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Lupine Publishers | In-Depth Review of Caregivers’ Nutrition Education effects, on Complementary Feeding Practices in Nigeria
Lupine Publishers | Scholarly Journal of Food and Nutrition
Abstract
This
study is an in-depth finding of the effect of nutrition education on
caregivers’ complementary feeding practices. The WHO recommendations for
optimal complementary feeding are based on continued breastfeeding, early
introduction of solid or soft diet, minimum meal frequency (MMF) and minimum
dietary diversity (MDD) in terms of food groups. Improved knowledge on adequate
complementary feeding could positively affect the attitude of caregivers
towards complementary feeding practices. Meanwhile, effect of demographic and
socio-economic status was also reviewed. Materials used for this study are
secondary data from archived materials and existing literature on effects of
nutrition education on complementary feeding in Nigeria and other developing.
The study showed that reports on complementary feeding practices in developing
countries are rated inadequate, with inappropriate early introduction of
complementary feeding. Complementary feeding was either introduced too early or
too late with thin and low iron rich and vitamin A rich diet. Study revealed
poor practices of Minimum Meal Frequency (MMF) and Minimum Dietary Diversity
(MDD). Force feeding overrides responsive feeding which attracts other
complicated health issues among the infants. The final summary showed that
nutrition education will be an effective tool to solve the problem of
inadequacy in complementary feeding practices.
Introduction
The
knowledge, attitude and practices of complementary feeding among caregivers in
the developing countries have been rated poor [1]. Caregivers’ nutrition
education on complementary feeding is an effective tool to improve the
complementary feeding practices. Other factors affecting the complementary
feeding as revealed by researchers are socio-demographic and socio-economic
status of the caregivers. The effects of nutrition education on knowledge,
attitude and complementary feeding practices of the caregivers and the
nutritional status of infants revealed by existing literature are discussed in
this chapter. Infants feeding practices reports available in some West African
nations showed poor practices of MAD by caregivers in Ghana (13%) and in Benin
Republic (9%) [2]. The report of the Nigerian National Demographic and Health
Survey [3] 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]. In the developing countries, malnutrition has been
proved to be responsible for over 41% of the deaths among children 6 to 24
months of age [4,5] revealed that under nutrition of protein and energy-giving
foods contributed to 45% of death, among children less than five years of age
in evidence-based research carried out in 34 countries in the world. The global
strategy for infants and young child feeding was based on the significance of
nutrition in the early months and years of life [6]. These strategies include
monitoring, assessing and promoting adequate infant nutrition, breastfeeding,
feeding behavior, national health programs and infants feeding guidelines. In
order to achieve adequate infant feeding practices in the developing nations,
the global strategies must be followed.
Research objectives are
a)
To ascertain the relationship between caregiver’s nutrition education on
caregivers’ complementary feeding knowledge, attitudes and practices
b)
To identify relative findings on effects of nutrition education on caregivers’
complementary feeding knowledge, attitudes and practices
c)
To establish the on effects of caregivers’ nutrition education on infant’s
nutrition status
Research Methods
Secondary
data from existing literatures on effects of nutrition education on
complementary feeding knowledge, attitude and practices as well as the infant’s
nutrition status was used to make compilations on these findings.
Demographic and
socio-economic factors influencing caregivers complementary feeding practices:
Demographic
and socio-economic status of caregivers is one of the major factors associated
with poor complementary feeding practices of caregivers and nutrition status of
infants in developing countries [7]. Maternal age, educational level and the
household’s income have been reported as factors associated with the
complementary feeding knowledge, attitudes and practices among the caregivers. The
caregivers’ age and low education level attainment have been revealed to
influence complementary feeding practices in countries such as India [8]. In
Nepal, indicated that mothers of infants aged 6-23 months working outside the
home were less likely to practice optimal complementary feeding that meet the
recommended dietary diversity. Also, [9] revealed that mothers that worked 8
hours outside their homes were unable to meet the recommended dietary diversity
and meal frequency for infants in Nigeria. This was associated with limited
time they had with their children. [10] revealed that food restrictions due to
cultural belief as well as economic status of mothers were contributing factors
to inappropriate feeding practices among mothers in Cross River State, Nigeria.
In Moretele District in South Africa, [11] showed that adherence to cultural
practices affects mothers’ attitude to complementary feeding practices.
