olive oil more than just oleic acid

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    Olive oil: more than just oleic acid

    Dear Sir:

    Recent articles in the Journal emphasized the role of olive oil in

    cardiovascular protection (1, 2). Many of the healthful effects of olive

    oil are usually attributed to olive oils high oleic acid content; how-

    ever, comparison of the proportion of oleic acid as a percentage of the

    energy intake in the Mediterranean diet with that of other Western

    diets (eg, North American and northern European) shows that oleic

    acid is present in comparable amounts. In fact, although most of the

    dietary lipids in the Mediterranean basin, where consumption of meat

    and animal fat is low, come from olive oil, other diets rich in chickenand pork meats provide similar quantities of oleic acid (3, 4). Finally,

    other vegetable oils, eg, canola, are high in monounsaturates.

    Extra virgin olive oil is a unique dietary lipid in the sense that it

    is not extracted from seeds by means of solvents. Rather, it is

    obtained from whole fruit (drupe) by using the cold-press tech-

    nique, which does not alter the chemical nature of the drupe or that

    of the resulting oil. In this way, the compounds that the fruit devel-

    ops in response to environmental stress, most of which are pheno-

    lic in structure, are transferred to the oil, where they constitute the

    polar, minor components fraction. The most abundant phenolic

    compound in the drupe is oleuropein, a bitter glycoside that consti-

    tutes up to 14% of the fruits dry weight. With the progression of

    blooming and maturation, oleuropein undergoes enzymatic and

    nonenzymatic hydrolysis and yields several simpler compounds,(eg, hydroxytyrosol, oleuropein aglycone, and ligstroside) that

    build up the full fruity taste that connoisseurs of olive oil search for.

    Note that these compounds are virtually absent in refined (rectified)

    oils (ie, the type of oil simply denominated olive oil), which is

    extracted by means of solvents and alkalinized with chemicals to

    reduce the excessive acidity (by law, 1% of fatty acids for extra

    virgin oils). Finally, the tocopherol content of olive oil is10 times

    lower than that of seed oils because of the lack of extraction of

    olive seeds, where most of the tocopherols are located.

    During the past few years, thanks to the availability of pure com-

    pounds, the biological activities of olive oil phenolics, namely

    oleuropein and hydroxytyrosol, have been thoroughly investigated

    in in vitro studies. These studies included, but were not limited to,

    the antioxidant capacity of these phenolics. The results indicatethat olive oil phenolics are potent free radical scavengers, inhibit

    chemically induced LDL oxidation, inhibit platelet aggregation and

    eicosanoid production by activated human leukocytes [and hence

    the potential antithrombotic activity described by Frost Larsen et al

    (1)], and potentiate the macrophagic response to endotoxin chal-

    lenge by increasing their production of nitric oxide (5). Finally,

    recent evidence of a dose-dependent absorption of olive oil pheno-

    lics by humans has been obtained (6). In turn, the use of extra vir-

    gin olive oil as the principal source of dietary fat and in substitu-

    tion of animal fat, in addition to providing a considerable amount

    of oleic acid, allows the intake of bioactive compounds whose

    potential healthful effects should be taken into consideration.

    Francesco Visioli

    Claudio Galli

    Institute of Pharmacological Sciences

    Via Balzaretti 9

    20133 Milan

    Italy

    E-mail: [email protected]

    REFERENCES

    1. Frost Larsen L, Jespersen J,Marckmann P. Are olive oil diets antithrom-

    botic? Diets enriched with olive, rapeseed, or sunflower oil affect post-

    prandial factor VII differently. Am J Clin Nutr 1999;70:97682.

    2. Kris-Etherton PM, Pearson TA, Wan Y, et al. High-monounsaturated

    fatty acid diets lower both plasma cholesterol and triacylglycerol

    concentrations. Am J Clin Nutr 1999;70:100915.

