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Lupine Publishers | Blood Characteristics and Tissue Histology of Nile Tilapia (Oreochromis Niloticus Niloticus) Fed A Diet Containing Cheese Skipper (Piophila Casei) Larvae

 Lupine Publishers | Scholarly Journal of Food and Nutrition

Abstract

A three-month laboratory feeding trial was conducted to evaluate the suitability of cheese skipper larvae [maggots] as an alternative protein source for Nile tilapia (Oreochromis niloticus niloticus) instead of fishmeal. The diets tested were a commercial diet (Diet 1, 0% maggot inclusion) and a maggot diet (Diet 2, 100% maggot inclusion). The values obtained for both treatment groups indicated nutritional adequacy of the diets. Non-significant differences were observed between both treatment groups for nearly all the hematological parameters. A marked increase in the total protein, ALT, AST and triglyceride levels was observed in the blood of fish fed the maggot diet compared to the levels in the blood of fish fed the commercial diet, suggesting health improvement in fish fed the maggot diet. The replacement of fishmeal with maggot meal is acceptable from a growth perspective and in terms of the observed histological architecture. The results show that the maggot diet can be conveniently used as a total replacement for fishmeal in the diet of Nile tilapia.

Abbreviation: Aquaculture; Maggot Diet; Nile Tilapia; Blood Characteristics; Histology

Introduction

Approximately 60% of the fish body is protein, representing a very good source of inexpensive protein for the growing world population. This aspect has led to the development of aquaculture to increase fish production to meet the demand [1]. The aquaculture industry is the fastest growing food production industry in the world, accounting for 50% of all fish consumed by humans [2]. The cost of aquafeed is the main cost factor in aquaculture, accounting for approximately 70% of a fish farming venture [3]. The major protein source and preferred choice in aquafeed is fishmeal due to the high quality of the protein with a nearly balanced amino acid profile [4]. Fishmeal is the most expensive component, leading to an exponential increase in the price of fish feed. Therefore, it was necessary to search for substitute protein sources such as inexpensive plant proteins [e.g., soybean meal, sunflower, cottonseed meal, rapeseed meal] or animal proteins [e.g., shrimp waste, earthworms and insect] [5-8]. These sources have high potential for supplying fish with the protein needed for maximum productivity [9, 10]. Insects have been employed to produce fish feed. Maggot larvae of flies or other insects have the ability to grow on a wide range of substrates and seem to be candidates for the replacement of fishmeal in fish diets [11-13]. Maggot meal has been reported to be highly nutritive, with the crude protein content ranging between 43.9 and 62.4%, lipid content between 12.5 and 21%, and crude fiber content between 5.8 and 8.2% [14-16]. Maggot meal is also rich in phosphorus, trace elements and vitamin B complex.

Blood characteristics are effective and sensitive indices for monitoring physiological changes in fishes. Analysis of blood indices has proven to be a valuable approach for examination of the health status of farmed fish, providing reliable information on metabolic disorders [17] and becoming a basic part of fish health monitoring programmes [18,19]. The ingestion of numerous dietary supplements has measurable effects on blood constituents [20]. According to Maxwell et al. [21], blood parameters are important for assessing the quality and suitability of feed ingredients for farm animals. Alteration in fish histology has been examined to identify changes, if any, in the tissue of fishes fed alternative feeds. The digestive system of teleostean fishes has been widely studied and described morphologically to determine the functions of many specialized anatomical structures in relation to different feeding adaptations [22]. Histological analysis of the digestive system is considered to be a good and immediate indicator of the nutritional status of fish [23,24]. Histological methods used for assessment of different feed effects on the livers and intestines of fishes were reviewed and explained by Raskovic et al. [25]. The intestine and the liver are the most important organs involved in the digestion and absorption of nutrients from ingested food; therefore, monitoring of these organs is considered to be necessary [26] for assessing the effects of ingredients used as raw materials of animal/plant origin. In this study, blood characteristics and tissue histology were used to evaluate the suitability of cheese skipper larvae [maggots] as an alternative protein source for tilapia (Oreochromis niloticus niloticus).

Material and Methods

Experimental design

A total of 120 healthy Nile tilapia (O. niloticus niloticus) were used in the present work. Nile tilapias [average initial weight 28-41 g and length 11-13.4 cm] were collected from the Nile River at Assiut, Egypt. The fish were acclimated in the laboratory for at least 21 days. During acclimatization, the fish were fed a commercial pellet diet twice per day and kept in a recirculation system, ensuring high water quality (dissolved oxygen: 5.6 mg/L, pH: 7.9, total NH3-N: 0.097 mg/L, and temperature: 25.5 °C). The composition of the commercial pellet diet is provided in Table 1. After acclimatization, the fish were divided into two groups. The first group was fed a commercial diet (Diet 1), and the second group was fed a maggot diet (Diet 2) (Table 1). Each group was assessed in triplicate. Experimental tanks were regularly cleaned, and faecal matter was siphoned out daily.

Sources of ingredients and diet preparation

Soybean meal, wheat bran, rice bran, mix oil, premix, dicalcium phosphate, and fishmeal were obtained locally from the market. The maggot meal used for this study was prepared in the laboratory during the experiment using the larval stage of Piophila casei skippers (fly larvae). The larvae were collected from conventionally prepared cheese by the floating method. The homemade cheese was mixed with running water, and the larvae that floated were collected with a sieve. Maggots were harvested, washed, killed in tepid water and dried for 36 hours at 60 °C in an oven. Dried samples were milled using mortar and pestle. The maggot powder was added to the components of the experimental fish food according to the recommended amounts listed in Table 1. Two test diets were formulated. Diet 1 (commercial diet) was formulated with the highest inclusion level of fishmeal and without maggot meal. Diet 2 (maggot diet) was formulated with the highest inclusion level of maggot meal and without fishmeal (Table 1). All dry diet components, including vitamins and mineral mixtures, were thoroughly mixed with oil. Water was added, and the feed was pressed into pellets that were 1 mm in diameter. The wet pellets were dried for 3 days at room temperature and stored at -2 °C until use.

Blood sampling

At the beginning and end of the experiment, 9 fish from each treatment were randomly selected for blood sampling. No anesthetic was applied to the fish, as anesthetics can affect blood parameters. Two samples of peripheral blood were collected by cardiac puncture as described by Osman et al. [27]. The first sample was freshly collected in small glass tubes containing heparin solution [0.2 ml/ml blood] as an anticoagulant. This sample was used for hematological analysis. The second sample was collected and left to coagulate for 15–20 min at 4 °C prior to centrifugation for 20 min at 3,000 rpm to separate the serum. The fresh serum was subjected to biochemical analysis.

Haematological analysis

Whole-blood samples were used for estimation of haemoglobin concentration (Hb), hematocrit(Hct), red blood cell count (RBC), and white blood cell count (WBC) using an automated technical analyzer (Celtic α MEK-6400J/K, TOKYO, JAPAN). The mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH) and mean corpuscular haemoglobin concentration [MCHC] were calculated as described by Dacia and Lewis [28].

MCHC [g/dl] = Hb / Hct × 100

MCH [pg] = Hb / RBC × 10

MCV [mm3] = Hct/RBC × 10

Biochemical analysis

Colorimetric determination of the selected biochemical parameters was performed using a spectrophotometer [Jasco-V530]. The absorbance of the sample was examined at an appropriate wavelength within a range of 340 to 546 nm according to the parameter tested. Commercial diagnostic kits from Biomatrix chemicals were used for assays of total protein content (g/dl) as described by Henry [29], cholesterol (mg/dl) as described by Thomas [30], triglycerides (mg/dl)as described by Friedewald et al. [31], calcium(Ca, mg/dl) as described by Fiereck [32], creatinine and urea (mg/dl) as described by Henry [29], glucose (mg/dl) as described by Trinder [33], and aspartate aminotransferase (AST, U/I)and alanine aminotransferase (ALT, U/I) as described by Reitman [34].