Households with lower wealth index were found to be the more likely to have
inappropriate complementary feeding practices in India, Bangladesh, Nepal,
Pakistan and Sri Lanka [12]. There was a significant association found between
caregivers’ socio-economic status and infant feeding practices in Nekemte,
Ethiopia. The study showed that caregivers in the low socio-economic strata
practiced sub-optima complementary feeding [13]. The effects of economic status
on nutrition status of children have also been illustrated by researchers. In
Ondo State, [14] discovered low intake of energy dense food and protein
containing food among children whose mother were living in rural communities of
Ondo state. The author stated further that the mothers were of low
socioeconomic status. This corroborates the research of [15] on effect of low
socio-economic status of rural market women in owo Local Government of Ondo
State on the nutrition status of their infants. The study reported a positive
correlation between low economic status of the market women and the feeding
practices as well as the nutritional status of the children. Research has
proved that caregivers required skilled support to adequately feed their
infants despite the limitations which could be caused by socio-economic and
demographic status of the caregivers [16]. Nutrition education is an effective
way of improving complementary feeding practices among mothers as [17] reported
that poor feeding practices are not necessarily due to lack of high quality of
foods at the household but lack of infants’ feeding knowledge by the
caregivers.
Complementary feeding knowledge,
attitude and practices:
Knowledge
is the understanding of any given topic [18]. In this study, knowledge referred
to the ability to understand specified aspects of complementary feeding
practices. Attitudes are emotions, motivations and perceptive as well as
cognitive beliefs that could either positively or negatively influence the
caregivers’ complementary feeding attitudes [18-20]. Caregivers complementary
feeding attitudes or infant’ feeding behavior is influenced by his/her
emotional, motivational and perceptional as well as thoughts [20]. Attitudes
have the ability to influence the future behavior of the caregivers’ knowledge
and could explain the reason why caregivers adopt complementary feeding
practices and no other alternatives [21]. The terms attitude, beliefs and
perceptions are interchangeable. In this study, “practices” is an observable
action of a caregiver that could affect his/her infants’ nutrition, such as
eating, feeding, water treatment, cooking and foods selection for the infants.
Practice and behavior are terms used interchangeable, though practice has a
connotation of longstanding or commonly practiced behavior [22].
Effect of nutrition
education on caregivers’ complementary feeding knowledge:
Knowledge
on complementary feeding by the caregivers has been revealed by [11] to be
limited in African countries. A Nigerian study showed that knowledge on benefit
of continued breastfeeding along complementary feeding till the infant’s age 24
months is low [23]. A descriptive study on maternal knowledge on complementary
feeding in India, established that 75% of caregivers had average knowledge on
appropriate consistency and safe preservation of infant’s meal [24]. The
circumstances are similar to Nigeria, Ondo State in particular. According to
[25], only 30% of the caregivers have adequate knowledge of complementary
feeding in Nigeria. In Ondo State, it is reported that 70% of the caregivers
used sorghum majorly as complementary foods [15]. The role of nutrition
education on caregivers feeding knowledge cannot be underrated. The [16] stated
that inadequate knowledge on appropriate complementary feeding is a determinant
of malnutrition among the infants in the developing countries. The effect of
organized and well-planned nutrition education on complementary feeding
knowledge have been proved by researchers [26] reported that 88% of caregivers
in North Shan State and Karachi State Republic of the Union of Myanmar were
able to plan infants’ meals from more than four food groups after nutrition
education on the infants feeding knowledge [27] showed that nutrition education
to improve maternal complementary feeding knowledge significantly impacts on
knowledge of meal preparation for children in Uganda. The authors stated that
71% of caregivers who received nutrition education intervention had improved
knowledge in complementary feeding and were able to improve in infants feeding
frequency. Furthermore, Nutrition education and counseling on infants feeding
improved the complementary feeding knowledge of caregivers significantly by 1.5
points in a study conducted in the Philippines. Ondo State, Nigeria still
suffers a setback in adequate complementary feeding as there is lack or low
knowledge of complementary feeding [15]. The author reported that caregivers in
Ondo State had low knowledge on food diversification. Intervention programs
which involve the caregivers and Community Health Extension Workers have been
confirmed to be limited in Ondo State thereby causing a research gap on
complementary feeding knowledge in Ondo State, Nigeria consistency. The study
of [15] was a cross-sectional study to determine the situation of feeding
practices and factors affecting the feeding practices of the infants. In
Nigeria, only 3.7% of households have access to an improved water resources
located on premises, free of E-coli and available when needed [28]. The report
showed that diarrhea is prevalent due to poor access to portable drinking
water. Caregivers knowledge to improved access to portable water was low as 63.4%
of caregivers used unprotected well in Biye community in Kaduna, Nigeria [29]
the author stated further that water boiling method is the cheapest way to
achieve portable water for the infants in the community.