    3. Dougherty RM, Galli C, Ferro-Luzzi A, Iacono JM. Lipid and phos-

    pholipid fatty acid composition of plasma red blood cells and platelets

    and how they are affected by dietary lipids: a study of normal subjects

    from Italy, Finland, and the USA. Am J Clin Nutr 1987;45:44355

    4. The British Nutrition Foundation. Unsaturated fatty acids. Nutritional

    and physiological significance. London: Chapman & Hall, 1992.5. Visioli F, Galli C. The effect of minor constituent of olive oil on car-

    diovascular disease: new findings. Nutr Rev 1998; 56:1427.

    6. Visioli F, Galli C, Bornet F, Mattei A, Galli G, Caruso D. Olive oil

    phenolics are dose-dependently absorbed in humans. FEBS Lett

    2000;468:15960.

    Fatty diets are unhealthyeven those basedon monounsaturates

    Dear Sir:

    In their recent study, Kris-Etherton et al (1) compared an aver-

    age American diet (AAD) rich in saturates (containing 34% total

    fat) with the American Heart Association (AHA) Step II diet

    (25% total fat) and 3 moderately fatty diets high in monounsatu-

    rates and poor in saturates (3436% total fat) that were based on

    olive oil, peanut oil, or peanut butter (1). The AHA Step II diet

    and the monoene diets were associated with identical reductions

    Am J Clin Nutr2000;72:8536. Printed in USA. 2000 American Society for Clinical Nutrition 853

    Letters to the Editor

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    in LDL cholesterol compared with the AAD. Similar to earlier

    studies, the low-fat Step II diet was found to raise triacylglycerol

    compared with the higher-fat diets. HDL cholesterol differed

    only marginally and insignificantly between diets. The authors

    concluded that a high-MUFA, cholesterol-lowering diet may be

    preferable to a low-fat diet in prevention of coronary heart dis-

    ease. The same opinion was expressed by other authors (2).

    We would like to warn people against considering high-fat

    monoene diets to be the most healthy diets. There are several rea-sons that high-fat dietseven those based on monoene fats

    should be avoided in modern societies in which physical activity

    and energy requirements are low. First, any high-fat diet

    increases the likelihood of developing obesity, as do most other

    highly energy-dense diets (3). Even the olive oilconsuming

    Greeks have become more obese during the past decades because

    of their increasingly sedentary lifestyle (4, 5).

    Second, in the recent study by Kris-Etherton et al and in most

    earlier trials comparing diets with various fat contents, energy

    intake was fixed and constant (ie, isoenergetic conditions were

    maintained) to keep body weight constant. This design is inap-

    propriate because spontaneous energy intake would normally dif-

    fer if diets with different fat contents were eaten ad libitum (6). It

    was shown very elegantly in a meta-analysis by Kris-Ethertonsown group that fat-reduced diets cause a dose-dependent decrease

    in energy intake and body weight (7). The spontaneous weight

    loss that would be expected with a low-fat Step II diet was thus

    inhibited by the design used in the recent study (1). Accordingly,

    the blood lipid response was importantly biased. It is well known

    that weight loss causes triacylglycerol to decline and that con-

    comitant increases in HDL cholesterol are often seen (8). In addi-

    tion, earlier long-term trials of healthy and hyperlipemic persons

    showed that diets comparable with the Step II diet had no adverse

    effects on triacylglycerol if eaten ad libitum (9, 10).

    Third, not only blood lipids but also several other cardiovas-

    cular risk factors are influenced by diet and therefore need to be

    considered in the overall evaluation of the health effect of a diet.

    We and other researchers showed that low-fat, high-fiber dietsmay affect blood coagulation and fibrinolysis strongly in an

    antithrombotic manner (11, 12). The effects on the hemostatic

    system seem to rely heavily on the carbohydrate quality of the

    diet, ie, the fiber content and the glycemic index (13). Therefore,

    it is unfortunate that Kris-Etherton et al did not report anything

    about these aspects of their experimental diets.