Histological analysis

At the end of the experimental period, three fish from each tank were sacrificed by decapitation. The livers and intestines were immediately dissected, fixed in 10% neutral buffered formalin, processed by conventional methods, sectioned at 3-5-μm thickness using a rotary microtome, and stained with hematoxylin-eosin [35]. PAS staining was also performed on the liver sections to discriminate the PAS-positive reactions caused by the presence of mucopolysaccharides and glycoproteins. The sections were examined under a light microscope (Motic microscope BA310 LED FL) and photographed using a DVC digital camera (HDCE-50 B). Twenty measurements of villus height (μm)were obtained using ImageJ (1.46) software. Baeverfjord and Krogdahl’s [36] method was used to count goblet cells.

Statistical analysis

Data are presented as the means ± standard deviations. The data were analysed by one-way analysis of variance [ANOVA] using a data analysis software system [37]. Means were tested using Fisher’s least significant difference [LSD] test. Two levels of significance were reported; *p<0.05; **p<0.01.

Results

Haematological parameters: Significantly (P<0.05) increased RBC, Hb, and MCH values were recorded in the blood of fish fed the commercial diet and those fed the maggot diet in the final samples compared to the initial blood samples (Table 2) Non-significant (P>0.05) differences were observed in the MCV, MCHC, Hct, and WBC values between the initial and final blood samples from fish fed the commercial diet and those fed the maggot diet (Table 2). Non-significant (P>0.05) differences were observed in the final RBC and WBC values between the blood samples from fish fed the commercial diet and those fed the maggot diet (Table 2). At the same time, the final values of Hb, MCH, MCV, and MCHC were higher in the blood samples from fish fed the commercial diet than in the blood samples from those fed the maggot diet (Table 2). In contrast, the final Hct concentration was higher in the blood samples from fish fed the maggot diet than in the blood samples from those fed the commercial diet (Table 2). The final lymphocyte concentration was lower than the initial lymphocyte concentration in the blood of fish fed the commercial diet. The lymphocyte concentration exhibited a non-significant (P>0.05) increase in the blood of fish fed the maggot diet compared to those fed the commercial diet (Table 2). The neutrophil concentration exhibited a non-significant decrease in the blood of fish fed the maggot diet. The final neutrophil concentration was higher in the blood of fish fed the commercial diet than in the blood of fish fed the maggot diet (Table 2). The monocyte concentration exhibited a marked decrease in the blood of fish fed the commercial diet and those fed the maggot diet. The final monocyte concentration was the same for both diets (Table 2). A significant (P<0.05) increase in the final concentration of eosinophils was observed compared to the initial concentration in the blood of fish fed the commercial diet and those fed the maggot diet. No significant difference was observed in the concentration of eosinophils between the fish fed the commercial diet and those fed the maggot diet (Table 2).

 

Blood Biochemistry: Significantly (P<0.05) increased final levels of total protein, cholesterol, and AST, compared to the initial levels, were observed in the blood samples from fish fed the commercial diet and those fed the maggot diet. Significantly (P<0.05)reduced final levels of glucose, triglycerides, and creatinine were observed in the blood samples from fish fed the commercial diet and those fed the maggot diet. The calcium level exhibited a significant (P<0.05) increase in the blood of fish fed the commercial diet and a significant (P<0.05)reduction in the blood of fish fed the maggot diet. Non-significant changes were observed in the levels of blood urea and ALT in the blood samples from fish fed the commercial diet and those fed the maggot diet (Table 3). Total protein, triglyceride, creatinine, ALT, and AST levels were significantly (P<0.05) higher in the blood of fish fed the maggot diet (Diet 2) than in the blood of those fed the commercial diet (Diet 1) (Table 3). In contrast, glucose, cholesterol, and calcium concentrations were significantly higher in the blood of fish fed the commercial diet than in the blood of those fed the maggot diet (Table 3). Non-significant changes were observed in the levels of urea and ALT in the blood of fish fed the commercial diet compared to the levels in the blood of those fed the maggot diet (Table 3).

Histological Alterations: The experimental diets used in the present study showed minor impacts on the histological structures of the intestine and liver tissues of Nile tilapia, O. niloticus niloticus. Analysis of the intestinal structures of fish fed the commercial diet and those fed the maggot diet showed normal architecture, with a mucosa, sub-mucosae, a muscular layer and a serosa (Figure 1). The anterior intestine of fish fed the commercial diet exhibited normal architecture, with circular muscles, longitudinal muscles, a serosa and short villi. A large number of small goblet cells were observed (Figure 1). The anterior intestine of fish fed the maggot diet exhibited normal architecture, with longer villi than those observed in fish fed the commercial diet. Small goblet cells were also observed in the intestines of fish fed the maggot diet (Table 4 and Figure 1). The posterior intestine of fish fed the commercial diet showed a narrow lumen and short and weak branched villi with a wide lamina propria. Normal appearance of circular muscles and sub-mucosae were observed. Large numbers of small goblet cells were observed (Table 4 & Figure 2). On the other hand, the posterior intestine of fish fed the maggot diet showed a wide lumen, long and branched villi, a narrow lamina propria, and normal appearance of the muscularis and sub-mucosae. Few goblet cells were observed in these samples (Table 4 and Figure 2).

The anterior and posterior intestines of fish fed the commercial diet showed detachment at the base of the villi between the circular muscles and villi (Figures 1 & 2). Lymphocyte infiltration in the villi, lamina propria and mucous membrane were observed in the intestines of fish fed the commercial diet. Blood cell congestion was observed in the lamina propria of fish fed the commercial diet. On the other hand, only slight lymphocyte infiltration was observed in the intestines of fish fed the maggot diet (Figures 1 & 2). Histological analysis of the livers of fish fed the commercial diet and those fed the maggot diet showed normal architecture of hepatocytes, with a regular shape and large centrally located nuclei. Large intracytoplasmic vacuoles and blood cell congestion in the sinusoidal blood vessels were observed in the livers of fish fed the commercial diet. Additionally, low glycogen levels were observed in the liver tissues. On the other hand, small intra-cytoplasmic vacuoles were observed in the livers of fish fed the maggot diet, and high glycogen levels were observed.

