displays a broad spectrum of anticarcinogenic properties as reviewed by Sung et al. [16]. Some of the well-studied mechanisms associated with the chemo-preventative capabilities of apigenin include its anti-inflammatory activity, its ability to suppress cell proliferation and oxidative stress, as well as its modulatory effect of autophagy and apoptosis [16, 17]. Interestingly, similar mechanisms have also been implicated in the development and aggravation of IR and its related complications. In a recent study, Jung et al. [18] showed that in addition to reducing circulating free fatty acids (FFAs), total cholesterol, and apolipoprotein B levels, apigenin modulated transcriptional factors linked with the development of obesity and related metabolic disturbances in high fat diet (HFD)-induced mice. This study showed that apigenin upregulated the expression of genes responsible for the regulation of beta-oxidation, oxidative phosphorylation, as well as electron transport chain and cholesterol homeostasis, which are all essential target sites for the control of substrate usage in cells. Although limited studies are reporting on its effect on skeletal muscle, two recent studies have shown that apigenin can regulate skeletal muscle function. For instance, Choi et al. [19] showed that this flavone improved mitochondrial function and exercise capacity by reducing the expression of atrophic genes such as RING-finger protein-1 and Atrogin 1 in mice fed HFD. Jang et al. [20] demonstrated that in C2C12 cells and skeletal muscle of C57BL/6 mice, this flavone promoted hypertrophy and myogenic differentiation by regulating protein arginine methyltransferase 7 (Prmt7)-peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)-G protein-coupled receptor 56 (GPR56) pathway, as well as the Prmt7-p38-myoD pathway. Although additional studies are required to further assess the impact of apigenin in the modulation of metabolic disease-related complications through the regulation of skeletal muscle function, the two aforementioned studies suggest that this flavone has a potential to protect against skeletal muscle weakness associated with metabolic complications.
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3. Aspalathin
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Aspalathin (PubChem CID: 11282394) is a natural C-glucosyl dihydrochalcone (3′-β-D-glucopyranosyl-2′,3,4,4′,6′- pentahydroxydihydrochalcone) with the molecular formula C21H24O11 (MW 452.412 g/mol) (Figure 2) [21]. Although aspalathin was known to be uniquely found in rooibos [22], recent evidence has shown that this C-linked dihydrochalcone glucoside can be detected in trace amounts in two other species of Acacia pendula [23]. Aspalathin is considered to have a poor bioavailability profile in different experimental settings as reviewed by Muller et al. [24] and Johnson et al. [25]. While Stalmach et al. [26], using high-performance liquid chromatography-mass spectrometry method, showed that O-methyl-aspalathin-O-glucuronide and eriodictyol-O-sulfate were the main metabolites excreted following ingestion of rooibos extract containing 10-fold higher levels of aspalathin in human subjects. In addition, a recent study by Bowles et al. [27] showed that aspalathin can be absorbed and metabolized to mostly sulfate conjugates detected in the urine of mice. However, additional evidence is required to establish the pharmacokinetic profile of aspalathin.
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Figure 2.
The chemical structure of aspalathin (3′-β-D-glucopyranosyl-2′,3,4,4′,6′- pentahydroxydihydrochalcone).
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Relevant to its biological activity, the initial evidence demonstrated that aspalathin possess strong antioxidant properties by scavenging 2,2-diphenyl-β-picrylhydrazyl (DPPH) radical in vitro [28]. This effect was important since experimental and clinical studies support the notion that drug compounds that enhance intracellular antioxidant properties can further exhibit a wide range of beneficial effects against the development of metabolic syndrome [29]. In addition to its robust antioxidant activity [28, 30, 31, 32, 33, 34], aspalathin can ameliorate inflammation [35, 36, 37, 38, 39], protect cardiac cells exposed to high glucose concentrations [40, 41, 42, 43, 44], and also display glucose lowering properties [45, 46, 47, 48, 49, 50]. In addition to work by our group [46, 48], studies conducted by Kawano et al. [51] and Son et al. [50] have reported on the effect of pure aspalathin or an aspalathin rich green rooibos extract on the signaling mechanisms that regulate glucose and lipid metabolism in skeletal muscle. Activation of 5\' AMP-activated protein kinase (AMPK), an important kinase in the regulation of energy production, as well as increasing the expression and translocation of glucose transporter (GLUT) 4 have been the key molecular targets by aspalathin in the skeletal muscle. Thus, although additional evidence such as assessing the therapeutic effect of this dihydrochalcone on skeletal muscle biopsies of insulin-resistant human subjects is still necessary, its aforementioned potential to target AMPK, and improve glucose uptake is of major importance for future therapeutic development.
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4. Berberine
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Berberine (PubChem CID: 2353) is a quaternary alkaloid (5,6-Dihydro-9,10-dimethoxybenzo[g]-1,3-benzodioxolo[5,6-a]quinolizinium) with the molecular formula C20H18 NO4+ (MW 336.37 g/mol) that is present in several plants including Hydrastis canadensis, Xanthorhiza simplicissima, Phellodendron amurense, and Berberis aristata (Figure 3) [52]. Berberrubine, thalifendine, demethyleneberberine, and jatrorrhizine are some of the major metabolites detected in plasma following the administration of berberine in rats, with the liver and intestinal bacteria identified to participate in the metabolism, and disposition of this compound in vivo [53]. Although a number of factors, including it being hydrophilic in nature and its containment of quaternary ammonium groups contribute to the low bioavailability of berberine [54]. Interestingly, the absorption of berberine in the small intestine can be enhanced by d-α-tocopheryl polyethylene glycol 1000 succinate [55]. Therefore, further research is required to better understand and inform on mechanisms that can add to our current knowledge on the bioavailability of berberine, which is crucial in improving its efficacy in vivo.
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Figure 3.
The chemical structure of berberine (5,6-dihydro-9,10-dimethoxybenzo[g]-1,3-benzodioxolo[5,6-a]quinolizinium).
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Berberine has a long history of medicinal use in traditional Chinese and Native American medicine [56] and has demonstrated a number of beneficial effects against metabolic complications, including amelioration of IR. Berberine demonstrated an enhanced effect to reduce body weight and raise plasma triglyceride levels while improving glucose tolerance and insulin action in both type 2 diabetic (db/db) mice and in FHD fed rats [57]. Interestingly, similar to aspalathin, an increase of glucose uptake through activation of AMPK as well as enhanced translocation of GLUT4 in skeletal muscle remains important in the ameliorative potential of berberine against IR [58, 59, 60, 61, 62]. However, it has been reported that berberine can alter muscle metabolism by altering mitochondrial function, resulting in the development of muscle atrophy in normal, and diabetic (db/db) mice [63]. Although the results were not in human subjects, these findings remain relevant since loss of muscle mass is an important feature that occurs in type 2 diabetic patients, especially in older individuals [64]. These results suggest that precaution should be taken when using these quaternary alkaloids, especially considering the toxicity of high doses [65]. In addition to acting by targeting the mitochondria [65], another mechanism by which berberine can reverse IR include downregulating toll-like receptor 4 (TLR4)/inhibitor of nuclear factor kappa-B kinase subunit beta (IKKbeta)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) inflammation signaling pathway, leading to reduced inflammation [66].
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5. Curcumin
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Curcumin, also known as diferuloylmethane (PubChem CID: 969516; (1E,6E)-1,7-Bis (4-hydroxy-3-methoxyphenyl) hepta-1,6-diene-3,5-dione), is a major polyphenolic derivative of turmeric (Curcuma longa) with the molecular formula C21H20O6 (MW 368.39 g/mol) (Figure 4) [67]. A single oral dose administration of curcumin can lead to the detection of its metabolites, glucuronide, and sulfate conjugates in plasma of human subjects [68]. Although is considered to have a safety profile, curcumin displays poor bioavailability profile that is coupled with quick metabolism and systemic removal [69]. However, recent developments such as blocking of metabolic pathways by concomitant administration with other agents, conjugation, and modification of structure, as well as modulation of route and medium of administration are some of the explored approaches to improve the bioavailability of curcumin as reviewed by Prasad et al. [70]. Indeed, increasing research over the past 30 years has focused on exploring the pharmacokinetics, safety profile, and efficacy of this natural product in order to enhance its therapeutic profile in humans [71].
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Figure 4.
The chemical structure of curcumin ((1E,6E)-1,7-bis(4-hydroxy-3-methoxyphenyl)hepta-1,6-diene-3,5-dione).
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An increasing number of reviews has been published to keep track of the cumulative literature informing on the therapeutic potential of curcumin, including anticancer, antioxidant, anti-inflammatory, and antibacterial activities [70, 71, 72]. Relevant to its effect on skeletal muscle function. A study published in 2005 by Farid et al. [73] showed that curcumin failed to inhibit NF-κB activity, leading to its inability to ameliorate loss of muscle mass in the soleus. However, in a follow-up study published in 2008, curcumin presented enhanced effect in blocking sepsis-induced muscle proteolysis, at least in part by inhibiting NF-κB, and p38 activities in rats [74]. In L6 or C2C12 myotubes exposed to high palmitate concentrations as a model of IR, curcumin reversed IR by increasing glucose and FFA oxidation, at least in part by mediating LKB1-AMPK pathways, as well as suppressing insulin receptor substrate 1 (IRS-1) Ser307 and protein kinase B (AKT) phosphorylation [75, 76, 77]. Although similar evidence has been supported by in vivo experiments on skeletal muscle tissue of either diabetic or nondiabetic rodents [75, 77], curcumin displays an enhanced capacity to protect against oxidative stress associated complications by improving mitochondrial biogenesis, and other antioxidant mechanisms [78, 79, 80, 81]. This involves activation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2) [82], an essential intracellular antioxidant response element that is a target of various natural products aiming to reduce metabolic disease-associated complications.