    Fourth, there is strong epidemiologic evidence that high

    intakes of fruit and vegetables are associated with less coronary

    heart disease and cancer morbidity. High-fat diets prevent high

    intakes of fruit and vegetables because of the low energy ceiling

    of modern sedentary societies. Remember that the Greeks of the

    1950s and 1960s were very physically active fishermen and farm-

    ers and that their high-fat, olive oilbased diets still allowed con-

    sumption of a large amount of bread, vegetables, and fruit (5, 14).For these 4 reasons (more could be added), we believe it is

    incorrect to consider high-fat monoene diets the most healthy

    choice for sedentary people. We can take good care of our body

    weight, our blood lipids, our hemostatic system, and our need for

    trace elements and unknown nonnutrients present in foods only

    if we allow plenty of our energy to be supplied from foods with

    low fat contents. Where to set the fat limit is a matter of discus-

    sion, but the epidemic of obesity tells us that we still eat more fat

    than is appropriate. We consider a population average fat intake

    of30% of total energy intake to be a wise recommendation.

    Peter Marckmann

    Arne Astrup

    Research Department of Human Nutrition

    Royal Veterinary and Agricultural University

    Rolighedsvej 30

    DK-1958 Frederiksberg

    Denmark

    E-mail: [email protected]

    REFERENCES

    1. Kris-Etherton PM, Pearson TA, Wan Y, et al. Highmonounsatu-

    rated fatty acid diets lower both plasma cholesterol and triacylglyc-

    erol concentrations. Am J Clin Nutr 1999;70:100915.

    2. Katan MB, Grundy SM, Willett WC. Should a low-fat, high-

    carbohydrate diet be recommended for everyone? Beyond low-fat

    diets. N Engl J Med 1997;337:5636.

    3. Bray GA, Popkin BM. Dietary fat intake does affect obesity! Am J

    Clin Nutr 1998;68:115773.

    4. Mamalakis G, Kafatos A. Prevalence of obesity in Greece. Int J

    Obes 1996;20:48892.

    5. Voukiklaris GE, Kafatos A, Dontas AS. Changing prevalence of coro-

    nary heart disease risk factors and cardiovascular diseases in men of

    a rural area of Crete from 1960 to 1991. Angiology 1996;47:439.

    6. Siggaard R, Raben A, Astrup A. Weight loss during 12 weeks ad

    libitum carbohydrate-rich diet in overweight and normal-weight

    subjects at a Danish work site. Obes Res 1996;4:34756.

    7. Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S, Kris-

    Etherton PM. Effects of the National Cholesterol Education Programs

    Step I and Step II dietary intervention programs on cardiovascular dis-

    ease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:63246.

    8. Marckmann P, Toubro S, Astrup A. Sustained improvement in blood

    lipids, coagulation, and fibrinolysis after major weight loss in obese

    subjects. Eur J Clin Nutr 1998;52:32933.

    9. Schaefer EJ, Lichtenstein AH, Lamon-Fava S, et al. Body weight

    and low-density lipoprotein cholesterol changes after consumption

    of a low-fat ad libitum diet. JAMA 1995;274:14505.

    10. Sandstrm B, Marckmann P, Bindslev N. An eight-month controlled

    study of a low-fat/high-fibre diet: effects on blood lipids and bloodpressure in healthy young subjects. Eur J Clin Nutr 1992;46:95109.

    11. Marckmann P, Sandstrm B, Jespersen J. Favorable long-term effect

    of a low-fat/high-fiber diet on human blood coagulation and fibri-

    nolysis. Arterioscler Thromb 1993;13:50511.

    12. Avellone G, Di Garbo V, Cordova R, Scaffidi L, Bompiani GD.

    Effects of Mediterranean diet on blood lipid, coagulative and fibri-

    nolytic parameters in two randomly selected population samples in

    western Sicily. Nutr Metab Cardiovasc Dis 1998;8:28796.