Discussion

The primary objective in fish nutrition is to provide a nutritionally balanced mixture of ingredients to support the vital functions of fishes at an acceptable cost [38]. Blood parameters are an important tool for monitoring both the nutritional status and health status of fishes [39]. In recent years, increasing attention has been given to haematological studies as an integral part of the examination of the health conditions and productivity of fishes. The effect of maggot meal as a feed supplement on the growth performance indicated that this component was well utilized by O. niloticus niloticus [40]. The same conclusion could be made based on the effects on the haematological and biochemical parameters as well as the results of the histological investigation. Changes in the blood indices of fish as a result of feed have been previously reported [41]. The haematological values obtained for both treated groups indicated the nutritional adequacy of the diets, as the values did not indicate nutritional deficiency [42]. Non-significant differences (P>0.05) were observed among the groups for nearly all the haematological parameters, except RBC, Hb and MCH. These parameters increased markedly after three months of exposure via the blood in Nile tilapia fed the commercial diet and those fed the maggot diet. The fish given the commercial diet exhibited the highest RBC and Hb values, although the values were within the normal ranges. Fish fed the maggot diet exhibited the lowest RBC and Hb values. The differences in the final values of RBC and Hb between the blood of Nile tilapia fed the commercial diet and those fed the maggot diet were non-significant. This finding seems to confirm that the fish were not negatively influenced by the inclusion of maggot meal in the experimental diet. The high values of MCV and MCH observed here, however, may not indicate a serious problem, because the PCV, RBC, WBC, Hb and MCHC in all the treatments were within the normal ranges for healthy fish. The non-significant differences in the evaluated parameters between the two diets implies that maggot meal can successfully replace commercial meal in fish diets. This result is consistent with the reports of other authors who have observed improved performance of fish fed diets containing maggot meal over those solely fed commercial meal. Thus, this finding reflects the nutritive quality and acceptance of this biomaterial [43]. The result also corroborates previous observations that maggot meal, similar to other animal protein sources, is well accepted and utilized by fish [44-46]. Some haematological values observed here appeared to be slightly lower than those reported for tilapia by some authors but were within the acceptable range. Notably, the variations in haematological values within species can be influenced by environmental conditions, sex, age, origin, breeding system, and feeding, among other factors [47]. There was no significant difference in WBC in fish fed the commercial diet and those fed the maggot diet. For both diets, the WBC decreased from an initial value of 19.16 × 103/μl to a final value of 19.08 × 103/μl. The values of WBC recorded here were within the range reported by Bittencourt et al. [45] for healthy Nile tilapia. These results indicate that the fish were healthy. Reduction in the WBC value to below the normal range [which is not the case here] is an indication of allergic conditions and can be harmful to fish because these cells play an important role in the innate immune system [48, 49]. Lymphocytes produce antibodies that provide defence against infection. Lymphocytes represented the highest proportion of the WBC in the blood of fish in this study. This finding is in contrast with the WBC composition in most livestock, with neutrophils exhibiting the highest proportion. Neutrophils were in the second most abundant, representing approximately 30% of the total WBC in the blood of Nile tilapia fed the commercial diet and those fed the maggot diet. At the end of the experiment, the percentage of lymphocytes was high in the blood of fish fed the maggot diet, while the percentage of neutrophils was high in the blood of fish fed the commercial diet. This finding can explain the constant percentage of monocytes and eosinophils in the blood of Nile tilapia fed the commercial diet and those fed the maggot diet. The concentration of monocytes in the blood of Nile tilapia in this study was within the normal range. The monocyte concentration in the blood of Nile tilapia fed the commercial diet and those fed the maggot diet ranged from 1.3% to 2.3%. This finding was consistent with the results of Kelly [50], who reported that monocytes constitute less than 10% of the total WBC in animals of all species. Basophils were not observed in the blood of fish in this study. This finding is similar to the results obtained in most livestock. Kelly [50] reported that basophils rarely occur in the blood of all species of livestock. Biochemical parameters vary among species and can be influenced by many biotic and abiotic factors, such as water temperature, seasonal pattern, food, age and sex [18]. A marked increase in the total protein level was observed in the blood of fish fed the maggot diet compared to that in the blood of fish fed the commercial diet. The low plasma protein level observed in Nile tilapia fed the commercial diet may be a consequence of decreased protein absorption by the relatively short villi observed in these fish. These results suggested that fish health was improved when the fish were fed the maggot diet. Although there was an increase in serum protein levels, the increased levels of ALT and AST suggest protein catabolism at the high dietary protein levels present in the maggot diet [51,52]. The increase in ALT and AST activities observed in Nile tilapia fed the maggot diet may reflect the use of excess hydrocarbons from amino acids to meet energy demands. Similar responses were observed in Oncorhynchus mykiss for ALT [53] and in Rhamdia quelen for AST and ALT [54]. Blood glucose levels may vary according to season and water temperature and may decrease with increasing ages and sizes of fishes [55]. Plasma glucose levels in fishes increase during stress, probably due to the action of catecholamine on stored glycogen in liver and other tissues [56]. Here, elevation of plasma glucose was not observed in either feeding group. The level of glucose was lower in the blood of fish fed the maggot diet than in the blood of those fed the commercial diet. In this study, cholesterol concentrations increased from 50.1 to 140 in fish fed the commercial diet (Diet 1), while in fish fed the maggot diet (Diet 2), cholesterol concentrations increased to only 119.17. The cholesterol concentration in the blood of fish fed the commercial diet was higher than that in the blood of fish fed the maggot diet due to the high proportion of fat in the chemical composition of the feed. Because glucose and cholesterol levels were within the normal range, possibilities of anorexia, diabetes, liver dysfunction and malabsorption of fat, which are symptoms of abnormal glucose and glucose levels in the blood [57], were ruled out. The triglyceride levels in the blood of fish fed the maggot diet were significantly higher and nearly twice those found in fish fed the commercial diet. Similar results were obtained in Liza klunzingeri by Mohammadizadeh et al. [58]. The triglyceride levels increased significantly due to the increase in protein levels in the maggot diet, which may be because the muscle is a pivotal compartment that is directly linked to amino acid turnover. The level of calcium was significantly low in the blood of fish fed the maggot diet. The creatinine level was high in the blood of fish fed the maggot diet. The urea level exhibited non-significant changes in the blood of fish fed the commercial diet and those fed the maggot diet during the experimental period. The histological structure of the fish digestive system has been well documented [59,60]. Examination of the intestinal histology of aquaculture species is important for understanding pathological alterations related to infectious diseases or promoted by nutritional sources [61]. Although fish histological studies provide much information regarding the gastro-intestinal tract [62], further information is needed regarding morphological adaptations to variations in diet nutrients, which could affect diet formulation. Histological analysis of the digestive system is considered to be a good method to determine the nutritional status of fishes [23,24], and identification of the structural variations is useful for studies on nutritional development [63,64]. Histopathological changes in the intestine may vary depending on the species and feed used in the experiments [65]. The flexibility of the piscine gastro-intestinal tract for adaptation to food availability has been well studied [65,66]. In the present study, the intestines of fish fed the commercial diet exhibited normal architecture, with short villi, a wide lamina propria, a large number of small goblet cells, lymphocyte infiltration, and blood congestion. In the case of Nile tilapia fed the maggot diet, the anterior intestine exhibited normal architecture, with long villi, a narrow lamina propria, few small goblet cells, and slight lymphocyte infiltration and blood cell congestion. The histological alteration observed in the intestines of fish fed the commercial diet, that is, shortening of the villi, widening of the lamina propria, lymphocyte infiltration, blood cell congestion, and increasing number of goblet cells, was previously identified as enteritis [67,37]. The same changes were also observed in the intestines of salmonids fed full-fat diets [68,67]. Generally, widening of the lamina propria was accompanied by profound infiltration of a mixed population of inflammatory cells such as lymphocytes, neutrophilic granulocytes, macrophages, and eosinophilic granular cells [67,68]. Similar results were observed when fishmeal was replaced with sunflower meal in the feed of sharpsnout sea bream (Dyploduspuntazzo Cetti) [69]. Villus length is a useful histological parameter that can be monitored not only in experiments regarding the replacement of fishmeal but also in the evaluation of different types of commercial feed.