Effect of nutrition
education on caregivers’ complementary feeding attitudes:
The
UNICEF [17] suggested that reduction of child mortality can be achieved when
IYCF awareness is improved. The poor complementary feeding attitudes have been
linked with communities’ beliefs and mothers’ perceptions [30]. Showed that
socio-cultural belief has a strong influence on infants feeding and determines
optimal infants feeding practices; breastfeeding and complementary feeding in
Kakamega County, Kenya. In Zambia, majority stopped breastfeeding before the
appropriate time because they believed that breast milk was not enough, and
that the child had lost interest in breastfeeding described how Mexican mothers
in a cross-sectional survey mostly fed their children liquid and semi liquid
foods with few vegetables, meats and legumes. The author stated that Mexican
mothers took this decision due to their perspective on the consistency of the
food for infants, that is, soft or solid foods are detrimental to infants’
health [31] confirmed that, despite the economic status and educational
attainments of mothers, they exhibit poor attitude to complementary feeding in
Shabelle Zone of Somalia due to influence of the cultural belief. Feeding thin
consistency feeds in small amounts and food restriction due to cultural beliefs
are common in Nigeria [32, 33] revealed that scientific knowledge on infant
feeding practices would improve complementary feeding attitude among mothers in
Republic of Kosovar. Meanwhile, the author’s opinion was in contrast to [34]
who revealed that despite the nutritional education on importance of
consumption of pulses to children’s wellbeing in Southern Ethiopia, there was
no significant difference between attitudes of mothers who received the
training and attitudes of mothers in the control group due to cultural belief
on effect of pulses on children [35] experienced low acceptability of blended
complementary food with pulses in Ethiopia. This study put into consideration
the fact that cultural beliefs may be influencing caregivers’ attitude and
therefore focused on other beneficial food items in the study area to improve
caregivers’ attitude on complementary feeding [36]. Showed that despite the
knowledge of complementary feeding among mothers in Lagos State, Nigeria, the
mothers had the poor attitude towards timely introduction of complementary
feeding as majority of the caregivers introduced complementary feeding too
early or too late. The author stated that this was prevalent among working
mothers. The intervention of nutrition education and counseling was proved to
improve mothers’ attitude towards complementary feeding [37] revealed that
caregivers had change in attitudes towards responsive feeding and their
infants’ nutrient intake was higher compared to the control group. Most studies
conducted both in Ondo State and in other locations in Nigeria were descriptive
and cross-sectional studies, leaving research gaps on effect of nutrition
education on complementary feeding attitudes in the area [23] conducted a
cross-sectional survey in Nigeria on factors affecting breastfeeding practices.
This was a cross sectional study which identified poor practices of
breastfeeding but could not profound solution through an intervention [25]
conducted a study in Lagos, Nigeria on factors associated with inadequate
complementary feeding. Also, [14] carried out a study on complementary feeding
in Ondo State, Nigeria on effect of socio-economic status on infant feeding.
The above two studies were cross-sectional studies on factors associated with
inadequate complementary feeding in Nigeria. The studies of [25,14] were unable
to improve the complementary feeding attitudes of the caregivers in the study
areas because they were cross-sectional studies and not an interventional
study. The above two studies had little or no effect on the participants,
although they could be included by Nigerian government’s program for policy
framework. The study of [38] and [39] was designed to assess complementary
feeding practices among caregivers and there was no intervention on
complementary feeding practices in these studies. There is limited literature
on the effect of nutrition education on maternal attitudes towards
complementary feeding.
Effect of nutrition
education on caregivers’ complementary feeding practices:
A
report by UNICEF showed that complementary feeding practices are globally poor
[2]. In Ireland, only 36% of infants had timely initiation of solid and semi
solid foods. According to [40], only 1.8% of caregivers in Uganda fed infants
with protein containing food products, especially meat during the period of complementary
feeding [41] stated that only 28% of caregivers in Ghana were able to feed
their infants 2-3 times daily with adequate complementary meals. The level of
inadequate complementary feeding in Nigeria is worse than that of Ghana as only
11% of exclusively breastfed infants receive complementary meals from four food
groups and only 7% of the non-exclusive breastfed infants were fed with
adequate complementary feeding in Nigeria. These show the poor practices of
complementary feeding among caregivers in the region. United States Agency for
International Development [42] in an assessment of infant and young child
feeding practices in Nigeria affirmed that there are challenges to improve on
complementary feeding behaviors among caregivers with infants. However, the
author indicated that with well-trained health workers, coordinated and
targeted messaging to caregivers and influencing groups in the communities,
there will be a great deal of progress towards increasing optimal infant and
young child feeding practices in Nigeria. To corroborate the above, [38] and
[39] observed that nutrition education intervention among caregivers in Nigeria
will improve the caregivers’ complementary feeding practices [43] discovered
that nutrition education on complementary feeding carried out by 30 several
studies in developing countries showed statistical evidences of improved
complementary feeding practices of mothers. Therefore, the study recommended
nutrition education among mothers to improve complementary feeding practices.