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6. Epigallocatechin gallate
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Epigallocatechin gallate (PubChem CID: 65064) is an ester of epigallocatechin and gallic acid ([(2R,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)chroman-3-yl] 3,4,5-trihydroxybenzoate, with the molecular formula C22H18O11 (MW 458.375 g/mol), that is abundantly found in tea (Figure 5) [83]. Due to the popularity of green tea and as one of its major components, epigallocatechin gallate remains one of the highly consumed polyphenolic compounds [84]. Although it is detectable in its original form in human plasma after oral administration [85], epigallocatechin gallate is considered to have very low oral bioavailability profile as reviewed by Mereles and colleagues [86]. Although additional evidence is required to improve its bioavailability, there has been an extensive exploration of this polyphenolic compound for its chemopreventive properties. Among the 10 polyphenols present in green tea, epigallocatechin gallate was found to exhibit the most antiproliferative and antiapoptotic effects [87].
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Figure 5.
The chemical structure of epigallocatechin gallate ([(2R,3R)-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)chroman-3-yl] 3,4,5-trihydroxybenzoate).
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It has already been established that epigallocatechin gallate can ameliorate complications linked with the development of the metabolic syndrome, by improving insulin sensitivity in both obese rodents and patients [88, 89, 90]. The enhanced therapeutic effect of this catechin has been associated with the modulation of various signaling pathways, including targeting of genes involved in cell survival, FFA regulation, mitochondrial energetics, intracellular antioxidant response, and others as reviewed by Singh and colleagues [91]. A number of studies have demonstrated several mechanisms associated with the ameliorative effect of epigallocatechin gallate on IR and associated complications in skeletal muscle. In addition to strengthening muscle integrity [92, 93, 94], accumulative data has been presented that this catechin can improve insulin sensitivity by enhancing glucose uptake, reduce lactate concentrations, enhancing mitochondrial capacity and stimulating beta-oxidation in cultured cells, or rodents as well as obese human subjects [95, 96, 97, 98, 99, 100]. Inhibition of oxidative stress, activation of AMPK, increased expression of PGC-1α, NAD-dependent protein deacetylase sirtuin-1 (SIRT1), nuclear respiratory factor 1, medium chain acyl coA decarboxylase, uncoupling protein 3 (UCP3), AKT, and peroxisome proliferator-activated receptor alpha (PPARα) are some of the mechanisms targeted by epigallocatechin to enhance skeletal muscle function in a diseased state [101, 102, 103, 104].
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7. Hesperidin
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Hesperidin (PubChem CID: 10621) is a flavanone glycoside ((2S)-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxy-2,3-dihydrochromen-4-one) with the molecular formula C28H34O15 (MW 610.565 g/mol) that is present in high amounts in citrus fruits (Figure 6) [105]. Although it has a low bioavailability due to the rutinoside moiety attached to the flavonoid [106], hesperidin can be converted to glucuronides and sulfoglucuronides, which have been shown to be excreted in urine nearly 24 hours after the orange juice ingestion [107]. In a randomized controlled trial, Nielsen et al. [108] demonstrated that removal of the rhamnose group to yield hesperetin-7-glucoside improved the bioavailability of the aglycone hesperetin. Suggesting that additional interventions are required to improve the bioavailability of citrus flavonoids such as hesperidin.
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Figure 6.
The chemical structure of hesperidin ((2S)-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxy-2,3-dihydrochromen-4-one).
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Increasing data has supported the notion that hesperidin possesses increased potential to lower raised blood glucose and lipid levels in various models of type 2 diabetes [109, 110, 111]. When administered in rats subjected to swimming exercise, this citrus flavonoid improved the biochemical and antioxidant profile of the animals [112]. This compound may induce its therapeutic effect through the regulation of genes implicated in insulin signaling such as insulin receptor substrate 1, GLUT2/4, and those linked with lipid metabolism, including sterol regulatory element–binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and acetyl-CoA carboxylase [113]. Although data on its effect on skeletal muscle is currently limited, it can reverse IR by reducing muscle glycogen content and ischemia–reperfusion injury while promoting myogenic differentiation through the activation of MyoD-mediated myogenin expression in cultured cells and animals [109, 114, 115].
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8. Luteolin
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Luteolin (PubChem CID: 5280445) is a flavone glycoside (2-(3,4-Dihydroxyphenyl)- 5,7-dihydroxy-4-chromenone) with the molecular formula C15H10O6 (MW 286.239 g/mol) that is rich in various dietary sources such as fruits, vegetables, and teas (Figure 7) [116]. As with most flavonoids, during its metabolism luteolin is broken down to its glucuronides, which can eventually pass through intestinal mucosa as shown by Yasuda and colleagues [117]. Although studies reporting on the pharmacokinetic profile of luteolin in human subjects are limited, this flavone is quickly absorbed in rats and can be detected in urine and feces while showing a slow elimination rate [118]. Furthermore, luteolin from peanut hull extract can be easily absorbed compared to the pure compound, with its absorption more efficient in the jejunum and duodenum than in the colon and ileum [119]. Alternatively, luteolin-loaded solid lipid nanoparticles prepared by hot microemulsion ultrasonic technique can also improve the solubility and increase the compound concentration in plasma of rats [120].
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Figure 7.
The chemical structure of luteolin (2-(3,4-dihydroxyphenyl)- 5,7-dihydroxy-4-chromenone).
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In addition to its strong antioxidant effects [121], in vitro experiments have provided evidence that luteolin possesses chemopreventive and anti-inflammatory properties [122, 123]. Hydroxyl groups and 2–3 double bond remain key structural features of luteolin that are linked to its enhanced therapeutic effect [124]. Recent studies show that this flavone attenuates hepatic steatosis and IR by upregulating PPARγ protein expression and activating AMPKα1 signaling, which may be linked to the improvement in circulating FFA levels in diet-induced obese mice [125, 126]. However, only a few studies have reported on the effect of luteolin on the skeletal muscle. Available literature has reported on its effect in preventing lipopolysaccharide-induced muscle atrophy, oxidative stress-induced tissue injury and inflammation, partly through regulation of atrogin-1/MAFbx expression, and c-Jun N-terminal kinases (JNK) phosphorylation reported on [127, 128, 129].
\n
\n
\n
9. Naringenin
\n
Naringenin (PubChem CID: 932) is a flavanone (5,7-dihydroxy-2-(4-hydroxyphenyl)chroman-4-one) with the molecular formula C15H12O5 (MW 272.256 g/mol) that is also predominantly found in citrus fruits (Figure 8) [130]. The chemical structure of naringenin comprises three hydroxy groups at the 4′, 5, and 7 carbons while its glycoside, naringin contains an additional disaccharide neohesperidose that is linked via its carbon end. Although naringenin can be detected as monoglucuronides in plasma and urine after ingestion of orange fruit juice in human subjects [131], the bioavailability of naringenin can be influenced by its glycosidic moiety. Felgines et al. [132] demonstrated that kinetics of absorption of naringenin and naringenin-7-glucoside was similar. In addition, naringenin-7-rhamnoglucoside exhibited a delay in its intestinal absorption, resulting in decreased bioavailability after ingestion in rats. On the other hand, complexation of naringenin with hydroxypropoyl-β-cyclodextrin has been another viable alternative to improve the bioavailability of naringenin, which is important to enhance its therapeutic potential [133].
\n
Figure 8.
The chemical structure of naringenin (5,7-dihydroxy-2-(4-hydroxyphenyl)chroman-4-one).
\n
Naringenin is among the well-studied citrus flavonoids shown to prevent complications associated with IR and the metabolic syndrome. Its role in preventing the deterioration in skeletal muscle mass and protecting against metabolic associated complication is summarized. In low-density lipoprotein (LDL) receptor–null (Ldlr−/−) mice fed HFD, this flavanone reduced fasting hyperinsulinemia, improved glucose utilization and increased insulin sensitivity through regulation of SREBP-1c–mediated lipogenesis [134]. It stimulated glucose uptake but failed to have a significant effect on basal or insulin-stimulated AKT phosphorylation while significantly increasing AMPK phosphorylation/activation in cultured L6 myotubes [135]. Bhattacharya and colleagues showed that naringenin stimulates glucose uptake, indicating a dependence on GLUT4 activity as well as phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and/or p38MAPK activity [136]. Maintenance of muscle mass by reducing muscle diacylglycerol content, improving hyperinsulinemia, promoting phosphorylation of p38/MAPK via estrogen receptor beta (ERβ), lowering reactive oxygen species (ROS) production, and enhancing tyrosine phosphorylation are other mechanisms associated with protective effect of naringenin in either cultured cells or in vivo animal models [137, 138, 139, 140].
\n
\n
\n
10. Quercetin
\n
Quercetin (PubChem CID: 5280343) is classified as a flavonol (2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one) with the molecular formula C15H10O7 (MW 302.238 g/mol) that is abundantly found in various fruits and vegetables (Figure 9) [141]. Quercetin is one of the most abundant dietary flavonoids that is rapidly metabolized to glucuronides and sulfates that can be detected in plasma and urine [142]. Although oral bioavailability of quercetin remains low, the type of sugar moiety attached to its structure may affect its absorption. This has been as demonstrated with quercetin glycosides from onion which have a higher absorption rate compared to apple-derived quercetin [143, 144]. Quercetin-4’-O-glucoside and quercetin-3-O-rutinoside (rutin) are one the accomplished glycosides of quercetin, and their absorption rate and extent can be influenced by plant matrix as demonstrated by Graefe and colleagues [145]. However, it is clear that further investigations into improvement strategies for pure quercetin aglycone are required to improve the therapeutic potential of this flavonol.
\n
Figure 9.
The chemical structure of quercetin (2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one).