Based on the present results, we can conclude that the selected commercial diet is rich in fat and proteins of plant origin compared to the maggot diet, which is a 100% animal protein product. An increase in villus length is associated with an increase in the surface area for absorption of nutrients [70]. The long villi found in fish fed the maggot diet indicate high efficiency in the absorption process [24,71]. This high efficiency was evidenced by the improved growth performance of fish fed this diet [12]. This finding shows that the maggot diet promoted an increase in villus length in these fish. A decrease in villus length leads to reduced surface area for nutrient absorption [71], which may also explain the poor condition of the liver observed in fish fed the commercial diet. The number of goblet cells could vary with feeding habits or starvation [72]. A higher number of goblet cells was observed in the intestines of fish fed the commercial diet than in those of fish fed the maggot diet. Goblet cells are associated with the immune system and act through the mucus as a lubricant. The increase in the number of goblet cells may be an indication of increased irritation [71], as these cells produce the mucus lining the brush border. This mucus serves as a lubricant, providing protection against chemical and mechanical damage. The increase in goblet cell number may also be an immune response against anti-nutrients [73]. The liver is of significant importance for nutrition and homeostasis in fishes. The liver of O. niloticus niloticus fed the commercial diet showed normal architecture, with normal hepatocytes and blood sinusoids. Large intra-cytoplasmic vacuoles and blood cell congestion in the sinusoidal blood vessels were observed. Low glycogen levels were recorded. Additionally, a normal architecture was observed in the liver of Nile tilapia fed the maggot diet, with normal hepatocytes and blood sinusoids, small intracytoplasmatic vacuoles, and high glycogen content. In conclusion, the haematological and blood biochemical analyses suggest improvement of fish health upon dietary administration of maggotsupplemented feed. The obtained results showed no negative effect on the histology of the visceral organs of Nile tilapia fed the maggot diet, suggesting that this diet is essentially good in terms of growth and utilization [72-74]. The replacement of fishmeal with maggot meal is acceptable from a growth perspective and in terms of the observed histological architecture. Thus, maggot meal could be an alternative animal protein source in fish diets to lower the production cost of fish diets. In future experiments in the area of fish nutrition, the histological status of the intestine should always be considered. This analysis should provide additional information regarding the state of this organ if any of the mentioned methods are used [75,76]. These methods are valuable in field experiments as well as in the laboratory. Maggots are a good alternative protein source for O. niloticus niloticus. However, further studies with tilapia and other fish species are needed to validate this conclusion.

Acknowledgement

The first author is grateful for the continuous support from the Alexander von Humboldt Foundation

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Lupine Publishers | How Beneficial are Statins and PCSK9-Inhibitors?

 Lupine Publishers | Scholarly Journal of Food and Nutrition

 

Abstract

Everyday people take their cars into the mechanic to be worked on. Sometimes it’s for routine maintenance, other times it’s because a warning light has come on or something just doesn’t feel or sound right when the car is running. People frequently visit their doctors for the same reason. Either something just doesn’t feel right – perhaps an unusual ache or pain, sometimes that pain is in your chest - or one of your blood tests (warning lights) came back in an abnormal range. Your doctor will frequently run blood tests looking for a problem, much like the mechanic will check the oil in your engine. Except the auto mechanic shuts the car off to run his tests; something your doctor doesn’t have the luxury of doing. You can infer a lot by looking at the engine oil, or getting a blood test. But you can only infer something is going on. Neither the engine oil nor the blood test tells you what the problem actually is – only hopefully where to look for the answer to the problem When people get their cholesterol levels checked, it’s usually because they’re worried about their heart – even though cholesterol by itself doesn’t cause heart disease (Figure 1) – inflammation does. To begin with you should also know there is more than one type of cholesterol in your body.

The combination of these various types of cholesterol, when put together, are called your total cholesterol (TC). It’s the sum of your good (HDL) and bad (LDL) cholesterol, along with the fats (triglycerides) in your blood, which are either made in your liver (very low density lipoprotein cholesterol; VLDL) or consumed (fats and chylomicrons) by you in the foods you eat. Another type of cholesterol is called intermediate density lipoprotein cholesterol (IDL), because it is intermediate in density, compared with the other types, and when compared with the other types of cholesterol IDL is composed almost equally of cholesterol and fat.

TC = HDL + LDL + VLDL/5 + Chylomicrons + IDL

You probably already realize this, but you do need cholesterol for your body to work. You need cholesterol for your cells to grow and maintain themselves and you need cholesterol for hormones, for the lining of the axons of nerves in your body – including your brain. You really don’t need to worry about eating it because your liver is designed to make it. In fact, most people only absorb about 10% of the cholesterol they eat, which means for most people, they are absorbing somewhere between 25 and 50 mg each day from the food they eat. If you had to depend upon that, you would probably either die or become seriously ill. Fortunately you don’t need to depend upon what you absorb from the foods you eat, because your liver will make around 1000 mg each day – 20 to 40 times the amount you get from your diet – as long as you don’t have liver disease. One of the interesting characteristics of carnivores is that their livers don’t make cholesterol to meet their needs, so carnivores have to consume cholesterol from the foods they eat to survive.

All this begs the question, if we need cholesterol, why do so many doctors say cholesterol is bad for you? The answer is both simpler and much more complex (Figure 1), than many people think. Most foods that are high in cholesterol are also high in saturated fat and it is this saturated fat, once oxidized, which is a primary, although not only, cause of inflammation, within the walls of the arteries of the heart that produces coronary artery (CAD)/heart disease [1,2], angina and death.

Increased dietary saturated fat intake not only increases the amount of cholesterol made by your liver, but it can also reduce the ability of cells in your body to remove the LDL cholesterol (Figures 1 & 3) from the blood, by interfering with the LDL receptors themselves–i.e., the part of your cells responsible for recognizing cholesterol and removing it from the blood for use by the body. Just like insulin receptors, which respond to increased levels of glucose (sugar) in the blood stream, so too do the LDL receptors, respond to increased levels of LDL cholesterol. However, there is no actual relationship between measured changes in blood tests like cholesterol and measured changes in CAD [3], when physiologically measured [4], as shown in (Figure 2) [2]. These changes cannot be measured using mere coronary arteriograms [5]-the basis for most if not all of the clinical data supporting the use of cholesterol lowering medicines - as coronary arteriograms neither measure the ability of the coronary arteries to respond to increased demand for coronary blood flow, nor the inflammation within the walls of the arteries themselves. This is an extremely important point and one that is frequently overlooked, given that up to 70% of all myocardial infarctions (heart attacks) occur in people whose arteries have less than 30% narrowing of the lumen – the area where the blood flows - and it is only this lumen narrowing, which coronary arteriograms can evaluate.

What types of foods raise your cholesterol levels?

While there are many studies which reveal that many different types of diets may initially show improvements in weight loss and blood cholesterol levels, most (not all) people would agree that there are three basic types of foods, which have been associated with increased cholesterol levels. These include:

a. Saturated Fat

b. Trans Fats, and

c. Highly refined, processed foods.

An increased consumption of any, or a combination of these, can be associated with increased cholesterol levels, increased insulin resistance, increased LDL receptor resistance, and increased weightobesity. Consequently resulting in heart disease, strokes, diabetes and a variety of other diseases. One of the common themes running through medicine and social media is the belief, that medicines can solve your problems or at least ameliorate them, thereby shifting the burden of responsibility. Something Big Pharma and Big Food are all too happy to accept, as this shift in responsibility results in profits for these corporations. Clearly you don’t solve what you put in your mouth by putting something else in your mouth–including medications or more of another type of food. You solve the problem by not putting the first problem in your mouth.