The study of [29] on improved hygiene practices among caregivers showed that
79.6% caregivers boiled their drinking water in Biye community, Kaduna,
Nigeria. Interventions that improved complementary feeding practices among
caregivers were carried out in some part of the world such as Cambodia,
Zimbabwe, Mali and Ghana with different degrees of success. In Bangladesh, [44]
revealed that breastfeeding counseling improved exclusive breastfeeding among
mothers. The author revealed that when mothers received counseling on exclusive
breastfeeding, they practiced it until 135 days while the control group
practiced exclusive breastfeeding for 75 days. This improvement achieved was
due to interventional research by the researcher. Another instance was the successful
report of FAO [20] in a program titled “Promoting improved complementary
feeding” in Cambodia. The program was based on counseling, training and cooking
demonstration. This program was carried out by conducting home visits to assist
households who were encountering challenges in adopting the improved
complementary feeding and the caregivers were trained with improved recipe. The
program was recorded to be a success as the caregivers had improved knowledge,
attitude and complementary feeding practices. However, a similar nutrition
education program which trained the caregivers on improving complementary
feeding in Zimbabwe proved unsuccessful due to inadequate monitoring system and
lack of trained personnel for continuity [27] stated that women who receive
nutrition education on complementary feeding were able to prepare complementary
diet from over four food groups, compared to their attitude towards dietary
diversity before the nutrition education. The success report of Cambodia
nutrition education and training program was particularly based on the current
caregivers with infants at the time of the program in the study area. The
program did not plan for the sustainability of the program on subsequent
caregivers; as there were no community-based personnel that were involved to
receive the training [20]. Also, in Zimbabwe, the nutrition program to promote
adequate complementary feeding practices was unsuccessful due to lack of
trained personnel educating caregivers to continue with the programs among the
caregivers. There has been limited documentation of complementary feeding on
nutrition education targeted at the caregivers as well as health personnel
within the health care system who deals with maternal and child’s health in
Ondo State. Surveys on infants’ feeding practices available were mainly on
cross-sectional survey of the situation and no known intervention was found.
Effect of caregivers’
nutrition education on nutrition status of infants
The
National Demographic and Health Survey carried out by revealed that 43% of
children less than five years of age in rural areas of Nigeria were stunted and
29% of Nigerian children were underweight and too thin for age. In Ondo State,
26% of children less than five years were stunted while 43% were underweight
[45]. Inadequacy in complementary feeding practices can result to malnutrition
in children during the complementary feeding period [46]. Declared the period
of complementary feeding as a period of windows of opportunity for growth
flattering. Revealed that there were suboptimal complementary feeding practices
among mothers studied in different geographical area in Nigeria which leads to
growth flattering of infants in the area. Interventions that can bring about
improvement in the nutrition status of infants could be achieved by nutrition
education [5] revealed that weight and height increased among children 6-24
months of age after maternal nutrition education on complementary feeding in
Sri Lanka and Tanzania. Concluded that nutrition education intervention was
successful in reducing malnutrition in Pakistan as 36% malnourished children
progressed to normal nutrition status [47] showed that there was an increase in
weight (350g) and length (0.66cm) among the infants of caregivers in
intervention group that received complementary feeding nutrition education in
Karachi, Pakistan [48] stated that pooled-effect sizes from three recent
systematic reviews suggested a modest nutrition education but there was a
significant effect of the types of complementary feeding interventions on
weight and length gain [49] revealed the effectiveness of nutrition education
as a tool to improve mothers’ knowledge and complementary feeding practices
which improved the nutrition status of the infants. The author reported in a postprogram
comparison research carried out among mothers in Uganda. Mother who
participated in the program had significant improvement on complementary
feeding practices which in turn had positive impact on the nutrition status of
their infants. In Nigeria there is limited literature on benefit of nutrition
education on nutrition status of the infants. The above interventional studies
on nutrition education on complementary feeding were carried out to determine
the effect of the intervention on complementary feeding practices as well as
the effects on the nutritional status of the infants.