    13. Jrvi AE, Karlstrm BE, Granfeldt YE, Bjrck IE, Asp NGL,Vessby

    BOH. Improved glycemic control and lipid profile and normalized

    fibrinolytic activity on a low-glycemic index diet in type 2 diabetic

    patients. Diabetes Care 1999;22:108.

    14. Kafatos A, Kouroumalis I, Vlachonikolis I, Theodorou C, Labadar-

    ios D. Coronary-heart-disease risk-factor status of the Cretan urban

    population in the 1980s. Am J Clin Nutr 1991;54:5918.

    Reply to P Marckmann

    Dear Sir:

    Numerous studies, including one we published recently (1),

    have shown beneficial effects of a weight-maintenance, high

    monounsaturated fatty acid (MUFA), blood cholesterollowering

    854 LETTERS TO THE EDITOR

    http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/
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    diet compared with a high-carbohydrate, low-fat diet on impor-

    tant cardiovascular disease (CVD) risk factors, notably triacyl-

    glycerol, HDL-cholesterol, and plasma glucose and insulin

    concentrations (2, 3). It is clear that elevated triacylglycerol and

    glucose and insulin concentrations increase the risk of CVD, as

    does a low HDL-cholesterol concentration. Lowering plasma tri-

    acylglycerol, glucose, and insulin and increasing HDL choles-

    terol decrease the risk of CVD. Although not measured in our

    recent study, a weight-maintenance, high-carbohydrate, low-fatdiet has also been shown to increase fibrinogen concentrations,

    whereas a high-MUFA, blood cholesterollowering diet does not

    (4). An elevated fibrinogen concentration was shown to increase

    the risk of CVD. Thus, the evidence is convincing that a weight-

    maintenance, high-MUFA, blood cholesterollowering diet

    beneficially affects CVD risk.

    As noted by Marckmann and Astrup, body weight is an impor-

    tant factor that must be considered in contemporary dietary rec-

    ommendations. The key questions are 1) What is the best diet for

    weight loss and weight maintenance? and 2) Will a higher-fat

    diet promote weight gain?

    In our recent meta-analysis (5), we observed a linear relation

    between decreasing percentage of energy from fat and a

    decrease in body weight. Although this finding suggests thathigher-fat diets promote weight gain, 3 important limitations of

    this study must be noted. First, a higher-fat weight-loss diet was

    not tested, so one can question whether weight loss might be

    less, the same, or maybe even greater because of better adher-

    ence to the higher-fat (ie, high MUFA), energy-reduced diet. It

    is generally accepted that a calorie is a calorie regardless of

    whether the energy is derived from fat, carbohydrate, or protein.

    Thus, weight loss with any energy-reduced diet is due to the

    reduction in energy intake relative to expenditure. What is not

    clear is whether macronutrient-manipulated weight-loss diets

    have any effect on adherence and, hence, on long-term weight

    loss and weight maintenance. Second, the weight loss was small

    despite a large reduction in energy intake from fat (ie, 2.6-kg

    weight loss associated with an 8percentage point decrease inpercentage of energy from fat). A smaller decrease in fat, con-

    sistent with current intake recommendations, would be expected

    to result in less weight loss (only 1.3 kg for a 4percentage

    point decrease in fat intake). Finally, in long-term studies over a

    period of 24 y, only small changes in body weight were shown

    (0.5-kg weight loss).

    Targeting fat reduction as the sole means of affecting the

    global epidemic of overweight and obesity is not justified. Obe-

    sity is a complex problemits causes are not fully understood.

    Although it is clear that an energy imbalance is the root cause,

    there is no compelling evidence that this is due to changes in fat

    intake. A case in point relates to the ongoing increase in the inci-

    dence of overweight and obesity in the United States that is con-

    current with little or no change in absolute intake of fat and adecrease in percentage of energy from fat (6). It is clear that an

    increase in energy intake in conjunction with a more sedentary

    lifestyle (ie, less physical activity) accounts, in part, for the fat-

    tening of Americans. Further evidence comes from Sweden,

    where a small increase in overweight occurred despite virtually

    no change in the diet (8, 9). In addition, there is ample evidence

    from other countries that there is no consistent association

    between increasing overweight and obesity and fat intake (7, 8).