\n
Quercetin exhibits a wide range of biological functions. Although Stewart et al. [146] failed to show any beneficial effect of quercetin against IR in diet induced-obese mice, other researchers have shown that this flavonol plays a major role in modulating several signaling pathways to reverse metabolic syndrome and improve skeletal muscle function, either in vitro on cultured cells or in vivo in animals and samples from human subjects [148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168]. In L6 myotubes and skeletal muscle of genetical modified (ob/ob) mice, quercetin improved insulin sensitivity by increasing GLUT4 expression [147]. Several studies using different experimental models have also demonstrated the positive effect of quercetin in improving skeletal muscle insulin sensitivity through enhanced uptake of glucose, and reducing oxidative stress or inflammation-induced damage, with modulation of tumor necrosis alpha (TNF-α), AKT, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and AMPK as prime pathways involved in the process [148, 149, 150, 151, 152, 153, 154, 155, 156, 157, 158]. The therapeutic potential of quercetin extends to its preventative effect against ischemia–reperfusion injury, as well as strengthening muscle fibers through the modulation of calcium homeostasis, and enhancing intracellular antioxidants [159, 160, 161, 162, 163, 164, 165, 166, 167, 168].
\n
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11. Resveratrol
\n
Resveratrol (PubChem CID: 445154) is a phytoalexin stilbenoid (3,5,4′-trihydroxy-trans-stilbene) with the molecular formula C14H12O3 (MW 228.247 g/mol) that is present in abundant amounts in various food sources such as grapes, blueberries, and red wine (Figure 10) [169]. Upon ingestion, resveratrol can be metabolized to form conjugated sulfates and glucuronides, namely resveratrol monosulfate, monosulfate dihydroresveratrol, and monoglucuronide dihydroresveratrol, as reviewed by Gambini and colleagues [170]. Although the bioavailability of resveratrol is considered low, it can vary depending on the method of administration and type of dietary source ingested [171]. The dimethyl ether analog of resveratrol, pterostilbene, has been shown to exhibit a higher bioavailability, in terms of total plasma levels of both the parent compound and metabolites than does resveratrol [172]. However, Li et al. [173] showed that intravenous and oral pharmacokinetic characteristics of trans-resveratrol can be improved through encapsulating with PP123 self-assembling lecithin-based mixed polymeric micelles. Suggesting that alternative methods to improve the bioavailability of resveratrol are required, which may translate to enhanced therapeutic potential in vivo.
\n
Figure 10.
The chemical structure of resveratrol (3,5,4′-trihydroxy-trans-stilbene).
\n
Resveratrol has displayed a variety of antidiabetic effects in rodent models. In addition, resveratrol attenuates thermal hyperalgesia, cold allodynia, as well as raised serum lipid levels [174, 175, 176]. In diabetic individuals, resveratrol administration is associated with significantly improved glucose and insulin control [177]. The systematic search of evidence linking resveratrol and IR in skeletal muscle revealed up to 18 studies published between 2007 and 2017, with 9 papers produced between 2016 and 2017, suggesting that this phytoalexin stilbenoid is increasingly explored for therapeutic effect against metabolic associated complications. Although Williams and colleagues showed no effect on insulin signaling pathways [178], stimulation of glucose uptake by resveratrol in cultured C2C12 cells or skeletal muscle has been linked with activation of extracellular signal-related kinase/p38/PI3K [179]. Its effect in promoting glucose uptake and improving insulin sensitivity was also associated with increased NAD-dependent protein deacetylase sirtuin-1 (SIRT1) expression, activation of AMPK while abolishing phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), JNK, and IκB kinase α/β (IKKα/IKKβ) [180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190]. Other documented beneficial effect of resveratrol includes inhibiting ischemia–reperfusion injury through its potent antioxidant properties [191], reducing cell proliferation through upregulating PGC-1α [192], promoting muscle regeneration and attenuating the impact of ROS [193], and elevated forearm skeletal muscle mitochondrial capacity [194].
\n
\n
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12. Rutin
\n
Rutin (PubChem CID: 5280805) is a glycoside combining the flavonol quercetin and the disaccharide rutinose (2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[α-L-rhamnopyranosyl-(1→6)-β- D-glucopyranosyloxy]-4H-chromen-4-one) with the molecular formula C27H30O16 (MW 610.521 g/mol) that is found in many plants and fruits, as well as tea infusions (Figure 11) [195]. Upon oral administration, rutin can be metabolized into sulfates and glucuronides of quercetin that are detected in blood, whereas unchanged forms of rutin and quercetin were not detected [142, 196]. Although quercetin glycosides from onions demonstrate an enhanced absorptive capacity than pure aglycones [143, 144], some studies have showed that rutin has a lower oral absorption rate than quercetin [142, 197]. However, as with the use of natural deep eutectic solvents [198], alternative methods to improve the absorptive capacity of rutin is tested to improve therapeutic effect in vivo.
\n
Figure 11.
The chemical structure of rutin (2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-3-[α-L-rhamnopyranosyl-(1→6)-β-D-glucopyranosyloxy]-4H-chromen-4-one).
\n
Like quercetin, rutin exhibits a wide variety of biological properties, mostly attributed to its strong antioxidant properties [199, 200]. It is accomplished that rutin displays enhanced potential to improve insulin sensitivity by regulating genes involved in glucose and lipid metabolism such as GLUT4, PPARγ, and tyrosine phosphatase 1B in cultured cells or skeletal muscle of rodents [201, 202, 203, 204]. However, from the study by Zyma et al. [205], that demonstrated that rutin induces conformational changes in the myosin structure of skeletal muscle of rabbits accompanied by an increase in ATPase activity, accumulative evidence has supported muscle strengthening capacity of this polyphenol. For example, Su et al. [206] presented data showing that rutin promoted skeletal muscle endurance capacity by modulating markers of mitochondrial biogenesis such as PGC-1α and SIRT1 expression in ICR mice subjected to a weight-loaded forced swim test. These findings were further supported by data showing that rutin increased the mitochondrial size and mitochondrial DNA content as well as gene expression related to mitochondrial biogenesis, such as PGC1-α, NRF-1, transcription factor A, and SIRT1 [207, 208].
\n
\n
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13. Sulforaphane
\n
Sulforaphane (PubChem CID: 5350) is an isothiocyanate (1-isothiocyanato-4-methylsulfinylbutane) with the molecular formula C6H11NOS2 (MW 177.28 g/mol) that is found in cruciferous vegetables such as cabbages, broccoli, and brussels sprouts (Figure 12) [209]. Although sulforaphane displays a dose-dependent pharmacokinetic behavior, as higher doses show reduced absorptive potential, lower doses of the compound can be rapidly absorbed in rats following intravenous administration, with the absolute bioavailability being able to reach 82% [210]. In human subjects consuming fresh broccoli sprouts or the broccoli sprout extract, with each estimated to provide 200 μmol sulforaphane daily, the compound metabolites were found to be three times higher in plasma and urine of sprout consumers, suggesting enhanced sulforaphane absorption from sprouts [211]. Therefore, dietary form and dosing schedule of sulforaphane may influence impact absorption and therapeutic potential in human subjects.
\n
Figure 12.
The chemical structure of sulforaphane (1-isothiocyanato-4-methylsulfinylbutane).
\n
Sulforaphane has received a considerable interest due to its ability to simultaneously control multiple cellular targets involved in various metabolic complications. For instance, in rats fed HFD, this isothiocyanate has displayed an enhanced hypoglycemic potential as well as the elevation of GLUT3 expression in the cerebral cortex and hypothalamus, leading to improved glucose tolerance [212]. Other studies [213, 214] have supported the beneficial effect of sulforaphane or its stable precursor glucoraphanin, to reverse IR, mostly through its robust antioxidant properties. In skeletal muscle, sulforaphane has exhaustive exercise-induced muscle damage, reducing muscle glycogen content, and enhanced exercise endurance capacity through inhibition of pro-inflammatory response and enhancing antioxidant response by upregulating NRF2 expression [215, 216, 217, 218, 219, 220].
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\n
\n
14. Conclusions
\n
Natural compounds have gained popularity for their potential beneficial effect to fight metabolic diseases due to their less adverse effect compared to synthetic drugs. Furthermore, natural compounds serve as a valuable source for the discovery of new drugs. Currently, knowledge shows that natural compounds can ameliorate IR, however, the gap in scientific evidence of plant-derived therapeutic benefits still exist due to the slow rate of translation of animal studies findings into human clinical trials. In this chapter, evidently reported the great potential and the future promise of natural compounds for the management and treatment of metabolic disorders, specifically IR, obesity, and T2D. Therefore, further research is required to assess the use of natural compounds alone or in combination with well know antidiabetic drugs might result in synergistic and enhanced effects in combating metabolic diseases.
\n
\n
Acknowledgments
\n
This work was supported by the Biomedical Research and Innovation Platform of the South African Medical Research Council (SAMRC) baseline funding and the South African National Research Foundation (NRF; grant number 87836 to SE Mazibuko-Mbeje). The grant holders acknowledge that opinions, findings, and conclusions or recommendations expressed in any publication generated by the SAMRC or NRF supported research are those of the authors, and that the SAMRC and NRF accept no liability whatsoever in this regard. PVD was partially supported as a Post-Doctoral Fellow by funding from the SAMRC.
\n
Conflicts of interests
The authors report no conflicts of interest. All authors are responsible for the content and writing of the chapter.