Discussion
The
literatures reviewed for this study showed that the complementary feeding
knowledge, attitude and practices among the caregivers is inadequate, and this
affects the nutrition status of infants. The caregivers especially in the
developing countries such as Nigeria and some African nations have limited or
low knowledge of appropriate complementary feeding practices. The caregivers’
complementary feeding practices are not in line with the WHO recommended
guidelines for infants feeding. The knowledge on the appropriate time of
introducing complementary feeding among the caregivers was established.
Majority of the caregivers had knowledge on timely introduction of
complementary feeding (6 months), although not all of them. It means that some
introduced early while some introduced it late. This is similar to the report
of [47]. The author reported that in Karachi, Pakistan 17% of the mothers
lacked knowledge of appropriate time of introducing complementary feeding and
83% had good knowledge. Although, [13] revealed that 44.2% of mothers in
Nekemte, Ethiopia lacked knowledge on rightful time of introducing
complementary feeding. The literature reviewed further showed that the
attitudes of the caregivers towards complementary feeding were influenced by
the culture and the belief of the caregivers as an individual and the
communities. It is an established fact that nutrition education would be an
effective means of improving complementary feeding practices among caregivers
on; timely introduction of complementary feeding, soft/solid food consistency,
good hygiene practices, food diversification, consumption of iron rich foods
and minimum acceptable diet. Effect of caregivers’ belief on dietary diversity
as indicated by [30] revealed that mothers’ attitude towards infants feeding
played a significant role in food they fed the children in Kakamega County,
Kenya [34] reported that mothers’ negative attitude towards pulses in feeding
the infants was the factor preventing mothers to diversify complementary foods
with pulses in Southern Ethiopia but the knowledge of the caregivers in the
intervention group was improved on dietary diversity after nutrition education.
According to [50] knowledge either directly contributes to attitude formation
or indirectly affects attitudes. Complementary feeding practices by caregivers
globally were rated poor [16]. The author stated further that the situation
does not exclude the caregivers in the developed world; it is a global problem
[16]. The effect of poor complementary feeding practices on the infants’
wellbeing has been identified and determined to be, increase in morbidity and
mortality rate [16]. Survival rate of infants before their first birthday has
been associated with feeding practices of the caregivers [51]. Intervention on
complementary feeding practices rated the second to reduce mortality rate in
infancy. It has been shown that infant and young child feeding is a key area to
improve child survival, promote healthy growth and development [52].
Acknowledgement
The
researchers acknowledge TETFUND and Rufus Giwa Polytechnic, Owo, Ondo State.
Conflict of interest
The
researchers declare no conflict of interest regarding this study.
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Friday, June 10, 2022
Lupine Publishers | Do Low Carb Diets Cause Heart Disease or Cancer?
Lupine Publ;ishers | Scholarly Journal of Food and Nutrition
Keywords
Keywords: Fmtvdm; lowcarb; heart disease; cancer;
atkins; pritikin
Introduction
It
is well recognized that coronary artery disease and cancer are the result of
inflammatory changes, which occur within the tissues of the body - specifically
the walls of the coronary arteries (CAD) and within the specific organ (e.g.
breast, colon) tissue in question [1-3] – and not the blood. Despite this
obvious difference between blood and tissue, medical studies looking at the
impact of diets and drugs have primarily utilized changes in qualitative or at
best semi-quantitative imaging [4-6], weight and blood tests to monitor
presumed changes in heart disease and cancer. However, changes in heart disease
and cancer cannot be measured through the mere use of blood tests alone, since
these blood tests merely tell us what is happening within the blood and not
what is happening in the tissues of the body proper [7,8] – hence, the
persistent debate about the consequences of different diets or drugs, and the
potential risk for CAD and cancer [9-14] – and the persistent doubt and
confusion by the public and media [15-18]. Frankly, if I hadn’t spent more than
three decades working out some of the details and limitations in our knowledge
and published studies - based upon what I read in the lay press - I would be
just as confused [19-25].
Case example in point - consequence
or coincidence?