While the approach of putting more food or medications in your mouth is lucrative for Big Food and Big Pharma, it has been disastrous for everyone else. Let’s be very clear here-there has not been a shift in genetics in the last 100 years. Evolutionary mutations don’t work that way and such changes when they do occur, provide a survival benefit or they become extinguished. As Figure 4 shows [6], there is little, if any, survival benefit from this increased expenditure of healthcare monies being thrown at the problem and no appreciable increased life expectancy. One of, if not the, major health care expenditure currently confronting us, is the cost of prescription medications; with statins, PCSK9-inhibitors and diabetes medications leading the way. Before we address how these medications work, lets first look at the issue of cholesterol itself.

How much cholesterol is too much?

People unfortunately have a tendency to think of things in black and white, true false, right wrong - absolutes. For decades physicians have talked about levels of cholesterol that we want to keep your blood cholesterol below to reduce your risk of heart disease. The truth is that there is no absolute value, which is safe for everyone. What may be safe for you may kill someone else and vice-versa.

In the 1980’s and 1990’s, the first author was a member of the American Heart Association - Physician Cholesterol Education Faculty, and we used to tell people that total cholesterol levels should be kept below 150 milligrams/deciliter (mg/dl or %) or 3.879 mmol/l (millimole per liter) in standard international (SI) units. The use of this number was somewhat arbitrary as 50% (half) of all people who have heart attacks, have total cholesterol levels less than 150 mg/dl. At the same time, other people with higher cholesterol levels do not have heart attacks. There are a number of reasons for this including the differences in genetic handling of cholesterol levels, the other factors involved in the inflammatory process (Figure 1) and our sheer lack of real data about tissue levels of cholesterol and CAD where the real problem lies, versus blood levels of cholesterol and CAD.

The important take away point is that oxidized cholesterol builds up in the walls of the arteries of the heart and elsewhere, interfering with the ability of these arteries of the heart to do their job and the result, which isn’t measured by looking at the cholesterol in the blood, is a heart attack, stroke, loss of limb, etc. Cholesterol flowing through the blood stream without depositing is not actually causing an issue, at least not while flowing freely through the blood.

The cholesterol causing heart disease isn’t the cholesterol floating around in your blood stream to be sampled by your doctor

Only about 7% of your total BODY cholesterol is found in your BLOOD. The remaining 93%, which we don’t measure, is stored inside the cells of your body. Within the cells, the cholesterol is being used for cell growth, repair and to make hormones along with other substances needed by your body. It is also here where cholesterol is undergoing oxidation and participating in the inflammation within the walls of your arteries - where the real problem exists. When too much cholesterol is stored in the walls of your arteries, and oxidized, inflammation will occur (Figure 1) and these arteries will not be able to do their job. When that happens, you can have a heart attack, stroke, need kidney dialysis or lose a limb. It will just depend upon which artery is being damaged. The smaller the artery the sooner the damage is likely to occur and be noticed.

LDL receptor resistance is just as important, if not more so, than Insulin resistance (Figures 1 & 3)

A lot of people are talking about insulin resistance - the reason why many people ultimately develop diabetes. When you have more sugar than the cells of your body need, the cells protect themselves by becoming less responsive to the insulin. Less responsive = insulin resistance.

The same thing happens with cholesterol. Most, but not all, of your cholesterol is taken up for use by the cells of your body via LDL cholesterol receptors. Just like the insulin receptors for glucose (sugar), when the cells in your body don’t need more cholesterol, the LDL cholesterol receptors become less response (Figure 3). Less responsive = LDL resistance. When these LDL receptors become less responsive, the LDL cholesterol remains in your blood stream longer, where with time it becomes damaged (oxidized). This oxidized cholesterol can enter the walls of the arteries which supply blood to your brain, heart, kidneys, liver; in other words, everywhere. Once inside the walls of your arteries, this oxidized cholesterol - which is an inflammatory irritant to the artery - is taken up or consumed (phagocytized) by a special type of cell, called a macrophage.

Macrophages are specialized cells intended to protect your body. They are part of your defensive immune system designed to fight disease and foreign invaders. By consuming the oxidized cholesterol, the damaged cholesterol is removed from the wall of the arteries. Unfortunately, this results in the death of these macrophages, which have died in defense of your body; thus beginning an inflammatory build up within the walls of your artery, which we call atherosclerosis - or coronary artery (heart) disease.

This inflammatory buildup within the walls of arteries interferes with the ability of the coronary arteries to relax and carry more blood flow to the heart when needed [4,5]. This is atherosclerosis and it is not seen by conventional cardiology tests. Coronary arteriograms with their limitations and reliability problems [5], do not see this buildup within the walls of the artery. Coronary calcium (CAC) scoring, which looks for the presence of calcium – which may or may not be present (Figure 1) - only sees calcium (if present) but tells us nothing about the ability of the arteries to increase their blood flow when needed.

Both arteriograms and CAC scoring are merely anatomic tests. They are limited to seeing a narrowing or calcium, but their failure to see something and their inability to tell you what the arteries are capable of doing [4], provide us limited information. Up to eightyfive percent of people will have a heart attack due to the rupture of this built up inflammatory material, inflammation, which began years earlier within the walls of the arteries. As such the use of coronary arteriograms and CAC scores for assessing the impact of cholesterol lowering drugs is extremely limited and should be cautiously considered.

How do the cholesterol lowering drugs work?

Ninety-three (93) percent of the low-density lipoprotein (LDL) cholesterol in your body, the cholesterol we call the bad cholesterol - because it is this cholesterol, which eventually causes most of the harm to the arteries of your body once oxidized, causing heart attacks, strokes and other major medical problems – is actually in the cells of your body and not the blood stream. It is in the cells of your body, where this LDL is needed – where it is actually being used for cell growth, repair, hormone production, et cetera, where it cannot be measured. However, even too much of a good thing, can be a problem.

This 93% of your body’s cholesterol isn’t measured by sampling your blood for cholesterol. This cholesterol is inside the cells and cannot be measured, at least without taking biopsies (pieces) of your muscles, heart, brain, liver, et cetera. To get this LDL inside your cells to be used requires, as we have mentioned, a special receptor that recognizes the LDL - just like there are insulin receptors that recognize insulin to bring glucose into the cells.

Many of the drugs physicians use to lower your cholesterol, work either by slowing down how much cholesterol your liver makes (that 1000 mg per day) or they work by trying to increase how much LDL cholesterol is taken up from the blood, into the cells of your body. Just because you lower the amount of LDL in your blood, doesn’t mean you are reducing the amount of LDL in your body. In fact if you’re removing it from the blood and putting it inside the cells, you’re clearly not removing it from the body. The consequence of this is an increase in the amount of cholesterol within the cells of the body proper. When those cells are within the walls of the coronary arteries, inflammation can worsen promoting CAD. Coronary arteriograms and CAC scores are not going to see this.

The main drugs for slowing the production of cholesterol by your liver are HMG Co-A reductase inhibitors - affectionately called statins. This is the slowest step in the production of cholesterol by your liver. There is ample evidence that these drugs interfere with co-enzyme Q 10, needed for normal cellular function. There is also unpublished data, showing that damage to muscles, resulting from the use of statins is much higher than previously thought, with studies showing muscle damage even when blood tests for that muscle damage are not elevated.

Another older group of drugs, included here for purpose of being complete, are the bile acid sequestrants. These drugs work inside your gastrointestinal (GI) tract, where they combine with the cholesterol in the bile secreted through your liver and gallbladder to help digest fats you have eaten. By binding with the cholesterol in your bile, the cholesterol is removed from your body when you evacuate your bowels. Thus these drugs actually lower the total body cholesterol burden.