Abbreviations
AKT
protein kinase B
AMPK
5\' AMP-activated protein kinase
ATP
adenosine triphosphate
CD36
cluster of differentiation 36
DPPH
2,2-diphenyl-β-picrylhydrazyl
ERβ
estrogen receptor beta
FAS
fatty acid synthase
FFA
free fatty acid
GLUT
glucose transporter
HFD
high fat diet
IR
insulin resistance
IRS-1
suppressing insulin receptor substrate 1
JNK
c-Jun N-terminal kinases
LDL
low density lipoprotein
LKB1
serine/threonine kinase 11
MAPK
mitogen-activated protein kinase
MW
molecular weight
NF-κB
nuclear factor kappa-light-chain-enhancer of activated B cells
\n',keywords:"skeletal muscle, metabolic syndrome, insulin resistance, type 2 diabetes, natural products",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/62500.pdf",chapterXML:"https://mts.intechopen.com/source/xml/62500.xml",downloadPdfUrl:"/chapter/pdf-download/62500",previewPdfUrl:"/chapter/pdf-preview/62500",totalDownloads:614,totalViews:211,totalCrossrefCites:2,totalDimensionsCites:3,hasAltmetrics:0,dateSubmitted:"April 6th 2018",dateReviewed:"May 14th 2018",datePrePublished:"November 5th 2018",datePublished:"October 10th 2018",dateFinished:null,readingETA:"0",abstract:"Natural compounds, especially polyphenols have become a popular area of research mainly due to their apparent health benefits. Increasing the phenolic content of a diet, apart from its antioxidant benefit, has a beneficial effect on signaling molecules involved in carbohydrate and lipid metabolism. These effects could potentially protect against metabolic syndrome, a cluster of metabolic complications such as obesity, insulin resistance and type 2 diabetes that is characterized by a dysregulated carbohydrate, and lipid metabolism. Research continues to investigate various natural compounds for their amelioration of impaired signaling mechanisms that may lead to dysregulated metabolism to find means to improve the life expectancy of patients with metabolic syndrome. In this chapter, a systematic search through major databases such as MEDLINE/PubMed, EMBASE, and Google Scholar of literature reporting on the ameliorative potential of commonly investigated natural products that target skeletal muscle to ameliorate metabolic syndrome associated complications was conducted. The selected natural products that are discussed include apigenin, aspalathin, berberine, curcumin, epigallocatechin gallate, hesperidin, luteolin, naringenin, quercetin, resveratrol, rutin, and sulforaphane.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/62500",risUrl:"/chapter/ris/62500",book:{slug:"muscle-cell-and-tissue-current-status-of-research-field"},signatures:"Sithandiwe Eunice Mazibuko-Mbeje, Phiwayinkosi V. Dludla,\nBongani B. Nkambule, Nnini Obonye and Johan Louw",authors:[{id:"229061",title:"Dr.",name:"Sithandiwe",middleName:"Eunice",surname:"Mazibuko-Mbeje",fullName:"Sithandiwe Mazibuko-Mbeje",slug:"sithandiwe-mazibuko-mbeje",email:"sithandiwe.mazibuko@mrc.ac.za",position:null,institution:{name:"South African Medical Research Council",institutionURL:null,country:{name:"South Africa"}}}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Apigenin",level:"1"},{id:"sec_3",title:"3. Aspalathin",level:"1"},{id:"sec_4",title:"4. Berberine",level:"1"},{id:"sec_5",title:"5. Curcumin",level:"1"},{id:"sec_6",title:"6. Epigallocatechin gallate",level:"1"},{id:"sec_7",title:"7. Hesperidin",level:"1"},{id:"sec_8",title:"8. Luteolin",level:"1"},{id:"sec_9",title:"9. Naringenin",level:"1"},{id:"sec_10",title:"10. Quercetin",level:"1"},{id:"sec_11",title:"11. Resveratrol",level:"1"},{id:"sec_12",title:"12. Rutin",level:"1"},{id:"sec_13",title:"13. Sulforaphane",level:"1"},{id:"sec_14",title:"14. Conclusions",level:"1"},{id:"sec_15",title:"Acknowledgments",level:"1"},{id:"sec_18",title:"Conflicts of interests",level:"1"},{id:"sec_17",title:"Abbreviations",level:"1"}],chapterReferences:[{id:"B1",body:'Garg N et al. Natural products as mediators of disease. Natural Product Reports. 2017;34(2):194-219\n'},{id:"B2",body:'Ansari N, Khodagholi F. Natural products as promising drug candidates for the treatment of Alzheimer\'s disease: Molecular mechanism aspect. 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An examination of resveratrol\'s mechanisms of action in human tissue: Impact of a single dose in vivo and dose responses in skeletal muscle ex vivo. PLoS One. 2014;9(7):e102406\n'},{id:"B179",body:'Deng JY et al. Activation of estrogen receptor is crucial for resveratrol-stimulating muscular glucose uptake via both insulin-dependent and -independent pathways. Diabetes. 2008;57(7):1814-1823\n'},{id:"B180",body:'Bruckbauer A et al. Synergistic effects of leucine and resveratrol on insulin sensitivity and fat metabolism in adipocytes and mice. Nutrition & Metabolism (London). 2012;9(1):77\n'},{id:"B181",body:'Goh KP et al. Effects of resveratrol in patients with type 2 diabetes mellitus on skeletal muscle SIRT1 expression and energy expenditure. International Journal of Sport Nutrition and Exercise Metabolism. 2014;24(1):2-13\n'},{id:"B182",body:'Sin TK et al. SIRT1-dependent myoprotective effects of resveratrol on muscle injury induced by compression. Frontiers in Physiology. 2015;6:293\n'},{id:"B183",body:'Frendo-Cumbo S, MacPherson RE, Wright DC. Beneficial effects of combined resveratrol and metformin therapy in treating diet-induced insulin resistance. Physiological Reports. 2016;4(15):e12877\n'},{id:"B184",body:'Gospin R et al. Resveratrol improves insulin resistance with anti-inflammatory and “browning” effect in adipose tissue of overweight humans. JIM. 2016;64:814-815\n'},{id:"B185",body:'Dugdale HF et al. The role of resveratrol on skeletal muscle cell differentiation and myotube hypertrophy during glucose restriction. Molecular and Cellular Biochemistry. 2018;444(1-2):109-123\n'},{id:"B186",body:'Godínez Salas ET et al. Effect of the bioactive compounds genistein and resveratrol on insulin resistance in patients with metabolic syndrome. The FASEB Journal. 2017;31(1)\n'},{id:"B187",body:'Sadeghi A et al. Resveratrol ameliorates palmitate-induced inflammation in skeletal muscle cells by attenuating oxidative stress and JNK/NF-kappaB pathway in a SIRT1-independent mechanism. Journal of Cellular Biochemistry. 2017;118(9):2654-2663\n'},{id:"B188",body:'Sung MM et al. Resveratrol improves exercise performance and skeletal muscle oxidative capacity in heart failure. American Journal of Physiology. Heart and Circulatory Physiology. 2017;312(4):H842-h853\n'},{id:"B189",body:'Tran HT et al. Resveratrol ameliorates the chemical and microbial induction of inflammation and insulin resistance in human placenta, adipose tissue and skeletal muscle. PLoS One. 2017;12(3):e0173373\n'},{id:"B190",body:'Zheng J et al. Resveratrol improves insulin resistance of catch-up growth by increasing mitochondrial complexes and antioxidant function in skeletal muscle. Metabolism. 2012;61(7):954-965\n'},{id:"B191",body:'Elmali N et al. Effects of resveratrol on skeletal muscle in ischemia-reperfusion injury. Ulusal Travma ve Acil Cerrahi Dergisi. 2007;13(4):274-280\n'},{id:"B192",body:'Kaminski J et al. Dietary resveratrol modulates metabolic functions in skeletal muscle cells. Journal of Food and Drug Analysis. 2012;20(Suppl 1):398-401\n'},{id:"B193",body:'Bosutti A, Degens H. The impact of resveratrol and hydrogen peroxide on muscle cell plasticity shows a dose-dependent interaction. Scientific Reports. 2015;5:8093\n'},{id:"B194",body:'Polley KR et al. Influence of exercise training with resveratrol supplementation on skeletal muscle mitochondrial capacity. Applied Physiology, Nutrition, and Metabolism. 2016;41(1):26-32\n'},{id:"B195",body:'PubChem Compound Database CID: 5280805. National Center for Biotechnology Information. Available from: https://pubchem.ncbi.nlm.nih.gov/compound/5280805. [Accessed: 11 January 2018]\n'},{id:"B196",body:'Yang C et al. Bioavailability and metabolic pharmacokinetics of rutin and quercetin in rats. Journal of Food and Drug Analysis. 2005;13(3):244-250\n'},{id:"B197",body:'Manach C et al. Bioavailability of rutin and quercetin in rats. FEBS Letters. 1997;409(1):12-16\n'},{id:"B198",body:'Faggian M et al. Natural deep eutectic solvents (NADES) as a tool for bioavailability improvement: Pharmacokinetics of rutin dissolved in proline/glycine after oral administration in rats: Possible application in nutraceuticals. Molecules. 2016;21(11):1531\n'},{id:"B199",body:'Yang J, Guo J, Yuan J. In vitro antioxidant properties of rutin. LWT - Food Science and Technology. 2008;41(6):1060-1066\n'},{id:"B200",body:'Gatineau E et al. Chronic intake of sucrose accelerates sarcopenia in older male rats through alterations in insulin sensitivity and muscle protein synthesis. The Journal of Nutrition. 2015;145(5):923-930\n'},{id:"B201",body:'Cai Y et al. Effects of rutin on the expression of PPARgamma in skeletal muscles of db/db mice. Planta Medica. 2012;78(9):861-865\n'},{id:"B202",body:'Lee DG et al. Effect of rutin from tartary buckwheat sprout on serum glucose-lowering in animal model of type 2 diabetes. Acta Pharmaceutica. 2016;66(2):297-302\n'},{id:"B203",body:'Hsu CY et al. Rutin potentiates insulin receptor kinase to enhance insulin-dependent glucose transporter 4 translocation. Molecular Nutrition & Food Research. 2014;58(6):1168-1176\n'},{id:"B204",body:'Kappel VD et al. Rutin potentiates calcium uptake via voltage-dependent calcium channel associated with stimulation of glucose uptake in skeletal muscle. Archives of Biochemistry and Biophysics. 2013;532(2):55-60\n'},{id:"B205",body:'Zyma VL et al. Interaction of flavonoid compounds with contractile proteins of skeletal muscle. General Physiology and Biophysics. 1988;7(2):165-175\n'},{id:"B206",body:'Su KY et al. Rutin, a flavonoid and principal component of Saussurea involucrata, attenuates physical fatigue in a forced swimming mouse model. International Journal of Medical Sciences. 2014;11:528-537\n'},{id:"B207",body:'Seo S et al. Rutin increases muscle mitochondrial biogenesis with AMPK activation in high-fat diet-induced obese rats. Nutrients. 2015;7(9):8152-8169\n'},{id:"B208",body:'Nieman DC et al. Quercetin\'s influence on exercise performance and muscle mitochondrial biogenesis. Medicine and Science in Sports and Exercise. 2010;42(2):338-345\n'},{id:"B209",body:'PubChem Compound Database CID: 5350. National Center for Biotechnology Information. Available from: https://pubchem.ncbi.nlm.nih.gov/compound/5350. [Accessed: 12 January 2018]\n'},{id:"B210",body:'Hanlon N et al. Absolute bioavailability and dose-dependent pharmacokinetic behaviour of dietary doses of the chemopreventive isothiocyanate sulforaphane in rat. The British Journal of Nutrition. 2008;99(3):559-564\n'},{id:"B211",body:'Atwell LL et al. Absorption and chemopreventive targets of sulforaphane in humans following consumption of broccoli sprouts or a myrosinase-treated broccoli sprout extract. Molecular Nutrition & Food Research. 2015;59(3):424-433\n'},{id:"B212",body:'Souza CG et al. Chronic sulforaphane oral treatment accentuates blood glucose impairment and may affect GLUT3 expression in the cerebral cortex and hypothalamus of rats fed with a highly palatable diet. Food & Function. 2013;4(8):1271-1276\n'},{id:"B213",body:'Nagata N et al. Glucoraphanin ameliorates obesity and insulin resistance through adipose tissue browning and reduction of metabolic endotoxemia in mice. Diabetes. 2017;66(5):1222-1236\n'},{id:"B214",body:'Fu J et al. Divergent effects of sulforaphane on basal and glucose-stimulated insulin secretion in beta-cells: Role of reactive oxygen species and induction of endogenous antioxidants. Pharmaceutical Research. 2013;30(9):2248-2259\n'},{id:"B215",body:'Malaguti M et al. Sulforaphane treatment protects skeletal muscle against damage induced by exhaustive exercise in rats. Journal of Applied Physiology. 2009;107(4):1028-1036\n'},{id:"B216",body:'Fan H et al. Sulforaphane causes a major epigenetic repression of myostatin in porcine satellite cells. Epigenetics. 2012;7(12):1379-1390\n'},{id:"B217",body:'Whitman SA et al. Nrf2 modulates contractile and metabolic properties of skeletal muscle in streptozotocin-induced diabetic atrophy. Experimental Cell Research. 2013;319(17):2673-2683\n'},{id:"B218",body:'Sun CC et al. Sulforaphane attenuates muscle inflammation in dystrophin-deficient mdx mice via NF-E2-related factor 2 (Nrf2)-mediated inhibition of NF-kappaB signaling pathway. The Journal of Biological Chemistry. 2015;290(29):17784-17795\n'},{id:"B219",body:'Oh S et al. Nuclear factor (erythroid derived 2)-like 2 activation increases exercise endurance capacity via redox modulation in skeletal muscles. Scientific Reports. 2017;7\n'},{id:"B220",body:'Uruno A et al. Nrf2-mediated regulation of skeletal muscle glycogen metabolism. Molecular and Cellular Biology. 2016;36(11):1655-1672\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Sithandiwe Eunice Mazibuko-Mbeje",address:"sithandiwe.mazibuko@mrc.ac.za",affiliation:'