A
middle-aged man with chest discomfort, had per his report, been following a
LowCarb diet for six months. His already borderline elevated total blood
cholesterol level prior to beginning the LowCarb diet had increased by almost
100 mg/dl or 2.59 mmol/l after being on the diet. His physician ordered a
coronary artery calcium (CAC) study, shown in Figure 1, which revealed no
evidence of calcification (Table 1). The absence of measurable calcium on a CAC
study does not eliminate CAD [1], although, elevated numbers – which are
semi-quantitative, can be helpful. In this instance they were not. Following
persistent angina chest pain, a coronary arteriogram (cardiac catheterization),
shown in Figure 2, was performed reportedly revealing a 99% narrowing of the
proximal part of the patients left anterior descending (LAD) coronary artery.
This was treated with stent placement. The real question here isn’t does he
have CAD – which he still has despite having stents because having a stent doesn’t
mean you are now free of CAD, only that you are receiving continued treatment
for the CAD – but WHY? Clearly the answer is that he has inflammation within
the wall of his LAD. But the more fundamental question is why did this
inflammation occur and was the LowCarb diet, which he reported following, the
cause of that inflammation or was it merely a coincidence?.
Discussion
Beyond
the obvious information from the patients case, including his reported history
of changing his diet, the already borderline elevated blood cholesterol level
which reportedly increased further on the LowCarb diet and the CAC study, which
failed to detect CAD because, after all, CAC studies only detect calcium –
which when present is a good indicator of something going on but the absence of
which as seen in this case does not eliminate the question of CAD – the
question then becomes, Did the LowCarb diet produce the patients CAD and angina
[19,20]? It is unlikely that in six-months he went from pristine arteries to an
almost totally occluded LAD – although as previously documented using Positron
Emission Tomography (PET) this could have happened [26]. Notwithstanding this
possibility, we simply have no prior information about the state of health of
this gentleman’s coronary arteries prior to this original cardiac
catheterization. Was this the same amount of narrowing that was present prior
to the dietary change? Is this worse or better than what existed before? While
we now know that Dr. Robert Atkins died with CAD and reportedly had stents
placed for treatment years before his death - it is not known whether the
Atkins diet was the cause of his CAD. Perhaps it was coincidental, perhaps his
heart disease would have been worse without the diet, perhaps it was the cause
or perhaps the diet had no effect at all. We also know that Nathan Pritikin
died with leukemia and followed the Pritikin vegetarian diet. While much
attention has been paid to reports that Pritikin had heart disease diagnosed
earlier in life, which was reportedly absent at the time of his death – we
truly don’t know if the original diagnosis of heart disease was accurate, or
not. Perhaps he never had heart disease and simple didn’t develop it over time
following his diet. The bigger question – one I never hear raised – is What
role, if any; did his diet play in his leukemia? Was it the cause, or would he
have died earlier had he not been following his diet? Or perhaps the Pritikin
diet had no effect on the leukemia.
Despite
all the social media, advertising, marketing, Google searches, tweeting, blogs,
Facebook postings, and bickering, we will never know the answer to how these
diets affected the overall health of - or the role, if any, they played in -
Atkins heart disease or Pritikin’s cancer. Anyone who tells you otherwise is
probably trying to sell you something. It is one thing to say there is a
correlation and something else altogether to say there is causation [27]. What
we do know is inflammation is the cause of heart disease and the early changes
associated with cancer [1]. This inflammation is caused by a host of factors,
which play different roles in different individuals, based upon their genetic
response to environmental factors – environmental factors, which include inter
alia diet, lifestyle, medications, and smoking. We also know that merely taking
blood samples to look for cholesterol levels, or C-reactive protein, or
homocysteine, or anything else is ersatz and is not going to tell us what is
happening to the coronary arteries themselves or to tissue (e.g. breast)
undergoing an environmental barrage on its way to becoming cancer [7,8]. If we
as physicians are going to talk to our patients, or publish papers in medical
journals, or talk to the media – so the media can write second hand stories,
which someone else will write third hand stories about – then we need to get
our facts straight and to do that will require that we objectively measure [28]
what we are talking about. Until then, we are only doing everyone a disservice
by pretending we know exactly what these diets are doing to people. If we are
right, then we have just been lucky. If we are wrong – then we are potentially
violating our Hippocratic Oath, “Primum non nocere”.
Conclusion
Before
we continue to tell people which diets are safe, which are harmful, and which
may have no impact on heart disease or cancer, we should first objectively
measure the true effect these diets have on the arteries of the heart and the
potential areas of the body, where we are concerned about the risk of cancer
occurring. Then and only then will we be able to have an intelligent objective
conversation with our patients about diets and their causative role in heart
disease and cancer.
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Friday, May 27, 2022
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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Friday, April 29, 2022
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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