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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 4, July/August 2019
208
AFRICA
Natural cocoa inhibits maternal hypercholesterolaemia-
induced atherogenesis in rabbit pups
Richard Michael Blay, Saviour Kweku Adjenti, Kevin Kofi Adutwum-Ofosu, Bismarck Afedo Hottor,
John Ahenkorah, Benjamin Arko-Boham, Frederick Kwaku Addai
Abstract
Atherosclerosis begins during foetal development and is
enhanced by maternal hypercholesterolaemia during preg-
nancy. This study assessed the effect of natural cocoa on
atherosclerosis in offspring conceived in maternal hypercho-
lesterolaemia. Female rabbits were fed a cholesterol-enriched
diet for two weeks and hypercholesterolaemia was confirmed,
after which they were crossed with normocholesterolaemic
males. One group of hypercholesterolaemic mothers (HCC)
received natural cocoa powder (NCP) in their drinking
water, whereas the other group (HC) received only water.
Histological analysis of three segments of the aorta (arch,
thoracic and abdominal) from offspring of both groups was
compared with a control group (NC). Intima–media thick-
ness of the aortic arch in offspring born to hypercholester-
olaemic rabbits (HC: 146 µm) was higher compared to HCC
(99 µm) and control rabbits (58.5 µm). All the sections from
the aortic arch of the HC group had atherosclerotic lesions
while none of the sections of the aortic arch from the NC
and HCC groups had lesions present. Inferentially, regular
and voluntary consumption of NCP during pregnancy may
inhibit aortic atherogenesis in offspring of hypercholesterol-
aemic mothers.
Keywords:
atherosclerosis, maternal hypercholesterolaemia,
intima–media thickness, cocoa, antioxidants, foetal
Submitted 22/9/18, accepted 16/4/19
Published online 24/5/19
Cardiovasc J Afr
2019; 30: 208–215
www.cvja.co.zaDOI: 10.5830/CVJA-2019-019
Atherosclerosis is a progressive disease that is initiated by
turbulent blood flow and the accumulation of lipids in the walls
of large arteries, leading to dysfunction of the endothelium, and
subsequently, the formation of lesions.
1,2
The disease leads to
complications such as myocardial infarction and stroke, which
are known to cause the death of about 17 million people globally
each year.
3-5
In humans, the process of atherogenesis begins during
foetal development, and early lesions known as fatty streaks,
containing cholesterol-rich macrophages or foam cells, occur in
the first decade of life.
6
There is therefore a long time lag between
the onset of atherogenesis and clinical manifestation,
7
and fatty
streaks become precursors to advanced lesions later on in life.
1
The relationship between serum cholesterol levels and
atherosclerosis has long been established, and cholesterol-
lowering therapy is known to reduce atherosclerosis.
8
The specific
process that initiates atherosclerosis, however, needs to be further
understood in order to develop effective therapeutic measures.
Three hypotheses have been proposed concerning the initiation
of atherosclerosis, namely, the response-to-injury, the response-to-
retention and the oxidative-modification hypotheses.
9
According
to the response-to-injury theory, atherosclerosis is initiated
when endothelial cells are denuded due to damage to the cells.
10
It is now known that endothelial injury alone does not initiate
atherosclerosis, but injury results in the initiation of oxidation of
low-density lipoprotein (LDL) and the activation of monocytes,
which differentiate into macrophages and foam cells.
11,12
In the response-to-retention hypothesis, sub-endothelial
retention of apolipoprotein B-containing lipoproteins in the walls
of arteries is the key pathological event during atherosclerosis.
9,13
The oxidative-modification hypothesis suggests that native LDL
is oxidised in the vessel wall and the uptake of modified or
oxidised LDL by macrophages leads to the formation of foam
cells,
14
which become the pivot for the development of advanced
atherosclerotic lesions.
Putting together the evidence supporting the various
hypotheses, accumulation of cholesterol and its oxidation are
key in the initiation of atherosclerosis. Hypercholesterolaemia,
a condition characterised by elevated cholesterol levels in blood,
is therefore the principal risk factor for cardiovascular diseases,
15
and understanding the role it plays during atherosclerosis is
therefore likely to provide several novel treatment solutions.
Maternal hypercholesterolaemia during pregnancy results
in the formation of significantly larger atherosclerotic lesions
in foetuses,
7
and the formation of advanced lesions in adult life
progresses faster in offspring of hypercholesterolaemic mothers.
16
Maternal hypercholesterolaemia may enhance atherosclerosis
by differentially dysregulating the expression of aortic genes in
the offspring,
17
resulting in a cascade of processes later in life
that will increase lipid deposition and inflammation. Moreover,
hypercholesterolaemia in pregnancy enhances endothelial
dysfunction in foetal arteries and placental vasculature,
18
thereby
decreasing nitric oxide-dependent vasodilation while increasing
oxidative stress.
19
On the other hand, dietary intervention in
humans using antioxidant-rich foods has an inverse relationship
with the risk of cardiovascular diseases.
20,21
Department of Anatomy, School of Biomedical and Allied
Health Sciences, College of Health Sciences, University of
Ghana, Korle-Bu campus, Accra, Ghana
Richard Michael Blay, PhD,
rmblay@ug.edu.ghSaviour Kweku Adjenti, PhD
Kevin Kofi Adutwum-Ofosu, PhD
Bismarck Afedo Hottor, PhD
John Ahenkorah, PhD
Benjamin Arko-Boham, PhD
Frederick Kwaku Addai, PhD