Biomedical Research and Innovation Platform, South African Medical Research Council, South Africa
Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, South Africa
'},{corresp:null,contributorFullName:"Phiwayinkosi V. Dludla",address:null,affiliation:'
Biomedical Research and Innovation Platform, South African Medical Research Council, South Africa
'},{corresp:null,contributorFullName:"Bongani B. Nkambule",address:null,affiliation:'
School of Laboratory Medicine and Medical Sciences (SLMMS), College of Health Sciences, University of KwaZulu-Natal, South Africa
Biomedical Research and Innovation Platform, South African Medical Research Council, South Africa
Department of Biochemistry and Microbiology, University of Zululand, South Africa
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1. Introduction: conceptualizing health promotion
According to Tannahill [1], health promotion is an umbrella term covering overlapping fields of health education, prevention and attempts to protect public health through social engineering, legislations, fiscal measures and institutional policies which entail the combination of the best in terms of both theory and practice from a wide range of expert groups (educationists, behavioral scientists, medical practitioners) and non-professionals including the communities involved. For him, health promotion stems largely from a new focus for health services that recognize some basic facts: many contemporary health problems are preventable or avoidable through lifestyle change; modern technology is a bundle of mixed blessings bringing both benefits and risks to health; medical technology is at the phase of diminishing returns (losing efficacy and connection to ordinary people); such non-medical factors as better nutrition, improved living conditions and public health measures have contributed to both health and longevity even more than medical measures; that doctors can cause as well as cure disease; and increasing public desire to attain better or improved quality of life and at the same time demystifying and demedicalising the attainment (achievement) of good health [1].
For the World Health Organization (WHO), health promotion is essentially about engendering a context in which the health and well-being of whole populations or groups are owned mainly by the people concerned, i.e., enabling citizens of local communities to achieve political control and determination of their health [2, 3]. Therefore, health promotion goes beyond mere healthcare but puts health on the policymaking agenda in all sectors and at all levels, directing policymakers to be cognisant or conscious of the health consequences of their decisions and accept responsibilities for health.
Health promotion can be seen as the whole process of enabling or empowering people to increase control over and improve their overall health. It focuses on creating awareness of health issues, engendering behaviour modification consistent with prevention and attitudes to ill health and motivating increased usage of available health facilities. In the pursuit of good health (physical, mental and social well-being), individuals and groups through health promotion are enabled to identify and realize aspirations, satisfy needs and change or cope with the environment in manners consistent with complete good health.
Health promotion is expected to contribute to programme impact by enabling prevention of disease, reduction of the risk factors or behaviors associated with given diseases, promoting and fostering lifestyles and conditions that are conducive to good health and enabling increasing use of available health facilities. Therefore, health promotion creates both the awareness and conscientisation that leads to disease prevention, control of health situations and usage of health services and facilities. It implies individual and collective control and participation in health focusing on behavioral change, socio-economic lifestyles and the physical environment.
Without doubt the WHO’s Ottawa Charter definition of health promotion is very comprehensive and encompasses the core values and guiding objectives of health promotions [3]. It summarily sees health promotion as the process of enabling people to increase control over and improve their health. In line with the above definition, Macdonald and Davies [4] contend that it calls attention to the critical role of the concepts of process and control as the real essence of health promotion. For them, “the key concepts in this definition are ‘process’ and ‘control’, and therefore effectiveness and quality assurance in health promotion must focus on enablement and empowerment. If the activity under consideration is not enabling and empowering it is not health promotion” [4], p. 6.
As the burgeoning literature on health promotion over the years indicate it is a community-driven (inspired), multifaceted and multidisciplinary area of concern that also involves critical sociopolitical, economic and environmental elements and dynamics (see [4, 5, 6, 7, 8, 9, 10]).
It is important to also understand that even though one can make a distinction between public health and health promotion, in reality both are interconnected and hardly practically separable. In other words, public health is built on health promotion and health promotion is imperative for public health delivery. As has been argued, public health “is synonymous with health promotion in that it aims to implement co-ordinated community action to produce a healthier society” [11], p. 315.
There is no gainsaying the fact that health promotion nowadays has an overwhelming sociopolitical component that is really definitive. In fact, as has been posited, “health promotion activities are by their nature inherently politically based and driven, thus making it impossible to divorce them from the political arena” [11], p. 314. Health promotion becomes a dynamic area of interface between public policy institutions (the state and its agencies), the public (community/people) and the professionals (ranging from the media professionals, public health advocates, social workers to medical practitioners).
The chapter depended on the desk review of extant literature and documents for its information. The main exclusionary criteria in this regard were materials not related to health promotion and materials published before 1984, which were considered extreme-dated. The inclusive criteria were determined by such concepts as public health, public health in Africa, health promotion, health education and awareness and theories and models in health promotion. Such prominent Internet information sites like the WHO, American Public Health Association (APHA), Health Resources and Services Administration (HRSA) and the Universitats Bibliothek Leipzig (UBL) Online Resources were utilized in gathering materials for the chapter.
2. Theories and models of health promotion
There is no gainsaying the fact that effective and result-oriented health promotion practice depends on sound theory [12]. In other words, theory becomes very informative of health promotion practice and activities. In recognition of the above, one would examine briefly the main theories that have implicated health promotion globally. It is important, however, to state here that the choice of a theory or model to guide health promotion should be determined largely by the specific nature of the health issue being addressed, the community or population in view and the sociopolitical context in question. This is because theories and models are simply used in practice in order to plan health programmes, explain and understand health behaviour as well as underpin the identification of appropriate intervention and implement such intervention in ways that are both effective and sustainable.
Despite a plethora of theories and models utilized in health promotion, I will only focus on five of the most popular and commonly used. These are ecological models of health promotion, the Health Belief Model (HBM), Stages of Change Model or the Trans-theoretical Model, Theory of Reasoned Action or Planned Behaviour and the Social Cognitive Theory.
2.1 The ecological models of health promotion
As the name implies, these models focus on the interaction of people with their physical and sociocultural environments. The approach thus recognizes that there are multiple levels of influence on health and health behaviour especially the health seeking behaviour and choices that people make. The ecological models are anchored on five overriding influences which determine and guide health behaviour and response to health issues [13, 14, 15, 16]. These influences are intrapersonal or individual factors (these impact on individual behaviour, e.g., beliefs, knowledge, attitude, etc.); interpersonal factors (these are produced through living with and interacting with other people, e.g., family, friends and social groups/networks; these other people can function as both the source of solidarity and support as well as sources of barriers and constraints to health-promoting behaviour of the individual, e.g., dwelling among chronic smokers or having intense interaction with them may expose one to the dangers of either smoking or the influence of second-hand smoke); community factors (these make reference to social norms that are shared by groups or communities, and such norms whether formal or informal can influence health behaviour and health seeking behaviour of the individual and group members, e.g., relationship between institutions, groups and organizations); institutional factors (policies, rules, regulations and institutional structures that may constrain or even promote healthy behaviour in a given society, e.g., the workplace and voluntary organizations to which the individual belongs are prime examples); public policy factors (policies at different level of governance that regulate, structure or support actions and practices targeted at health outcomes like disease prevention policies and structures enabling early detection, control or response and management of health crisis in the society; these stem from the position of the government and are critical in achieving the goals of public health delivery) (Figure 1).
