Frequency of eating and concentrations of serum cholesterol in the Norfolk population of the European prospective investigation into cancer (EPIC-Norfolk): cross sectional study
BMJ 2001; 323 doi: https://doi.org/10.1136/bmj.323.7324.1286 (Published 01 December 2001) Cite this as: BMJ 2001;323:1286
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In my response to the paper by Dr. Titan and coworkers (1)references
3 and 4 should be 5 and 6, respectively, and vice versa.
1. Titan SMO, Bingham S, Welch A, Luben R, Oakes S, Day N, Khaw KT.
Frequency of eating and concentration of serum cholesterol in the Norfolk
population of the European prospective investigation into cancer (EPIC-
Norfolk): cross sectional study. BMJ 2001; 323: 1286-90.
Competing interests: No competing interests
Dr. Titan and her co-workers’ suggestion that frequent eating lowers
cholesterol may be right, but their data allow other explanations to their
findings (1). From table 2 it appears that intake of energy increased in a
continuous relation with eating frequency. Indeed, those who ate six times
daily or more often, consumed almost 30 percent more kilojoules per day
than those who only ate once or twice although their body mass was almost
the same. The only valid explanation is that their physical activity has
been underestimated. Furthermore, smoking decreased, also in a continuous
relation with eating frequency. Meta-analyses have found that exercise
results in small but significant decreases of low-density-lipoprotein- and
total cholesterol (2), and that smoking is associated with a small, but
significant higher concentration of these lipids (3). The habit of eating
once or twice a day also reflects a stressful life with little control of
one’s daily activities, and many studies have shown that mental stress may
rise the cholesterol concentration considerably (4).
Therefore, the advice
to eat more often to prevent cardiovascular disease is not backed up by
this study. Even if the habit of eating frequently, or exercising
regularly, or abstaining from smoking, or living a non-stressed life may
lower the cholesterol concentration, there is no evidence either that this
effect may influence the risk of cardiovascular disease by itself. A high
physical activity may lower the risk by improving endothelial function (5)
or the formation of collateral vessels (6); non-smoking by lowering the
burden of oxidant exposure; and freedom from mental stress by beneficial
influences on adrenal hormone secretion. The higher cholesterol
concentration of the physically inactive, smoking and stressed individual
may just be an innocent bystander telling that something is wrong.
1. Silvia M O Titan, Sheila Bingham, Ailsa Welch, Robert Luben, Suzy
Oakes, Nicholas Day, and Kay-Tee Khaw. Frequency of eating and
concentrations of serum cholesterol in the Norfolk population of the
European prospective investigation into cancer (EPIC-Norfolk): cross
sectional study. BMJ 2001; 323: 1286-90.
2. Halbert JA, Silagy CA, Finucane P, Withers RT, Hamdorf PA.Exercise
training and blood lipids in hyperlipidemic and normolipidemic adults: a
meta-analysis of randomized, controlled trials. Eur J Clin Nutr 1999; 53:
514-22.
3. Hambrecht R, Wolf A, Gielen S, et al. Effect of exercise on coronary
endothelial function in patients with coronary artery disease. N Engl J
Med 2000; 342: 454-60
4. Belardinelli R, Georgiou D, Ginzton L, Cianci G, Purcaro A. Effects of
moderate exercise training on thallium uptake and contractile response to
low-dose dobutamine of dysfunctional myocardium in patients with ischemic
cardiomyopathy. Circulation 1998; 97: 553-61
5. Craig WY, Palomaki GE, Haddow JE. Cigarette smoking and serum lipid and
lipoprotein concentrations: an analysis of published data. BMJ.
1989;298:784-8.
6. Ravnskov U. The Cholesterol Myths. Washington DC: New Trends
Publishing, 2000
I have no competing interests
Competing interests: No competing interests
[ Full
size article on "Cholesterol as Alzheimer's cause" ]
[ Authors
Preface ] [ Lay
summary ] [ Meeting
abstracts ]
Dietary habits define
body lipid and systemic and tissue cholesterol status [ BMJ
(2001) Vol 323, 1286 ] that was implicated this year in mortality rate
[ Lancet
(2001) Vol 358, 351 ] and in the development of Alzheimer's disease,
the subject of our research.
It is important to note that the lack of consistent relation between
eating frequency and high density lipoprotein (HDL) cholesterol reported
in today BMJ
contribution by Titan et al.likely reflects the importance
of HDL in routing tissue cholesterol to liver and bile for excretion, a
process called reverse cholesterol transport. In contrast, LDL (reported
in the study to be negatively and consistently associated with frequency
of eating) route cholesterol and other lipids from liver (managing dietary
fat) to different tissues (except of the brain that creates its own cholesterol,
see below).