A relatively new group of drugs are the PCSK9 inhibitors. These drugs are antibodies to proprotein convertase subtilisin kexin9 (PCSK9). PCSK9 removes LDL receptors from your liver as part of the naturally occurring clean up (recycling) sequence. The function of PCSK9 is to reduce the number of LDL receptors your liver has, which will reduce the amount of LDL your liver can remove from your blood. Block this with a PCSK9 inhibitor, and the LDL receptors remain in place, resulting in more LDL being removed from your blood by your liver; thereby lowering your blood LDL cholesterol, while increasing your liver LDL cholesterol.

Finally, we have Niacin - also known as vitamin B3. Niacin increases your good (HDL) cholesterol, which you can also do by exercising, not smoking if you are a smoker and reduce the fats and refined foods in your diet. Again, not putting the first thing in your mouth.

HDL is a scavenger mechanism. By removing LDL from other parts of the body, HDL can reduce the level of LDL in your blood - but not your body. HDL merely moves the cholesterol around from one place to another, to be dealt with another day. In some instances, HDL can actually harm your body. If the HDL is dysfunctional, which happens either due to genetics or when you have diabetes, inflammation or oxidative stress, this same HDL that was once thought to be only helpful, can actually be pro-inflammatory and cause atherosclerotic heart disease.

Conclusion

The focus of using cholesterol lowering medications, is to lower blood cholesterol levels. However, as we have seen, the real harm occurs within the cells of the body and in particular within the walls of the arteries, where inflammatory plaques result from a combination of factors (Figure 1), including but not limited to oxidized LDL cholesterol. By actually lowering the serum LDL levels, many of these drugs work by increasing the uptake of LDL into the cells of the body proper.

The proposed benefit of these medications, are based upon the lowering of blood LDL cholesterol levels, and reported changes in coronary arteriograms. However, the lack of correlation between changes in blood cholesterol levels and changes in measured physiologic CAD [3] - by simply removing the LDL cholesterol from the blood and placing it into the cells of the body where oxidation may occur – raise significant questions as to the real cost benefit ratios of these drugs.

Given these limitations, it would appear that greater emphasis should be placed on lowering total body cholesterol burden, either through the use of medications which actually lower LDL body cholesterol levels, or through dietary and lifestyle changes which limit the oxidative impact of LDL cholesterol in addition to the other components (Figure 1) responsible for inflammatory coronary artery disease.

Acknowledgment

FMTVDM is issued to the first author. The “Inflammation and Heart Disease” theory was developed by the first author. All figures reproduced with the expressed consent of the first author.

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Lupine Publishers | Does Nutrition Education Improved Complementary Feeding Practices in Ondo State, Nigeria? a Cluster Randomized Controlled Trial

 Lupine Publishers | Scholarly Journal of Food and Nutrition

Abstract

This study showed the effect of nutrition education on complementary feeding practices among caregivers in Ondo State, Nigeria. The study was a cluster randomized controlled-trial design. The study participants were in two groups. One was intervention and the other one was the control group in a ratio of 1:1. The sample size was 282; the intervention group was 142 and the control group was 142. Intervention on complementary feeding was carried out inform of nutrition education among the caregivers in the intervention group and the control group received no intervention. The intervention group received four 4 lesson sessions per group. The sessions were based on continued breastfeeding, timely introduction of complementary feeding, minimum meal frequency, minimum dietary diversity, minimum acceptable diet, feeding with iron rich foods, responsive feeding and hygiene. Data were analyzed using SPSS version 22.0. From Kaplan-Meier analysis, continued breastfeeding survival at age 11 months was 94.4% in the intervention group and it was 69.7% in the control group. Adjusted Relative Risk [ARR] was used to determine the effect of nutrition education on the intervention group and control group for variables such as Minimum Acceptable Diet [ARR: 3.13; CI: 2.53-5.16; P<0.001] at the end line. This study concluded that nutrition education based on complementary feeding guidelines improved the feeding practices of the caregivers. Therefore, the study recommends that Ministry of Health in Ondo State should encourage complementary feeding training for caregivers and CHEWs at the various Basic Health Centers in the State.

Abbreviation: ARR: Adjusted Relative Risk; BHC: Basic Health Centre; CFP: Complementary Feeding Practices; CHEW: Community Health Extension Workers; EBF: Exclusive Breastfeeding; FAO: Food and Agriculture Organization; HIV: Human Immunodeficiency Virus; ICF: International Classification of Functions, disability and health; IEC: Information Education Communication; IG: Intervention Group; IYCF: Infant and Young Child Feeding; LGA: Local Government Areas; MDD: Minimum Dietary Diversity; MMF: Minimum Meal Frequency; MAD: Minimum Acceptable Diet; NCP: National Population Commission [Nigeria]; NDHS: Nigeria Demographic and Health Survey; NGOs: Non-governmental organizations; NNHS: National Nutrition and Health Survey; OSHREC: Ondo State Health Research Ethics Committee; OSPHCDB: Ondo State Primary Health Care Development Board; SMART: Standardized Monitory and Assessment of Relief and Transition

Introduction

The UNICEF showed that globally 66% of children aged 6 to 8 months received semi-solid, solid or soft foods, with cases of nutrition deficiencies due to untimely introduction of complementary foods [1]. The timely introduction of complementary feeding among caregivers in sub-Sahara Africa was 71% and 68% for West and Central African countries while it was 67% for Nigeria [1]. Children receiving MAD was 11% in sub-Sahara Africa, 9% in West and Central African countries and 10% in Nigeria [1]. Infants feeding practices reports available in some other West African nations showed poor practices of MAD by caregivers in Ghana [13%] and in Benin Republic [9%] [1]. The report of the Nigerian National Demographic and Health Survey [2] indicated that only 11% of the breastfed infants received complementary foods from at least

four food groups. Globally, about 45% of infants less than 6 months of age were exclusively breastfed [EBF], with 42% in sub-Sahara Africa and 29% for West and Central African countries. In Nigeria, EBF rate is at 17%, which implies that 83% have had untimely introduction of complementary feeding [1]. The issues of poor infants feeding knowledge and practices among caregivers which result to poor nutrition status among the infants call for action due to the present level of malnutrition in Nigeria.

Standardized Monitory and Assessment of Relief and Transition reported that 21.1% of children less than five years of age in South West Nigeria, the Geo-political Zone of this study were stunted [3]. Malnutrition caused the death of 53% of children less than five years of age in Nigeria [4]. It also showed that 13% of the death could be averted if 90% of mothers in Nigeria practiced exclusive breastfeeding for the first six months. If the same mothers practiced timely introduction of complementary feeding, a further 6% of the death rate could be prevented [5]. Inadequacy in complementary feeding during infancy and childhood has been demonstrated by researchers as a factor that leads to malnutrition, resulting in higher mortality and morbidity rate among the children [6]. In Nigeria, poor infants feeding practices rate is high. Apart from lack of adequate complementary feed being provided to the infants, force-feeding practices rather than responsive feeding is reported among 83.8% respondents in Enugu, Nigeria [7]. Only 10% of infants received minimum acceptable diet in the country [1]. The report of National Demographic and Health Survey showed that only 17.6% of infants in the South West Geo-Political Zone received minimum adequate diet [2].

Objectives

a) To implement a nutrition education program using World Health Organization guidelines on complementary feeding for caregivers in Ondo State, based on complementary feeding practices, knowledge and attitudes.

b) Establish the effects of nutrition education on complementary feeding, knowledge, attitudes and practices among caregivers in Ondo State.

Materials and Methods

Research Design

This was a cluster-randomized controlled trial. A randomized controlled trial reduces bias in interventional studies by controlling for known and unknown confounders. It also provides evidence of a causal-effect relationship between the intervention and the outcomes [8,9]. The Basic Health Centres were randomized and not the caregivers to enhance participation by caregivers, by reducing loss to follow-up.