Figure 1.
Ecological models of health promotion (simplified).
As the above pyramid, suggests the individual, interpersonal and community factors are at the base. These factors therefore exert more influence and pressure over the individual’s health behaviour than the institutional and public policy factors as these are more important. In other words, the institutional and public policy factors are literally far from the individual and do not exert as much pressure on his behaviour as those factors that are very close to him both spatially and otherwise. In an age of increasing pessimism in government, people are much driven by interpersonal and community factors than what comes from a typical further off entity.
Given the above, it is obvious that the ecological approach is very pertinent in the understanding of the range of factors that influence people’s health. Its main strength is that it can provide what is called a complete perspective on factors that affect health behaviour and response to health issues especially the role of social and cultural factors or normative patterns on health in the society. It is perhaps very well suited to health intervention and practice in developing societies with an overbearing influence of sociocultural factors on behaviour, attitudes and practice of the people.
2.2 The health belief model (HBM)
This is a theoretical model that has been found useful in guiding both health promotion and strategies for disease prevention. As the name suggests, it focuses on individual beliefs about specific health conditions which predict or direct individual health behaviour [17, 18]. The specific components of this belief that influence health behaviour include perceived susceptibility to the disease; perceived severity of the disease in question; perceived benefits of action (positive benefits of such action) as well as cues to action (awareness of factors that engender action); self-efficacy (belief that action would lead to success); and perceived barriers or obstacles to action (especially if such obstacles are seen as daunting or insurmountable or otherwise).
In the utilization of the HBM in health promotion, there are five main action-related segments that would help in identifying key decision-making points and thus facilitate the utilization of knowledge in guiding health intervention. These are: collection of information (through needs assessments; rapid rural appraisal, etc. in order to determine those at risk of the disease or affliction and specify which population or component of the population to be targeted in the intervention); conveying in unambiguous and clear terms the likely consequences of the health issue in question and its associated risk behaviors in order to facilitate a clear apprehension of its severity; communication (getting information to the target population on the recommended steps to take and the perceived or likely benefits of the recommended action); provision of needed assistance (help the people in both the identification of and reduction of barriers or constraints to action); and demonstration (actions and activities that enable skill development and support aimed at enhancing self-efficacy and increased chances of successful behaviour modification targeted at the health issue in question) (Figure 2).
Figure 2.
Health belief model (HBM).
In Africa, the HBM has been very useful in understanding people’s response and behaviour to HIV/AIDS and other chronic diseases. Being a society very flushed with beliefs, the degree of responsiveness to a health situation is often the direct product of a set of beliefs held by the individual and/or by his immediate community.
2.3 Stages of change model (aka trans-theoretical model)
This model is focused on examining and explaining the individual’s readiness to change his behaviour and sees such change as occurring or happening in successive stages. It therefore adopts a quasi-evolutionary framing of behaviour change in which behaviour change, sustenance and termination are encompassed in six stages. These stages are pre-contemplation (existence of no intention to take any action by the individual); contemplation (thinking about taking action and ruminating on plans to do this soon); preparation (signifies intention to take action and includes the possibility that some steps or preliminary steps to action have been taken already); action (discernible change in behaviour for a brief period of time); maintenance (sustenance of the action taken; behaviour change that is maintained in the long run or long-term behaviour change); and termination (the expressed and discernible desire never to return to prior negative behaviour by the individual concerned).
The above stages are very important in planning behaviour change or modification and recognize that behaviour change is both gradual and takes time. What is needed from the health promoter is that at each of these stages specific interventions or programmes are devised to help the individual progress to the next stage. Also, the recognition that the model may in reality be cyclical rather than lineal, i.e., individuals may progress to the next stage or even regress to previous or lower stages, is important in planning health promotion interventions utilizing this model. It also calls attention to understanding that there are individual differences in the adoption of change, i.e., some people may be swift in behaviour modification, while others may take longer time; but each needs support in order to pull through.
2.4 Theory of reasoned action (theory of planned action)
The main contention of this theory is that an individual’s health behaviour is usually determined by his intention to exhibit or display a given behaviour. Therefore, the intention to exhibit a given behaviour (or behaviour intention) is predicated upon or predicted by two main factors, viz. personal attitude to the behaviour in question and subjective or personal norms (an individual’s social and environmental context and the perception the individual has over that behaviour) related to that behaviour.
The basic assumption here is that both positive attitudes and positive subjective norms will generate greater perceived control of behaviour and increase the chances of intentions towards changes in behaviour. The theory generally provides information that can be used in predicting people’s health behaviour and thus in planning and driving through health interventions. It anchors in recognizing the predictors of behaviour-oriented action and the need for supportive social and environmental contexts that facilitate and sustain desirable health behaviour.
2.5 The social cognitive theory (SCT)
This theory combines both the cognition of the individual and the social context of the individual in offering explanation and understanding of health behaviour and response. It seeks to describe the influence of the experience of the individual, his perception of the actions of other people near him and the factors in the person’s immediate environment on health behaviour of the individual. It moves from this general perspective to provide opportunities for social support (defined as conducive to healthy behaviour) and reinforcements that generate behaviour change or modification. In this sense, the SCT depends on the idea of reciprocal determinism which denotes the continuing or uninterrupted interaction among the person’s characteristics, his behaviour and the social context or environment in which the behaviour takes place.
However, the best way to appreciate the SCT is to examine the main components the theory isolates as related to behaviour change at the individual level. These are self-efficacy (belief in one’s ability to control and execute behaviour within a given context); behaviour capability (thorough comprehension of behaviour and the ability to exhibit or perform it); expectations (outcomes or outputs of the behaviour change in question); expectancies (the assignation of value to the above outcome of behaviour and which is important in sustaining the behaviour); self- control (the regulation and monitoring of behaviour of the individual); observational learning (the act of watching others performing the desired behaviour and the outcomes therein as well as modeling that behaviour in question); and reinforcements (incentives and rewards seen as eliciting, encouraging and sustaining behaviour change in the individual) [19].
The three components as the above diagram shows reinforce each other and in the process condition and determine behaviour of the individual even in the context of health as well as choices made therein (Figure 3). The SCT is very pertinent in contexts where desirable health outcomes can be achieved by behaviour modification or change. For instance, certain chronic diseases or health conditions can be tackled through healthy lifestyles and dieting that reduce risk factors and chances of individuals succumbing to such conditions. Therefore, the theory can help frame intervention programmes in this area that focus on changing people’s behaviour and in the process achieve desirable health outcomes.
Figure 3.
Illustration of the social cognitive theory (SCT).
Theories and perspectives or models as already indicated are critical in providing explanations of a problem or issue (broadening our understanding and perspective as it were) and also very important in the effort to tackle a given problem or issue in the society especially by way of developing and implementing programmes and interventions. Perhaps, the above underscores why some scholars [20, 21, 22] would highlight the difference between the so-called theories of the problem and theories of action, meaning that while the former aids our apprehension of a given issue or social reality, the latter is important in terms of taking actions or evolving activities to tackle the issue in question.
3. Health promotion as sociopolitical engagement
Health promotion generally implicates a huge element of politics and power dynamics in the sense that only political will and cognition can build discernible changes in health. Lobbying and advocacy are critical tools of health promotion and function within the political arena. The sociopolitical contexts and influences are especially recognizable in the public health sector in the developing world where political will and doggedness are often necessary to drive through even the most salutary change or innovation in the health sector. Also, political forces are equally dominant in the provision of crucial health infrastructure and facilities as well as the reasonable funding demanded by any effective public health system. As Harrison opines health promotion “requires concerted, sophisticated and integrated political action to bring about change and requires professionals concerned with public health to engage with the politics of systems and organizations” [5], 165.
Therefore, health promotion seeks to empower and transform communities by getting them involved in activities that influence public health especially through agenda setting, lobbying and advocacy, consciousness raising and social education [11, 22]. All these are accomplished on terms that are either defined or strictly affected by the socio-economic realities of the people themselves. By its emphasis on the community, health promotion has a heavy sociological frame that prioritizes the values of society as well as mobilization and solidarity in the quest for good and sustainable health. It thus makes assumption that individual members of the society would give equal weight to their own health and the health of their neighbors. In other words, it is often anchored on the uncanny assumption that the health of the individual member of a given society is intertwined with the health of the community as a collective. This means the reference point of health promotion is that one’s health is as good as the health of the members of the community or society as a whole, i.e., common health destiny. Therefore, such things as community empowerment, community competence and overwhelming sense of community are all apprehended as contributing to the health of the communities [23].
4. Approaches to health promotion
Traditionally there are five approaches utilized in health promotion. These are medical (the focus here is to make people free from medically defined diseases and afflictions; it is mainly anchored on prevention strategies and the role of the medical practitioner or expert in ensuring that the patients comply with recommendations); behavioural change (behaviour modification approach that recognizes that people’s behaviour and lifestyles can be changed in order to enable them attain good health, i.e., facilitate adoption of healthy lifestyle); educational (provision of information and knowledge that enable understanding of health issues and build awareness for informed decision-making and choice among people); client-centred (in this situation health practitioners work with clients in order to identify what they know about a given disease and take appropriate action; emphasis on perceiving the client as equal and building the clients self-empowerment that enable them make good choices and control their health outcomes); and societal change (the focus here is on the society or community rather than the individual and seeks to change or modify both the physical and social environments in order to make them consistent with or conducive to good health).