Based on above, recent Neurology article on the correlation of
Alzheimer’s histochemical features with systemic HDL cholesterol [ 1
] in association with our Neuroscience Letters article [ 2
] and another earlier Neurobiol Aging contribution [ 3
] set the notion that HDL cholesterol represents "the imprint of Alzheimer's
brain cholesterol pathology".
Most recent article (published at BMJ ClinMed
on November 27, 2001 [
4 ] and based on experimental
evidence and comprehensive analysis of the data published previously) concludes
that fundamental pathophysiological event in most common sporadic forms
of Alzheimer's disease is accurate brain cholesterol homeostasis failure.
This article also discusses how and why diet affect brain cholesterol and
may lead to the disease.
Read ClinMed contribution [ 4 ] to learn
the facts. It is free, click away, and available as scientific paper and
as lay language articles (written by authors and reprinted from the press
book of the Society for Neuroscience Meeting held November 10-15,
2001 in San Diego, CA).
[ Full
size article on "Cholesterol as Alzheimer's cause" ]
[ Authors
Preface ] [ Lay
summary ] [ Meeting
abstracts ]
REFERENCES
1. Launer LJ, White LR, Petrovitch
H, Ross GW, Curb JD. Cholesterol and neuropathologic markers of AD: A population-based
autopsy study. Neurology 2001; 57: 1447-1452 [ PubMed
] [ Full
Text ] [ eLetter
to editor ].
2. Koudinov AR, Berezov TT,
Koudinova NV. The levels of soluble amyloid beta in different high density
lipoprotein subfractions distinguish Alzheimer’s and normal aging CSF:
implication for brain cholesterol pathology?
Neurosci. Lett. 2001;
314:
115-118 [ Full
Text ] [ PubMed
] [ Reprint
Order ].
3. Merched A, Xia Y, Visvikis
S, Serot JM, Siest G. Decreased high-density lipoprotein cholesterol and
serum apolipoprotein AI concentrations are highly correlated with the severity
of Alzheimer's disease.
Neurobiol Aging. 2000; 21: 27-30 [ PubMed
].
4.Koudinov
AR, Koudinova NV. Brain Cholesterol Pathology is the Cause of Alzheimer's
Disease. Clin. Med. Health Res. published online November 27, 2001,
clinmed/2001100005 [ Article
Preface at the authors WEB site ] [ Abstract
and Full text at Clin Med J ] [ Lay
language article 1
] [ Lay
language article 2
] [ Lay
language article 3
] [ Authors
related eLetters to editor ] [ Inform
a colleague ].
Competing interests: No competing interests
Increased frequency of meals and water intake
We have read with interest the “Frequency of eating and
concentrations of serum cholesterol in the Norfolk population of the
European prospective investigation into cancer (EPIC- Norfolk):cross
sectional study” by Dr Titan and her coworkers in BMJ. Vol. 323, 1
December 2001, 1286-90.(1).
In this article a decrease in serum concentration of both total
cholesterol and low density lipoprotein cholesterol
has been noted with increased frequency of eating in men and women. In
people who ate more frequently there was an increase in energy intake and
fat intake. Bile is an important vehicle for bile acid and cholesterol
excretion (2). Ingestion of hypoosmolar nutrient solution (volume 237 ml,
188 mOsmol / kg water) in cholecystectomised patients with T- tube biliary
drainage causes an increase in bile flow and a decrease in cholesterol
and triglyceride content of bile compared to that seen after ingestion of
hyperosmolar nutrient solution ( volume 237 ml , 550 mOsmol / kg water )
(3) . Hence amount of water intake along with meal can alter the bile flow
and concentration of its constituents and this can influence the
cholesterol excretion and serum cholesterol
concentration.
References :
1) Titan SMO, Bingham S, Welch A , Luben R, Oakes S, Day N , Khaw K-T
Frequency of eating and concentrations of serum cholesterol in the Norfolk
population of the European prospective investigation into cancer (EPIC-
Norfolk):cross sectional study. BMJ, 1 December 2001, . Vol. 323; 1286-90.
2) Mayes PA Digestion and absorption. In Murray RB ,Granner DK, Mayes
PA, Rodwell VW eds. Harper’s Biochemistry McGraw Hill New York 25th
edition 2000 Page 662 – 74 .
3) Math MV , Nambiar RM and Jacob E Effect of ingestion of hyperosmolar
and hypoosmolar nutrient solutions on bile flow and bile constituents in
cholecystectomised patients . Med. Sci . Res ,1990 ,18 , 171-73.
Dr. Mahantayya V. Math.
Mr. Basil Sunil Fernandes
Dr. P. Balasubramaniam.
(Prof. & Head, Department of Physiology.)
Department of Physiology.
Kamothe , Navi Mumbai
M. G. M’S MEDICAL COLLEGE
Maharastra. India. 410209
Competing interests: No competing interests