The study had two phases: the needs assessment phase and the intervention phase.

Sample Size

Sample size was determined using [10] for continuous assessment. A total of 290 caregivers were achieved. During the study 6 caregivers were lost to follow-up which resulted to 284 caregivers that completed the study. They were distributed as follows; This resulted into 70 caregivers in the first Basic Health Center for intervention group, 72 in the second BHC for intervention group, 69 in the first BHC for control group and 73 in the second BHC at the end of the study depending on eligibility criteria and willingness of the caregivers to participate in the different communities.

Sampling Techniques

Multi-stage sampling method was adopted for this study. Purposive sampling method was used for the selection of Ondo North Senatorial District out of the three Senatorial Districts in the State. Owo Local Government Area [LGA] due to existing literature [11]. Simple random sampling method was used for the selection of the 4 Basic Health Centres [BHC] out of ten [10] BHCs in the LGA. Randomization was then conducted to assign the BHCs into intervention groups and control group by a biostatistician using MS EXEL at a ratio of 1:1, with each study group having two BHCs. Caregivers were allocated to study group based on the BHCs they attend for post-natal care.

The recruitment of study participants into the study

The study participants were recruited by the researcher, assisted by the Community Health Extension Workers [CHEWs]. The researcher together with the CHEWs in the selected BHCs recruited and registered eligible participants [caregivers with infants] into the study at the weekly routine meetings in the BHCs. Daily recruitment was carried out when the caregivers visited the health centres for routine meetings for immunization, appointments and check-ups. Eligible caregivers were recruited in 13, 11 and 10 in numbers in each Basic Health Centres, until the required sample size was achieved. The screening was conducted by the researcher and the Community Health Extension Workers (Figures 1 & 2).

The Training

Caregivers in the control group were selected from 2 BHCs and did not receive any intervention from the research team. Meanwhile, the caregivers in the intervention group which were also selected from 2 BHCs received the complementary feeding nutrition education from the research team. The education session began with creating rapport between the researcher [assisted by CHEWs in the research group] and the participants. The training was conducted in the local Yoruba language for better understanding. The content of the nutrition education on complementary feeding was based on the guidelines [12] as well as the knowledge, attitude and practices gaps identified during the need’s assessment. The caregivers received training on continued breastfeeding, dietary diversity, meal frequency, responsive feeding techniques, meal planning for infants, infants’ meal planning during illness and recovery and hygiene [water treatment]. This training was carried out in three consecutive weekends as the caregivers were recruited per group in the respective health centers weekly. After the recruitment and training, the caregivers were followed up during the program. The phone numbers of the caregivers and the CHEW in that zone, where the caregivers resided were also written down by the researchers in case of questions or if need arises to attend to some unclear area of the training pertaining to the study. Two days to and on the eve of visitation day, the enumerator allocated to the area would call to remind the caregivers about the visitation day.

Research Instruments

WHO [2010a] IYCF indicators [13]

WHO [2010b] 24hr. dietary recall on complementary feeding practices [14]

WHO [2004] Complementary feeding guidelines [12] Data analysis

Pilot study was carried out. During the pilot study, training was conducted for caregivers in the intervention group and there was standardization of data collection procedures. Each questionnaire was administered twice on the same group of participants at an interval of two days. A correlation co-efficient of more than 0.7 was considered adequate [Mukaka, 2012]. They are as follows:

a) Baseline questionnaire for the caregivers: 0.89[0.82- 0.92].

b) Second questionnaire for all the caregivers: 0.77[0.61- 0.84].

c) Third questionnaire for all the caregivers: 0.88[0.71- 0.91].

Complementary feeding practices were determined based on the [13] IYCF indicators. Early initiation of breastfeeding was determined thus; proportion of infants who were put to breast within one hour of birth; for exclusive breastfeeding; [proportion of infants 0-5 months who were fed exclusively with breast milk]. For continued breastfeeding, [proportion of infants fed with breast milk in the previous day], For meal frequency [a frequency of 2 times for ages 6-8 months and 3 times for 9-11 months was considered adequate and milk feeding frequency for non-breastfed infants [proportion of infants 6-11 months who received at least 2 milk feedings during the previous day] was considered adequate]. For dietary diversity, a daily intake of 4 or more out of 7 food groups was considered adequate [15]. For consumption of iron rich and iron fortified foods, proportion of infants who received iron rich food or iron fortified food that is designed for infants or that is fortified at home. For responsive feeding, caregivers were expected to encourage the infant to eat the food served. Also, for hygiene, treatment of water by boiling water to boiling point and allow it to cool in a clean container was the acceptable practice.

Feeding practices was determined using the feeding practices variable for the questionnaire according to 24hr. dietary recall on complementary feeding practices [14]. The caregivers that answered yes to right practices was awarded 1 while the caregivers that answered no to right complementary feeding practices was awarded 0. The proportion of each variable was subjected to regression analysis. In addition, adjustment/ controlling for the covariates such as caregivers age and parity was done during the analysis to cater for the design effect because it was the BHCs that were randomized into study groups and not the caregivers.

Logistical and ethical considerations

Ethical clearance was obtained from Ondo State Health Research Ethics Committee [OSHREC]. Letter of introduction to the coordinator of Owo LGA, BHCs was obtained from Ondo State Primary Health Care Development Board [OSPHCDB], Nigeria.

Results

The influence of nutrition education on complementary feeding practices of the caregivers

A regression analysis using Adjusted Relative Risk was carried out to determine the effect of the nutrition education on the feeding practices of the caregivers. The caregivers in the intervention group were 8 times more likely to feed the infant with minimum meal frequency than the caregivers in the control group at the midline [ARR: 8.13; CI: 3.12-21.19; p<0.001] and 3.4 times at the end line [ARR: 3.41; CI: 2.36-5.22; p<0.001]. The result showed that caregivers in the intervention group were 7 times more likely to feed their infants with diversified diet in terms of the complementary foods at midline [ARR: 7.89; CI: [4.47-13.92; p<0.001] and 6.7 times at the end line [ARR: 6.66; CI: 4.43-8.84; p p<0.001]. Feeding the infants with minimum acceptable diet was 6.4 times more likely among the caregivers in the intervention group [ARR: 6.42; CI: 2.42-18.33; p<0.001] at the midline and 3 times more likely at the end line [ARR: 3.13; CI: 2.53-5.16; p<0.001] compared to the control group. This shows that the infants in the intervention group were more like to meet the minimum acceptable diet requirement compared to the infants in the control group, both at the midline and at the end line of the study.

Responsive feeding was more likely to be practiced among the caregivers in the intervention group than the caregivers in the control group [ARR: 2.12; CI: 1.72-2.65; p<0.001] at the midline and 6 times more likely at the end line [ARR: 6.60; CI: 4.43-8.84; p<0.001]. The responsive feeding practices were also established by caregivers during the FGDs. This was what a caregiver from the intervention group had to say; I did not believe that the different ways of encouraging the infants to accept complementary food could be achievable because of my experience with my first daughter, but this training helped me. Since the time we were taught on responsive feeding which was demonstrated to us in the health centre, I practiced responsive feeding on my infant and it was achievable.” [CAREGIVER3, FGD2 2017] (Table 1).