    Energy balance and, if needed, weight loss in individuals

    who are following any diet is dependent on energy intake irre-

    spective of the macronutrient profile. In the context of a high-

    MUFA, blood cholesterollowering diet, it is clear that this diet

    has beneficial effects on CVD risk factors in weight-stable indi-

    viduals. Although it has not been tested as a weight-loss diet

    compared with a high-carbohydrate, low-fat diet in free-living

    subjects, such a diet could be planned that would have a low

    energy density (ie, high in fruit and vegetables) to provide bulk

    and promote satiety. The key issue for controlling energy intake

    may not be the macronutrient profile of the diet but rather theenergy density, because the fat content and energy density of

    foods are not always perfectly correlated. As argued by Rolls

    and Bell (9), energy density is more closely related to factors

    such as the water and fiber contents of foods. In that study and

    others, subjects ate less when consuming foods of low energy

    density compared with foods of high energy density, regardless

    of fat content. Thus, focusing solely on the fat content of foods

    when designing weight-loss diets may limit the effectiveness of

    the diets if the effects of energy density are not considered.

    We advocate a reexamination of the effects of the macronutri-

    ent content of the diet on risk of CVD. While acknowledging that

    the ultimate test of higher-fat diets will be in free-living individ-

    uals consuming foods ad libitum, we believe that by promoting

    the addition of fruit, vegetables, whole grains, and legumes tothese diets, it may be possible to achieve long-term success in

    terms of both weight control and CVD risk reduction.

    Penny M Kris-Etherton

    Christine L Pelkman

    Guixiang Zhao

    Thomas A Pearson

    Ying Wan

    Terry D Etherton

    The Pennsylvania State University

    Nutrition Department

    S-126 Henderson Building

    University Park, PA 16802E-mail: [email protected]

    REFERENCES

    1. Kris-Etherton PM, Pearson TA, Wan Y, et al. Highmonounsaturated

    fatty acid diets lower both plasma cholesterol and triacylglycerol

    concentrations. Am J Clin Nutr 1999;70:100915.

    2. Mensink RP, Katan MB. Effect of monounsaturated fatty acids ver-

    sus complex carbohydrates on high-density lipoproteins in healthy

    men and women. Lancet 1987;1:1225.

    3. Lerman-Garber I, Ichazo-Cerro S, Zamora-Gonzalez J, Cardoso-

    Saldana G, Posadas-Romero C. Effect of a high-monounsaturated

    fat diet enriched with avocado in NIDDM patients. Diabetes Care

    1994;17:3115.

    4. Kris-Etherton PM, for the DELTA investigators. Effects of replacingsaturated fat (SFA) with monounsaturated fat (MUFA) or carbohy-

    drate (CHO) on plasma lipids and lipoproteins in individuals with

    markers for insulin resistance. FASEB J 1996;10:2666.

    5. Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S, Kris-

    Etherton PM. Effects of the National Cholesterol Education Pro-

    grams Step I and Step II dietary intervention programs on cardiovas-

    cular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:

    63246.

    6. Ernst ND, Obarzanek E, Clark MB, Briefel RR, Brown CD, Donato

    K. Cardiovascular health risks related to overweight. J Am Diet

    Assoc 1997;97(suppl):S4751.

    LETTERS TO THE EDITOR 855

    http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/http://www.ajcn.org/
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    7. Seidell JC. Obesity in Europe: scaling an epidemic. Int J Obes Relat

    Metab Disord 1995;19(suppl):S14.

    8. Epstein FH. The relationship of lifestyle to international trends in

    CHD. Int J Epidemiol 1989;18(suppl):S2039.

    9. Rolls BJ, Bell EA. Intake of fat and carbohydrate: role of energy

    density. Eur J Clin Nutr 1999;53(suppl 1):S6673.

