Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Cholesterol misregulation causes Alzheimer's disease: diet likely involved
- Alexei R Koudinov, Natalia V Koudinova (1 December 2001)
-
Non-dietary factors explain the lower cholesterol concentration associated with frequent eating
- Uffe Ravnskov (18 January 2002)
-
Correction
- Uffe Ravnskov (26 January 2002)
-
Increased frequency of meals and water intake
- Mahantayya V Math, Basil Sunil Fernandes, P. Balasubramaniam (8 February 2002)
|
|
|||
|
Alexei R Koudinov, neuroscientists Berezov Academic Lab, Moscow, Russia; Weizmann Inst., Dept. Biol. Regul, Rehovot, 76100 Israel, Natalia V Koudinova
Send response to journal:
|
[ Full
size article on "Cholesterol as Alzheimer's cause" ]
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" ]
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.
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 ].
<CTRL><D> TO BOOKMARK |
|||
|
|
|||
|
Uffe Ravnskov, Independent researcher Magle Stora Kyrkogata 9, S-22350, Lund, Sweden
Send response to journal:
|
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 |
|||
|
|
|||
|
Uffe Ravnskov, Independent researcher Magle Stora Kyrkogata 9, S-22350, Lund, Sweden
Send response to journal:
|
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. |
|||
|
|
|||
|
Mahantayya V Math, Assistant Lecturer Dept. of Physiology MGM Medical College, Kamothe NaviMumbai, Basil Sunil Fernandes, P. Balasubramaniam
Send response to journal:
|
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 |
|||