Continued breastfeeding survival analysis

Adjusted Relative Risk analysis showed that 30% of the caregivers in the control group were less likely to continue breastfeeding, compared to the intervention group at the end line [ ARR 0.30; CI: 0.16-0.56; p<0.001]. Additionally, survival analysis was performed on the continued breastfeeding practices of the caregivers in both groups to determine the probability of continued breastfeeding along with complementary feeding among the caregivers. From Kaplan-meire analysis, 69.7% of the caregivers in the control group continued with breastfeeding at age 11 months, compared to 94.4% of the caregivers in the intervention group [p<0.001].

Discussion

Despite research-based evidence on association of adequate complementary feeding practices and child survival. In Nigeria, 70% of caregivers did not have good adequate complementary feeding practices [16,17]. Only 17.5% of Nigerian infants received minimum acceptable diet during complementary feeding by the caregivers [18]. In South western Nigeria, the geopolitical zone where this study was carried out, only 17.8% of infants received minimum acceptable diet [MAD] while in Ondo State, only 11.4% received MAD [2]. This study showed the effect of nutrition education which improved the caregivers’ complementary feeding practices. Prior to the commencement of complementary feeding practices at the baseline, there was no significant difference in the complementary feeding practices in the two groups. Some of the caregivers that introduced complementary feeding earlier than six months were among caregivers that participated in this study. Whether they introduced complementary feeding earlier or at appropriate time there was a significant improvement in the feeding practices among the caregivers that received nutrition education (Figure 3 & 4).

Force feeding ways of introducing complementary feeding among the caregivers in the control group showed poor feeding practices of the caregivers. There was lack of knowledge on responsive feeding which made the caregivers in the control group lack confidence to feed the infants. This resulted to force feeding as determined in this study, which could affect the timely introduction of the complementary feeding practices. Majority of the caregivers in the control group started force feeding due to the refusal of the complementary foods by the infants. The issue of early intolerance of the complementary foods by the infants was handled during the nutrition education using different techniques of responsive feeding through posters and food demonstrations. This study is in line with guiding principle of complementary feeding stated by the National Policy on infant and young child feeding in Nigeria [19], which declared that responsive feeding using psycho-social care should be adopted by mothers in Nigeria. To foster a reciprocal relationship between the parent or caregiver and the child, and thus practicing responsive feeding, was hypothesized to be beneficial to both parties [20]. Accelerated rate of death and pneumonia as a result of force feeding was a concern [21]. They further stated that force feeding leads to infections, collapsed lungs, digestive and pancreatic problems. Acceptable ways of introducing complementary feeding that will be acceptable by the infants and will not frustrate the effort of the caregivers which could lead to introduction of force feeding, was learnt by the caregivers in the intervention group during the nutrition education on complementary feeding. Lack of responsive feeding practices caused growth flattering among the infants in low- and middle-income countries [22].

Therefore, responsive feeding techniques should be among the package for complementary feeding guidelines. To corroborate the effectiveness of nutrition education on responsive feeding, it was revealed that there was an improvement in the complementary feeding practices of caregivers in the intervention group as the caregivers in Kosova were able to see more reasons to have patience and encourage the infants to eat complementary foods [23]. Consumption of iron rich foods was high among the infants in both groups and this agrees with the reports on consumption of iron rich foods in South-West Nigeria by [19]. The report revealed that 60.1% of infants in this geo-political zone consumed iron rich foods. Despite the high rate of consumption of iron rich foods in both groups, there was a wide margin of iron rich foods intake between the infants in the intervention group and control group in the present study. Increase in the intake of iron rich foods was due to the nutrition education that the caregivers in the intervention group received. Intakes of iron were lower by 16% among infants of 6-12 months than children of 13-36 months in an observational study in Brazilian Well Child Clinic [24]. There was an association between complementary foods and haemoglobin concentration among Indian infants [25]. The author stated that there was a positive association between the infants’ haemoglobin concentration and fortified baby foods, breast milk and infant formula as well as fruits and vegetables to a lesser extent on the contrary to porridge or gruel. Iron deficiency [ID] is the most common micronutrient deficiency world-wide and young children are the special risk group because their rapid growth leads to high iron requirements [26].

Early initiation of complementary food using semi-solid, solid/ soft food consistency and food diversification was improved among the caregivers in the intervention group. The knowledge acquired during the nutrition education was put into practice during the period of complementary feeding before the first birthday of the infants [age 12 months]. It was recommended that nutrition education is needed in West African countries to improve the knowledge of caregivers on complementary foods consistency as majority of mothers in West African countries feed the infants with thin gruel during complementary feeding [27]. Poor timing of initiation of complementary feeding led to 70% malnutrition among infants in Konaseema region of India therefore recommended nutrition intervention on complementary feeding [28]. Untimely initiation of complementary feeding was prevalent among caregivers in North eastern part of Ethiopia and that nutrition education on timely introduction of complementary feeding could improve the practices among mothers [29]. The infants in the intervention group had higher minimum meal frequency rates than the infants in the control group. This was similar to the findings which revealed that meal frequency increased according to the age of children study in South eastern of Ethiopia [30]. The increase in the percentage of the infants who were fed with minimum meal frequency was higher in the intervention group than the control group due to the effect of the nutrition education on the intervention group. This is in line with the findings which showed that there was an increase in meal frequency of infants whose mothers were in intervention group than the infants whose mothers were in the control group in Ethiopia [31]. The intervention group caregivers increased the meal frequency during illness of the infants during the study compared to the caregivers in the control group. Children poor appetite induced by illness can contribute to perpetuate vicious cycle of infectious diseases [32].

Dietary diversity during complementary feeding was achieved among the caregivers in the intervention earlier at midline of the study than the caregivers in the control group. The effect of the knowledge of the caregivers in the intervention group was noticeable in the minimum dietary diversity achieved during the feeding practices. There was higher number of infants who were fed on minimum dietary diversity in the intervention group than the control group. This study was in line with the study which showed significant difference between dietary diversity, meal frequency and feeding infants with iron containing foods among caregivers the intervention group and those in the control group in Uganda [33]. However, literature on intervention to improve the feeding practices of caregivers prior the commencement of the complementary feeding practices, and at different age of the infants’ months was limited. Nutrition education improved dietary diversity among caregivers of infants between 6-23 months in Malawi [34]. Also, UNICEF showed that nutrition education is a catalyst for improving dietary diversity among caregivers in Lilongwe, Malawi [35]. Treatment of drinking water by the caregivers showed that the caregivers in the intervention group practiced good hygiene as compared to the caregivers in the control group. This could be the effect of the nutrition education received by the intervention group. The underlying determinants of undernutrition include food insecurity, inappropriate care practices, poor access to health care, and an unhealthy environment, including access to portable water, sanitation, and hygiene [36] in [37]. In 2018 UNICEF declared that 88% of diarrhea deaths were due to lack of access to safe drinking water, poor sanitation and hygiene [38]. World Health Organization stated that nutrition outcome could be improved with better intervention on water, sanitation and hygiene [39].

The improvement in complementary feeding practices in the intervention group could be linked to the knowledge acquired during nutrition education. The intended feeding practices as noted at the baseline study as well as during FGDs and KIIs was to feed the infants with thin consistency. However, nutrition education was able to change the understanding of the caregivers on food consistency which in turn improved the feeding practices among the caregivers in the intervention group. Several studies have proved the need for nutrition education to improve complementary feeding practices of caregivers. Nutrition education was recommended as a viable tool to improve complementary feeding practices among mothers in Cross River State, Nigeria [18]. Nutrition education on complementary feeding is needed by caregivers in Sagamu, Nigeria to improve the infant feeding practices among mothers [40]. It was 30% of infants in Nigeria were adequately fed and therefore recommended nutrition education for the improvement of caregivers feeding practices [41].

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