The conventional health promotion methods (modes of operationalizing health promotion and achieving its goals) include health education (the conscious and systematic effort at providing education or knowledge to people on particular and general aspects of health; it is about enabling people through proper and right knowledge on what to do and how to do it; it is empowering and improving people’s capacity to act with regard to their health issues and conditions), information, communication (the above three are often captured in the popular acronym IEC), social mobilization, mediation, community theater and advocacy and lobbying. However, while these methods are okay in differing contexts, a decision on the specific medium to use should be guided by both environment (community conditions) and the nature of the health issue involved. The use of more than one method in any given case is highly recommended especially in Africa where there are broad inequalities in access to social goods and the media. The increasing use of social media especially among young Africans calls attention to their deployment equally in core health promotion. Social media platforms like WhatsApp and blogs can be very potent in this regard.
5. Health promotion research in Africa
There is an undeniable need to give high priority to health promotion research in Africa. Such research should aim at enabling a realistic and focused achievement of the goals of health promotion. Broadly, health promotion aims inter alia at:
The prevention of communicable and non-communicable diseases
The reduction of risk factors associated with diseases
The fostering of lifestyles and conditions in the general population that are consistent with overall well-being or good health
The effective/maximal utilization of existing health services and stimulating demand for others where/when necessary
According to the WHO [24] Health Promotion Strategy for the African Region, the contributions of health promotion to the achievement of health objectives include increasing individual knowledge and skills especially through IEC; strengthening community action through the use of social mobilization; enabling the emergence of environments supportive and protective of health by making optimal use of mediation and negotiation; enabling the development of public policies, legislation and fiscal controls which enhance and support health and overall development using advocacy and lobbying; and making prevention and consumer needs the core focus of health services delivery. All these can be positively influenced by research and studies which evaluate the effectiveness of what has been done as well as explore new strategies suitable to the socio-environmental context in question.
However, while research is very critical to achieving the goals of health promotion, it should be concise and focus essentially on the priority health programmes which have been identified by the WHO for the continent. Some of such programmes include the Global Fund for Malaria, HIV/AIDS and Tuberculosis, Immunization, Mental Health, the Tobacco Free Initiative and Reproductive Health as well as the fight against recurrent scourge of Ebola, etc. Such research should focus on identifying effective health promotion approaches and communication media to embody and convey the outcomes to communities through community participation; the extent or effectiveness of these means and seeking to still improve overall programme effectiveness and sustainability. Therefore, health promotion research should focus on ascertaining goals/outcomes of health promotion (to guide policy), provide reliable conditions associated with these outcomes or goals, precisely define the changes intended and delineate reliable mechanisms and indicators of M and E of health promotion strategies in specific country/community contexts.
The importance of research is essentially derived from the fact that it calls attention to the need for verification and evidence-based activities in health promotion. These are without doubt the ways of knowing if real empowerment and enabling has been achieved in the process. Thus,
Health promotion is about enabling people to improve their health; and secondly, evidence relevant to health promotion should bear directly on factors that support or prevent enablement and empowerment (determinants of health) activities that support enablement and empowerment (health promotion) and assessing whether these activities have been successful (evaluation of health promotion). [25], p. 357
The above clearly suggest that health promotion should be anchored on evidence or should rest on experience and reality regarding what works or what is possible and effective in any context. In this manner, “evidence-based health promotion involves explicit application of quality research evidence when making decisions” [26], p. 126. Research is even more foundational in health promotion since health promotion efforts need to be anchored on agreed definitions and values of health promotion. As Seedhouse contends the failure to be explicit about definitions and values generates conceptual confusion in research as well as sloppy practice [27].
The evaluation of health promotion which should be a core research activity may be based on the three main forms of evidence/knowledge associated with health promotion [28]: instrumental (controlling social and physical environments), interactive (understanding of diseases/health issues; lived experiences; solidarity) and critical (reflection and action; raising consciousness regarding causes and means of overcoming them). These three evidences are anchored on the given scientific/philosophical traditions, viz. instrumental (positivism, quantitative, experimental, scientific knowledge), interactive (constructivist, naturalistic, ethnographic/qualitative knowledge) and critical (materialist, structural and feminist theory).
There is also an overwhelming need for health promotion research to be aware of the difference between health promotion outcomes and health outcomes. Health outcomes crudely imply the consequences or benefits of healthcare delivery (e.g., reduction of mortality rate) related to a disease (which may be the case in spite of an increment in number of those affected by the disease). But health promotion outcomes signify the form of control and attitudinal re-orientation groups and individuals adopt in facing a given disease which may impact on the number of people affected by the disease and improve attitudes and behaviour towards those affected by the disease. Health promotion outcomes can be seen directly through community members’ perception and interpretations of a given health issue which makes the achievement of control possible.
Health promotion research should utilize both quantitative and qualitative methods. In addition to complementing quantitative methods in health promotion research, qualitative research enables the researcher reach the heart of issues in engagement with community members. In Africa, where a good percentage of the population are still domiciled in the rural areas, qualitative approach offers the possibility of profound insights into the why and how of health behaviors which may not be possible or easily achieved with the quantitative or traditional biomedical approaches. As a result, “the increasing popularity of qualitative methods is as a result of perceived failure of traditional methods to provide insights into the determinants – both structural and personal – of whether people pursue or do not pursue health-promoting actions” [25], p. 359.
6. Challenges to health promotion in Africa
It is important to recognize that in spite of apparent good intentions, health promotion can actually generate negative or counterproductive effects when not well managed. Thus, “negative outcomes occur where professionally paternalistic and disempowering health policy decisions force health-related outcomes that are irrelevant to sustained community development and are not based on or resourced according to the social reality of the community” [11], p. 315. The above sentiments caution one against embarking on health promotion activities and initiatives that are not anchored on the health realities of the community concerned. Often, overzealous health professionals unintentionally betray the health priorities of communities by assuming knowledge of all there is to know about the health situations and needs of the people.
Perhaps a critical shortfall of some health promotion activities and processes is the adoption of what can be termed the pathogenic paradigm which over-relies on risk instead of emphasizing protective mechanisms. This essentially entails a focus on the failure of communities and individuals to avoid disease or their apparent susceptibility to diseases instead of seeking to unleash their potential and capacity to engender and sustain good health and development. It is an approach that relies too much on health practitioners and experts and hardly gives voice to the people and their own knowledge cum realities.
Generally health promotion in Africa suffers from some of the debilitating challenges which confront the practice of health promotion broadly in many countries in the continent. These challenges, among others, include:
Poor definition and rudimentary elaboration of expected health outcomes
Ambiguous elaboration of factors and conditions to be targeted in health promotions
Ambiguity of health promotion policies and guidelines
Lack of capacity (or inadequate capacity) to develop, implement and evaluate health promotion programmes
A general context of inadequate investment in health promotion
Underdeveloped sectoral collaboration
Low political will and commitment to health promotion programmes as well as institutional corruption and resource mismanagement
The above challenges have implications for research in health promotions in the continent. There is no gainsaying the need for health promotion to be evidence based because essentially it is the only way to make it responsive to the health needs and interests of the people.
7. Resituating and reinforcing health promotion in Africa
Health promotion combines varied but complementary indicators like legislation, health finance including fiscal measures and taxation, gender inclusiveness, mapping of priorities and organizational change. In spite of their differences, these issues are in reality intertwined or systematically connected in the sense that, for the public health system to function well and optimally, there should be a synergy between these indicators. Briefly:
7.1 Legislation
This revolves around having the political will to make and drive through policies and laws that improve and sustain healthcare delivery. It also involves public health sector governance and leadership which aim at ensuring that only competent and qualified people lead the sector and that activities are governed by a democratic and free process which place emphasis on human rights, dignity and self-worth of all stakeholders.
7.2 Finance
Without doubt efficient health promotion and by implication the entire health delivery system cannot function without finance. In fact, the extent and impact of health promotion depend to a significant extent on the availability of funds. The problem of finance is especially critical in developing nations in Africa where political corruption and competing needs whittle down whatever gets to health from the yearly appropriation of government. However, there is a need to understand that a lot needs to be done in terms of the fiscal policies in these nations in order to achieve the desire for good health and improved life expectancy. In other words, the process of fiscal policymaking and budgetary allocation should prioritize health promotion and health delivery in these countries.
7.3 Organizational change
There is no gainsaying the fact that the health system as a whole is dynamic especially so in Africa where apart from battling known ailments new ones (or novel presentation of the old ailments) spring up now and then. The above entails that the health system calls for dynamic organizational setting that is robust enough to deal with changes while making improvements in the system. There is apparently no denying the fact that health promotion as a critical component of health delivery would benefit from organizational change. This is particularly so in the face of the reality that health promotion in most of the continent is still below the expectation. This is not to deny that health promotion has worked well in specific instances like the HIV/AID scourge and maternal health. However, such grab and slash system which focuses on only one of such delimited issues in the system cannot be seen as either robust or effective in the long run.
7.4 Gender inclusiveness
There is an obvious need to ‘en-gender’ health promotion as a very critical issue in Africa. This would entail ensuring that those involved in health promotion ensure that in all key phases of health promotion (planning, implementation and evaluation) women and men should be equal partners and collaborators. Gender, in this case, while calling attention to the needs of women, should also ensure that the men are not left behind even in approaching health issues traditionally seen as the concerns of women. Typical example here is in the area of family planning or reproductive health which demands the active collaboration or participation of both men and women to achieve desired results.
7.5 Mapping of priorities
For the WHO [24], the priority interventions in Africa in respect of health promotions include capacity building, development of plans, incorporation of health promotion components in non-health sectors and strengthening of priority programmes using health promotion interventions. These essentially mean pursuing health promotion through capacity building, action planning, advocacy and multisectoral orientation. They are also in tune with relating to the determinants of health promotion in the continent. These include socio-economic conditions and physical (environment), biological, and behavioral lifestyles which impact on health in Africa. Countries can be encouraged to map out their priorities taking into consideration such factors as disease and financial burdens, threats, intervention tools and agencies, acuity, management capabilities, persistent challenges, etc.