    All cereals may not be equal

    Dear Sir:

    I wish to comment on the article by Liu et al in your September

    1999 issue (1), which found an inverse relation between the prevalence

    of coronary heart disease and whole-grain consumption in a large

    prospective study of nurses. In 1988, I carried out a statistical study (2)

    in which the consumption of60 food items in 21 countries belong-

    ing to the Organization of Economic Cooperation and Development

    (OECD) was correlated with mortality from coronary disease. My

    results, regarding cereal consumption, were as follows in Table 1:

    As far as correlation with coronary disease is concerned, all cere-als appear to be different. A negative correlation was found only with

    rice consumption, and even this could be due to an indirect linkage.

    Coronary mortality in eastern Asia could be low on account of low fat

    and milk consumption but give the appearance of a negative correla-

    tion with high rice consumption. Similarly, the high positive correla-

    tion with oats consumption could be indirect. Appreciable quantities

    of oats are consumed only in a few countries of northern Europe. The

    true correlation could be between coronary disease mortality and

    environmental temperature. The world leaders in coronary disease

    mortality are Russia and its neighbors, which all have cold climates.

    In warmer countries, coronary mortality tends to be lower, and very

    low in the tropics. In my opinion, the connection between coronary

    disease and grain consumption must be treated with caution.

    Stephen Seely

    3 Truro Drive

    Sale, Cheshire M33 5DF

    United Kingdom

    REFERENCES

    1. Liu S, Stampfer MJ, Hu FB, et al. Whole-grain consumption and

    risk of coronary heart disease: results from the Nurses Health

    Study. Am J Clin Nutr 1999;70:4129.

    2. Seely S. Diet and coronary arterial disease: a statistical study. Int J

    Cardiol 1988;20:18392.

    Reply to S Seely

    Dear Sir:

    We appreciate Seelys proposition that all cereals my not be

    equal in affecting risk of coronary heart disease mortality. We

    would like to emphasize 2 main points. First, in a prospective

    cohort study, we reported an inverse relation between whole-

    grain consumption and the incidence, not prevalence, of coro-

    nary heart disease (1). The difference between prevalence and

    incidence is subtle but important. Prevalence includes people

    with coronary heart disease at baseline who may have changedtheir diet after disease diagnosis.Incidence studies can provide a

    direct assessment of the association between diet and disease

    that would not be confounded by factors modified after disease

    diagnosis (2). Second, the study by Seely can at best suggest a

    hypothesis to be explored because of important limitations inher-

    ent in any such international correlation or ecologic study,

    including the crude assessment of diet, lack of information on

    individual diets, and the lack of adjustment for confounding fac-

    tors including genetic predisposition, environment, and lifestyle

    practices (3). Seely noted only a few of the many differences

    between these countries. Large prospective cohort studies with

    detailed dietary assessment, long-term follow-up, and careful

    control of multiple confounding factors are better suited to

    examine diet-disease associations.

    Simin Liu

    JoAnn E Manson

    Walter C Willett

    Brigham and Womens Hospital

    Division of Preventive Medicine

    900 Commonwealth Avenue East

    Boston, MA 02215-1204

    REFERENCES

    1. Liu S, Stampfer M, Hu F, et al. Whole-grain consumption and risk

    of coronary heart disease: results from the Nurses Health Study.Am J Clin Nutr 1999;70:4129.

    2. Rothman KJ, Greenland S. Modern epidemiology. 2nd ed. Philadel-

    phia: Lippincott-Raven Publishers, 1998.

    3. Willett WC. Nutritional epidemiology. 2nd ed. New York: Oxford

    University Press, 1998.

    856 LETTERS TO THE EDITOR

    TABLE 1

    Correlation between cereal consumption and mortality from coronary

    disease

    Food item

    Wheat 0.03

    Rye 0.33

    Barley 0.20

    Oats 0.95

    Maize 0.27

    Rice 0.55

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