8. Conclusion and recommendations
Generally, there is a need for stepping up health promotion research in Africa in the areas of family and reproductive health targeting such issues as VVF, antenatal care, diabetes, cardiovascular issues, new disease forms/resurgence of old diseases (including Ebola), etc. especially in terms of communicating with those who are marginal to the formal sector of the society or who are less privileged by virtue of education, economic opportunities or physical/mental challenges, etc. in both urban and rural contexts. Health promotion can profit from an acute awareness of the fact that what works in one socio-geographical setting may not work in another since no two societies are exactly the same. This would entail designing programmes that even where the general principles or goals remain the same embody recognition of the socio-geographical peculiarities of the society/community concerned.
Given the usual paucity of funds in the continent, it makes sense that to minimize cost and save time, there should be incorporation of both needs assessment and evaluation into ongoing health promotion activities. This approach offers a smart way of pursuing health promotion goals without elaborate budget.
In spite of country differences and specific structural challenges, there is a need to build a culture of sharing and documenting outcomes and evidences of health promotion between different countries and organizations. This is a step towards achieving the desirable goal of multinational coordination especially for infectious diseases and epidemics. Equally, African nations need to invest more in capacity building for media and theater practitioners in both private and public sectors on health promotion. There is no gainsaying the media’s crucial role in health information dissemination. Actually, health promotion is largely media driven and should be programmed as such.
In addition to media practitioners, there should be health programme or intervention specific to health promotion capacity building for different cadres of public sector workers. Such capacity building or training should be anchored on acute awareness of current research trends and best practices globally. There should also be increased attention to the need for specific health promotion for under-represented health issues and priority to non-communicable diseases should be targeted. It should also improve capacity on how to incorporate methods of targeting members of the society marginal or vulnerable within each country context.
\n',keywords:"health promotion, public health, challenges, Africa, health education, theories",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/71667.pdf",chapterXML:"https://mts.intechopen.com/source/xml/71667.xml",downloadPdfUrl:"/chapter/pdf-download/71667",previewPdfUrl:"/chapter/pdf-preview/71667",totalDownloads:494,totalViews:0,totalCrossrefCites:0,dateSubmitted:"July 5th 2019",dateReviewed:"February 21st 2020",datePrePublished:"April 5th 2020",datePublished:"September 9th 2020",dateFinished:null,readingETA:"0",abstract:"The chapter examines the place and role of health promotion in the drive for sustainable and effective public health delivery in Africa. It conceptualizes health promotion from a multifaceted and multi-professional perspective hinged on the empowerment of communities and individuals to play active roles and adopt behaviour consistent with the goals of good health. The paper drawing on documentary data sees health promotion as critical to the achievement of health goals in the continent and equally reflects on the theories of health promotion, strategies for health promotion and challenges to health promotion in Africa. It argues that health promotion in the continent can be strengthened through such measures as appropriate legislations, robust funding, gender inclusiveness, stepping up research, regular needs assessment and evaluation, setting needs-driven priorities and building capacity of health promotion to target vulnerable and marginal members of the society, among others.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/71667",risUrl:"/chapter/ris/71667",signatures:"Edlyne Eze Anugwom",book:{id:"9138",title:"Public Health in Developing Countries",subtitle:"Challenges and Opportunities",fullTitle:"Public Health in Developing Countries - Challenges and Opportunities",slug:"public-health-in-developing-countries-challenges-and-opportunities",publishedDate:"September 9th 2020",bookSignature:"Edlyne Eze Anugwom and Niyi Awofeso",coverURL:"https://cdn.intechopen.com/books/images_new/9138.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",editors:[{id:"293469",title:null,name:"Edlyne Eze",middleName:null,surname:"Anugwom",slug:"edlyne-eze-anugwom",fullName:"Edlyne Eze Anugwom"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"293469",title:null,name:"Edlyne Eze",middleName:null,surname:"Anugwom",fullName:"Edlyne Eze Anugwom",slug:"edlyne-eze-anugwom",email:"akommiri@gmail.com",position:null,institution:{name:"University of Nigeria, Nsukka",institutionURL:null,country:{name:"Nigeria"}}}],sections:[{id:"sec_1",title:"1. Introduction: conceptualizing health promotion",level:"1"},{id:"sec_2",title:"2. Theories and models of health promotion",level:"1"},{id:"sec_2_2",title:"2.1 The ecological models of health promotion",level:"2"},{id:"sec_3_2",title:"2.2 The health belief model (HBM)",level:"2"},{id:"sec_4_2",title:"2.3 Stages of change model (aka trans-theoretical model)",level:"2"},{id:"sec_5_2",title:"2.4 Theory of reasoned action (theory of planned action)",level:"2"},{id:"sec_6_2",title:"2.5 The social cognitive theory (SCT)",level:"2"},{id:"sec_8",title:"3. Health promotion as sociopolitical engagement",level:"1"},{id:"sec_9",title:"4. Approaches to health promotion",level:"1"},{id:"sec_10",title:"5. Health promotion research in Africa",level:"1"},{id:"sec_11",title:"6. Challenges to health promotion in Africa",level:"1"},{id:"sec_12",title:"7. Resituating and reinforcing health promotion in Africa",level:"1"},{id:"sec_12_2",title:"7.1 Legislation",level:"2"},{id:"sec_13_2",title:"7.2 Finance",level:"2"},{id:"sec_14_2",title:"7.3 Organizational change",level:"2"},{id:"sec_15_2",title:"7.4 Gender inclusiveness",level:"2"},{id:"sec_16_2",title:"7.5 Mapping of priorities",level:"2"},{id:"sec_18",title:"8. Conclusion and recommendations",level:"1"}],chapterReferences:[{id:"B1",body:'Tannahill A. Health promotion – Caring concern. Journal of Medical Ethics. 1984;10:196-198'},{id:"B2",body:'World Health Organization. Health Promotion: A Discussion Document on Concepts and Principles. Geneva: WHO; 1984'},{id:"B3",body:'World Health Organization. The Ottawa Charter for Health Promotion. Geneva: WHO; 1986'},{id:"B4",body:'Macdonald G, Davies J. Reflection and vision: Proving and improving the promotion of health. In: Macdonald G, Davies J, editors. Quality, Evidence and Effectiveness in Health Promotion: Striving for Certainties. London: Routledge; 1998. pp. 5-18'},{id:"B5",body:'Harrison D. Health promotion and politics. In: Bunton R, Macdonald G, editors. Health Promotion: Disciplines, Diversity and Developments. 2nd ed. London: Routledge; 2002. pp. 158-177'},{id:"B6",body:'Tones K. Why theorise? Ideology in health promotion. Health Education Journal. 1990;49(1):2-6'},{id:"B7",body:'Jones L. The politics of health promotion. In: Jones L, Sidell M, editors. The Challenge of Promoting Health: Exploration and Action. London: Macmillan; 1997. pp. 131-157'},{id:"B8",body:'MacDonald TH. Rethinking Health Promotion: A Global Approach. London: Routledge; 1998'},{id:"B9",body:'Victor C. Inequalities in health and health promotion. In: Pike S, Forster D, editors. Health Promotion for all. Edinburgh: Churchill Livingstone; 1995. pp. 157-170'},{id:"B10",body:'Webster C, French J. The circle of conflict: The history of the public health and health promotion movements. In: Adams L, Amos M, Munro J, editors. Promoting Health: Politics and Practice. London: Sage; 2002. pp. 5-12'},{id:"B11",body:'Whitehead D. Health promotion and health education: Advancing the concepts. Journal of Advanced Nursing. 2004;47(3):311-320'},{id:"B12",body:'Caplan R, Holland R. Rethinking health education theory. Health Education Journal. 1990;49(1):10-12'},{id:"B13",body:'McLeroy KR, Bibeau D, Steckler A, Glanz K. An ecological perspective on health promotion programmes. Health Education Quarterly. 1988;15:351-375'},{id:"B14",body:'Sallis JF, Owen N. Ecological Models. In: Glanz K, Rimer BK, Lewis FM, editors. Health Behaviour and Health Education: Theory, Research and Practice. 2nd ed. San Francisco: John Wiley; 1997. pp. 403-424'},{id:"B15",body:'Stokols D. Establishing and maintaining healthy environments: Towards a social ecology of health promotion. The American Psychologist. 1992;47(1):6-22'},{id:"B16",body:'Hancock T. Health, human development and the community ecosystem: Three ecological models. 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Journal of General Internal Medicine. 2003;18(7):558-567'},{id:"B21",body:'Parker E. Application of health promotion theories and models for environmental health. Health Education and Behaviour. 2004;31(4):491-509. DOI: 10.1177/1090198104265601'},{id:"B22",body:'Whitehead D. Incorporating socio-political health promotion activities in clinical practice. Journal of Clinical Nursing. 2003;12:668-677'},{id:"B23",body:'Edmondson R. Social capital: A strategy for enhancing health? Social Science & Medicine. 2003;57:1723-1733'},{id:"B24",body:'World Health Organization. Health Promotion: A Strategy for the African Region. Geneva: WHO; 2001'},{id:"B25",body:'Raphael D. The question of evidence in health promotion. Health Promotion International. 2000;15(4):356-367'},{id:"B26",body:'Wiggers J, Sanson-Fisher R. Evidence-based health promotion. In: Scott D, Weston R, editors. Evaluating Health Promotion. Cheltenham, UK: Stanley Thornes; 1998. pp. 31-49'},{id:"B27",body:'Seedhouse D. 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UK Research and Innovation (former Research Councils UK (RCUK) - including AHRC, BBSRC, ESRC, EPSRC, MRC, NERC, STFC.) Processing charges for books/book chapters can be covered through RCUK block grants which are allocated to most universities in the UK, which then handle the OA publication funding requests. It is at the discretion of the university whether it will approve the request.)
UK Research and Innovation (former Research Councils UK (RCUK) - including AHRC, BBSRC, ESRC, EPSRC, MRC, NERC, STFC.) Processing charges for books/book chapters can be covered through RCUK block grants which are allocated to most universities in the UK, which then handle the OA publication funding requests. It is at the discretion of the university whether it will approve the request.)
Wellcome Trust (Funding available only to Wellcome-funded researchers/grantees)
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